R 5th Year OSCE - Part 2

The H Book for 5th Year OSCE 2012-2013 Part 2
Table of Content
Part 1
Part 2
Preface
Chapter 3 Notes/Make-up scenarios
Table of Topics of Past OSCE
Notes/Make-up scenarios: Medicine
Chapter 1 Past OSCE (from 2002 to 2012)
Notes/Make-up scenarios: GP
2012 OSCE
Notes/Make-up scenarios: Peds
2011 OSCE
Notes/Make-up scenarios: Oncology
2010 OSCE
Notes/Make-up scenarios: Eyes
2009 OSCE
Notes/Make-up scenarios: Aboriginal
2008 OSCE
2007 OSCE
2006 OSCE
2005 OSCE
2004 OSCE
2003 OSCE
2002 OSCE
Chapter 2 Real Marking Guides

-
2007
2006
2005
2004
2003
Unknown Year
List of topics to know (Important)

Chapter 3 Notes/Make-up scenarios
-
Notes/Make-up scenarios: O&G
Last Page
Last Page
Notes/Make-up scenarios: Medicine

Station 1 - ECG
Level 1
- MI
- LBBB, RBBB
- Heart Block
- AF, AF (flutter)
- Premature Beats
- Supraventricular Tachycardia
- Hyperkalemia (Usually not a ECG station, but
a lab interpretation station)
- Palpitation/Chest Pain
Level 2
- Ventricular Hypertrophy
- AV dissociation
- Pericarditis
- Pulmonary embolism
- Dyspnea
Station 1 - CXR
Level 1
- Pulmonary effusion/Pleural effusion
- Pulmonary edema (HF management)
- Consolidation (Pneumonia)
- COPD
- Atelectesis
- Pneumothorax
Level 2
- Interstitial lung diseases E.g. Fibrosis
- Cystic Bronchiectasis (CXR+CT)
- Pulmonary nodules
Station 2 - Lab Interpretation

Level 1
- Hyperkalemia
- Hyponatremia
- Spirometry
- Thyroid function test
- Liver function test Diseases Pattern
- Renal function test
- Anemia
- Diabetic ketoacidosis
- MI
- Iron study
- Metabolic acidosis
- Pancytopenia
- CFS Interpretation
- Pleural effusion interpretation
- DVT/PE/Thrombophilia
Level 2
- Proteinuria/Hematuria
- Osteoporosis
- Hypercalcemia
- Hypernatremia
- Jaundice
- Heart failure BNP
- Coagulations
- Thrombocytopenia
Level 3
- Hepatitis B
- Hypokalemia
- Lipid
- WCC differential
- Hemolysis
- ANA, ANCA, Complements
Station 3 History + Physical Examination (Verbal only) + DDx + Investigation + Management - (Usually a renal/neuro/gastro/endo case)
Cardio Most of the time a ECG or CXR station
Respiratory Most of the time a ECG or CXR
Renal
station
Level 1
Level 1
Level 1
- Chest Pain, Dyspnea
- Cough, Dyspnea
- Dysuria, Oliguria
Hypertension Primary + Secondary

Heart Failure
Hypotension Shock, Postural hypotension
DVT/PE/Thrombophilia
Ulcers
Gastro
Level 1
- Abdominal Pain, Hematemesis, PR bleeding,
Jaundice, Dysphagia, Melena
- IBD
- Pancreatitis
- Cholestatic liver disease
- Hemochromatosis
Level 2
- Cirrhosis
- Liver failure
- Peptic ulcer
Hematology
Level 1
- Anemia (Lab interpretation)
- Bleeding disorders
- Thrombophilia
- Pancytopenia
- Multiple myeloma
Level 2
- Transfusion products + Side effects
Usually there are 3 stations and they are:
- COPD
- Asthma
- Pulmonary Embolism
Level 2
- Respiratory failure type 1, II
Endo
Level 1
- Weight loss, Polyuria
- Thyroid
- Hypercalcemia
- DM Complication/Examinations
- DKA
- Lipid
Station 1: ECG/CXR, As only CXR in 2012, ECG (+/- CXR) 99% will come out in 2013
Station 2: Lap interpretation, Renal function test in 2012
- Acute renal failure

- Chronic renal failure
- Glomerular diseases
- Proteinuria/Hematuria
- Stones
- UTI
Neuro
Level 1
- Syncope, Delirium/acute confusion, Dementia,
Weakness/Paralysis, Seizures
- Headache, Facial Pain Can be a GP Station
- Stroke
- Periphery polyneuropathy
- Alzheimers
- Intracranial hemorrhage
- Multiple sclerosis
Level 2
- Tremor, Parkinsonism, Polyneuropathy,
Mononeuropathy
- Head Injury
- AV Malformations
- Intracranial aneurysm
- Intracranial venous thrombosis
- Primary Tumors
- Brain abscess
- MG Myasthenia gravis
-
Station 3: History taking + Physical Examination (Verbally) + DDx + Investigation + Management (Usually a neuro/gastro/endo case), Peripheral polyneuropathy
in 2012
-
Knowing level 1 stuff should be safe enough to pass
Minimal to Know: ECG level 1, CXR level 1, Lab interpretation level 1 + Neuro/Renal/Gastro level 1
(ECG 99% +/- CXR will come out in 2013 OSCE)

Notes/Make-up scenarios: Medicine ECG
A Quick ECG Guide Work out 1 to 11 for the following ECG!!
1. Rate
2. Rhythm Atrial Rhythm E.g. AF, Atrial flutter, SVT, Ventricular Rhythm E.g. VT, VF
3. Check Heart Block
4. Axis
5. Check BBBB
5. P Wave
6. PR - Transmission from SA to AV nodes
7. QRS Depolarization of ventricles, Duration <0.12s, Range 0.06-0.1s
8. QT Interval, Represents the depolarization and the repolarization of ventricles (Not really checked)
9. ST Segment
10. T Wave, Repolarization of the ventricles
11. J Wave = Osborn wave (Note really checked)
Bradycardia
Tachycardia
- Causes: Hypothyroidism, Increased vagal tone, Sleep, Hypothermia,
- Causes: Fever, exercise, emotion, pain, anemia, heart failure, shock,
Intrinsic disease of SA node (Sick sinus syndrome), Athletes
thyrotoxicosis, alcohol, alcohol withdrawal
Left Axis Deviations
Right Axis Deviation
- Left ventricular hypertrophy
- Chronic lung disease
- Inferior myocardial infarction
- Right ventricular hypertrophy
- Left anterior fascicular block
- Lateral MI
- Can be normal, particularly in obese people
- Left posterior fascicular block
- May associate with Wolff-Parkinson-White Syndrome
- Dextrocardia
- Lead reversal
P Wave
Absent P Waves
Dissociation between P and QRS Complex
- AF, Nodal (Junctional) rhythm, SA block
- Complete Heart Block
Bifid P Waves
P pulmonale / Peaked P wave
- Left atrial hypertrophy E.g. Mitral stenosis
- Right atrial hypertrophy E.g. Pulmonary hypertension, Tricuspid stenosis
- Pseudo P Pulmonale in Hypokalemia
LBBB
RBBB
Diagnosis
- More common than LBBB
It is diagnosed when QRS duration is > 0.12 seconds (if <0.12 and LBBB QRS
morphology = Incomplete LBBB)
QS or rS complex in V1
M pattern in V6
V1
V6
Associated Conditions
- Cardiomyopathy
- Valvular heart diseases
- Congenital heart diseases
Important Note
- LBBB interferes with ECG diagnosis of QRS axis, acute MI, ventricular
hypertrophy
QRS duration > - 0.12s
Important Note
- It does not interfere with ECG diagnosis of ventricular hypertrophy or Q
wave MI
Causes - The right bundle branch is vulnerable to stretch and trauma

- Chronically increased right ventricular pressure E.g. Cor pulmonale
- A sudden increase in right ventricular pressure with stretch E.g. PE
- MI
- Myocarditis
- Other Causes: HTN, Cardiomyopathy, Congenital heart disease,
Mechanical damage
PR - Transmission from SA to AV nodes (PR range 3-5 small squares)
Prolonged PR - >0.2s
Shortened PR - <0.12s
- First degree heart block
- Pre-excitation syndrome E.g. No delay in the AV node to the Bundles of
- Associated with hypokalemia, acute rheumatic fever
His (as there are other pathways)
- Example of Pre-Excitation Syndrome = Wolff-Parkinson White Syndrome
PR depression
- Pericarditis
QRS Depolarization of ventricles, Duration <0.12s, Range 0.06-0.1s (Smaller than 3 small squares)
Prolonged QRS, >0.12s
Increased Amplitude, Normal R+S <4.5mV in a precordial lead E.g. V1-V6
1. The beat is ventricular in origin

2. There is a bundle branch block
Hyperkalemia
Bundle branch block
Amplitude increased in cardiac hypertrophy
Note: VAT = Ventricular activation time, and is

measured in increased QRS amplitude
Axis Deviation Determined by the QRS complex
Q Wave, Normal <0.04s

- Q wave: Represents normal depolarization, Can be seen in V5, V6, I, aVL
- Pathological Q wave may occur within a few hours of a MI
- Pathological Q waves are usually >0.04s wide and >2mm deep
QT Interval, Represents the depolarization and the repolarization of ventricles

Background
Prolonged
- QT interval is dependent on the HR, so need to calculate the corrected QT - MI
interval
- Myocarditis
- Normal corrected QT Interval: 0.38 to 0.42s
- Bradycardia E.g. AV block
- Hypothemia
- U&E Imbalances E.g. Decreased K+/Ca++/Mg++
- Medications: Sotalol, Quinidine, Antihistamines, Macrolides
ST Segment
- Normal ST segment is slightly upwards
- Flat, depressed ST segments may indicated coronary ischemia
- ST elevation: MI (elevation >1mm, longer than 0.08s), Acute pericarditis,
Left ventricular aneurysm
- ST depression: Hypokalemia or digoxin toxicity, Acute posterior MI
T Wave, Repolarization of the ventricles
Background
T Inversion
- Abnormal if inverted in I, II, V4, V5, V6
- V1-V3: Normal (Black and children), RBBB, PE
- T-wave inversion: Coronary ischemia, Left ventricular hypertrophy,
- V2-V5: Subendocardial MI, HCM, Subarachnoid hemorrhage, lithium
Wellens syndrome
- V4-V6: Ischemia, LVH, LBBB
- Tall and Narrow T waves (peaked): Hyperkalemia
- Flat T wave: Cononary ischemia, Hypokalemia
J Wave = Osborn wave
- Seen in hypothermia, Subarachnoid hemorrhage, Hypercalcemia
ECG-L1-MI
3. What is the above ECG showing you?

Anterior Wall MI
4. What is the below ECG showing you?

Posterior Wall MI
Acute Anterior MI ST elevation in anterior lead V3 and V4

(sometimes and septal and lateral leads), ST elevation is concave
downward, Usually overwhelms the T wave forming a tombstoning
type appearance
Old: Q waves in V1 and V2
1. Explain the ECG changes you can see in a MI.

- Tall T waves seen in the first few minutes, then inverted T waves from
hours to days
- ST elevation generally lasts for several hours
- Dominant R wave in V1-V3
2. How can you decide the location of MI?

- Anterior MI: ST elevation in V1-V3
- Posterior MI: ST depression in V1-V3
- Antero-Lateral MI: ST elevation in V4-V6
- Inferior MI: ST elevation in II, III, aVF
- Lateral MI: ST elevation in I, aVL
Normal ECG prior to MI
Hyperacute T wave changes - increased T wave amplitude and

width; may also see ST elevation
Marked ST elevation with hyperacute T wave changes

(transmural injury)
Pathologic Q waves, less ST elevation, terminal T wave

inversion (necrosis)
o
5. What is myocardial ischemia?

- Hypoxia of the myocardium may occur in the absence of infarction and necrosis. The
changes may occur following stress (physical or emotional) or even spontaneously.

Significant degrees of ischaemia may exist with no evidence of ECG abnormalities. The
changes, when present, are confined to the ST segment and T waves. There will be no
change in the QRS complexes.
The following ECG changes may accompany myocardial ischaemia:
1) Flattening of T waves
2) Inverted T waves
3) Abnormally tall T waves
4) "Normalisation" of primarily abnormal T waves
5) Sloping ST segment depression
6) Horizontal ST segment depression
7) ST segment elevation
8) Any combination of the above changes
(Pathologic Q waves are usually defined as duration

0.04 s or 25% of R-wave amplitude)
Pathologic Q waves, T wave inversion (necrosis and fibrosis)
Pathologic Q waves, upright T waves (fibrosis)
Ischemic changes with exercise
ECG-L1-LBBB, RBBB
Generally in the OSCE, LBBB or RBBB is only part of the abnormalities.
1. What is above?
- LBBB
- Also left atrial hypertrophy
2. What is below ECG?

- RBBB
- Also first degree heart block
LBBB
RBBB
Diagnosis
It is diagnosed when QRS duration is > 0.12 seconds (if <0.12 and
LBBB QRS morphology = Incomplete LBBB)
QS or rS complex in V1
M pattern in V6
More common than LBBB

QRS duration > - 0.12s
Important Note
-
It does not interfere with ECG diagnosis of ventricular hypertrophy or Q wave

MI
Causes - The right bundle branch is vulnerable to stretch and trauma
V1
V6
Associated Conditions
- Cardiomyopathy
- Valvular heart diseases
- Congenital heart diseases
Important Note
-
LBBB interferes with ECG diagnosis of QRS axis, acute MI, ventricular
hypertrophy
Chronically increased right ventricular pressure E.g. Cor pulmonale

A sudden increase in right ventricular pressure with stretch E.g. PE
MI
Myocarditis
Other Causes: HTN, Cardiomyopathy, Congenital heart disease,
Mechanical damage
ECG-L1-Heart Block
1. What is this?
- First degree heart block
- Increased PR interval
2. What are the causes of 1st degree heart block?

- AV nodal diseases
- Enhanced vagal tone E.g. Athletes
- Myocarditis
- Acute MI
- Electrolyte Imbalances E.g. Hypo/Hyper-kalemia, Hypomagnesemia
- Medications: Beta blocker, Ca++ blocker, Digoxin
3. How would you investigate?

-
History, Physical examination, Investigation

History: MI? Medications
Physical examination: Sick? Murmur?
Investigations: FBC, U&E, CRP, Troponin
1. What is this?
- 2nd Degree Heart Block: Type I Wenckebach
- Progressive lengthening of the PR interval and the failure of conduction of
an atrial beat
- In healthy individual, this is often due to increased vagal tone and is
abolished by exercise
4. The blood tests are unremarkable. What is the treatment for 1st degree
heart block?
- In general no treatment required for asymptomatic
- People with symptoms try to identify and correct the cause (see
causes above)
- Note: Small risk of developing into higher heart block
2. What are the causes of Type I Wenckebach?

- Similar to the 1st degree heart block
4. The blood tests are unremarkable. What is the treatment for 1st degree
heart block?
Similar to the 1st degree heart block
Similar to the 1st degree heart block
1. What is this?
- 2nd Degree Heart Block: Type 2 Mobitz
- Most beats are conducted with a constant PR interval, but occasionally
there is an atrial contraction without a subsequent ventricular contraction
- Does not go away with exercise
2. What are the causes of Type 2?

- Almost always due to an organic diseases
- AV nodal diseases
- Myocarditis
- Acute MI
- Electrolyte Imbalances E.g. Hypo/Hyper-kalemia, Hypomagnesemia
- Medications: Beta blocker, Ca++ blocker, Digoxin
4. How to manage?
History, Physical examination, Investigation

History: MI? Medications
Physical examination: Sick? Murmur?
Investigations: FBC, U&E, CRP, Troponin
1. What is this?
- Complete heart block/3rd degree HB
- Progressive lengthening of the PR interval and the failure of conduction of
an atrial beat
More likely to progress to complete HB treatment almost always

indicated
In selected cases, Atropine is used in transient AV block
Otherwise, permanent pacing
2. What are the causes of complete?

- Congenital: Relatively asymptomatic at rest
Acquired
- Medications Class I-IV Anti-arrhythmias
- Degenerative diseases and Lev diseases (calcification of the conduction
system)
- Rheumatic fever, Myocarditis
- Autoimmune disease E.g. RA, Scleroderma
- Infiltrative Diseases E.g. Amyloidosis
- IHD
- Electrolyte Imbalances (potassium and magnesium)
3. How would they present?

- Asymptomatic
- Fatigue
- Dizziness
- Impaired exercise tolerance
- Chest pain
- More serious symptoms: Syncope, Confusion, Sudden death
4. What is the treatment?

- New onset complete heart block is a medical emergency
- Treatment depends on the level of the block
- First withdrawal medications that aggravate the conduction
- Oxygen, IV access
- Transcutaneous pacing / Transvenous pacing
- Implantation of pacemaker
ECG-L1-SVT
What is this?
- Heart rate may be 140-240 beats/min and is regular (different from AF E.g. irregular in AF)
- The P wave is often buried in the QRS complex
Ans = AV nodal reentrant tachycardia
Paroxysmal Supraventricular Tachycardia
Background From Wiki 2012
- Supraventricular tachycardia is any rapid heart rhythm originating from
above the ventricle
Essential of Diagnosis
- Frequently associated with palpitation
- Sudden onset and termination
- Rapid, regular rhythm
The term often refer to one specific cause of SVT, namely paroxysmal
supraventricular tachycardia
- 2 common types: Atrioventricular reciprocating tachycardia (E.g. WolffParkinson-White Syndrome) and AV nodal reentrant tachycardia
General Consideration
- Often occurs in patient without structural heart disease
- Most common mechanism is reentry, which is most commonly seen within
the AV node = AV nodal reentrant tachycardia
- Less commonly, reentry is due to an accessory pathway between the
atria and ventricles = AV reentrant tachycardia or Atrioventricular
reciprocating tachycardia
Treatment
- Mechanical Measures: Valsalva maneuver, Carotid sinus massage (often
performed by physicians, should be avoided in carotid bruits), Others
Coughing, Stretching the arms and body, Splashing cold water on the face
- Drug Therapy: IV Adenosine, Calcium blockers (E.g. Verapamil)
- Cardioversion: 2 electrode pads are used
Supraventricular Tachycardia due to Accessory AV Pathways
- Frequently associated with palpitation
- Can be associated with syncope
- Rapid, regular rhythm
- May have narrow or wide QRS complex on ECG
- Often have pre-excitation (delta wave) on baseline ECG
Treatment
- Catheter ablation
- Drugs: Managed differently from the reentry type, use class III E.g.
Amiodarone = Potassium blockers
ECG
- Most commonly seen in young adults

- Rarely cause syncope
- Usually have narrow QRS complex on ECG
- Often responsive to vagal maneuvers, AV nodal blockers or Adenosine
Clinical Signs and Symptoms
- Asymptomatic
- Palpitation
- Mild chest pain or dyspnea
- Episodes begin and end suddenly, may last for few seconds to hours or
longer
Prevention
- Catheter ablation = An invasive procedure to remove a faulty electrical
pathway from hears E.g. AF, AF, SVT, Wolff-Parkinson-White Syndrome
- Drugs: Beta blocker or calcium blocker E.g. Diltiazem, Verapamil
- If there is a direct connection between the atria and ventricle through
Kent bundles = Wolff-Parkinson-White Syndrome
- Often a short PR interval and a delta wave
- Up to 30% of patients with WPW syndrome will develop AF or Atrial
flutter
Atrioventricular reciprocating tachycardia (E.g. Wolff-Parkinson-White Syndrome)
ECG-L1-AF
What is this?
Ans: AF
Atrial Fibrillation Current Medicine 2012
- Irregular heart rhythm
- Usually tachycardic
- Often associated with palpitation (acute onset) or fatigue (chronic)
- High incidence and prevalence in the elderly population
General Considerations
- AF is the most common chronic arrhythmias
- Affects about 10% who aged <80
- Also occurs in rheumatic and valvular heart disease, dilated
cardiomyopathy, ASD, hypertension, coronary heart disease
- Also occurs in patients with no apparent cardiac disease
- It may be the initial presenting sign in thyrotoxicosis, and this should be
excluded with the initial episode
- ECG: Typically demonstrates disorganized atrial activity with QRS
- AF often paroxysmal before becoming the established rhythm
- Alcohol excess, withdrawal may precipitate AF
Symptoms and Signs

- Rarely life threatening, but a major preventable cause of stroke
- Some have few symptoms, others find it very uncomfortable
- Most patients will complain of fatigue
- HR range from slow to extremely rapid, but is regular unless underlying
heart block and a permanent ventricular pacemaker
- Because of the varying stroke volumes resulting from varying periods of
diastolic filling, not all ventricular beats produce a palpable peripheral
pulse
Most serious consequence of AF = Thrombus formation due to stasis in

the atria (particularly the left atria) and consequent embolization
stroke
Management
New Diagnosed AF
- Anticoagulants
- Rate control or elective cardioversion
Paroxysmal AF
- Anticoagulants
- Anti-arrhythmias E.g. Amiodarone
Refractory AF
- Beta-blocker, calcium blocker, digoxin
- If no drugs work AV node ablation and permanent pacing
AF Therapeutic Guidelines
General Issues
- AF usually presents with an irregular ventricular rate of around 160-180
beats a minute in untreated patients with a normal AV nodes
- If patient presents for the first time attempt to identify causes E.g.
high BP, mitral valvular disease, thyrotoxicosis, HF
3 Types
- Paroxysmal AF: Episodes come on suddenly, generally revert in next 1-2
days without any intervention
- Persistent AF: Abrupt onset, but episodes persists for days or weeks
- Permanent (Chronic) AF
- All 3 types have similar risk of thromboembolism
Treatment
- 3 areas to consider: Rate control, Rhythm control, Prophylaxis against
thromboembolic complications
Rhythm Control and Cardioversion
- If the patient has severe symptoms or a compromised hemodynamic
state, cardioversion should always be considered immediately, it is safe
to cardiovert is the episode has lasted less than 48 hours
- If >48 hours, risk of thromboembolism increased
- Conversion with drug therapy: Amiodarone
Synchronized Electrical Cardioversion
- Requires a DC shock, starting with 100 joules
- But consider 200 or 300 in a larger patient
Rate Control
- Use: Atenolol, Metoprolol, Diltiazem, Verapamil
- Also Ventricular rate has been traditionally been controlled with digoxin
Anticoagulants
- Aspirin 100-300 mg orally, daily
- Warfarin or Dabigatran
- Prophylaxis of Stroke: Aspirin and Clopidogrel
ECG-L1-AF1
ECG
What is this?
Ans: AF = Atrial Flutter
- Regular heart rhythm
- Usually tachycardia 100-150 bpm
- Often wit palpitation or fatigue
- ECG show sawtooth pattern in leads II, III and aVF
- Often seen in conjunction with structural heart disease or chronic
obstructive pulmonary disease
- Less common than AF
- Occurs most often in patients with COPD
- The reentrant circuit generates atrial rates of 250-350 bpm
Treatment
- Ventricular rate control: Same agents for AF, nit more difficult with flutter
- Anticoagulants
ECG-L1-VPB
What is this ECG?
Ans: Ventricular Premature Beats (Ventricular Extra-systoles)

Background
- Also called premature ventricular contractions
- Sudden death occurs more frequently in the presence of organic heart
disease
Treatment
- If asymptomatic, no therapy
- Electrolyte imbalances, hyperthyroidism, occult heart disease should be
excluded if they are frequent
Clinical Findings
- The patient may sense it as a skipped beat
- PVB the QRS complexes is differ from the normal ones, usually not
preceded by a P wave
-
Drugs: Beta blockers

Catheter ablation
ECG-L1-High K
DDx
Background
Ineffective Elimination
Medications: K+ sparing diuretics, ACEi, NSAIDs, Trimethoprim, Digoxin

overdose
- Renal insufficiency (renal US for renal failure)
- Mineralocorticoid Resistance E.g. Addisons, Aldosterone deficiency
Excessive Release from Cells
-
A plasma potassium >6 mmol/L is an emergency and require urgent

treatment
Complications: Ventricular fibrillation and cardiac arrest
If the patient look artefactual result?
- Rhabdomyolysis,
- Massive blood transfusion
- Burns
- Shift out of cells by Metabolic acidosis, Low insulin level
Excessive Intake
- Excessive K+ supplement
Artefactual results
- Hemolysis E.g. Difficult puncture
- Contamination with potassium EDTA anticoagulant in FBC bottles
- Thrombocythaemia (K+ leaks out of platelets during clotting)
- Delayed analysis (K+ leaks out of RBCs)
Signs and Symptoms
Treatment in Non-Urgent Cases
Fast irregular pulse, chest pain, weakness, palpitation, light-headedness

ECG changes: tall tented T waves, small P waves, a wide QRS complex,
ventricular filbrilation
Review medications
Polystyrene sulfonate resin, binds to K+ and prevent absorption, lower
level over a few days
Frusemide
Emergency
Stabilizing Cardiac Cell Membrane
- Adults: 10ml of 10% calcium gluconate, slow IV over 2-5 mins

- Avoid use of Digoxin
Shifting K+ into Cells
- Glucose and Insulin
- Salbutamol may be needed
Long Term
- Frusemide
- Polystyrene sulfonate resins
ECG-L2-AV Dissociation
1. What is AV dissociation?
- The ventricular rate is the same or faster than atrial
rate 2 rhythms present
- Atrial impulses arriving at the AV node when it is
refractory so not conducted
2 Types
- Complete dissociation, none of the P wave conduct
- Incomplete, some P wave capture the ventricles
3. What are the causes of it?
- Surgical and anesthesia interventions E.g. intubation
- Medications
- Sinus node diseases
- Digoxin
- MI
- Electrolyte imbalances
5. How to treat?
- Treatment directed on the cause
2. How is it different from complete heart block?

- There is a block where atrial impulses cant reach AV node
- The atrial rate is faster than the ventricular rate
4. What is the presentation?

- Exertional dyspnea
- Light-headedness
- Palpitation
- Throbbing sensation in neck
- Fatigue, Malaise
6. What is the ECG above showing you?
There are p-waves and there are QRS complexes and many seem to have no relation to
each other. It is easy to believe there is complete AV block. But there is not AV block,
this is AV dissociation
The Black arrows show p-waves that do not conduct

The green arrows show normal sinus beats that are
conducted before the AV node can initiate a beat on
its own.
The thick blue arrow shows a capture or fusion beat:
The narrow blue arrow is also a fusion beat
This is AV Block
This is AV Dissociation
ECG-L2-Bradyarrhythmias
1. Define bradyarrhythmias.
- HR < 60 bpm
3. What would you ask in the history?

- Syncope
- Light-Headedness
- Dyspnea
- Angina
- See above causes
2. What are the causes?

- Professional athletes asymptomatic, sinus bradycardia
- Cardiac Diseases: IHD, Rheumatic heart diseases, Degeneration of the
conduction system (most seen in elderly), Heart block, Sick sinus
syndrome
- Medications: Beta blockers, Ca++ blockers, Digoxin (always ask and
assess level of Digoxin)
- Hypothermia
- Hypothyroidism
- Hypoxia
- Hyperkalemia
- Increased in ICP
-
Make-Up Scenario Medicine (CXR)

CXR-L1-Pulmonary Effusion+ Pulmonary Edema
Case 1
1. What is case 1?
- Pulmonary effusion
3. What symptoms?
- Dyspnoea
- Dull chest pain
5. The fluid is drawn from the pleura. What is this procedure called?
- Thoracentesis
7. Any other investigations you would organize?

- Blood: FBC, U&E, ESR, CRP, Blood culture, Albumin, Amylase, TFT, LFT
- CXR
- If exudate consider a pleural biopsy
Case 2
2. What is pleural effusion?
- Fluid in the pleural cavity
4. What clinical signs?
- Displacement of the trachea away from a large effusion
- Reduced movement of the affected side
- Dull on percussion
- Breath sounds are reduced or absent over a pleural effusion
- Reduced vocal fremitus over a pleural effusion
6. What can be done on the fluid drawn?
- pH, Glucose, Protein, Albumin, LDH, Amylase
- Gram stain, Culture
- Cell count and differential
- Cytopathology to identify cancer cells
8. What are the 2 types of fluid and their causes?
Transudative (protein <25g, due to increase in hydrostatic pressure )
- Left ventricular failure/Congestive heart failure
- Cirrhosis
- Nephrotic syndrome/Renal failure
9. What can you do in recurrent pleural effusion?

- Pleurodesis (chemical or surgical)
- In malignant effusions
1. What is case 2?
- Pulmonary edema (fluid in the air sac)
3. What symptoms?
- Shortness of breath
- Exertional dyspnea
- Cough
- Tachypnea
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Later: Blood stained sputum, cyanosis
5. What investigations?
- CXR, ECG (look for MI)
- U&E
- ABG
- Lung function test (not in an emergency setting)
- Hypothyroidism
Exudative (protein >35g, due to inflammation)
- Bacterial pneumonia
- Cancer
- Viral infection
- TB/Lupus
- Pancreatitis
10. How to manage this patient?
- Depends on the underlying cause
- Chest drain
2. What are the causes of pulmonary edema?
Increase in the Capillary Permeability
- Pneumonia, Renal failure, ARDS
Increase in the Capillary Pressure
- Left heart failure, Fluid overloaded E.g. Renal/Liver failure
Reduction in the Oncotic Pressure
- Hypoalbuminemia E.g. Liver failure, Nephrotic sydrome
4. What signs?
- Cheyne stokes respiration in severe cases
- JVP elevated
- Basal crepitations
- Triple or gallop rhythm HS
- A pleural effusion may also be present
6. How to manage?
Acute Management
- ABC
- IV access
- Sit upright
- Oxygen (make sure no underlying chronic lung diseases)
- Frusemide + GTN Spray
- Consider morphine
- Put in an urinary catheter
- If severe CPAP
- If AF Amiodarone
- If still fails Dobutamine, a sympathomimetic drug used in heart failure
and cardiogenic shock
7. What are the findings of pulmonary edema?
CXR-L1- Pneumonia vs Collapse/Atelectesis
Case 1:
1. What is case 1?
- Pneumonia (increase in opacity)
Case 2:
2. What are the causes of community and hospital acquired pneumonia?
Community
3. How would you assess the severity of the patient presenting to ED?
- CORB
- Confusion/O2 sat<90%/RR >30 breaths a min/SBP <90mmHg
5. What antibiotics would you use?

Moderate Pneumonia
- Azithromycin to cover atypical organism
- Benzylpenicillin
Severe
- Use Ceftrixone instead of Azithromycin
Streptococcus pneumoniae, Hemophilus influenzae

Other: Mycoplasma pneumoniae, Chlamydophila and Legionella
pneumoniae
Hospital
- MRSA, Pseudomonas aeruginosa, Stenotrophomonas maltophilia
- Others: Legionella, Aspergillis species, Respiratory viruses
- Also consider aspiration
4. You decided to admit this patient. What investigation would you do?
- CXR
- Blood: Culture, FBC, U&E, ABG, CRP, ESR
- Sputum culture, Throat swab
- Urinalysis
- Consider myoplasma serology and bronchoalveolar lavage
6. How to treat hospital acquired pneumonia?
- Commonly used: Gentamicin + Benzylpenicillin
7. What is this?
Pneumocystic jiroveci pneumonia
Treated by Trimethoprim + Sulfamethoxazole
8. What are the sings of consolidation?

- History: Sudden onset malaise, Chest pain, Dyspnea, Fever, Ill-appearing
- Signs: Reduced chest expansion on the affected side, Dull percussion,
Bronchial breath sounds, Crackles, Increased resonance
1. What is happening in case 2?
- Collapse
- There is loss of volume
3. What are the clinical features of it?

- Occurs within 2 days of the operation
- Dyspnea, Rapid pulse, fever
- May be cyanosis
- Coughing is painful
- Sputum clear at first, then become purulent
Signs
- Tracheal deviation to the collapse side
- Chest wall expansion reduced to the affected side
- Dull percussion
- Breath sounds reduce, bronchial breath sounds above the area of collapse
5. How can you prevent this from happening?
- Stop smoking
- Deep breathing and coughing
- Adequate analgesia
2. What is collapse? What are the causes?

- A bronchus is obstructed (E.g. tumor, foreign objects, retained
secretion), the air in the part of lung is absorbed and collapse
Causes
- Most common = After surgery retained secretion
- Foreign body/Tumor
4. How to manage?
- Removal of impacted secretion by coughing, managed by a
physiotherapist
- Ensure adequate analgesia
- If severe aspiration through the nose or an endotracheal tube
- If fever lasts longer than 2 days likely a chest infection treat with
Augmentin
CXR-L1-COPD + Pneumothorax
1.
2.
-
What is this?
COPD
What is your acute management?
Bronchodilator: Salbutamol by inhalation, up to 10 inhalations or
Ipratropium up to 6 inhalations
- If not adequate nebulized therapy
- Systemic Corticosteroids E.g. Prednisolone 30-50mg orally daily
- Antibiotics: Amoxycillin 500mg orally, 8 hourly for 5 days
Oxygen Therapy
- Maintain O2 sat about 88-92%
- Be aware, cos this may inhibit the respiratory drive relying on CO2, in
generally if PaO2 is >65 (or if O2 sat is > 92%) Reduce O2
3. What is your long term management?

- Bronchodilator
1.
2.
-
What is this?
Tension Pneumothorax
What is your acute management?
Tension pneumothorax is a medical emergency requiring urgent
decompression
- It is associated with severe SOB, tachycardia, hypotension and circulatory
collapse
- Commonly seen in traumatic patients
Management
- Urgent Needle Decompression Insert a cannula above the 3rd rib in the
mid-clavicular line, remove the needle from the cannula, a gush of air
confirm the diagnosis, once done a thoracostomy tube should be inserted
- Catheter Aspiration E.g. Venous catheter, insert above the 3rd rib along
the mid-clavicular line, repeat CXR, Catheter should be connected to a
continuous drainage
- Intercostal Tube Drainage Preferred in tension pneumothorax, the tube
should be connected to a continuous drainage or underwater seal, it is a
specialized procedure
3. What is the management for pneumothorax?
Primary Spontaneous Pneumothorax
Combination E.g. Seretide (Fluticasone + Salmeterol), Symbicort

(Budesonide + Eformoterol)
Mycolytic therapy If the patient is producing a lot of sputum can
reduce exacerbation
Vaccination to flu
Oxygen
Conservative: Symptoms usually resolve within 24-48 hours without

treatment, for patients who are able to speak in sentences, not short of
breath, RR<24m normal BP, PR <120, Analgesia is important, often
improve SOB, Give oxygen
Intervention: See above management for tension pneumothorax
Make-Up Scenario Medicine (Lab Interpretation)

Lab-L1- Blood Gases
1.
2.
3.
4.
5.
Ans: Respiratory Acidosis
Ans: Respiratory acidosis + Metabolic alkalosis = Compensated
1. Interpret the above results.
- Step 1 pH: Low = Acidosis, High = Alkalosis
- Step 2 bicarbonate: Low = Metabolic acidosis, High = Metabolic
alkalosis
- Step 3 PCO2: Low= Respiratory alkalosis, High = Respiratory acidosis
Case 1
Case 2
Case 3
- Low pH = Acidosis Respiratory acidosis
- High pH = Alkalosis
- Low pH = Acidosis
- Low bicarbonate = Metabolic acidosis
- High Bicarbonate = Metabolic alkalosis
- High bicarbonate = Metabolic alkalosis
- Low PCO2 = Respiratory alkalosis
- Normal PCO2
(Compensation)
(Compensation)
- Ans: Metabolic alkalosis
- High PCO2 = Respiratory acidosis
- Ans: Metabolic acidosis
- Ans: Respiratory acidosis
2. What is the role of lungs and kidneys in acid-base balance?

- Lungs quickly removes CO2
- Kidneys maintain the bicarbonate buffer system
4. What are the causes of metabolic alkalosis?

- Volume loss E.g. Vomiting, Diuretics, Gastric drainage
- Severe potassium deficiency
- Hypermineralocorticoid states E.g. Steroid treatment, Cushing syndrome
- Excessive alkali intake
6. Causes of respiratory alkalosis?
- Hyperventilation E.g. Asthma, Pulmonary edema, Pulmonary fibrosis,
Congenital heart diseases
- Increased respiratory drive E.g. Anxiety, Fever
- Pregnancy
- Cirrhosis
- Excessive mechanical ventilation
8. What are the consequences of metabolic acidosis?

- Impaired myocardial contractility
- Increased risk of ventricular fibrillation
- Pulmonary constriction
Lab-L1- LFT
Abnormal LFT
1. What are measured in a standard LFT?
- Albumin
- ALT
- AST
- Alkaline Phosphatase ALP
- GGT
- Total Bilirubin, Direct Bilirubin = Conjugated bilirubin
3. What are the causes of metabolic acidosis?

With increased anion gap
- Renal failure
- Ketoacidosis DM, Starvation, Alcohol
- Lactic acidosis inadequate tissue oxygenation, hepatic failure,
neoplasm
With normal anion gap
- Excessive acid intake
- Loss of base E.g. Diarrhea
- Potassium diuretics
5. Causes of respiratory acidosis?
- Acute respiratory failure E.g. Drug intoxication, Cardiopulmonary arrest
- Chronic respiratory failure E.g. COPD, Obesity
7. What is the management?

- Generally, if the underlying disturbance is corrected, the kidneys and
lungs restore acid-base balance
- Metabolic acidosis in the setting of chronic renal failure (administration
of oral bicarbonate),
- Severe uncorrectable metabolic acidosis in the setting of acute renal
failure (temporary hemodialysis)
- Metabolic alkalosis from volume and chloride loss (fluid replacement with
saline solution).
-
2. And what is their importance?

Albumin
- Protein produced by the liver
- Decrease in the chronic liver diseases E.g. Cirrhosis
- Also decreased in nephrotic syndrome loss via kidneys
ALT
- Presence in hepatocytes
- Increased in hepatocellular damage
AST
3. What other LFT can be tested?

- INR
- Serum glucose
- LDH Lactate dehydrogenase Indicate liver damage, can also elevated in
hemolysis, high tissue turnover
- Nucleotidase Similar to GGT
- Alpha-1-Antitrypsin Deficiency leading to liver cirrhosis
- Alpha-Fetoprotein Hepatocellular cancer
- Iron studies in hemochromatosis
- Copper in Wilsons disease
- Hepatitis serology
- Also raises in hepatocellular damage

- But also found in cardiac and skeletal muscles
- AST to ALT ratio >1 = Alcoholic Cirrhosis or Viral Hepatitis
ALP
- Found in cells lining the biliary ducts
- Increased in intrahepatic cholestasis, bile duct obstruction (E.g. Gall
stones), infiltrative diseases of liver
- ALP also presents in bones
GGT
- More sensitive marker than ALP
- May be elevated even in minor subclinical levels of liver dysfunction
- GGT is raised in chronic alcohol toxicity
Conjugated Bilirubin
- Elevated in post-hepatic causes
Cases
ALT and AST elevated hepatocellular damage

AST/ALT ratio <1, less likely to be alcoholic cirrhosis or viral hepatitis
Action: Hepatitis serology to confirm
- Ans: Turned out to be viral hepatitis
ALP is elevated in intrahepatic cholestasis, bile duct obstruction and

infiltrative liver disease
Given his age, must rule out liver met
AST to ALT ratio = 2 Alcoholic cirrhosis or viral hepatitis

GGT chronic alcohol toxicity
Ans: Cirrhosis on biopsy
Lab-L1- Iron Study
1. Explain the iron study.

Iron
- Very little values in assessing iron stores
Cancer of the head of pancreas
Ans: Hemolysis
26 Male
- Normal
Ferritin (acute phase protein, produced in liver)

- A low ferritin confirms a iron deficiency
- But raised by acute inflammation or liver disease masking iron
deficiency
Transferrin
- Transport iron
- Low = Chronic disease
- High = Iron deficiency, Pregnancy, Estrogen therapy
Transferrin Situation %
- Assessment of transport iron
- Low = Iron deficiency or chronic diseases
- High = Iron therapy or Iron overloaded
18 Female
- Iron deficiency as indicated by the low ferritin
41 Male
- Iron overloaded
67 Female
- Chronic disease
15 Female
- Intercurrent Illness
21 Female
- Pregnancy or estrogen therapy
2. Explain the iron metabolism in our body.
3. In 18 years old female, she has iron deficiency. What are the causes? How would
you manage her?
- Causes: Poor diet, Vegetarian, Blood loss (menorrhagia, ulcer), Malabsorption
(celiac disease)
- Signs: Koilonychia, Glossitis, Stomatitis
- Treatment: Oral ferrous, Then IM if intolerate (E.g. GI side effects,
Constipation)
Hepcidin, produced by the liver when the iron level is high, and
inhibits the absorption of iron in the intestines
- Hepcidin binds to the ferropotin in the enterocytes and inhibits
absorption of iron
- In hemochromatosis, impaired production of the Hepcidin
- Iron is transferred by transferring
- Stored in ferritin (intracellular protein that stores iron), but we test
for serum ferritin
4. She fails to improve. What are the possible causes?
-
5. The 41 males is iron overloaded. What is happening?
Non-compliance
Continued blood loss
Mal-absorption
Misdiagnosis E.g. Thalassemia
6. What is the mechanism behind anemia caused by chronic diseases?

- Cytokine production inhibits the production of RBC
- Investigation: Low or normal MCV, Ferritin normal or increased
- Treatment: Treat the underlying causes, Erythropoietin in chronic
renal failure
- Examples: Epoetin alfa, beta, Darbepoetin
- Either SC or IV
Lab-L1- Spirometry (can combine with acid-base interpretation)
Primary Hemochromatosis Impaired production of Hepcidin, Complications of

hemochromatosis = skin pigmenetation/DM/Testicular
failure/Cardiomyopathy/Cirrhosis/Joint iron deposition, Managed by venesection
Secondary Hemochromatosis
- Too frequent blood transfusion
- Excessive iron supplements
7. What Transferrin increases in pregnancy?
- Iron demand increases
1. Interpret this result.
2. What patterns is below showing?
Obstructive pattern reduced FEV1/FVC

Not really reversible changes after treatment <12%
Likely to be COPD
HOWEVER, the FVC is low.so this is actually a mixed pattern
Remember
-
Obstructive: FEV1/FVC reduced, FEF25-75% reduced E.g. Astham, COPD

Restrictive: Low FVC, normal or high FEV1/FVC E.g. Interstitial lung
disease, respiratory muscle weakness, thoracic cage deformities
- Mixed: Low FVC, Low FEV1/FVC E.g. Cystic fibrosis
What is spirometry?
Some Definitions
A measure of lung function, how much air and how quickly air can be
moved in and out of the lungs
FVC (forced vital capacity): The maximum air that can be inhaled or
exhaled
Differentiate between asthma and COPD

Tell between obtrusive and restrictive disease
Monitor disease
Response to therapy
Encourage and motivation to stop smoking
More accurate assessment
How to do?
-
Breath in fully
Seal the lips around the mouth piece
Blow out as long as possible, and as hard as possible
Repeat the test if necessary
Contraindications
- Recent eye or abdominal surgery
- Aneurysm
- Chest pain
- Abdominal pain, nausea, diarrhea
- Children below the age of seven
PFT Function
FEV1 (forced expiratory volume in 1 second): The volume that can be

exhaled in 1 second
- EFV1/FVC ratio: Useful indicator of obstruction, Normal valves about 80%
(decreased in obstructive disease, in restrictive disease it can be increased
or normal)
- FEF25-75% (forced expiratory flow): average flow over the middle half of
the expiration, more sensitive than FEV1
Common Causes of Errors
- Untrained
- Poor posture
- Failure to inflate lung
- Hesitation at the start of expiration
- Sub-maximal effort
- Leaks
- Cough
- Poorly calibrated spirometer
Interpretation
-
3. What are the causes of lung fibrosis?

-
Obstructive: FEV1/FVC ratio reduced, lower limit 70-75%, but depends on

age group, sex
- Restrictive: FEV1/FVC ratio typically >80%
ABG
Obstructive: FEV1/FVC reduced, FEF25-75% reduced E.g. Astham, COPD

Restrictive: Low FVC, normal or high FEV1/FVC E.g. Interstitial lung
disease, respiratory muscle weakness, thoracic cage deformities
Mixed: Low FVC, Low FEV1/FVC E.g. Cystic fibrosis
Upper Lobe: scharts Silicosis, Sarcoidosis, Histiocytosis, Ankylosing

spondylitis, Allergic bronchopulmonary aspergillosis, Radiation, TB
Lower Lobe: Rasco RA, asbestosis, scleroderma, cryptogenic fibrosing
alveolitis, others E.g. drugs Hydralazine, Methotrexate, Amiodarone
pH
PaO2 (normal 75-100mmHg), if low O2 = hypoxemic, is level < 60mmHg
oxygen, if lower than 26mmHg risk of death, must oxygenate
immediately
- PaCO2 (35-45mmHg), high level indicate hypoventilation (E.g. respiratory
acidosis or hypercapinia), low level indicate hyperventilation (E.g.
Respiratory alkalosis)
- HCO3-: Indicate if a metabolic problem is present, high = metabolic
alkalosis
- Base Excess: If high >+2 = There is metabolic alkalosis, If <-2 = Metabolic
acidosis
- Anion gap: Used to work out the causes of metabolic acidosis
Lab-L1- Anemia (make sure you know pernicious anemia)
- Whay are the cause of high, normal and low MCV anemia?
Background
-
Low hemoglobin
<135 g/L for men, <115 g/L for women
Symptoms: Fatigue, Dyspnea, Faintness, Palpitation, Headache, Tinnitus,
Anorexia
Signs: Pallor, Tachycardia, Flow murmur, cardiac enlargement, blood
transfusion can be fatal in cardiac failure
Normal MCV AAFFHHP Atrial fibrillation, HP printer

-
Acute blood loss

Anemia of chronic disease
Renal Failure, Bone marrow failure
Hypothyroidism, Hemolysis (E.g. Gram +ve bacteria, Sickle-cell disease,
G6PD deficiency)
Pregnancy
Types - Low MCV (microcytic)

Tails
- Thalassemia
- Anemia of chronic disease
- Iron deficiency
- Led poisoning
- Sideroblastic anemia (very rare)
High MCV (macrocytic) ABC MMHHR medical hair replacement
-
Alcohol excess or liver disease

B9 or B12 deficiency
Cytotoxics E.g. in Chemotherapy
Marrow infiltration
Myelodysplastic syndromes
Hypothyroidism
Hemolysis (E.g. Gram +ve bacteria, Sickle-cell disease, G6PD deficiency)
Reticulocytosis (Increase in immature RBC, may be caused by hemolytic
anemia)
Lab-L1- hemolysis
-
This 35 years old lady comes to see you because of SOB. Here is the result of the blood test.
1. What can you tell from the blood test?

- High MCV anemia
3. What further investigations would you ask for?

- Directed on the DDx
- LFT, Vit B9 and B12, FBC and blood film, TFT
- Hemolysis: High reticulocyte count, High bilirubin, High LDH, Blood films
(Sickle cells, Spherocytosis), Urine urobilinogen, Urine hemoglobin
4. What is this showing you?

-
Hemolysis
6. What is your next step?

To work out if this is an extravascular or intravascular hemolysis
- 1. Test urine for hemoglobin, +ve in intravascular hemolysis
2. What are the DDx?

ABC MMHHR
- Alcohol or liver disease
- Vit B9 or B12 deficiency
- Chemotherapy
- Marrow filtration
- Myelodysplastic syndrome
- Hypothyroidism
- Hemolysis E/g/ Gram +ve bacteria, Sickle cell disease, G6PD deficiency
- Reticulocytosis
Further Lab Result
5. There are 2 types of hemolysis: Explain intravascular and extravsacular

hemolysis. Indicate their causes. Outline how to tell which is which.
Extravascular
- RBC mainly destroyed in the spleen splenoemgaly
- Example: Sickle cell disease, Hereditary spherocytosis, Thalassemia, G6PD
deficiency
Intravacular
- Destruction within the vascular system release of free hemoglobin
detected in urine + increased serum haptoglobin
- Examples: Autoimmune hemolytic anemoia, Blood transfusion
incompatibility, Prosthetic heart valve, Infections E.g. Malaria
7. She turns out to have a +ve coombs test. How to manage?
- Consider blood transfusion if Hb low and symptomatic
- Acute management: Prednisolone
- 2. Test for serum haptoglobin, increased in intravascular hemolysis

If this is intravsacular hemolysis
- Direct Coombs test, +ve in autoimmune hemolytic anemia, transfusion
reaction and hemolytic disease of the newborns
If this is an extravascular hemolysis
- Sickle solubility test (for sickle cell anemia, a mixture of HbS in a reducing
solution makes it cloudy, normal Hb gives a clear solution)
- Hb electrophoresis, HbA2, Hb F (for thalassemia)
- G6PD deficiency Test for G6PD in red cells
- Hereditary spherocytosis Blood film, -ve Coombs test
Long Term: Cyclophosphamide
Lab-L1-DKA
1. What is A and B?
- A: DKA Predominantly with type I
- B: HHS Hyperosmolar Hyperglycemia State With type II
3. What is the management of DKA?
- Fluid Management: Normal saline 1L/h over the first 2 hours, then 3-4
liters in the first 8 hours, when the glucose falls about 14, a 10% glucose
containing solution should be used (cerebral edema can develop due to
quick decline)
- Insulin Replacement: IV 0.1 unit per kg
- Potassium: As the acidosis is corrected, potassium will flow out of cells
be aware of hyperkalemia
2.
4.
-
How to make a diagnosis of DKA?

Diabetic = high glucose
Ketone
Acidosis
What are the management of HHS?
Management similar
- Sodium Carbonate: Use only in severe acidosis E.g. <7

- Phosphate: Replacement is seldom used
Lab-L1-Coagulation
Hematemesis
1.
-
3.
-
What are the causes of hematemesis?

Peptic ulcer disease
Esophageal varices
Mallory-Weiss tear
Gastritis, Esophagitis
Esophageal or gastric cancer
Medications: Anticoagulants
Arterovenous malformation E.g. Aorto-duodenal fistulae
Physical Examination
General Inspection
Vitals
GIT examination: Note sign of alcoholism, liver failure = portal
hypertension, Signs of liver failure (Leuconychia, Clubbing, Palmar
erythema, bruising, asterixis, jauncdice, fetor hepaticus, gynecomastia,
spider naevi, Hepatosplenomegaly, ascites, legs edema)
- Cardio examination: Liver failure right heart failure, Note perfusion,
5. Management
General Management
- ABC
- Fluid resuscitation
- Correct coagulation
- Upper endoscopy = Diagnostic and therapeutic
2. Please take a brief history.

- When did it happen? How much blood? Was it fresh or dark brown?
- What were you doing before this happened?
- Were you drinking a lot before it happened?
- Were you vomiting before vomited blood?
- Abdominal pain?
- Is this your first time you have had this?
- GIT: Constipation, Diarrhea, Bloody stools? Painful swallowing? Difficulty
swallowing?
- In general: Recent loss of weight? Night sweats? Fever?
- Px: Peptic ulcer? Liver disease? Cancer? Medications E.g. Anticoagulants?
Allergies?
- Fx
- Social: Alcohol, Smoking, Exercise
4. Investigations
- Upper endoscopy
- Blood: FBC, U&E, CRP, ESR, LFT, Coagulantion, Group and hold
Esophageal Varices
- Ligation upon endoscopy
Mallory-Weiss tear
- Treatment usually supportive, as persistent bleeding is uncommon
- But cauterization or injection of adrenaline to the bleeding site stop
the bleeding
Peptic Ulcer
- Omeprazole + Amoxycillin (if allergic use Metronidazole) + Clarithromycin
Lab-L1-DVT
65 years old female has a background of end stage renal failure, which was managed by hemodialysis. She received heparin 2 weeks ago as a thrombolytic
prophylaxis during the hemodialysis. Today she presented to you with a swollen left leg.
- Explain how to investigate of you suspect this is a DVT. You will be provided with the results later.
1. What is the DDx of a left swollen leg?
2. What is your approach to this patient?
- Arterial occlusion
- History (ask risk factors for DVT)
- DVT
- Physical Examination (tenderness, calf swelling, pitting edema)
- Cellulitis
- Investigations
3. What investigation would you order? Give reason.
4. How to manage DVT?
- D-dimer
- Clexane (low molecular heparin) SC 1.5mg/kg for at least 5 days
- Doppler US look for lack of compressibility
- Warfarin daily adjusted according to INR 2-3
- Coagulation studies (which includes APTT, PT, INR)
- Check platelets one week after starting LMWH risk of
- FBC (for cellulitis, for platelet counts)
thrombocytopenia
- Anti-phospholipid antibodies (HD/Bonus , to screen for anti- Duration of treatment 3-6 months
phospholipid syndrome)
5. The blood test came back. And the platelet count was abnormally low. How 6. What do they mean APTT, PT, INR?
will you explain this?
- Heparin induced thrombocytopenia
- PT Prothrombin Time, normall 10-14s
- Formation of antibodies that activates platelet predispose to
- APTT Activated Partial Thromboplastin Time, mainly used to monitor
thrombosis
effect of Heparin
- Type 1 Mild, self-limiting fall in platelet
- INR usually 1-2, Target INR for warfarin is 2-3
- Type 2 Severe form
- INR is a ratio of PTtest/PTnormal
7. What are the different types of anti-coagulants?
8. What are the types of anti-platelets?
- Warfarin Vitamin K antagonist, may lead to skin necrosis, can be
- Aspirin
reversed by FFP, INR
- Clopidogrel (Pivax) APD receptor inhibitors
- Heparin Binding to anti-thrombin III inactivate thrombin, APTT
monitoring, reversed by potamine
- Clexane Low molecular weight heparin
- Direct thrombin inhibitors Dabigatran, in AF
- Direct factor Xa inhibitors Apixaban
Others
- Citrate Use in the lab and in the dialysis machine

9. What are the thrombolytics?
- Streptokinase
- Plasminogen activators E.g. Alteplase
- Used in MI, Cerebral infarction, massive PE
11. What are anti-fibrinolytics?
- E.g. Tranexamic acid
- Inhibitor plasmin formation
13. How to measure the activity of low molecular weight heparin?
-
Measure the factor Xa
14. How to diagnosed heparin induced thrombocytopenia?

- Thrombocytopenia, usually 5-10 days since the commencement of
Heparin
- Detect antibodies against heparin-PF4 complexes if positive, mix the
platelets of the patients with heparin, a release of serotonin indicates
platelet activation
Lab-L1-PE
10. What are the fibrinolytics?

- Equal to thrombolytics
12. Can you use anti-platelets in DVT?

- Anti-platelets Used in the arterial thrombosis, not venous
13. You started her warfarin, but she later develops chest pain and shortness
of breath. What do you think is happening?
- Not coagulating her enough Under treatment
15. How to treat heparin induced thrombocytopenia?
- Stop heparin
- Warfarin if the platelet count is >150, if not very high risk of skin
necrosis
- Consider Dabigatran, Apixaban
Case 1: You are a GP. This 45 years old female presented to you because of sudden onset dyspnea. She said it was not her first time. 1 week ago she was
prescribed an ACEI by another GP to control her newly diagnosed HTN. She had a bad reaction to the ACEI (short of breath) and was changed to ACERB. She
has been taking the ACERB for the past 3 days without problems but today she was suddenly short of breath. She thinks it is the mediation that is causing the
symptom. You agreed and discontinued the medication. Next day you received a call from the hospital and were told that the patient died last night. Later
autopsy revealed a big pulmonary embolism.
1. What are the risk factors of PE?
2. What are the clinical features of PE?
- Age
- New or worsening dyspnea
- Obesity
- Chest pain pleuritic chest pain/retrosternal chest pain
- History of DVT/PE
- Tachypnea
- Hormone therapy
- Tachycardia
- Pregnancy
- Hemoptysis
- Immobility
- Syncope
- Surgery
- Cyanosis
- Shock
3. What would you do if you suspect the patient has PE?
- Pretest probability
- ECG: Often normal except for sinus tachycardia, AF may present,
Evidence of myocardial ischemia, the classic S1,Q3,T3 with right axis
Features
Scores
deviation and RBBB is uncommon
Clinical Signs and Symptoms of PE
3
CXR may show reduced vascular markings
Alternative Diagnosis Unlikely to be PE
3
- ABG
HR >100
1.5
Immobilization
1.5
Previous DVT or PE
1.5
Hemoptysis
1
Cancer
1
- Low (<2) Dimer, then Ventilation perfusion scan or CT pulmonary
angiography
- High (>6) Ventilation perfusion scan or CT pulmonary angiography
- If still non-diagnostic, do US of the leg veins
- Hemodynamic Compromise E.g. Right ventricular strains (as
demonstrated by Echo or elevated troponin and/or severe hypoxemia)
- Heparin 80 units/kg loading dose IV, then 18 units/kg/hour IV infusion
and adjust according to APTT (platelet count should also be monitored
because of heparin-induced thrombocytopenia) can use Clexane instead
- Warfarin should be started, adjust according to INR
If ongoing hypotension, right heart failure or severe hypoxemia, duration 3-6
months
- Human Plasminogen Activator: Alteplase
7. What are the indications of thrombophilic screen?
- <40-50 years old without obvious risk factors
- Fx of VTE in young patient
- Unusual site of VTE
- History of recurrent miscarriage, pre-eclampsia, placental abruption
- Skin necrosis after use of warfarin
-
9. What suggestions would you give to reduce risk VTE when flying?
- Low risk individuals: Keep mobile, drink plenty of fluid
- Medium risk: Addition of compression stockings
- High risk: SC Enoxoparin before flight and on the following day
Increased ESR due to pulmonary infarction

D-dimer
CT/Ventilation perfusion scan
6. What is the risk of recurrence?

- Risk of recurrence in 5 years about 20%
8. What does the screen include?

Venous Thrombosis
- Protein C and S
- Antithrombin
- Lupus anticoagulants Anticardiolipin antibodies
- FBC and clotting screen
Arterial Thrombosis
- Lupus anticoagulants
- Anticardiolipin antibodies
- Homocysteine
- Lipoprotein A
10. What advices to give after surgery?
- Stop estrogen containing oral contraceptives 4 weeks before surgery
- Rehydration
- Mobile
- DO NOT regard aspirin or other anti-platelet agents as adequate
prophylaxis for VTE
- Temporary IVC filter to very high risk patients
- Compression stocking
Lab-L1-Lipid
1.
-
What is the non-pharmacological management of it?

Promote dietary medication
Reduce saturated fat, Increases fiber
Limit alcohol intake
Weight loss
3. What are some cause of hyperlipidemia?

Increase in LDL
- Hypothyroidism, Nephrotic syndrome, Cholestasis, Anorexia
Increase in TG or decrease in HDL
- Type 2 DM, Obesity, Renal impairment, Smoking, Alcohol, Estrogen use
Lab-L1-TFT
1. What is happening?
- Hypothyroidism
2. How about the pharmacological management?

For high LDL
- Use statin E.g. Atorvastatin, Pravastatin, Simvastatin, maximum
responses within 4 weeks or dose increase
- SE: Myopathy, GI symptoms, Elevated LFT, Headache, Sleep disturbances
E.g. Insomina, Nightmares
- Each doubling the statin dose, reduce LDL by 5-10%
- Add ons: Ezetimibe, Cholestyramine, Nicotinic acid, Fibrate
For predominant high TG
- Fibrate +/- fish oil
- Add ons: Nicotinic acid
-
2. What are the causes of hypothyroidism?

Autoimmune
Primary atrophic hypothyroidism diffuse lymphocytic infiltration of the

thyroid leading to atrophy
- Hashimotos Thyroiditis Goiter due to cell infiltration
- In the acute phase of subacute viral thyroiditis which will then
progress into hyperthyroidism
Secondary Hypothyroidism
- Very rare, not enough TSH
Others
- Radioiodine treatment, Surgery
- Drug induced E.g. Amiodarone, 2% users get hypo or hyperthyroidism,
Interferon
- Pregnancy
Hypothyroidism Association
- Turners and Downs syndromes, CF
-
3. What are the signs and symptoms?

- Symptoms: Tired, Sleepy, Lethargic, Mood decreased, Cold intolerance,
Weight increases but loss of appetite, Constipation, Hoarse voice,
Menorrhagia, Memory decreased, Dementia
- Signs: Bradycardia, Reflexes slowly relax, Dry skin, Yawning, Cold hands,
Ascites, Non-pitting edema, Pleural effusion, Round puffy face, Immobile
5. What are the causes of goiter?
Treatment
- Levothyroxine
4. How to diagnose?
For Screening: Thyroid Function Test
- Particularly important to determine free T3 and T4, as oral estrogen can
increase the level of throxine-binding protein
- TSH, low in primary, high in secondary
For Hypothyroidism
- Add antithyroglobulin and antithyroperoxidase antibodies for Hashimoto
thyroiditis
- Remember to do lipid profile, hypothyroidism associate with high LDL
and TG
For Hyperthyroidism
- Graves Disease: Antithyroglobulin and antimicrosomal antibodies
(elevated in graves disease), TSH receptor antibodies (usually 65% in
Graves Disease)
- 123 Iodine uptake scan Increase uptake hot areas on scan
For Thyroid Nodules
- FNA, guided by US
- 123 Iodine uptake
MRI
- Usually not necessary, also often pituitary gland is enlarged due to
hyperplasia from secreting much more TSH, which can be mistaken as
tumors
6. What are the complications of hypothyroidism?
Thyroiditis
Iodine deficiency
Medications E.g. Amiodarone
Infiltration E.g. Sarcoidosis
1. What is happening?
- Hyperthyroidism
Cardiac complications
Increased susceptibility to bacterial pneumonia
Depression
If untreated in pregnancy can lead to miscarriage
Myxedema crisis
2. What are the causes?

Graves Diseases
- 2/3 of cases of hyperthyroidism
- Typically 40-60 years of age
- Circulating antibodies that activates TSH receptor, causes smooth
enlargement of the thyroid
- Patients often hyper, but can be normal or hypothyroidism
- May associate with other autoimmune diseases E.g. Viltiligo, type 1 DM,
Addisons
Toxic Multi-nodular Goiter
- Due to iodine deficiency induction of thyroid cell hyperplasia
- Dont associate with infiltrative ophthalmopathy
Toxic Adenomas
- A benign tumor producing T3 and T4, Isotope scan is hot
Subacute Thyroiditis
- Typically with a moderately enlarged and tender thyroid
- Thought to be due to a viral infection
Others
- Ectopic thyroid tissue E.g. Thyroid tissue in ovarian tumor, Teratomas
- Over-replacement
- Pituitary tumor
- Pregnancy
- Amiodarone
4. How to diagnose?
Symptoms: Diarrhea, weight loss, increase in appetite, over active,

sweats, heat intolerance, palpitation, tremor, irritability,
oligomenorrhea, rarely psychosis, chorea, panic, ithc, alopecia
Signs: pulse fast irregular, warm moist skin, fine tremor, palmar
erythema, thin hair, lid lag (immobility of the lid when looking down), lid
retraction, may be goiter, thyroid nodules
Signs of graves disease: exophthalmos
, ophthalmoplegia
, pretibial myxoedema, clubbing, painful finger
5. How to manage?
- Drugs: beta blockers for rapid control of symptoms
- Anti-thyroid medications: Carbimazole +/- Thyroxine (to reduce the risk
of hypothyrodism), in Graves maintain regime for 12-18 months then
withdraw, about 50% will relapse, require radioiodine or surgery, Side
effects of Carbimazole: agranulocytosis (decrease in white blood cells)
stop if signs of infection E.g. sore throat, mouth ulcer
- Radioiodine: Most become hypothyroid post treatment, no evidence of
birth defects, caution in active hyperthyroidism as risk of thyroid storm
- Thyroidectomy: Risk of damage to the recurrent laryngeal nerve and
hypoparathyroidism, patients may become hypo or hyperthyroid
For Screening: Thyroid Function Test

- Particularly important to determine free T3 and T4, as oral estrogen can
increase the level of throxine-binding protein
- TSH, low in primary, high in secondary
For Hypothyroidism
- Add antithyroglobulin and antithyroperoxidase antibodies for Hashimoto
thyroiditis
- Remember to do lipid profile, hypothyroidism associate with high LDL
and TG
For Hyperthyroidism
- Graves Disease: Antithyroglobulin and antimicrosomal antibodies
(elevated in graves disease), TSH receptor antibodies (usually 65% in
Graves Disease)
- 123 Iodine uptake scan Increase uptake hot areas on scan
For Thyroid Nodules
- FNA, guided by US
- 123 Iodine uptake
MRI
- Usually not necessary, also often pituitary gland is enlarged due to
hyperplasia from secreting much more TSH, which can be mistaken as
tumors
6. What are the complications?
- Complications: heart failure (thyrotoxic cardiomyopathy), angina, AF,
osteoporosis, ophthalmopathy, gynaecomastia, thyroid storm
Lab-L1-Pancytopenia/MM
1.
-
What does it mean by pancytopenia?

Leukopenia
Anemia
Thrombocytopenia
3. What does it mean by hypersplenism?

- It is an overactive spleen, it removes the blood cells to quickly
Causes
- Basically the cases of splenomegaly
- For Examples: Cirrhosis, Lymphoma, Malaria, Tuberculosis, Inflammatory
diseases
5. What is aplastic anemia?

- The bone marrow does not produce enough blood cells
- In aplastic anemia, patients have pancytopenia E.g. Low red and white
cells and platelet
- Signs and symptoms: Pancytopenia
- Causes: Many cases idiopathic, Autoimmune disorder, Medications
(Carbamazepine, Chloramphenicol, Quinin, Phenytoin), Exposure to
2. What are the possible causes?

Impaired marrow production
- Aplastic anemia
- Infiltration E.g. Acute leukemia, Myelodysplasia, Myeloma, Lymphoma,
Solid tumors, TB, Megaloblastic anemia = B12 or folate B9 deficiency
Peripheral Destruction
- Hypersplenism
4. What would you ask in the history?
- Symptoms of anemia (E.g. SOB), Leukopenia (Infection), bleeding
Ask about symptoms of the possible causes (consider causes of
splenomegaly)
- Weight loss, night sweat in tumor, leukemia
- Coughing in TB
- Recent travelling
- Abdominal tenderness
- Liver diseases
- FBC, RFT, U&E, LFT, LFL, B12 and B9
- Screen for MM
- Bone marrow biopsy
radiation, Parvovirus can cause short lived aplastic anemia (but most
cases go unnoticed as the RBC live up to 180 days)
- Diagnosis: Can only be confirmed on bone marrow biopsy, but blood tests
should be done before the bone biopsy (E.g. FBC, RFT, U&E, LFT, LTL, B12
and B9)
- Treatment: Suppression of the immune system, in more severe cases a
bone marrow transplant, Mild chemotherapy with cyclophosphamide
may be effective
- Prognosis: Untreated leads to death in 6 months, with prompt treatment
survival from 5-10 years, and many live well beyond that length of time
- Occasionally milder cases resolve on their own, relapses are common
7. Explain multiple myeloma?
- Cancer of the plasma cells, which are derived from B lymphocytes
- Important: Do a serum protein electrophoresis & ESR on all over 50
presented with back pain
Symptoms
- Anemia, Recurrent infection, Bleeding
- Renal impairment
- Osteolytic lesions E.g. back pain, pathological fractures, vertebral collapse
- Hypercalcemia E.g. Stones, Bones, Groans, Psychiatric overtones
Investigations
- Serum and urine electrophoresis
- Also FBC, increased urea, Ca++, ESR
Diagnosis
- Protein band on electrophoresis
+
- CRAB Calcium/Renal/Anemia/Back pain
Lab-L1-CFS interpretation
1. What is measured in a LP that is not shown here?

- Pressure, Appearance, Amount, Lactate
3.
-
2. What tell you tell from pressure?

Increased Pressure
- Cerebral edema, Subarachnoid hemorrhage, Congestive heart failure,
Meningitis, Hydrocephalus
Decreased Pressure
- Severe dehydration, Leakage of spinal fluid, complete subarachnoid
blockage, Circulatory collapse
4. What is the significance of finding red cells?
- Can indicate peripheral contamination from the lumbar puncture
- But if phagocytosed erythrocytes hemorrhage into CSF
What does it mean by the presence of white cells count?

Pleocytosis = Presence of WC in CSF
Small number of monocytes = Normal
Present of granulocytes = Abnormal
A large number of granulocytes = Bacterial meningitis
DDx: Reaction to the lumber puncture, reactions prior to the injections of
medicine, recent epileptic seizures
5. How about glucose level?
6. How about level of protein?
Decreased Level
- Increased in meningitis, neurosyphilis, abscesses, subarachnoid
- Fungal or bacterial infection, Hypoglycemia
hemorrhage
Increased Level
- DM
7. How about lactate?
- Increased in CNS cancer, multiple sclerosis, respiratory alkalosis
Make-Up Scenario Medicine (Lab Interpretation/Renal) Pleural effusion interpretation
- Transudate vs exudate E.g. Charaters, Causes
- Risk of pleural tap? (Pneumothorax, always do a CXR after)
Lab-L1-Hyperkalemia (a common complication of acute and chronic renal failure)
You are a RMO. You were notified that one of the patient has a potassium level of 6.1mmol/L.
Explain your approach. (Always history, physical examination and investigation.)
1. What are the causes of hyperkalemia?
- Artefactual Results: Difficult puncture, Delayed analysis, Contamination
- Fast irregular pulse
with potassium EDTA anticoagulants in FBC bottles
- Chest pain
- Ineffective Elimination: Renal failure, K+ sparing diuretics, ACEI, NSAIDs,
- Weakness
Addisons
- Palpitation
- Light-headedness
- Excessive Intake: Excessive K+ supplements
- Excessive Release from Cells: Massive blood transfusion, Rhabdomyolysis,
Shift out of cells by metabolic acidosis/low insulin
3. What would you worry most?
4. What 2 things you would do before treatment?
- Ventricular fibrillation
- Physical examination and ECG to rule out artefactual result and
monitor heart
5. You did an ECG. Is this normal?
- Tall T wave
- Wide QRS complex
- Absent T wave
- Flattening of P wave?
6. What is the immediate treatment?
Stabilizing Cardiac Cell Membrane
- Adults: 10ml of 10% calcium gluconate, slow IV over 10 mins
- Avoid use of Digoxin
Shifting K+ into Cells
- Glucose and Insulin Short acting insulin 10 unit bolus + 50% glucose 50ml
IV over 5 mins
- Salbutamol may be needed, 0.5mg IV, have the potential to precipirate
cardiac arrhythmias
8. What food is high in potassium?
- Bananas
- Avocados
- Salmon
- Yogurt
- Dried apricots
- Baked potatoes
- Spinach
6. What are the ECG changes of hyperkalemia?

- Wide QRS complex
- Tall T wave
- Small P wave
- Ventricular fibrillation
7. What are the long term treatments?

Long Term for hyperkalemia
- Frusemide
- Polystyrene sulfonate resins = Resonium 15g 3-4 times orally daily,
suspended in 45-60ml of water
Long Term for chronic renal failure
8. What is a serious side effect of giving too much resonium?

- Colonic necrosis perforation
- Mild laxatives may be used to prevent constipation, but do not use
sorbitol increase risk of colonic necrosis
Lab-L1-Hyponatremia
Case 1
55 years old man was admitted to ED after running marathon for 3 hours. He has a sodium level of 118. How do you explain this? He looks sick. What to look
for on clinical examination? What is your immediate management?
Case 2
67 years old female, on a background of chronic renal failure secondary to her DM, was noted to have a sodium level of 125. How do you explain this? She
looks fine on clinical examination, why? What is your immediate management?
1. What is the normal range of sodium?
2. What are the signs and symptoms you are looking for?
- Normal Range 135-145
- N+V, Headache, Confusion, Lethargy, Fatigue, Appetite loss,
- Hypo when <135
Restlessness, Irritability
- Mild = 125-135
- Muscle weakness, Cramps, Seizures
- Moderate = 115-124
- Neurological Signs: Due to brain edema, most often when sodium <115
- Severe when <115 neurological signs
- Worse case herniation brain stem compression respiratory
arrest
- Severity of symptoms, severe if acute drop
- Chronic neurological adaptation
3. What are the possible causes of hyponatremia?
4. How to manage the patient in case 1 and 2?
Both water and sodium increases Hypervolemic Hyponatremia
In Case 1
- Liver/Renal/Cardiac failure water overloaded (most common)
- Since he has been running marathon, the likely cause = loss of sodium
- Nephrotic syndrome
- He is sick acute severe symptomatic hyponatremia
- Inappropriate IV therapy
- Require immediate IV sodium chloride 3%
Slightly increased water, sodium remains the same Normovolemic
In Case 2
Hyponatremia
- Likely cause = water overloaded chronic hyponatremia
- Hypothyroidism
- Management: Fluid restriction
- Glucocorticoid deficiency
- Loop diuretics may be added watch out for volume depletion
- Prolonged Exercise Marathon
- SIADH CNS disorder, Medications
How can you determine if this is hypovolemic, hypervolemic or normovolemic
Sodium Loss Hypovolemic Hyponatremia
hyponatremia?
- Diuretics use
Clinical Examination if the patient is dehydrated or water overloaded
- Prolonged vomiting/diarrhea
Investigations:
- Mineralocorticoid deficiency - Addisons disease, Congenital adrenal
1. Serum Osmolarity:
hyperplasia
If low Can be hypovolemic, hypervolemic or normovolemic
Hypo and hyper can usually can clinically determined
In Normovolemic Blood urea normal or slightly reduced
If normal or high Consider hyperglycemia, hyperlipidemia,
hyperproteinemia
2. Urine Sodium
If you determine the patient to be dehydrated, urine sodium helps to
determine the causes
6. You decided to give sodium chloride infusion to patient 1. What is the

infusion rate?
- Acute: Half the weight x Rate of change (1)
- Chronic: Half the weight x Rate of change (0.5)
Urine sodium <10 = Dehydration, Diarrhea, Vomiting

Urine sodium >20 = Diuretics, Stones, Mineralocorticoid deficiency
5. If the sodium for patient in case 2 was noted to be 113 from the beginning.
Will your management be different?
- For sodium <120 all require 3% sodium chloride IV
- But in chronic hyponatermia (patient 2), rate of change should not be
more than 0.5/ hour (1/h in acute setting E.g. patient 1)
- Increase 6-8 in the first 24 hours, noted that demyelination has been
reported in changes of 8
- Remember to check the sodium level 4 hourly to make sure you dont
overshoot the limit
- Otherwise risk of demyelination permanent CNS damage (central
pontine myelinolysis)
Case 3
- This 45 years old man was admitted last night because of meningitis. This morning he developed hyponatremia of 128. Urinalysis showed a really high
osmolarity.
6. What is the cause?
- SIAHD = diagnosis of exclusion
Treat
- Treat meningitis
- Fluid restriction 1.2-1.8L a day
- If <120, Sodium chloride 3% IV
Lab-L1-Hypercalcemia
1. Briefly explain the calcium homeostasis in our body.
PTH
- Overall Effects: Increase in Ca++
Mechanism
- Stimulating osteoclast
- Increase Ca++ reabsorption in kidneys, but losing PO43- Increase renal production of Vitamin D
Calcitonin
- Made in C-cells of the thyroid
- Effects: Decrease in Ca++
Vitamin D and Calcitriol
- Vitamin D is first hydroxylated in the liver then in the kidney to Calcitriol
Actions
- Increase Ca++ absorption in guts
- Inhibit PTH release
- Enhanced bone turnover
2. What is corrected calcium?

- In plasma, 40% of calcium is bound to albumin
- As lab only measure unbound Ca++ Corrected total Ca++ for albumin
- Increase Ca++ and PO43- reabsorption in kidneys

3. What are the causes of hypercalcemia?
- Most common causes (90%): Primary hyperparathyroidism (mild
hypercalcemia) and Malignancy (Severe hypercalcemia)
- Increased Intake: Vitamin D excess, Milk-Alkali syndrome
- Endocrine: Primary, secondary (Usually low or normal Ca++) or tertiary
hyperparathyroidism, Adrenal insufficiency, Hyperthyroidism,
Pheochromocytoma
- Neoplastic Diseases: PTH related proteins, MM, Lymphoma
- Miscellaneous: Familial hypocalciuric hypercalcemia, Lithium intake,
Thiazide use, Paget disease of bone, Complications of renal
transplantation
- Granulomatous diseases E.g. Sarcoidosis, TB can cause hypercalcemia via
overproduction active vitamin D
5. What investigation would you order?
- Indicators for malignancy: Low plasma albumin, low chloride, raised
phosphate, raised alkaline phosphatase, alkalosis, hypokalemia
- Indicators for primary hyperparathyroidism: Normal or low albumin,
normal or reduced phosphate, raised PTH (or inappropriately normal)
- Check for thyroid, vitamin D, renal function (stones)
- Adrenal insufficiency

Bones, Stones, Groans and Psychiatric Overtones
- Kidney stones, bone fracture, anorexia, vomiting, constipation, weakness,
fatigue, altered mental status depression
- GIT: Constipation, N+V, Abdominal pain, Pancreatitis
- Neurological: Drowsiness to weakness, depression, lethargy, stupor,
coma if severe
- Renal Stones
- Skeletal: Bone pain, Osteoporosis
- Cardiovascular: ECG changes, shortened QT interval
- Calcification: Cornea
6. How to manage the patient?

- Stop medication E.g. Thiazide
- Hydration
If severe
- Refer to ED
- IV normal saline +/- loop diuretics (assess fluid status)
- Monitor potassium, sodium and magnesium level
Bisphosphonate
- Used in hypercalcemia of malignancy
- May require 2-3 days to work
Calcitonin
- May be helpful in short term until bisphosphonate kicks in
Dialysis
- With low calcium dialysate
Lab-L2-Hypernatremia
A 45 years old man presented to ED because of 4 episodes of diarrhea and 2 episodes of diarrhea.
Case 1: Normal clinical examination, not confused
Case 2: Sodium was noted to be elevated at 140mmol/L
Case 3: In shock
1. How to manage case 1?
2. What are the causes of hypernatremia?
- Oral rehydration
- Inadequate intake of water
If severe E.g. Signs of dehydration
- Excessive water loss
Sodium Chloride 0.9%
- Glycosuria
Initial Bolus = 10ml/kg over 30 mins
- Diuretics
- Diabetes insipidus (inadequate ADH)
Maintenance = 100ml/kg/24 hours for the first 10kg, then 50 for the next
10kg, then 20 for the remaining kg
Add 70mmol K+ every 24 hours E.g. 20mmol K+ to each bag
E.g. 70kg man, require 2.5L of fluid + 100mmol Na+ + 70mmolK+ every 24
hours
Give
1L of sodium chloride
1L of 5% dextrose
1L of 5% dextrose
Add 20mmol K+ to each bag
- Alternative = 3L Hartmanns solution (sodium lactate, in extracellular
space only)
3. How to management case 2?
- Free access to water for mild cases
- 5% dextrose IV if severe
- Sodium concentration should not decreased by more than 0.5mmol/L per
hour and 10mmol/L in 24 hours
5. In case 3, the patient came in with shock, would you use sodium chloride
0.9% or 5% dextrose as the resuscitation fluid? Why?
- Use sodium chloride 0.9%, it has the osmotic effect of drawing fluid from
extravascular space into intravascular space
- 5% dextrose will just quickly distributed across the entire body
Lab-L2-Hypokalemia
1. What are the causes of hypokalemia?
Inadequate Intake
- Rare, except in starvation
GI Loss
- Diarrhea, Vomiting
- Pancreatic adenoma
Urinary Loss
- Diuretics E.g. Thiazide, Furosemide
- Other medications: Amphotericin B
- Diabetic ketoacidosis polyuria
- Alkalosis shift K+ into cells
- High aldosterone E.g. Renal artery stenosis, Conns, Cushing
Shifting into Cells
- Insulin
- Adrenaline
- Beta agonists
4. If the patient in case 3 came in with signs and symptoms of shock,

- Give 20ml/kg sodium chloride 0.9% until BP stabilize around 90/60mmHg
- Give it as fast as possible
- Correct electrolyte + maintenance
Signs and Symptoms

- Muscle weakness
- Hypotonia
- Hyporeflexia
- Cramps
- Palpitation
- Light headedness
- Rhabdomyolysis may been seen with severe hypokalemia E.g. <2.5
- If HTN presence think about aldosterone excess
Treatment
Mild to Moderate
- Oral K+ supplement
Severe E.g. <2.5mmol/L
- IV potassium carefully, not more than 20mmol/hour
- Continuous ECG monitoring
- Check K+ every 3-6 hours
- Magnesium deficiency should be corrected
- Do not give K+ if oliguria
3. Name one genetic disorder that is associated with hypokalemia.
- Type II Bartter Syndrome Mutation of the ROMK renal outer medullary
potassium channels
- Type 1 to 5
2. What serious complication can hypokalemia cause?

- Dangerous arrhythmias and rhabdomyolysis
3. What investigations will be useful in determine the cause?

Urinary Potassium
- If high indicates urinary loss E.g. Aldosterone/Mineralocorticoid excess,
Batter syndrome
Plasma renin and aldosterone level would be useful if high urinary potassium
ECG
- Broadening of T wave, Prominent U waves, Premature ventricular
contractions
Lab-L2-Hypokalemia
1. Briefly explain the calcium homeostasis in our body.
PTH
- Overall Effects: Increase in Ca++
Mechanism
- Stimulating osteoclast
- Increase Ca++ reabsorption in kidneys, but losing PO43- Increase renal production of Vitamin D
Calcitonin
- Made in C-cells of the thyroid
- Effects: Decrease in Ca++
Vitamin D and Calcitriol
- Vitamin D is first hydroxylated in the liver then in the kidney to Calcitriol
Actions
- Increase Ca++ absorption in guts
- Inhibit PTH release
- Enhanced bone turnover
- Increase Ca++ and PO43- reabsorption in kidneys
3. What are the causes of hypocalcemia?
- The most common causes = Hypoalbuminemia
Decreased Intake or Absorption
- Malabsorption
2. What is corrected calcium?

- In plasma, 40% of calcium is bound to albumin
- As lab only measure unbound Ca++ Corrected total Ca++ for albumin
4. What physical signs would you look for?

- Spasm (Trousseaus sign)
- Perioral paraesthesiae
- Anxious, Irritable
- Vit D deficiency
Increased Loss
- Alcoholism
- Chronic renal disease
- Diuretics
Endocrine Causes
- Hypoparathyroidism
- Parathyroidectomy
- Thyroid carcinoma with Calcitonin secretion
Associated Diseases
- Pancreatitis
- Rhabdomyolysis
- Septic shock
Physiological
- Associated with decreased serum albumin
- Hyperphosphatemia
- Induced by aminoglycoside antibiotics
5. What investigations would you order?
- Serum calcium concentration is low
- In true hypocalcemia, the ionized serum calcium is also low
- Serum phosphate is usually elevated in hypoparathyroidism or in
advanced CKD
- Serum phosphate is low in early CKD or vitamin D deficiency
- Important to check for PTH, vitamin D level
- Renal function
- ECG: Lengthening of the QT interval
Lab-L2-Hematuria
Seizures
Muscle tone increased in smooth muscle E.g. colic, wheeze, dysphagia
Orientation impaired E.g. time, place, person and confusion
Dermatitis
Impetigo
Chvosteks sign, Cataract, Cardiomyopathy, Choreoathetosis (Chorea +
athetosis = twisting movements of fingers, arms, legs and neck)

Symptomatic hypocalcemia and level <1.875
- IV calcium until symptoms stops
- 15mg/kg over 4-6 hours
Chronic Asymptomatic Mild Hypocalcemia
- Usually treated with oral supplements
- Calcium is best taken between meals
- Other treatment depends on causes
This 45 years female comes to you for routine check-ups. Urinalysis indicates RBC +.
Task: Take a history, Indicate what would you look for on examination, give a DDx, Outline investigations, Then answer questions from the examiner.
1. What are the causes of hematuria?
2. For macroscopic hematuria, why is it important to ask about the color of
the initial and terminal stream?
- Commonest: UTI
- Blood at the beginning of the stream only: from lower UT E.g. urethra
- Common: Stones
- Blood at the end of the stream only: from high up E.g. Bladder neck or
- Less Common: Renal trauma, BPH, Benign microscopic hematuria, GN,
base of the bladder
Malignant HTN, Anticoagulants
- Uncommon: PKD, Carcinoma, Hydronephrosis
- Rare: Vasculitis, SlE, Polyarteritis nodosa, AF (Microemboli in kidneys)
3. History
4. Physical examination
- Flank Pain Pyelonephritis, Stones, GN
- Skin lesions Vasculitis
Dysuria
Urethral discharge
Weight loss Tumor
Fever
Nocturia BPH, Cystitis, Pyelonephritis
In women, menstrual history is important (blood from vagina is not
uncommon)
Others
- Recent Streptococcal infection Post-streptococcal GN
- Painless hematuria bladder cancer
- History of stones
- Heavy exercise
- Medications
- Fx: Alport syndrome, IgA nephropathy
4. What investigations would you organize?
- Urinalysis
- Urine protein to creatinine ratio
- Microscopy (morphology of the RBC, dysmorphic from glomerular
diseases) and culture
- Blood: FBC, U&E, Coagulations
- US of urinary tract + kidneys
- PSA if the patient complain of back pain, weight loss, erectile dysfunction
Others Usually if patient >50 years and no clear cause found
- Cytoscopy
- CT Scan
- Biopsy
If after all still not clear follow-up every 6 months
6. What can make the urine red in color? Apart from hematuria.
- Beetroot
- Rifampicin
Abdo tenderness/Mass
Urethral discharge
Suprapubic tenderness cystitis
Enlarged prostate BPH
Tender prostate Prostatitis
5. What symptoms would you ask?

- Symptoms of DDx
- Ask back pain, abdominal pain, dysuria, fever, N+V
7. When will you urgently refer the patients?

Possible Prostate Cancer
- Hard, irregular prostate prostate carcinoma
- Rising PSA
Possible Bladder and Renal Cancer
- Any age with painless macroscopic hematuria
- >40 with recurrent UTI
- >50 with unexplained microscopic hematuria
- Abdominal mass
Lab-L2-Proteinuria
You are a GP. 25 years old male comes in for a routine test. On urinalysis, the protein was noted to be ++.
1. He asks you what are the possible causes the +?
2. What is you next step? What would you do?
Functional Proteinuria
- History - Exercise, Sick, Hx of UTI, renal disease, drugs, sore throat, Px of
- Acute illness E.g. UTI
DM, HTN, Fx of kidney disease, autoimmune disease
- Exercise
- Physical examination Look for nephrotic syndrome, HF, HTN, uremia,
- Orthostatic proteinuria: Protein not found in the morning, uncommon in
enlarged kidneys
patients >30 years of age (orthostatic proteinuria can occur in some
Investigations
glomerular diseases)
- Simplest method is to collect an urine sample in the morning, send the
Overloaded Proteinuria
urine to lab to note the ratio of protein to creatinine (rather than a 24
- Hemolysis
hours urine collection)
- Rhabdomyolysis
- Use morning sample to rule out orthostatic proteinuria
- Bence Jones protein associated with MM
Also
- Glomerular diseases
- Acute tubular necrosis
- O&G: Pre-eclampsia
3. The protein : creatinine ratio 100 mg/ml (normal <35) confirmed
4. If the urinalysis from the beginning indicates protein of + (instead of ++),
proteinuria. What would you do?
would you do things differently?
- Refer to a nephrologist
- Usually + is insignificant if the patient has no remarkable medical history
- If referring, consider initiating renal tract US, immunology (serum and
- You may repeat the urinalysis 1-2 weeks instead of doing the
urine electrophoresis, ANA, ANCA, Complements), hepatitis B and C
protein/creatinine ratio
serology
Case 2: This diabetic patient has persistent proteinuria. What medications are used in the management of persistent proteinuria?
Case 3: You are a GP. This 45 years female was diagnosed with focal segmental GS at the age of 35. Chatting with her you found out that she has a 14 years old
son who is completely healthy.
Case 2: Medications
For case 3, will you do anything to his son?
- ACEI
- Yes, yearly urinalysis
- ACERB
- Renal diseases, most of the time are asymptomatic (a bit too late when
- Spironolactone
the symptoms appear)
Lab-L2-Thrombocytopenia
25 years old female presented to you (GP) for a general check up. She noticed that her gym bleed every time she brushes. You did a FBC and her platelet is
low.
1. She asks you the possible causes.
2. What would you do?
- Decreased Production: Vitamin B12 or folic acid deficiency, Leukemia,
- History (Spontaneous bruises, Nose bleeds, Menorrhagia, Medications,
Decreased thrombopoietin in liver failure, Uremia, Dengue, Alport
Weight loss)
syndrome
- Physical Examination (examine for splenomegaly)
- Investigations
- Increased Destruction: ITP, TTP, HUS, DIC, Anti-phospholipid syndrome,
Lupus
- Medications: Heparin, Valproic acid, Methotrexate
3. Investigations in Primary Care
4. Referral to a hematologist.
- FBC, Request blood film
- Platelet count 100 in a well patient non-urgent referral
- Renal function
- LFT
- Viral serology (EBV, hepatitis screen), consider HIV
- ANA, ANCA E.g. Lupus
- B12, Folate
- Immunoglobulin To exclude common variable immunodeficiency
- Clotting studies (related to liver function)
- For anti-phospholipid anti-cardiolipin antibodies, Lupus anticoagulant
Lab-L3-Hepatitis B
1
2
It sounds confusing, but it is not!!!
- Step 1: Indentify IgM = Acute infection
- Step 2: Indentify IgG = Chronic Infection or Recovered
- Step 3: Indentify Surface antigen (+ ve = chronic infection, -ve = Recovered)
- Step 4: Check vaccination = +ve for the antibody for surface antigen (-ve
for core)
50-100 fairly urgent referral

<50 urgent referral
3
4
5
In a Hepatitis B report, there are 5 things they measure
- Hepatitis B surface antigen HBsAg
- Antibody to the surface antigen Anti-HBs / HBsAb
- Hepatitis B core antigen HBeAg (e = extracellular form)
- IgM to core antigen Anti-HBc IgM / HBc IgM
- IgG to core antigen Anti-HBc IgG / HBC IgG
in acute illness: +ve for hepatitis surface antigen, +ve IgM for the core
In chronic illness: +ve for hepatitis surface antigen, +ve IgG for the core
In vaccination: +ve for the antibody for surface antigen (-ve for core)
In recovered person: +ve for the antibody for surface antigen, and IgG for
the core
Case 2 4
- All +ve IgG = Chronic infection or infection in the past
- Case 2: -ve for HBsAg Recovered
- Case 3 + 4: Both +ve for HBsAg both chronic infection
-
Case 1
- Since +ve for IgM acute infection
Case 5
- Vaccination = +ve for the antibody for surface antigen (-ve for core)
2. How would you manage a patient with acute hepatitis B?
- Case 3 = Anti-HBe ve chronic infection

- Case 4 = Anti-HBe +ve chronic infection
1. How is hepatitis B transmitted?
- Body fluids
3. This patient with acute hepatitis B wonders if he will develop chronic
hepatitis B and what treatment if available if this happens?
Chronic infection 2-10% adults
- +ve hepatitis surface antigen for longer than 6 months, also +ve IgG for
core
Chronic Hepatitis B
- Antiviral E.g. Entecavir, once daily for 12 months
- Cessation of oral therapy may result in severe flare of hepatitis, which
can occasionally be fatal
Resistance
- Consider Lamivudine, Tenofovir
5. How to prevent hepatitis B?
- Vaccination
In 95% of healthy people, immune system will clear hepatitis B

recovery
- No antivirals required in most of patients
- Rarely, 1% will develop fulminant hepatic failure antiviral +
transplantation
Otherwise
- Supportive treatment only
- Recheck IgG and surface antigen after 6 months for detection of chronic
hepatitis B
4. What would happen if the patient resist on treatment of chronic hepatitis B?
- Warn the patient this risk of development or cirrhosis and hepatocellular
cancer
Hepatitis A
- Causes acute viral hepatitis
- Does not lead to chronic hepatitis
- Most caused by exposure to contaminated food or water
- Vaccination or previous exposure gives long term immunity
- Time from exposure to acute hepatitis A about 30 days (range from 15-50)
- Symptoms: Jaundice, Anorexia, Nausea, Vomiting, Abdominal pain, Mild
fever
- Diagnosis: Anti-Hep A IgM antibody during acute illness
- Jaundice recovers after an average of 6 weeks
- Adults and adolescents with acute hepatitis A are more likely to develop
severe hepatitis or fulminant hepatitis
- Occasionally, a cholestatic form of hepatitis A with prolonged pruritis a
short course corticosteroid may help seek expert advice
Hepatitis C
Acute Hepatitis
Chronic Hepatitis C
- Not all patients with acute hepatitis C need antiviral treatment
- Acute infection 20-40%, chronic infection 60-80%
- 55% of symptomatic patients clear the virus
- 5-20% with chronic infection progress to cirrhosis
- Early treatment with Peg-Interferon alfa may lead to resolution and
- +ve antibody to Hep C, and + ve for Hep C RNA
prevent progression to chronic infection
Management
- Diagnosis: Detection of serum hepatitis C virus
- No alcohol
-
Hepatitis D
It requires the present of hepatitis B surface antigen to be infectious
Vaccination against Hep A and B

Long Term Peg-Interferon + antiviral E.g. Ribavirin
Hepatitis E
The infection often resolves spontaneously
In older patients, risk of fulminant hepatic failure
Neuro-L1-Acute Confusion/Delirium
This 78 years old female was brought into ED after noted by the staff at the nursing home of being confused and disorientated.
- Please take a history from her carer.
- Outline your DDx and investigations to the carer.
- You will then be given investigations result and you are required to explain to her the result and the management.
1. What are the causes of acute confusion?
2. What is delirium?
I Watch Death
- Impairment of cognitive function, not progressive, reversible
- Infection: UTI
- Often worse at night
- Withdrawal
- Disorders of attention, perception, thinking, memory, psychomotor
- Acute metabolic: Metabolic acidosis, Hyperosmolar hyperglycemic state,
behaviours
Hypoglycemia
- Delirium can be hyperactive or hypoactive
- Trauma
- Sometimes difficult to tell from dementia as some may have both
- CNS Pathology
conditions
- Hypoxia
- Deficiency: Vitamin B12, Thiamine deficiency
- Endocrine causes: Thyroid storm
- Acute vascular: Stroke
- Toxins
- Constipation can be a cause in elderly
History
3. What are the risk factors for delirium?
Confusion
- Age 65 or over
- Onset, Triggering factors
- Past or present cognitive impairment
- Changes in conscious level? Progressively worse? Worse at night?
- Current hip fracture
- Head trauma?
- Severe illness
- Symptoms?
- Premorbidity Important in elderly E.g. Walking aid? Incontinence?
Px
- First time?
- Px medical conditions E.g. MI, Stroke
- Medications
- Recent hospitalization?
- Allergies
Fx
Social
- Smoking
- Alcohol
4. Outline investigations.
- CXR: Pneumonia, Heart failure
- ECG: MI, Arrhythmias
- FBC: Anemia, WBC for infection
- U&E: Hydration state, Renal function, Electrolyte imbalances
- Blood Glucose: Hypoglycemia
- Urinalysis
- Cultures: Blood if febrile, Sputum if available, Urine as a routine
- Consider blood gases
- Others: Vitamin B12, Thyroid, ESR (vasculitis), CT scan
Neuro-L1-Chronic Confusion/Dementia
This 78 years old female is confusesd.
1. What are the causes of dementia?
- Degenerative: Alzheimers disease, Vascular dementia, Lewy body, Picks
disease
- Infection: HIV, Syphilis, Whipples disease
- Inflammation: Vasculitis, SLE, MS, Sarcoidosis
- Trauma: Head injury, Intracranial hemorrhage
- Tumor: Brain tumor, Metastases
- Toxic: Alcohol, Lead
- Metabolic: Vitamin B12, Myxoedema (hypothyroidism), Hypoglycemia
- Inherited: Huntingtons, Wilsons disease
Screening Tests for Dementia
MMSE
- 21-24 points mild impairment
- 10-20 moderate
- <9 severe
IQCODE
- Questionnaire
- Memory (family, fds, occupation), Learning, Decision making, Problem
solving
- 16 questions
Clocking Drawing Test
- Score of 6
- Draw a clock, put in numbers, set the hands at ten past eleven
4. What is Alzheimers disease?
5. How to manage her?

Initial Management
- Identify and treat possible causes
- Effective communication and reorientation
Distressed People
- If the patient is consider a risk to the other consider giving short time
(<1 week) haloperidol or Olanzapine
- If patient is anxious Midazolam, Diazepam
- Use with caution, not in people with Parkinson or dementia
2. What are the clinical features?

- Memory loss
- Language impairment
- Disorientation
- Changes in personality
- Difficulty in carrying out activities
- Psy: Apathy, Depression, Psychosis
- Aggression, Sleep disturbances, Disinhibited sexual behaviors
- Head turning signs look at caere for an answer
3. What investigations to order?
- FBC, ESR, CRP, U&E, Ca++, LFT Coagulation - Albumin, TSH,
Autoantibodies, B12/folate
- CT/MRI
- Syphilis serology
- EEG
- CSF
- HIV
- PET scan
5. What is Parkinsons disease?
Background
- Progressive degenerative diseases, causing 50% of the dementia
- Histological changes of neurofibrillary tangles and senile plagues
- Diagnosis requires confirmation at post-mortem
Clinical Features
- Initial memory loss
- Language and visuospatial changes
- Later snout, sucking, rooting, grasp reflexes appear
Diagnosis
- According to DSM IV criteria
- 1. Memory impairment
- 2. Aphasia, Apraxia, Agnosia, Executive dysfunction
Investigations
- FBC, U&E, Clotting, LFT, Glucose, B12, TFT, ESR, CXR, ECG, Urinalysis
- CT/MRI
- HIV, Syphilis
Management - Drugs
- Cholinesterase Inhibitor E.g. Donepezil, Rivastigmine, Galantamine
- Memantine in moderate to severe Alzheimers disease
Management Non-Drugs
- Avoid alcohol
- Social and community support Multidisciplinary approach
- Exercise
Prognosis
- The mean life expectancy following diagnosis is about 7 years
- <3% of people live more than 14 years
- Death is most commonly due to bronchopneumonia
Background
- Second most common neurodegenerative disease
- Degeneration of dopaminergic neurons in the substantia nigra
Features
- Signs: Hypokinesia, Bradykinesia, Rigidity, Rest tremor
- Others: Slurred speech, Small handwriting, Lack of facial expression,
Shuffling gait
- A degree of cognitive impairment
DDx
- Alzheimers diseases
- Multiple cerebral infarction
- Drug induced Parkinsonism E.g. Metoclopramide
Diagnosis
- Generally base on history and physical examination
- CT/MRI
Management Medications
- No functional impairment does not require medications
- Initial choice depends on the age, occupation, economic situation
- Levodopa: Most effective, but if long term motor fluctuation and drug
induced dyskinesia
- Dopamine Agonist: May be used as monotherapy in early Parkinsons
disease, Possible SE of pathological shopping, eating, gambling, hypersexuality
Surgery
- Deep brain stimulation of the subthalamic nuclei or internal segment of
the globus pallidus
- Indications: Intolerant of higher dose of dopaminergic drugs or motor
complications uncontrolled by medications
Neuro-L1-Syncope/Collapse
This patient presemted with a sudden loss of concisousness and is a bit confused now.
DDx
History
- Syncope: Cough, Micturition, Vasovagal, Emotion
- I would like to know what happen before, during and after your collapse.
- Cardio: Stroke, MI, Carotid stenosis, Arrhythmias
Before: What were you doing when this happen?
- Hypotension E.g. Postural hypotension
- Postural Hypo: Standing from sitting?
- Neurological: Epilepsy, Neoplasm, Vertigo, Peripheral polyneuropathy,
- Syncope: Were you coughing? Were you in any emotional distress?
Previous head injury
- Hypoglycemia: Any warning signs? For example, blurred vision? Any
- Geriatric: Alzheimers, Parkinsons, Loss of balance, Vision? Falls? Home
vertigo?
environment?
- Head Injury
- Endo: Hypoglycemia, Alcohol
Medications: Benzo, Beta-blockers
Geriatrics: Loss of balance? Do you use any walking aid? Weakness of the
arms?
- Alcohol
- Also: Is this your first time? How many times in past 1 month?
During the attack: Do you know what happened during the attack?
- Did you lose your consciousness?
- How long did you lose you consciousness?
- Any bystander? Any jerky movement?
After the attack
Px
How long did it take for you to get up?

Did you injury yourself?
Were you confused?
Any urine leakage?
Did you bite your tongue
Heart conditions? (Aortic stenosis, Arrhythmias) Cholesterol? (Risk of

carotid stenosis) History of stroke? (HTN?) DM? Head trauma? Epilepsy?
- Medications? (Benzo, Beta blocker) Allergies
Fx: Alzeimers? Parkinsons?
Social: Smoking, Exercise
DDx
General Inspection: Distress? Color? Assess consciousness level? Glasgow

coma scale?
Vitals: BP, temp., EE, PR
Overall, focus on cardiovascular and neurological examination
Hands: Any injury? Poor perfusion? Signs of dupuytrens or palmar
erythema alcohol related fall?
Arms: Take BP, examine for injury E.g. Bruises, Fracture, Test for power
(weakness in stroke)
Head: Check for injury, Tongue biting, Cranial nerves, check for vision,
Nystagmus
Chest: Heart sounds, Murmur? Aortic stenosis? Carotid bruit?
Urine leakage?
Investigations
-
Syncope: Cough, Micturition, Vasovagal, Emotion

Cardio: Stroke, MI, Carotid stenosis, Arrhythmias
Hypotension E.g. Postural hypotension
Syncope
Cardio: Aortic stenosis, carotid stenosis, stroke/Transient ischemic attack,
Arrhythmias
Epilepsy
Neurological: Epilepsy, Neoplasm, Vertigo, Peripheral polyneuropathy,

Previous head injury
- Geriatric: Alzheimers, Parkinsons, Loss of balance, Vision? Falls? Home
environment?
- Endo: Hypoglycemia, Alcohol
- Medications: Benzo, Beta-blockers
Neuro-L1-Headache
-
This patient present with headach.

DDx Vitamin D (Vascular, Infections, Trauma, Autoimmune,
DDx
Metabolic/Muscular, Inherited, Neoplastic, Drugs)

Primary
Acute Single Episode
- Migraine, Tension, Cluster

Secondary
- Meningitis, Encephalitis
- Subarachnoid hemorrhage
- Head injury
- Venous sinus thrombosis (with papilloedema)
- Sinusitis
- Acute glaucoma
Recurrent Acute Attacks
Vascular: Hemorrhage, Stroke, Severe hypertension

Infections: Meningitis, Sinusitis, Abscess
Trauma
Autoimmune: Giant cell arteritis
Muscular: Neck pathology, Dental or temporomadibular joint
dysfunction
- Neoplastic: Intracranial masses E.g. Primary tumors, Metastasis
- Medications: Beta-blockers, Sildenafil
- Pschy
Facial Pain
-
Neurological: Giant cell arteritis, Neuralgia (Trigeminal neuralgia,

Glossopharyngeal neuralgia), Migraine
- Local Causes: Trauma, Sinusitis, Dental disease, Temporomandibular
joint dysfunction, Nasopharyngeal tumors, Referred cardiac pain
Alarm Symptoms
-
Visual Loss Acute angle-closure glaucoma

Loss of Balance Stroke, Tumor
Confusion Meningitis
Seizures Stroke, Encephalitis, Tumor
LOW
Thunderclap Headache Subarachnoid hemorrhage, Cluster headache
New onset after age of 50
Diplopia
Aphasia
- Migraine
- Cluster headache
- Trigeminal neuralgia
- Giant cell arteritis
Chronic Headache
-
Tension
Raised intracranial pressure
Medication
History
-
When: When did it start?

Location: On one side?
Constant? How long does it last for? How often?
How bad? On a pain scale 1-10?
Describe the pain? Dull? Sharp? Pin and needles?
Anything make it worse or better?
How does it affect sleep or appetite?
Wake up at night? Have it in the morning?
Night sweats? Loss of weight?
Neck stiffness Meningitis
Head Injury?
Associated Symptoms: Visual disturbances? Loss of balance? Weakness of
body? Numbness? Neck stiffness? Fever? Nausea? Photophobia?
Seizures?
Investigations
- BP
- Temporal artery tenderness
- Ophthalmologic: Papilloedema, Glaucoma
- Cranial
- Upper and lower neurological for focal lesions
- Cerebellar signs in elevated ICP
Tension
Features
Feature Pound
- Dull
- Band like
- Worse at the end of the day
- Bilateral
Management
- Pulsatile, Photophobia, Phonophobia

- Hours: 4-72 hours
- Unilateral
- Nausea, Vomiting
- Disabling
Management
Often respond to paracetamol, aspirin, NSAIDs
Cluster
Features
- Unilateral
- Retro-orbital
- Sharp
- Awakening
- Associate with lacrimation and nasal congestion
- Often restless and agitated
Management
-
Unique response to high flow oxygen

Triptans can also be effective
Prevention: Verapamil
Hemorrhage Subarachnoid Hemorrhage
If neurological findings, papilledema, alarming symptoms, cluster

headaches CT, MRI
ESR, CRP may be elevated in temporal arteritis
A LP to diagnose meningitis
Migraine
- Mild to moderate: Aspirin, Paracetamol

- Severe: Triptans
- Metoclopromide/Prochlorperazine for nausea
- Prevention: Propanolol, Amitriptyline
Venous Sinus thrombosis
-
Most commonly sagittal sinus thrombosis or transverse sinus thrombosis

Symptoms come over gradually over days or weeks
Thrombosis may extend into cortical veins and cause infarction
Sagittal Sinus: Headache, Vomiting, Seizures, Decrease vision,
Papilloedema
- Transverse Sinus: Headache, Focal CNS signs, Seizures
- Sigmoid Sinus:
- Inferior Petrosal Sinus:
- Cavernous Sinus:
- Management: Heparin improves outcomes, Fibrinolytics, Thrombophilia
screen (FBC, PT, APTT, Protein S/C, Antithrombin, Lupus anticoagulants)
and ENT review helps to identify the cause
Subdural Hemorrhage
Spontaneous bleeding into the subarachnoid space

Typical Age: 36-65
Causes: Rupture of a saccular aneurysm (80%), AVM arterio-venous
malformation (15%), 5% no causes found
Berry Aneurysm: Common sites in junctions of the communicating
branches, associated with polycystic kidneys, coarctation, Ehlers-Danlos
syndrome
Symptoms: Devastating occipital headache, Vomiting, Collapse, Seizures,
Coma may follow and last for few days
Signs: Neck stiffness, Kernigs sign (develop in 6 hours, resistance to knee
extension when hip is flxed), Retinal hemorrhage
DDx: Cluster, No causes, Meningitis, Intra-cerebral bleeds
Investigations: CT, LP if CT ve
Management: Refer to a neurosurgeon immediately, Maintain cerebral
perfusion by keeping the SBP >160mmHg, Ca++ blocker (to prevention
ischemic neurological deficits following subarachnoid hemorrahge),
Endovascular coiling is preferable to surgical clipping, CT angiography
before intervention to identify multiple aneurysms
Complications: Re-bleeding, Cerebral ischemia, Hydrocephalus (due to
blockage of arachnoid granulation), Hypo-natremia (manage with fluid
restriction)
Hematoma between the dura and arachnoid

Gradually increases in the ICP, Shifting mid-line structures away from the
clot, if untreated eventually herniation and coning
Most are caused by trauma, but is often forgotten as it was so minor or
long ago (up to 9 months)
May also occur without trauma E.g. Decreased ICP, Dural metastases
Symptoms: Fluctuating consciousness (35%), Physical or intellectual
slowing, Sleepiness, Headache, Personality changes
Imaging: CT shows clot, Midline shift, Crescent shaped hematoma
(differentiate from epidural hemorrhage)
DDx: Stroke, Dementia, CNS masses
Treatments: 1st line Drill or burr hole craniostomy, 2nd line Craniostomy
Extradural Hemorrhage
Stroke
Suspect if after head injury conscious level falls or is slow to improve, or

there is a lucid interval (temporary improvement in a patients condition
after a traumatic brain injury, and is indicative of an epidural hematoma)
- Causes: Often due to a fractured temporal or parietal bone causing the
laceration of the middle meningeal artery and vein
- Symptoms and Signs: Deteriorating consciousness, Lucid interval can last
for few hours or days, then decreased in GCS, severe headache, vomiting,
confusion, fits, hemiparesis, coma, dilated pupils, limb weakness, Deaths
following coma is usually due to respiratory arrest
- Tests: CT, Lens-shaped, Skull XR may show fracture, LP is contraindicated
- Management: Transfer to a neurosurgical unit for clot evacuation +/ligation of the blood vessels
- Prognosis: Excellent if diagnosed and operated early
Neuro-L1-Seizures/Epilepsy
Someone came in with 3 episodes of seizires in 1 week.
1. What are the causes of recurrent seizures?
Metabolic
- Withdrawal from alcohol or drugs, also uremia/hypo-hyperglycemia
CNS Pathology
- Trauma: Posttraumatic epilepsy, generally manifest within 2 years after
injury, but seizure within the first week of injury does not mean future
attacks will occur
- Tumors: Considered in all patients >30 with new seizure onset
- Vascular Diseases: More in patients >60, E.g. Infarction, hemorrhage,
aneurysm
- Degenerative: Alzheimer disease
- Infectious: Meningitis, Encephalitis, Sepsis
2. What are the DDx of seizures?

DDx of Focal Seizures
- Transient ischemic attack Longer duration, level of consciousness
unaltered, loss of sensory or motor function, Symptoms E.g. Convulsive
jerking or paresthesias
- Panic attack Evidence of anxiety
DDx of Generalized Seizures
- Syncope E.g. Postural changes, emotional stress, pain, straining,
typically preceded by pallor, sweating, nausea, malaise, recovers occurs
rapidly, there is no postical confusion
3. What are the types of seizures?

Focal Seizures
- Involved a part of the brain, with or without impairment of consciousness
Generalized Seizures
- Absence seizures: Consciousness impaired briefly, patients often unaware
of the attack
- Myoclonic: single or multiple jerks
- Tonic-clonic: Tonic = sudden loss of consciousness with rigidity and arrest
of respiration, Clonic = Jerking, may followed by flaccid coma
- Rule out CNS and metabolic causes
- EEG but should not be used in isolation to make a diagnosis of epilepsy
- CT/MRI
- Blood: FBC, U&E
- ECG E.g. Cerebral hypoperfusion
7. It turns out to be epilepsy. What is your management?
Lifestyles
- Avoid triggers E.g. Sleep deprivation, excess alcohol, stress
- Abrupt discontinuation of antiepileptics can provoke status epilepticus
- Avoid swimming, bathing alone, climbing, operating machine
Medications Usually start by neurologist
- Generalized seizures: Sodium valproate, then Lamotrigine
- Focal seizures: Carbamazepine, thenso many 2nd line
- Tonic-clonic seizure where generalized or focal onset is unclear: Sodium
valporate
Neuro-L1-Weakness/Paralysis
Cardiac Diseases Cerebral hypoperfusion due to a disturbance of cardiac

rhythm should be suspected in patients well known for cardiac or
vascular disease, repeat Holter monitoring may be necessary
- Brain stem ischemia
- Psychological
4. What are the signs and symptoms that may associate with seizure?
- Headache, mood alterations, lethargy in some patients hours before
seizure occurs
- But in most patients, seizures occurs unpredictably
- In few patients, seizures can be triggered by flashing light or flickering tv
6. What is your management if the investigations are all normal?

- 50% of patients experiencing their first seizure will never have another
seizure no treatment
This 67 years old man with long standing history of HTN and DM presented to ED with sudden onset weakness.
- Please take a history
- What would you look for on examination
- Outline DDx, investigation, management
1. What are the possible causes of muscle weakness?
2. How to tell if this is a nerve or muscle problem?
- CNS diseases affecting upper or lower motor neurons from peripheral
- Always history, physical examination and investigations
nerves to root or plexus
Upper Motor Neuron
- Also disorders of the neuromuscular transmissions E.g. Myasthenia gravis
Also primary disorders of muscles
History
Presenting Compliant
- Onset E.g. Acute onset in TIA and stroke, Chronic in MG and muscular
dystrophy
- Triggering factors?? Trauma cranial hemorrhage
Transient Ischemic Attack
1. What are the causes of transient ischemic attack?
Important Cause = Embolization
- Artheroscleotic changes in carotid bifurcation
- Cardiac Causes: AF, Rheumatic heart disease, Mitral valve disease, IE,
Mural thrombus complicating MI
- Also consider patient foramen ovale
Less Common Cause = Abnormal blood vessels
- Giant cell arteritis, SLE, Polyarteritis
Subclavian Steal Syndrome (see http://www.ultrasoundpaedia.com/normalcarotids)
- Proximal stenosis/occlusion of the subclavian artery
Caused by lesion anywhere from the frontal cortex, through the internal
capsule, brain stem and spinal cord to the anterior horn cells
- Affect muscle groups
- Characteristics: Increased tone, Increased reflexes (plantars are upgoing
= Babinski sign)
- UMN lesion can mimic LMN lesion in the first few hours before the
increased tone and hyperreflexia develops
Lower Motor Neuron
- Caused by lesion from anterior horn cells, nerve roots, plexi to the
peripheral nerves
- Affect muscle supplied by the nerves
- Characteristics: Muscle wasting, Hyporeflexia, Decreased tone,
Fasciculations
Neuromuscular Transmission Problems
- Patchy in distribution
- Often fluctuates
- No sensory change
Myopathic Disorders
- Marked proximally in limbs
- No sensory disturbance
- No muscle wasting or loss of tendon reflexes, at least not until an
advanced stage
-
2. What are the symptoms and signs?

- Symptoms in a given individual tend to be constant in type
- Onset is abrupt without warning, recovery usually occurs rapidly within a
few minutes
Obstruction of Carotid Circulation
- Occlusion of the Ophthalmic Artery Symptomless or amaurosis fugax
- Middle Cerebral Artery Occlusion Contralateral hemiplegia,
hemisensory loss, homonymous hemianopia, eyes deviated to the
affected side, if dominant hemisphere is involved -> aphasia, if
hemisphere swelling -> drowsiness, stupor and coma
May lead to transient vertebrobasilar ischemia

Signs: A bruit in the supraclavicular fossa, Unequal radial pulses, a
difference of 20mmHg between the systolic BP in the arms
3. What is the risk of having a stroke?

- Some patient will have a major stroke after a few attacks, after have
frequent attacks for weeks or months without having a stroke
- The risk of stroke is high in the first 3 months, particularly in the first
month within the first 48 hours
Obstruction of Anterior Cerebral Artery Usually well tolerated due to

the collateral supply from the other side
- Obstruction of the Anterior Communicating Artery weakness and
cortical sensory loss in the contralateral leg, sometimes mild weakness of
the arm especially proximally, there may be a contralateral grasp reflex,
Also behavioral changes and memory disturbances if bilateral anterior
infarction
Obstruction of the Verterbrobasilar Circulation
- Posterior Cerebral Artery A thalamic syndrome -> contralateral
hemisensory disturbance, developed by the development of pain and
hyperpathia (higher level of pain), Usually a macular-sparing
homonymous hemianopia, sometimes involuntary movements and alexia
- Vertebral Artery Occlusion If distal usually clinically silent due to the
collateral circulation
- Occlusion of both vertebral arteries or Basilar artery Pinpoint pupils,
flaccid quadriplegia and sensory, variable cranial nerve abnormalities
- Posterior Inferior Cerebellar Artery Ipisilateral sensory loss of the face
and cranial nerve 9 and 10, limb ataxia, numbness and Horner syndrome,
contralateral sensory loss of limbs
- Any major Cerebellar Arteries Vertigo, N+V, Nystagmus, Ipsilateral
limb ataxia, contralateral sensory loss in limbs
- If superior cerebellar artery is involved contralateral sensory loss also
involves the face
- If anterior inferior cerebellar artery is involved ipsilateral sensory loss
involves the face
4. What is the management of a TIA?
- Hospitalization for patients seen in 72 hours of the attack, when they are
at risk of recurrence
- Assess risk of recurrence ABCD2 score
- A: Age >60
- B: BP >140/90
- C: Clinical symptoms of focal weakness
- D: Duration >10mins
- D: DM
- 3 or more hospital admission
- Carotid endarterectomy, reduces the risk of stroke when TIA <1 month
(for stenosis >50%)
- If poor operative candidates medical management, aim at the
prevention of further attacks and stroke E.g. Control BP and DM, Statin
Non-Cardioembolic Attack
-
1st line Aspirin 81 mg daily orally, significantly reduces the frequency of

TIA
- 1.5 line Aspirin + Dipyridamole
- 2nd line Clopidogrel (Usually not combine with Aspirin)
Embolization from the heart
- Warfarin if AF, can consider Dabigatran (direct thrombin inhibitor)
-
Stroke
1. What is the differences between a TIA and a stroke?
TIA
- Within 24 hours
- Symptoms similar to a stroke, but usually last only about few minutes to
an hour
- Symptoms able to resolve itself within 24 hours
- In stroke, there is a more distinctive neurological signs reflecting the
region of brain affected

Obstruction of Carotid Circulation
- Occlusion of the Ophthalmic Artery Symptomless or amaurosis fugax
- Middle Cerebral Artery Occlusion Contralateral hemiplegia,
hemisensory loss, homonymous hemianopia, eyes deviated to the
affected side, if dominant hemisphere is involved -> aphasia, if
hemisphere swelling -> drowsiness, stupor and coma
- Obstruction of Anterior Cerebral Artery Usually well tolerated due to
the collateral supply from the other side
- Obstruction of the Anterior Communicating Artery weakness and
cortical sensory loss in the contralateral leg, sometimes mild weakness of
the arm especially proximally, there may be a contralateral grasp reflex,
Also behavioral changes and memory disturbances if bilateral anterior
infarction
Obstruction of the Verterbrobasilar Circulation
- Posterior Cerebral Artery A thalamic syndrome -> contralateral
hemisensory disturbance, developed by the development of pain and
hyperpathia (higher level of pain), Usually a macular-sparing
homonymous hemianopia, sometimes involuntary movements and alexia
2. What is lacunar infarction?

- Small lesions (usually <5mm) that occur in the short penetrating
arterioles in the basal ganglia, pons, cerebellum, internal capsule,
thalamus
- Associated with poorly controlled HTN, DM
- Clinical features depends on the location, but worsen over first 24-36
hours
- Associated Clinical Syndromes: Contralateral pure motor or pure sensory
deficit, Ipsilateral ataxia with crural paresis, Dysarthria with clumsiness of
the hand
- Diagnosis: By MRI scan
- Management: Aspirin, Risk factors control
- Prognosis is good, usually partial or complete resolution in 4-6 weeks
4. What is the management? From Fremantle Guidelines
Emergency Medical Staff
- Basic ABC
- Finger-prick glucose
- Non-contrast CT scan
- IV access
- Blood: FBC, U&E, Coagulation, group and hold, BSL blood sugar level
- ECG, CXR both not necessary prior to thrombolysis therapy
Thrombolysis Therapy CT to rule out hemorrhagic stroke
Alteplase, tissue plasminogen activator, given within 4.5 hours of
symptoms onset, increases likelihood of independence by 30%
- Major complications: Intracranial hemorrhage in 6%,
- Carefully select the patients according to the criteria
- Contraindications: Uncertain about the time of stroke, Coma, HTN,
Bleeding tendency
Antiplatelet Therapy CT to rule out hemorrhagic stroke
-
- Aspirin, start on the first day after CT

Neurosurgical Hemi-craniectomy
Vertebral Artery Occlusion If distal usually clinically silent due to the

collateral circulation
Occlusion of both vertebral arteries or Basilar artery Pinpoint pupils,
flaccid quadriplegia and sensory, variable cranial nerve abnormalities
Posterior Inferior Cerebellar Artery Ipisilateral sensory loss of the face
and cranial nerve 9 and 10, limb ataxia, numbness and Horner syndrome,
contralateral sensory loss of limbs
Any major Cerebellar Arteries Vertigo, N+V, Nystagmus, Ipsilateral limb
ataxia, contralateral sensory loss in limbs
If superior cerebellar artery is involved contralateral sensory loss also
involves the face
If anterior inferior cerebellar artery is involved ipsilateral sensory loss
involves the face
- Extensive hemispheric infarction cerebral edema

General Measures
-
Assess ability to swallow before giving oral medications, check for gag
reflex
- Blood pressure medications should be avoided in 48 hours, unless with
malignancy hypertension
- Oxygen if hypoxic
- Control glucose level
- Prevention of DVT Compression stocking
Preventing Further Events
Antiplatelet Therapy
- Aspirin
- Clopidogrel (more effective than Aspirin), it binds to platelet receptor
Anticoagulants
- Warfarin, used if patient has AF, maintain INR 2-3
Blood Pressure
Cholesterol
-
Management of Carotid Stenosis
Neuro-L1-Intracranial Hemorrhage
Intracranial Hemorrhage
Subarachnoid Hemorrhage
- Spontaneous bleeding into the subarachnoid space
- Typical Age: 36-65
- Causes: Rupture of a saccular aneurysm 80%, Arterio-venous
malformation 15%, 5% no causes found
- Berry aneurysm: Common sites in junctions of the communicating
branches, associated with polycystic kidneys, coarctation, Ehlers-Danlos
syndrome
- Symptoms: Devastating occipital headache, vomiting, collapse, seizures,
coma may follow and last for few days
- Signs: Neck stiffness, Kernigs sign (develop in 6 hours, resistance to
knee extension when hip is flexed), Retinal hemorrhage
- DDx: Meningitis, Cluster, Intra-cerebral bleeds (Stroke)
- Investigations: CT, LP if CT ve
Management:
- Refer to a neurosurgeon immediately,
- Maintain cerebral perfusion by keeping the SBP >160mmHg
- Ca++ to prevent ischemic neurological deficits followings subarachnoid
hemorrhage
- CT angiography before intervention to identify multiple aneurysms
- Endovascular coiling is preferable to surgical clipping
- Complications: Re-bleeding, Cerebral ischemia, Hydrocephalus,
Hyponatremia
Subdural Hemorrhage
Hematoma between the dura and arachnoid

Causes: Most are caused by trauma, but is often forgotten as it was so
minor or long age (up to 9 months ago), Others causes = Dural
metastases, Decreased ICP
- Symptoms: Fluctuating consciousness 35%, Physical or intellectual
slowing, Sleepiness, Headache, Personality changes
- Gradually increases in ICP shifting mid-line structures away from the
clot, if
- Imaging: CT show clots, Midline shift, Crescent shaped hematoma
(differentiate from epidural hemorrahge)
- DDx: Stroke, Dementia, CNS masses
Treatment:
- 1st Line: Drill or burr hole craniostomy
- 2nd Line: Craniostomy
Extradural Hemorrhage
- Causes: Laceration of the middle meningeal artery and vein secondary
tp fractured temporal or parietal bone
- Symptoms and Signs: Deteriorating consciousness, Lucid interval can
last for few hours or days, then decreased in GCS, severe headache,
vomiting, confusion, fits, hemiparesis, coma, dilated pupils, limb
weakness, death due to respiratory arrest
- Investigations: CT, Lens shaped, Skull XR may show fracture, LP is
contraindicated
- Management: Transfer to a neurosurgical unit for clot evacuation +/ligation of the blood vessels
- Prognosis: Excellent if diagnosed and operated early
Acute Subdural Hemorrhage
Epidural Hemorrahge
Subarachnoid Hemorrhage
Intracerebral Hemorrhage
Acute on chronic subdural hemorrahge

Neuro-L1-Facial Pain (can be a GP station)
1.
-
What are the causes of facial pain?

Trigeminal Neuralgia, Glossopharyngeal Neuralgia, Shingles
Temporomandibular joint
Giant cell arteritis
Sinusitis
Glaucoma
Dental causes
Facial migraine (migraine that affects below the level of eyes, often
attributed to sinus pathology, treatment same for migraine)
- Angina
- Atypical facial pain
-
History
-
Investigations
- Make sure there is no CNS pathology causing the neuralgia E.g. CT/MRI
2. What are the clinical features of trigeminal neuralgia?

- Facial pain commonly arise from one side of the mouth shoot towards
the ear, eye or nostril on the same side
- Attacks usually lasts less than a minute
- Severe pain
- The pain may be triggered by touch, movement, eating, cold air
- Many patients try to hold the face still while talking
- No other neurological deficits
- Spontaneous remissions for several months or longer may occur, but as
the condition progresses, attacks become more frequent and remissions
become shorter and shorter
- Symptoms remain confined to the distribution of the trigeminal nerve
- Prognosis poor
4. What is the management of trigeminal neuralgia? ATG
- Carbamazepine controlled release 100mg orally, monitor liver function
- If ineffective try Phenytoin
- Consider combination with Baclofen (muscle relaxant) or Lamotrigine
- Also consider Gabapentin
Surgery Not in patients with MS
- Despite normal CT or MRI, surgical posterior fossa exploration frequently
revealed some structural cause of neuralgia, decompression and
separation of the abnormal vessels from the nerve root produces lasting
relief
- Others: Radiosurgery to the trigeminal root, side effect of facial
paresthesia (but better than pain)
6. What is glossopharyngeal neulragia?
- Uncommon
- Pain occurs in the throat, about the tonsillar fossa, sometimes deep in the
eat and at the back of the tongue
- MS is sometimes responsible
- Treatment similar to trigeminal neuralgia
8. What are some clinical features of MS?
- Patient presents with more than one episode of neurological dysfunction,
and affects different parts of the CNS
- Features: Optic neuritis, Bladder, Impotence, Sensory deficits, UMN
deficit, Cerebellar damage (Ataxia, Dysarthria, Nystagmus), Vertigo,
Dementia in latter stages
- The symptoms are slowing progressing
3.
-
What causes trigeminal neuralgia?

Most cases idiopathic
MS Multiple sclerosis (especially in young patients E.g. <40)
Vascular compression
5.
-
What is atypical facial pain?

Facial pain without the typical features of trigeminal neuralgia
Generally constant, often burning sensation
Many of them are depressed
Try Amitriptyline 10mg orally
Then Carbamazepine, Phenytoin, Opioids
7.
-
If you are a GP, when will you refer the patient?

Worsening pain unresponsive to simple measures
Continuing pain of uncertain cause
Consideration of surgical treatment
Investigations
- MRI Showing plaques
- CFS Slightly raised protein, 70% with raised IgG, Pleocytosis
- Visual evoked potential
Cardio-L1-Hypotension
1. Define hypotension.
- Systolic < 90
- Diastolic < 60
3. What are the causes of acute hypotension/shock?

- Hypovolemic E.g. Vomiting, Diarrhea, Diabetes insipidus, Blood loss
- Cardiogenic E.g. MI, Arrhythmias, Myocarditis, HF, Valvular problems
- Obstructive E.g. Cardiac tamponade, Constrictive pericarditis, Tension
pneumothorax, Aortic stenosis
- Distributive E.g. Septic shock, Anaphylactic shock
- Endocrine E.g. Addisons disease, Thyroid problems
5. How to define postural hypotension?

- A drop in the systolic BP >20mmHg upon standing
- Usually the patient will complain of blackouts, dizzy turns
- Should be investigated
2. What are the causes of chronic hypotension?

- Cardiovascular Diseases: Arrhythmias, Outflow obstruction, Myocardial
diseases
- Diuretics
- Diabetes insipidus
- Addison disease
- End-stage malignant diseases
- Autonomic neuropathy (postural hypotension) E.g. Secondary to DM,
Alcohol, MS, Parkinson
4. Management of acute hypotension/shock
- ABC
- Oxygen
- Lie the patient head down, Elevation of legs
- Obtain IV access
- Fluid resuscitation (Give 20ml/kg sodium chloride 0.9% until BP stabilize
around 90/60mmHg, Give it as fast as possible)
- If BP is nil, give 1mg of adrenaline
- Correct electrolyte + maintenance
- Cross match blood
Identify Causes
- ECG for arrhythmias
- Auscultation for tension pneumothorax
6. What are the causes of postural hypotension?
Venous Pooling of Blood
- Varicose veins
- Prolonged standing
Impaired Vasomotor Tone
- Diabetic autonomic neuropathy
- Shy Drager syndrome
Volume Depletion
Autonomic Neuropathy: DM, Alcohol, MS, Guillain Barre Syndrome, HIV,
Parkinson
7. Management
- History, Examination, Investigations
- Investigations: FBC, U&E, CRP, ESR, Glucose, TFT, LFT, Urinalysis, ECG
Cardio-L1-Secondary HTN
Medications: Diuretics, Anti-hypertensive, Abruption cessation of steroid

therapy
Endocrine: Addisons disease
-
This 25 years old man presented to you with HTN poorly controlled by an ACEI. Take a history, focusing on the causes of secondary HTN.
1. What is normal BP?
2. What are the causes of secondary HTN?
- Systolic <120
- Renal Causes leading to fluid retention E.g. Renal failure from GN, PKD,
- Diastolic <85
Systemic sclerosis, Diabetic nephropathy, Also renal artery stenosis
(hypoperfusion rennin-angiotensin system)
- Endocrine Causes: Cushings syndrome, Conns syndrome,
Phaeochromocytoma, Hyperparathyroidism
- Medications: Contraception, Corticosteroid, Antidepressants, NSAIDs
- Others: Coarctation, Pregnancy (Gestational HTN, Pre-eclampsia)
- Renal Function: Creatinine, Urea, GFR (for renal disease)
- So in the history: Focus on the causes E.g. Dysuria, Oliguria, History of
- ESR Can increase in polyarteritis nodosa, chronic pyelonephritis
autoimmune diseases, Fx of DM, Symptoms of Cushings syndrome
- Autoantibodies: ANA, ANCA (for systemic sclerosis)
- Renal artery stenosis Auscultation with a bruit, Captopril challenge
tests (considered +ve if renin level increased substantially), Angiography
- Hyperparathyroidism Ca++
- Cushings Syndrome: high level of cortisol in the blood, 70% caused by
adenoma of the pituitary gland high level of ACTH
- Conns Syndrome = Aldosterone producing adenoma, (Hypokalemia,
Aldosterone-renin ratio)
- Phaeochromocytoma (Often with headache, palpitation, sweating)
test urine and serum for free metadrenaline and normetadrenaline
Cardio-L1-Palpitation
General Considerations
Forceful, rapid or irregular beating of heart

Rate, duration and degree of regularity of heart beat
Age at first episode
Factors that precipitate or terminate episodes
Light-headedness or syncope
Neck pounding
Chest pain
Definition = Unpleasant awareness of forceful, rapid or irregular beating

of the heart
A common PC, usually benign
Occasionally the symptoms of life-threatening arrhythmias
54% of patients with supraventricular tachycardia were initially wrongly
diagnosed with panic, stress, anxiety disorder
Symptoms
Ask to tap out the rhythm

Palpitation that start and stop abruptly suggest supraventricular or
ventricular tachycardias
- Termination using vagal maneuvers (E.g. Valsalva maneuver) suggests
supraventricular tachycardia
3 Common Description
-
Flip-flopping (stop and start): Often caused by premature contraction of

the atrium or ventricle
- Fluttering in the chest: Regular fluttering Supraventricular or
ventricular arrhythmias, Irregular fluttering AF, Atrial flutter,
tachycardia with variable block
- Pounding in the neck: Often due to cannon A wave in the jugular venous
pulsation, that occurs when the right atrium contracts against a closed
tricuspid valve
- If associate with chest pain Ischemia heart disease, if relieved by
leaning forwards pericardial disease
- If associate with light-headedness, pre-syncope, syncope suggest
hypotension, may signify a life-threatening cardiac arrhythmias
- If occurs with exertion Hypertrophic cardiomyopathy, rate-dependent
bypass tract
- Weight loss may suggest hyperthyroidism
- Vomiting electrolyte disorders and hypovolemia
- Hyperventilation panic disorder
Diagnostic Studies
-
12 lead ECG and Holter monitor

Bradyarrhythmias and heart block can be associated with ventricular
ectopy or escape beats, may be experience as palpitation
Wolff-Parkinson-White syndrome is suggested by short PR interval and
delta wave
In patients with a prior MI, Holter monitoring is an appropriate next step
ECG exercise testing is appropriate in patients who have palpitation with
physical exertion and patients with suspected coronary artery disease
ECG Findings: Long QT syndrome, Bradycardia, 2nd or 3rd HB, Sustained
ventricular arrhythmias
Cardiovascular examination
Midsystolic click mitral valve prolapse, suggest supraventricular
arrhythmias
Murmur of hypertrophic cardiomyopathy Atrial fibrillation or
ventricular tachycardia
Dilated cardiomyopathy increases the likelihood of VT and AF
Look for signs of hyperthyroidism E.g. Tremulousness, brisk deep tendon
reflexes, fine hand tremor
DDX
Cardiac Arrhythmias
- Sinus bradycardia
- Sinus, supraventricular and ventricular tachycardia
- Premature atrial and ventricular contractions
- Sick sinus syndrome
- Advanced AV block
Non-Arrhythmic Cardiac Causes
-
Valvular heart disease E.g. Aortic stenosis, Atrial or ventricular septal

effect, cardiomyopathy, congenital heart disease, pericarditis
Non-Cardiac Causes
-
Fever, Dehydration, Anemia, Thyrotoxicosis, Hypoglycemia,

Pheochromocytoma
Medications: Cocaine, Alcohol, Caffetine, Pseudoephedrine
Treatment
Most patients are found to have benign atrial or ventricular ectopy and
non-sustained ventricular tachycardia
- In patients with structurally normal hearts, these are not with adverse
outcomes
- Often reassurance is enough
- In very symptomatic patients, a trial of beta block may be tried
- Otherwise, treatment depends on specific arrhythmias
Renal-L1-Acute Renal Failure
Also beta agonists, digoxin, phenothizeins

Psy: Aanxiety,
46 years old female patient was admitted yesterday because of diarrhea.

Px: DM, HTN, Taking Metformin and ACEI
Her diarrhea resolved last night. Here showing her routine blood taken this morning. And the renal function 4 months ago.
Creatinine up 300 (200 4 months ago)
1. The blood test indicates some renal impairment. What is the first thing you 2. What are the signs and symptoms of acute renal failure?
would like to ask or to clarify?
- To determine if this is acute or chronic renal injury
- Oliguria is often associated with acute renal failure
- By comparing to previous renal function tests
- Can be asymptomatic
Symptoms and Signs of Uremia
- General: Malaise, Weakness
- Non-Specific: Abdominal pain, Platelet dysfunction bleeding and
clotting disorders
- Neurological: Confusion, Seziures
- Neuromuscular: Restless legs, Numbness and cramps in legs
- Skin: Pruritis, Edema
- GIT: Metallic taste of mouth, Urinous breath
- Genitourinary: Nocturia, Erectile dysfunction
Cardiac
- Arrhythmias: hyperkalemia secondary to impaired renal potassium
excretion
- Pericardial effusion pericardial fiction rub
- Pericarditis
3. What are the lab findings you would expect to see in a patient with acute
4. What are the causes of acute renal failure?
renal failure?
Blood
- Pre-Renal (40-70%): Hypoperfusion, Cirrhosis (reduction in systemic
- Creatinine, Urea up
circulatory resistance release of ADH hypoperfusion of kidneys),
- Platelet dysfunction
Renal artery stenosis, ACEI, NSAIDs
- High K+
- High phosphate
- Metabolic acidosis
- Anemia (if over weeks)
ECG
- Changes of hyperkalemia
5. What investigations would you like to order to in order to determine the
cause of acute renal failure?
- Blood: FBC (anemia), U&E (hyperkalemia), CRP, ESR, LFT, Coagulation
study, Complement, ANA, ANCA, ABG (metabolic acidosis), culture
(sepsis), CK (rhabdomyolysis)
- ECG
- CXR Pulmonary edema
- Renal US
- Urine: Urinalysis, Microscopy
7. How to manage this patient?
- History, Physical Examination, Investigations
Management
- Ask for help from a nephrologists
- Keep patient hydrated (make sure the patient is not water overloaded)
- Stop any nephrotoxic drugs (ACEI, NASIDs, Metformin if creatinine
>250mmol/L, Gentamicin)
Monitoring
- ECG monitoring
- Urine Output Catheter insertion
- Pulse, BP
Indications of Dialysis
- Persistent hyperkalemia
- Severe metabolic acidosis
- Refractory pulmonary edema
- Uremic pericarditis
Renal-L1-Chronic Renal Failure
Renal (10-50%): Acute tubular necrosis (caused by ischemia, drugs,

radiological dye, uric acid crystals, rhabdomyolysis), Vasculitis, GN,
Interstitial nephritis
Post-Renal (10%): Stone, BPH
6. List 3 important complications.

-
Hyperkalemia
Bleeding
Pulmonary edema
8. Explain to what has been happening to this patients daughter.
66 years old male patient has a history of chronic renal failure. Today he is here for the renal clinic for a routine follow. You noted that his renal function has
been stable over the past 3 months.
- Please take a history and determine the likely cause of his chronic renal failure
- Please explain to him what are the possible complications of renal failure
- What is the management of chronic renal failure?
1. How do you define chronic renal failure?
2. What are the possible causes of chronic renal failure?
High urea/creatinine or decline in GFR over months to weeks

Bilateral small kidneys on US are diagnostic
Persistent proteinuria
3. What are the symptoms and signs?

- Can be asymptomatic
Symptoms and Signs of Uremia
- General: Malaise, Weakness
- Non-Specific: Abdominal pain, Platelet dysfunction bleeding and
clotting disorders
- Neurological: Confusion, Seziures
- Neuromuscular: Restless legs, Numbness and cramps in legs
- Skin: Pruritis, Edema
- GIT: Metallic taste of mouth, Urinous breath
- Genitourinary: Nocturia, Erectile dysfunction
Cardiac
- Arrhythmias: hyperkalemia secondary to impaired renal potassium
excretion
- Pericardial effusion pericardial fiction rub
- Pericarditis
5. Management
- Manage all the complications described above
- Manage the causes E.g. DM, HTN (Diuretics may be required for HTN)
- Protein/Potassium/Phosphorus/Salt and water restriction
- ACEI for proteinuria slow the progression of CKD
- Dialysis
- Renal transplantation
Primary Causes: Glomerulonephritis (non-proliferative E.g. Focal and

segmental GN, Membranous GN, and proliferative E.g. IgA nephropathy,
Membrano-proliferative GN, Post-infectious)
- Secondary Causes: DM, HTN, Amyloidosis
- Hereditary: PKD, Alport Syndrome (Hearing loss and GN)
- Obstructive: Prostatic disease, Renal artery stenosis, Stones
4. What are the complications of chronic renal failure?
Cardiovascular
- HTN, Congestive HF (water overloaded)
- Pericarditis (Uremia)
Mineral Complications
- High phosphate, Low calcium secondary hyperparathyroidism
- Managed by phrophous binder (E.g. Calcium gluconate) and vitamin D
(calcitriol)
Hematological
- Anemia (due to impaired Erythropoietin production, EPO is given IV or
SC)
- Many patient are iron deficient (due to increasing level of hepcidin) (iron
tablets)
- Coagulation (platelet count may be mildly decreased, use Desmopressin
in preparation for surgery)
Hyperkalemia
Metabolic Acidosis - Sodium bicarbonate
Others
- Neurological: Restless leg syndrome
- Endocrine: Hypoglycemia if DM
- Erectile dysfunction
6. This patient wonder what hemodialysis is. Please explain.
- Circulating patients blood in a machine
- Use a membrane to remove unwanted substances while adding other
desirable materials
- Dialysate (the solution the blood is equilibrated against) running in the
opposite direction
- A vascular access is required E.g. Cather for short term, Fistula for long
term, Graft may be needed (but more prone to infection/clotting)
- It takes 1-2 months for a fistula to mature
Frequency
- Typically 3 times a week
- Each session 3-4 hours
-
7. How about peritoneal dialysis?
The dialysate is placed via a catheter into the peritoneal cavity

Fluid and toxic substances transfer across the mesenteric capillary bed
The fluid is then removed via a catheter
The common method: CAPD continuous ambulatory peritoneal dialysis,
the patient carry 2L of the dialysis unit, the fluid is exchanged 4 times a
day
- No machines required, can be done anywhere
- More lifestyle freedom but requires patient responsibility
- Major complications: Peritonitis
Renal-L1-Glomerular Diseases
- The patient remains attached to the dialysis machine

- Hypotension is not uncommon during the procedure
- Psychiatric problems due to loss of independence
8. Im thinking of going to China or India to get a renal transplant from a
prisoner (so hard to get one in Perth). Can you tell me more about renal
transplantation?
- Successful renal transplant usually normalize most abnormalities
associated with renal failure
- Patient need to tolerate the immunosuppressive regimen
- Major complication: Rejection
Buying it outside Perth
- Unethical
- Risk of hepatitis B/C, HIV
This 45 years man presented to you with edema and fatigue. Urinalysis indicates proteinuria and hematuria.
1. What is the classification of glomerular diseases?
2. Why is classifying into nephritic and nephrotic spectrum important?
- 2 spectra: Nephritic or nephritic spectrum
- Each spectrum has their DDx
Nephritic Spectrum (Active urine sediment + Hematuria + Often proteinuria)
Nephritic Spectrum (Glomerular inflammation)
- Least severe nephritic spectrum: Hematuria
- Patients can present with Asymptomatic glomerular hematuria
- Mid-point of the nephritic spectrum: Nephritic Syndrome: Hematuria,
- Patients can present with Nephritic syndrome (a collection of symptoms)
Some proteinuria (<3g/d), Edema, Elevated creatinine
- Post-Infectious GN
- Most severe nephritic spectrum: Rapidly progressive glomerulonephritis - IgA Nephropathy (can present from nephritic to nephrotic)
Nephrotic Spectrum (Proteinuria + Bland urine sediment)
- Rapidly progressive glomerunonephritis (Lupus, Goodpasture
- Disease with proteinuria and a bland urine sediment
syndrome)
- More severe end: Nephrotic Syndrome, Proteinuria (>3g/L),
Nephrotic Spectrum (Glomerular increase in permeability)
- Patients can present with Asymptomatic proteinuria
hypoalbuminemia, edema, hyperlipidemia
- Patients can present with Nephrotic syndrome
- Minimal changes disease
- Focal segmental glomerulosclerosis
- Membranous nephropathy (always look for cancer)
- Membranoproliferative glomerulonephritis
3. What are the signs and symptoms of nephritic spectrum?
- Nephritic Syndrome: Edema (periorbital, scrotal), Hypertension, Gross
- FBC, U&E
hematuria, Oliguria
- Urinalysis to detect protein and blood
- Nephrotic Syndrome: Edema, Hyperlipidemia, Low albumin, Coagulation
- Microscopy Presence of dysmorphic RBC indicates glomerular
abnormalities
diseases
- CKD
- ANA, ANCA, Complements
Occasionally with hemoptysis in pulmonary hemorrhages E.g.

Goodpasture, SLE
4. What is post-infectious glomerularnephritis?
- A glomerular disease
- In the nephritic spectrum
Causes
- Streptococci Infection
- Often happens 1-3 weeks after impetigo or pharyngitis
Symptoms and Signs
- Hematuria, HTN, Oliguria, Edema, Cola-colored urine
Investigations
- Anti-Streptolysin O (usually high, unless previous antibiotic treatment)
- Hematuria, Proteinuria (<3g/d)
- Severe cases with elevated creatinine
Treatment
- Treat infection
- Supportive
- Antihypertensive, Salt restriction, Diuretics
Prognosis
- Children are more likely to fully recover
- Adults more prone to develop rapidly progressive GN
6. What are the causes of rapidly progressive GN?
- Lupus
- Goodpasture Syndrome (antibody to the basement membrane, GN +
pulmonary hemorrhage)
- Pauci-Immune (ANCA associated)
Renal biopsy if unclear
5. What is IgA Nephropathy? (Henoch-Schonlein Purpura)

- Proteinuria, Hematuria, +ve IgA staining on renal biopsy
Signs and Symptoms
- Gross hematuria
- Associated with upper respiratory infection, GI Infections, flu-like illness
- Urine becomes red or cola-colored 1-2 days after illness onset
- Diagnosed by renal biopsy
Treatment
- Control HTN Use ACEI
- Corticosteroid
- Really severe: Cyclophosphamide, Azathioprine
Prognosis
- 40-50% develop chronic kidney disease
7. Briefly talk about..

Minimal changes disease
- Electron microscopy: Fusion of foot processes of podocytes
Focal segmental glomerulosclerosis
- Focal (<half the total number of glomeruli) segmental (< half of each
glomerulus) sclerosis
Membranous nephropathy
- Light: Thickened GBM
Membranoproliferative glomerulonephritis
- Light: Increased mesangial cells
Renal-L1-CKD
1. How many genes are involved in autosomal dominant PKD?
- 2
- ADPKD1
- ADPKD2 slower progression, and longer life expectancy

- Abdominal pain/mass
- Hematuria
- History of UTI and stones are common
- Fx
- >50% with HTN
- Tends not to be anemia, as Erythropoietin is produced by the cysts
3. List 6 complications.
- Pain: Can be caused by infection/bleeding into cysts/stones managed
by bed rest
- Hematuria: Commonly due to rupture of a cyst, can also due to stones or
UTI, usually resolved in 7 days, if not consider renal cell carcinoma
- Renal Infection: Pain, Fever, Leukocytosis, CT scan can be helpful because
infected cysts have increased wall thickness antibiotics, 2 weeks IV
then long term oral
- Stones: Hydration is recommended
- HTN: Cyst-induced ischemia activation of rennin-angiotensin system
(Diuretics use with caution as effects on cyst remain unknown)
- Cerebral Aneurysm: 10-15% with arterial aneurysm in the circle of Willis,
screening not recommended unless Fx
- Others: Aortic aneurysm, Aortic valve abnormalities
Renal-L3-Diabetic Nephropathy
1. What is a typical picture about diabetic nephropathy?
- Typically over 10 years
- Albuminuria (Micro albuminuria develops 10-15 years, progress 3-7 years
to >300mg a day)
- Decline in GFR (Initially increase, then normal, and decreases)
- May associate with retinopathy
- Signs of diabetic nephropathy on renal biopsy (diffuse glomerulosclerosis)
4. Give examples of systemic disease with renal involvement.
- Multiple Myeloma
- Sickle cell diseases
- TB
- Gout
- Amyloidosis
- SLE
- HTN
- DM
Renal-L3-Tubulo-interstitial Diseases
US confirm the diagnosis

- With the onset of microalbuminuria aggressive treatment
- Strict DM control
- Management of HTN
- ACEI or ARB
-
This patient has chronic pain and has been using paracetamol 4 times a day for the past 4 years. On urinalysis you noted proteinuria. He also complains of
polyuria.
1. What is tubulo-interstitial disease?
2. What are the 4 main causes of tubulo-interstitial diseases?
- Pathology of the tubules and interstitium of kidney
- Most Common = Obstructive Uropathy E.g. Prostate in men, Carcinoma,
- Acute see acute renal injury
Stones
- Chronic
3. What are the causes of acute tubulo-interstitial diseases?

Medications
- Antibiotics: Penicillin, Ciprofloxacin, Erythromycin, Tetracycline,
Sulfonamides, Vancomycin, Rifampin
- NSIADs
- Diuretics: Thiazides, Furosemide
- Others: Allopurinol
Infections
- Strep
- EBV
5. What are the lab findings?
- Hyperkakemia
- Hyperchloremic acidosis
- Proteinuria
Renal-L3-Dialysis
1. What are the different types of dialysis?
- Hemodialysis
- Peritoneal dialysis
- Kid
2. What is hemo-dialysis?
- A constant flow of blood running alone a dialysate
- Diffusion to remove the unwanted substances from the blood
- AV fistula needed
- Native fistula has less infection/thrombosis/aneurysm than grafts
- Patients typically require hemodialysis 3 times a week
- Option: Nocturnal dialysis, Home hemodialysis
4. What are the advantages and disadvantages of peritoneal dialysis?
Advantages
- Phosphates are better cleared
- Cheaper
Second Most Common = Vesicoureteral Reflux Primarily a disorder in

childhood, result of incompetent sphincter, typically diagnosed in
children with recurrent UTI, detected by cysto-urethrogram, If diagnosed
in adult US will show renal scarring and hydronephrosis
- Analgesics E.g. use for chronic headaches, muscle pain, arthritis
- Heavy metals E.g. Lead
- Polyuria Due inability of the tubules to concentrate the urine
- Volume depletion

- Identify the cause
- If hydronephrosis relief of obstruction
- Withdrawals of all analgesics
2. What are the indications of dialysis?
- When GFR declines to 5-10ml/min
- Uremic symptoms
- Fluid overloaded, unresponsive to diuresis
- Refractory hyperkalemia
- Severe metabolic acidosis
3. What is peritoneal dialysis?
- Dialysate is introduced into the peritoneal cavity
- After equilibration, the dialysate is drained, and exchanged
3 Kinds
- CAPD Continuous ambulatory peritoneal dialysis Manual exchange
- CCPD Continuous cyclic peritoneal dialysis Cycler machine to exchange
- NIPD Nocturnal intermittent peritoneal dialysis A cycler machine at
night
5. What are the side effects of hemodialysis?
- Fluid removal through ultrafiltration Hypotension, fatigue, nausea,
headaches, chest pains, leg-cramps
- These may be avoided by dialyzing more often or longer per treatment
Disadvantages
- Removes large amount of albumin
- Complications: Peritonitis N+V, abdominal pain, dialysate is cloudy
6. What are different types of accesses?
- Catheter
- AV fistula
- AV graft
Renal-L3-Gout and Kidney
Case: This renal patient developed gout.
1. Why is gout associated with kidney diseases?
- Kidney is the primary organ for excretion of uric acid
- Patients with proximal tubular dysfunction have decreased excretion of
uric acid
Infection: Sepsis, Endocarditis, Osteomyelitis

Heparin (can be reversed by potamine)
2. What is the management of gout?

Acute Gout
- Colchicine 500mg orally, 6-8 hourly until attack abates or
- Prednisolone 20mg orally daily until symptoms abate
- Intra-articular corticosteroid injection
- Avoid changes to Allopurinol (changes in urate concentration can
exacerbate the attack)
- Once the attack has settled start Allopurinol 50mg orally + Colchicine
500mg orally twice daily until the target dose of Allopurinol is reached
Chronic Gout
- Allopurinol 50mg orally, daily for the first month, then increase the dose
by 50mg every 2-4 weeks depending on the renal function and plasma
urate level
- Covered by Colchicine until target dose achieved
Rheuma-L3-SLE
This patient was diagnosed with SLE. You are about to start her on Cyclophosphamide.
1. What are the side effects that you should warn this patient?
2. What is SLE?
Long Term
- Autoimmune disease
- Infertility
- Characterized by vasculitis and ANA
- Infection
- Chronic, remitting and relapsing disease
- Increased risk of cancer
- Often affect skin, joint, kidneys, serosal membrane
- Bone marrow suppression
- Virtually every organ in the body can be affected
- Hemorrhagic cystitis
3. What age group do you usually see?
- Age of onset 12-35 years
- Systemic: Fever, Malaise, Fatigue, Weight loss
- Female more common
- Skin: Photosensitivity, Rash (usually pruritic), Raynauds phenomenon,
- Causes unknown
Sjogrens syndrome
- Joint: Pain
- Renal: Proteinuria, Hematuria, GN, Renal failure
- Pulmonary: Pleurisy, Effusion, Interstitial pneumonia
4. What investigation to order if you want to diagnose SLE?

- ANA, ANCA, Complements, Lupus anticoagulants
- FBC, U&E, ESR, CRP
- + Clinical Features
6. She wants to get pregnant. What should you tell her?
- Maternal SLE may result in complete heart block in fetus
- Pregnancy can induce a flare-up
- Increased risk of pre-eclampsia
Cardio: Pericarditis
Neurological: Seizure, Headache
Ocular: Conjunctivitis, Episcleritis
GI: Hepatomegaly, Splenomegaly, N+V
Hematological: Anemia, Thrombocytopenia, Leukopenia,
Lymphadenopathy
5. What is the management of SLE?
- Sun cream
- Avoid estrogen containing pills (can induce a flare-up)
- Corticosteroid, Infliximab, Methotrexate
- If severe cyclophosphamide (Azathioprine less toxic)
ANA (Antinuclear Antibody)
- If positive test for Anti-dsDNA and ENA (E.g. Anti-Ro, Anti-La, Anti-Jo1,
Anti-RNP, Anti-centromere antibodies, Anti-Scl-70)
- Anti-dsDNA for SLE
- Anti-Scl-70 for systemic sclerosis
- Anti-centromere for CREST syndrome
- Anti-Ro, Anti-La both for Sjogrens Syndrome
ANCA
- C-ANCA Associate with Anti-PR-3 E.g. Wegeners granulomatosis
- P-ANCA Associated with MOP E.g. IBD
Other to known: RF, Anti-CCP
Notes/Make-up scenarios: GP
Station 1
- Preventative Measures
Station 2 and 3
Level 1
- Respiratory: Spirometry, Asthma (teach to use a ventilator/6 steps management plan), Allergic
Rhinitis / Sinusitis
- ENT: Vertigo, Sore thorat
- Sexual Health: Emergency Contraception, STD, Dysuria, UTI
- Chronic Pain: Back pain, Knee pain, Facial pain, Migraine
- Undifferentiated: Tiredness Dont miss gyne history
- Also: DM Management, Cardiovascular Factors Assessment
- Headache
- Skin Lesions
- Smoking, Alcohol Management
Level 2
- Gay Consultation
Level 3
- Suturing
GP There are 3 stations.

-
Overall, GP stations are ones of the easiest stations and are reasonably easy to pass all 3 GP stations
Usually:
-
A preventive health station: Need to know breast screening, prostate screening, colonic cancer screening
2 Stations from the following topics:

-
Chronic Pain: Back pain, Knee pain, Facial pain, Migraine
Sexual health: STD screening, Vaginal discharge, Dysuria, Contraception (covered in O&G), Pregnant woman with UTI, HRT and menopause (covered in O&G)
ENT: Vertigo, Sore throat
Respiratory: Chronic cough, Sinusitis, Asthma, Allergic rhinitis
Undifferentiated: Tiredness, Chronic abdo pain, Immunization
Difficult patient: Gay
Others: Skin E.g. Melanoma, Warts
Knowing all cases in the tutorial should be safe enough to pass.

Scenarios in the GP guidebookIm.too.lazy to put up the notes for GP
Week 3 Cases - [ENT] problems in General Practice
1.
2.
Your patient is a 4-year-old, whose parent brings him/her in because of earache. Your patient comes in and tells you s/he feels dreadful headache, feeling really
The child was awake and distressed for much of the night. The parent says the clogged up, and a toothache. S/he says she had a head cold about 10 days ago,
which s/he thought had finally gone, but then this started 2 days ago
child has been going to swimming lessons and wonders if this could be causing
the pain.
3.
A patient comes to see you about a cold that wont go away. The nasal discharge
is usually quite watery, but is often thicker in the morning. S/he sometimes
wakes with a scratchy throat, and sometimes feels some phlegm at the back of
the throat. S/he is adamant that it isnt hay fever, as s/he also gets that around
cats and dogs, and some flowers - and it only lasts for a couple of hours, with
sneezing and itchy eyes.
5.
A 36 year old woman, phones requesting a home visit. She says she is
dreadfully dizzy and nauseous, and every time she tries to get up the room
seems to spin. This started yesterday and is getting worse.
Week 4 Cases - Respiratory problems in General Practice
1
Your patient tells you s/he has the flu. S/he has had a head cold and sore
throat, and now a persistent productive cough for 5 days. S/he says s/he
wants something to get rid of it fast as s/he is travelling overseas for work next
week.
3
Your next patient comes to see you about her/his asthma. It has been worse
over the past few months, and s/he is needing to use a puffer a couple of times
a day.
5.
Your last patient has been feeling unwell for about 3 days with a cough and
fever. S/he thinks its flu, but feels really unwell, and is sometimes a bit
breathless. On examination you hear crackles in the left lower and mid zones.
Week 5 Cases - Chronic pain in general practice
1.
- Your patient tells you s/he has done his/her back in again. S/he says s/he
was lifting some groceries out of the car boot. When s/he turned s/he felt
the pain suddenly in her/his back, and found it difficult to straighten up.
You know this patient has a history of chronic lower back pain
3.
4.
Your next patient is a 20-year-old student, who works part time as a waiter. S/he
comes in with a 4-day history of a sore throat the worst Ive ever had. S/he
says s/he has a fever and a headache, and feels quite tired.
2
Your next patient, a middle aged woman, has had a cough for the last 3
months.
4
Your patient is 19 and tells you that s/he has recently started a triathlontraining course but finds s/he is still getting short of breath when training, and
feels his/her fitness should have improved by now.
-
2
A patient comes to see you for a Progress certificate for their Workers
Compensation claim. S/he says the back pain is about the same, but s/he's
getting increasingly frustrated about his/her slow recovery. S/he wonders if
acupuncture will help.
4.
Your patient comes in with knee pain. It's been present really for about six
months. It's getting worse thought it was just part of getting old, but now
worried it is gout or that really bad arthritis that cripples you
Patient comes in for something for her migraines says she has been getting
them for years, and nothing really seem to help, but shes heard of some nasal
sprays.
5.
Your next patient presents with facial pain.
Week 6 Cases - Sexual Health
1.
A woman comes in to see the doctor. She is extremely embarrassed to tell the
doctor that she has an unusual discharge.
3.
Your patient tells you of burning and stinging when they pass urine and are
worried they may have 'caught something' whilst on holiday overseas.
5.
A parent, a patient you know well, comes in to discuss their son's sexuality - he
'came out' last week.
Week 7 Cases - Difficult Patients
1.
- A 32 year old woman comes to see you, she is a smoker and wants to quit.
3.
You are seeing this patient who you know well with poorly controlled diabetes.
After your last consultation you made a note that you need to talk with this
obese patient about losing weight next time you see them. You did not
mention this to the patient.
-
5.
A 60 year old patient with a past history of Dukes B adenocarcinoma of the
bowel resected 3 years ago presents for results. You saw him last week and he
complained of right upper quadrant pain and weight loss so you arranged an
ultrasound. This has shown multiple lesions in the liver highly suggestive of
metastatic disease.
-
2
An adolescent visits the doctor because she thinks she has the flu.
4.
A woman requests the morning after pill.
2.
A 50 year old man has been sent along by his wife. He lost his license last
month for the 3rd time for DUI and she has insisted that he talk to you about
his alcohol use.
4.
A 40 year old male barrister has insisted that your receptionist give him an
urgent appointment with you even though you are heavily booked and running
late. He has a migraine and is adamant that he just needs a shot of pethidine.
He has never seen you before, his usual doctor is on leave and his medical
records are not available. Your receptionist tells you that he is becoming angry
as he has been waiting to see you for half an hour.
6.
-
Week 8 Cases - Undifferentiated illness in General Practice

1.
Your next patient is a mother of four, with six-month-old twins. She has brought
the babies in for their immunisations, and when you ask how she is, she tells you
she is really tired. She says she thought she would have been feeling better by
now.
3.
Your next patient has suffered from episodes of abdominal pain for several
months. She has seen another doctor about this and presents to you for a
second opinion.
5.
Your patient, who has recently had a moderately severe viral RTI, tells you they
have heart palpitations and chest tightness.
2.
Your next patient is new to the practice. He tells you he has seen a couple of
doctors about his problem, but nothing they have done has helped. He says he
has been tired for about eight months.
4.
Your patient tells you they have no energy, that they have lost their get up and
go.
6.
-
Notes Preventative Health Refer to the red book

12 years old girl
- Assess growth
- Progress at school
- Look for behavioral or emotional problems
Prevention Advice
- Injury prevention
- Sun protection
- Dental care
- Physical activity
- Nutrition
75 years old woman

- Falls, gait, balance
- Assess for risk factors E.g. Chronic disease, Dizziness, Vertigo
- Assess home hazards
- Depression
- Visual and hearing impairment snellen chart
- Memory, MMSE
48 years old woman

Assess
- SNAP behavioral risk factors
- DM, CVD risk
- Depression
- Osteoporosis
- Skin cancer
Measures
- Weight, Height
- BP
- Lipids
- Glucose
Perform
- Pap smear
- Mammography
15 years old boy.
- Reduce harm
- Assess potential risky behaviors
- Encourage delay in initiation of potentially risky behaviors
- Substance abuse, pregnancy prevention, injury prevention
- Immunization
- Incontinence
General
- BP
- Glucose, Cholesterol
- Pap Smears
- Contraception: Any contraceptive measures?
- Immunization: Flu vaccines
- Mammogram 50-69 years, every 2 years
- Smoking, Alcohol
- Nutrition
- FOBT 50-75 years old
- PSA considered for 50 years old
- STI screens
Notes/Make-up scenarios: Peds

- Usually there are 3 stations and they are:
-
Newborns, or very young child
Kids, Older child
Adolescent
- Knowing level 1 stuff should be safe enough to pass

Station 1 Newborns (First 28 days)
Level 1
- Video in respiratory distress
- Upper respiratory infection/Common
Cold/Cough
- Jaundice
- Sepsis, Fever
- Ambiguous genitalia
- Vomiting, Diarrhea
- Crying baby
- Rash E.g. Diaper rash, Eczema, Urticaria
- FFT
- Prematurity
Level 2
- Snoring
- Newborn Screening tests
- Murmur
- Cerebral palsy
- Down syndrome
Station 2 Kids
Level 1
- Abuse
- 6 weeks check, Breast feeding issues
- UTI
- Burns
- Anaphylaxis
- Juvinile onset DM
- Rehydration/Gastroenteritis
- Ped resuscitation
- Immunization
- Febrile convulsion
- Otitis media
- Developmental stage determination (Video)
- Vomiting E.g. DKA
- Diarrhea Acute + Chronic
- FFT, Celiac disease
- Rash
- Abdo Pain
- Asthma
Level 2
- Developmental delay E.g. Kid have not been
speaking for 3 years, Autism
- Precious puberty
- Delayed puberty
- Short statue
- Septic arthritis
- Limping
- Trauma
- Testicular Pain
- Lymphadenopathy
- Constipation
Station 3 Adolescent
Level 1
- Sadness E.g. Chronic disease, Smoking, Drugs
- History taking (Difficulty history taking)
E.g. Denied smoking even though smoking
E.g. Ask the mother out to see the adolescent alone,
but the mum refuses to do so (you are supposed to
insist on seeing the adolescent alone)
E.g. 14 years old asking for contraceptions
Newborns-L1-Video in respiratory distress

- Whooping Cough, Croup, Grunting, Wheezing, Intercostal recession (Dont really tell you the diagnosis, just signs of respiratory distress)
- If there is a video station, usually show you a whooping cough or croup baby (otherwise pneumonia or bronchiolitis) + some signs of respiratory distress
(Usually on oxygen or NGT tube)
1. http://www.youtube.com/watch?v=ag6QUWjiZvA
2. http://www.youtube.com/watch?v=51Zku19JpLI
3. http://www.youtube.com/watch?v=Eg9cpb9WZRU
4. http://www.youtube.com/watch?v=ViRQM1m_z2k
5. http://www.youtube.com/watch?v=XY9zv0BvFHc
Ans see question 5
1. What are the possible causes of a 26 days old newborn presented with
respiratory distress?
Bacterial Infection: Pneumonia, Pertussis (whooping cough), TB, Sinusitis, always
think about meningitis in a very sick patient
Viral Infection: Viral pneumonia, Bronchiolitis, Croup, Influenza
Inflammatory: Asthma (diagnose as young as 5 years old), Allergies E.g. allergic
rhinitis (suggested by eosinophilia)
Genetic: Cystic fibrosis, Anemia E.g. Sickle cell anemia
Congenital: Pulmonary/Vascular malformation, Congenital heart disease
General: Height and weight, Degree of stress
Skin: Rashes
Head, Ears, Eyes, Nose, Throat: Watery eyes, Sinus tenderness, Nasal discharge
Lungs: RR, Chest appearance, Retraction, Breath sounds
Heart: Murmur
Extremities: Cyanosis and clubbing (E.g. CF, Bronchiectasis)
3.
What is your management?
Depends on the history, physical examination and results from lab
History
Presenting Illness
Cough: Duration, Frequency, Characters, Productive, Non-Productive (children
frequently swallow sputum), Triggering factors E.g. Allergies, foreign Cold air in
asthma
Associated symptoms: Rhinorrhea, watery eyes, headaches, fever, poor weight
gain
How many days of school missed
Medication?
Travel history
Family members ill?
Px
Birth history
Vaccination
Previous illness or surgery
Fx
Asthma, Allergies, CF, TB, Sarcoidosis, Emphysema
Environmental
Smokers at home, pets, Child care
2. What is your investigation?
Do a septic screen
FBC (WCC differential will give you info about viral vs bacterial vs allergy), U&E,
Glucose, Blood culture, Chest radiology (may not be useful, also ve does not
rule out pneumonia), LP (consider if severe), Urinalysis
Also nose and throat swab
Stools culture
If suspect pertussis (E.g. you hear a whooping cough),
If suspect TB,
Others: Flu, test for CF
4. Will you DDx be different if the patient was just born 1 hours earlier (instead of
26 days old)?
Pulmonary
Generally, monitor O2, give when needed, Mechanical ventilation if required

Put in IV access, Monitor vitals
Supportive management before lab tests available E.g. Fluid rehydration, try
orally, then IV
Feeding: Encourage when possible, if not, consider NGT
If lab results indicate bacterial infection antibiotics
If +ve for croup corticosteroid
Common: Transient tachypnea of the newborn

Less Common: Meconium aspiration, Pneumonia, Reparatory distress
syndrome, Pneumothorax, Milk aspiration, Persistent pulmonary hypertension
of the newborn
Rare: Diaphragmatic hernia, Tracheo-esophageal fistula, Pulmonary hypoplasia,
Airway obstructions, Pulmonary hemorrahge
Non-Pulmonary
5. What are the video showing you?

1 = Grunting
2 = Baby with Croup Stridor Barking Cough
3 = Whooping Cough in Baby (12 weeks old)
4 = Infant with pertussis (3 month old baby with whooping cough)
5 = Infant Respiratory Distress Signs, turns out to be pneumonia
7. How much do you know about whooping cough?
Pertussis
Caused by Bordertella pertussis
Clinically: A persistent cough for more than 2 weeks +/- 1. Paroxysmal coughing
2. Inspiratory whoop 3. Post-tussive vomiting
Diagnosis: NAT Nucleic acid test, include nasopharyngeal aspirate or swab in
children, and nasopharyngeal swab in adults (Immunofluoresecnt staining of the
swabs)
Cases of pertussis should be notified, also patients are selfdom infectious after
coughing for 3 weeks
Treatment
Azithromycin, Erythromycin
Prophylaxis
Recent contacts should be identified, antibiotic prophylaxis should be given to
vulnerable individuals E.g. Women in the last month of pregnancy, Very young
Vaccination, needs 3 injections, so..cant be used to control an outbreak
9. Acute bronchiolitis.
Acute Bronchiolitis
The most common LRTI in infants, diagnosis is limited to the first 12 months
It affects both lower and upper RT, has a peak prevalence and severity in those
less than 6 months old
Diagnosis is clinical: Typical history of nasal discharge, fever, wheezy cough,
examination with inspiratory crackles +/- expiratory wheeze
Congenital heart disease

Intracranial birth trauma
Severe Anemia
Metabolic acidosis
In order of frequency: Surfactant deficiency > Transient tachypnea > meconium
aspiration > Pneumothorax > pneumonia > diaphragmatic hernia > upper airway
obstruction
6. What is grunting?
It is a sign of respiratory distress, most often in the newborn or infants
It is an end-expiratory sound
Causes
See DDx in Q1
8. How about croup?
Croup
Presents with a coryzal syndrome, hoarseness, inspiratory stridor, barking cough,
variable airway obstruction
Most common in 1-3 years old children
Parainfluenzae viruses are the most common cause
Assessment
Loudness of stridor is not a good guide to the severity of obstruction
Blood tests, oxygen, nasopharyngeal aspirate are rarely indicated
Mild: Mild chest wall retraction, tachycardia
Moderate: Stridor at rest, chest wall retractions
Severe: Stridor at rest, fatigue, marked tachycardia, restlessness
Management
Dexamethasone 0.15mg/kg orally
In severe croup + Nebulized adrenaline
10. Explain pneumonia.
In the first 3 days of life
Acquired from maternal perineal flora E.g. Streptococcus agalactiae, E. coli
After the 3 days of life
Streptococcus pneumoniae
Mycoplasma pneumoniae
Causes: Respiratory syncytial virus, Rhinovirus, Human metapneumovirus,

Prainfluenzae, Influenzae
Most children present to GP have mild bronchiolitis, main management =
reassurance and education
Indications for admission: O2 <94%, difficulty feeding, moderate to severe work
of breathing, Increased RR
Hospital management: O2, IV fluid, NGT if required, bronchodilator can be added
but not been shown to shorten hospital stay
Chlamydia trachomatis should be considered in infants up to 3 months of age,

particularly if fever is absent, as many as 50% of infants with C. trachomatis
pneumonia will have conjunctivitis
While uncommon, Staphylococcus aureus can cause severe pneumonia in all
ages
How to Diagnosis
Fever in an unwell or toxic child with acute respiratory distress + evidence of
infiltration on CXR
Usually present with fever, cough, tachypnea, possibly grunting
Can also present with fever without a source, occasionally abdominal
pain/meningism
Neither CXR, WCC, Neutrophil count, nor CRP is reliable in trying to tell
between viral and bacterial pneumonia
Causes
Viruses E.g. RSV, influenzae, parainfluenzae, adenovirus
Bacteria E.g. see above
Generally Strep. If <5y and Myco. If >5y
But viral is still more common than bacterial
Clinical Features
If wheeze present, bacterial pneumonia is unlikely
Bilateral wheeze +/- crackles are more suggestive of a viral pneumonia
Investigations
CXR is those who are unwell
Blood culture
PNA Pre-nasal aspirate/Nasopharyngeal aspirate
Newborns-L1-Respiratory distress + Fever/Sepsis

Ken was born 5 hours ago. A nurse called you that he seems to be a bit short of breath and quite hot on palpation.
1. What information would you like to know more about Ken?
2. What to look for on clinical examination?
3. The nurse asked you what the possible causes are.
4. What investigation would you ask?
5. What are the management before the results become available?
History
Responsive? Unconscious? If stable take a more detailed history
General
Antepartum History: Antenatal screening (HIV, Chlamydia), Complications during Take vitals, Monitor O2
pregnancy, Trauma, GBS status, Single or twin?
Look for lethargy, hypotonia, Temperature instabilitu, Poor skin perfusion,
During Labour: Maternal fever, ARM, Induced, Any invasive procedure E.g. Scalp
Jaundice, Unstable plasma glucose, Apnoea, Seizures
electrode, Prolonged labour, Meconium stained liquor
Specific
Post-Partum: Resuscitation? Birth weight? Term?
GIT: Vomiting, Diarrhea, Abdominal distension
PC
CNS: Seizures, Irritability,
SOB: Since when? Color? Fever? In distress? Any other symptoms?
Skin: Septic lesions
Poor feeding? Skin lesions?
Eyes, Umbilicus: Discharge
Other symptoms: Vomiting, Diarrhea, Seizure, Umbilical discharge, Eye

discharge, Abdominal distension
Plasma glucose ok?
Vaccination
1. Possible causes.
Infection
In order of frequency: Surfactant deficiency > Transient tachypnea > meconium
aspiration > Pneumothorax > pneumonia > diaphragmatic hernia > upper airway
obstruction
3. Management
If signs of sepsis antibiotics = Penicillin + Gentamicin
Monitor O2, give O2 if required
Encourage feeding
Monitor glucose level
Monitor vital signs regularly
4. What are the risk factors of neonatal sepsis?

-
Premature rupture of the membranes

Discolored liquor
Preterm labour and birth
Maternal peripartum pyrexia
Maternal GBS, UTI
Resuscitation required at birth
Multiple gestations
Invasive procedures E.g. Endotracheal tubes
Inadequate hand washing
More Information
Transient Tachypnoea of the Newborn
-
Commonest cause of respiratory distress in term infants

Caused by the delay in the resorption of lung liquid and is more common in Csection
CXR may show fluid in the horizontal fissure
Additional oxygen may be required
Usually settles within the first day of life, can take several days
A diagnosis of exclusion
Pneumonia
2. Investigation.
Do a septic screen: Blood culture, Gastric aspirate, Ear swab, Eye swab,
Nasopharyngeal swab, Suprapubic urine
FBC, U&E, PGL, CRP
Consider LP
CXR.if indicated...
CRP
-
Synthesized in liver to inflammatory process

A single normal value cannot rule out infection, as the sampling may have
preceded the CRP rise
Serial estimations useful
There is an increase in 4-6 hours, peak at 36-50 hours
Quick decrease with resolution of infection, half-life about 4-7 hours
Meconium Aspiration
-
Meconium is passed before birth by 8-20% of babies

It may be passed in response to fetal hypoxia
At birth, these infants may inhale thick meconium
Asphyxiated infants may start gasping and aspirate meconium before delivery
Meconicum can result in mechanical obstruction and chemical pneumonitis
Lungs are over-inflated, accompanied by patches of collapse and consolidation
High incidence of airleak, leading to pneumothorax
Artificial ventilation is often required
May develop persistent pulmonary hypertension, make it hard to achieve
adequate oxygenation despite high pressure ventilation
Pneumothorax
Prolonged rupture of membranes, chorioamnionitis and low birth weight

predispose to pneumonia
Broad-Spectrum antibiotics are started early
Milk Aspiration
-
Occurs more frequently in preterm infants

Babies with bronchopulmonary dysplasia often have gastro-esophageal reflux
Infants with cleft palate
May occur spontaneously in up to 2% of deliveries

Usually asymptomatic and may cause respiratory distress
Can also occur secondary to meconium aspiration
Persistent Pulmonary Hypertension of the Newborn
-
Diaphragmatic Hernia
-
This occurs in 1 in 4000 births

Many are diagnosed on antenatal US screening
Most cases there is a left-sided herniation of abdominal content through the
foramen of the diaphragm
The apex and heart sounds will then be displaced to the right side of the chest
Poor air entry into the left chest
Once diagnosed, a nastrogastric tube is passes and suction is applied to prevent
distension of the intra-thoracic bowel
Life threatening condition

Usually with birth asphyxia, meconium aspiration, septicaemia or respiratory
distress syndrome
Sometimes occur as a primary disorder
High pulmonary resistance right to left shunting
Cyanosis occurs after birth
Heart murmurs and signs of heart failure are often absent
An urgent Echo is required to establish that the child does not have congenital
heart disease
Most infants require mechanical ventilation and circulatory support
Inhaled NO, a potent vasodilator
In severe cases, infants placed on heart and lung bypass for several days
John was born at term 20 hours ago. The routine blood test indicated elevated CRP.
1.
2.
3.
4.
Please take a brief history from the mother?

What are the signs and symptoms in neonatal sepsis?
What are your investigations?
How to manage?
1.
2.
Antepartum: Antenatal screening test normal? Especially those for infection
General or Non-Specific
E.g. Hepatitis B/C, GBS, Any complications? PPROM? UTI?
During Labour: Maternal fever? ARM? Invasive procedure? (scalp electrode),

Prolonged labour? Instrumental?
Post-Partum: Resuscitation?
Hypotonic, Lethargy
Pyrexia, Hypothermia, Temperature instability
Poor skin perfusion
Poor feeding, Intolerance of feeds
Unexplained jaundice
Unstable plasma glucose
Apnoea and seizures
Neutropenia
- DIC
Suggestive or Specific
- Respiratory distress
- GIT: Vomiting, Diarrhoea, Abdominal distension
- CNS: Irritability, Seizures, Full fontanelle
- Skin: Septic lesions
Eyes, Umbilicus: Discharge
3.
4.
Early Onset First 24 Hours

-
Blood culture
Gastric aspirate (if has not fed)
Ear swab
Tracheal aspirate (if intubated)
FBC, U&E, PGL for baseline
Consider LP
CRP
CXR (in indicated)
Late Onset Beyond 24 Hours

-
Blood culture
Culture of specific sites as
indicated E.g. Skin, Umbilicus
FBC, U&E, PGL for baseline
CSF (LP should be performed in
all cases of proven septicemia)
CRP
CXR
Suprapubic urine
Early Onset
-
Antibiotics if clinical signs of
Late Onset
-
Common organism: S
sepsis
epidermidis, Gram ve E.g.
Common organism: GBS,
Pseudomonas and Klebsiella
Gram ve, E. coil, H. influenza
species
Parental therapy: Penicillin
and Gentamicin
Septic workup: Blood culture, LP,

Suprapubic urine
Empirical treatment:
Vancomycin + Gentamicin
If a GIT cause is suspected:

Metronidazole can be added
Newborns-L1-Jaundice
Jeffrey was born by vacuum-assisted delivery 3 days ago. His mother has brought his yellow skin to mid-wifes attention. The yellow color extends all over the
childs body. Take a brief history from the mother and outline your investigations and management of his problem.
1. Is this jaundice significant?
2. What is the most likely cause of the jaundice?
3. Why is the management of jaundice important? What are the possible sequelae?
Introduction
PC
My name is . Im one of the doctors working here today. I understand that
your son was born by vacuum-assisted delivery and has been yellow. Before
we go on to talk about what should be done, I will need to take a more
detailed history. Is that alright.
Birth History
-
When was your son born?

Full term? How many weeks?
What is the reason for the vacuum-assisted delivery?
Any complications during the pregnancy? E.g. IUGR
Any abnormal antenatal screenings? Are you aware of your blood
group? Were you even given anti-D? Are you rhesus +ve?
Low birth weight at birth? What is the weight now?
How was he at birth? Breathing problems? Any complications?
Any birth trauma?

Did they do any screening tests for the newborn? What were the
results?
Newborn Screening Tests: PKD, Congenital hypothyroidism,
Galactosemia, CF, Amnio acid disorders, Fatty acid oxidations
disorders, Organic acid disorders
PC
- When did the yellow skin first start?
- Can you describe the pattern? What part of body was first affected?
- How is he in general? Appear to be distress?
- Has he opened his bowel? What is the color?
- Have you been breast feeding? Any problems with the feeding
Px, Fx (Fx of blood disorders), Medications, Allergies
-
Investigations
Since your son is not here, I am not able to examine your son
Management
-
The management will depend on the blood tests results, and also the
underlying causes.
But in general, we need to control the level of bilirubin within a safe level.
It is because too high level of bilirubin can cause Kernicterus, which can
cause damage to the brain.
Phototherapy: Aim to lower the bilirubin level and avoid exchange
transfusion, whether to start this therapy depends on the age, weight and
The yellow skin is what we call jaundice.

And the substance responsive for this is called bilirubin, which is the
breakdown product of red blood cells.
There are a number of causes that could lead to an increased level in
bilirubin.
Conditions that causes too much red blood cells to be destroyed or
conditions that directly or indirectly affects the liver can lead to
jaundice.
Because you told me that the jaundice appears on 2nd day, it is likely
that the jaundice is caused by the immature liver.
However, we still need to do some blood tests to rule out other
possible causes.
Bloods: FBC, U&E, CRP, ESR, Bilirubin level (with
unconjugated/conjugated ration), glucose, TFT
If Sepsis blood culture, urine culture, CFS
May consider repeating the newborn screening tests
the level of bilirubin. Infants under phototherapy requires additional fluid

as a result of increased water losses we will make sure you son is
hydrated, Also cover the infants eyes with pad
Very occasionally, exchange transfusion will be needed. Indications: Sickle
cell disease, TTP, Hemolytic disease of newborn
More Info
History
Pregnancy, Labor, Delivery
- Maternal blood group (Ah and ABO incompatibility )
- Pregnancy infection (Infection in newborn can cause jaundice)
- Abnormal fetal US E.g. GIT obstruction
- Traumatic delivery E.g. Use of instrumental delivery hematoma
- Maternal Medications
Infant Hx
-
Gestational age, Postnatal age, Ethnicity

Newborn screen results, Infant blood type
Nutrition
Voiding and stooling pattern
Symptoms and signs of sepsis
Hematological Disorder, Splenectomy, Gallstones
Fx
DDx in term of timing of onset
1. Jaundice appearing in the first 24 hours
- Always important and must be investigated, most likely due to hemolytic disease
(ABO incompatibility, rhesus immunization)
- If shows skin hemorrahges (E.g. petechiae), a non-bacterial transplacental
infection E.g. CMV, toxoplasmosis, herpes, rubella is possible
2. Jaundice occurring after the first day
- On the 2nd or 3rd day, most likely to be physiological, if the infants appear sick
other causes must be considered
- Physiological jaundice is a diagnosis after exclusion of more serious conditions
3. Occurring beyond the 4th or 5th day of life
- Generally not due to hemolytic disease
- Look out for bacterial infection E.g. UTI, Septicemia
- Infants of Asian or Mediterranean: Glucose 6-phosphate dehydrogenase
deficiency should be considered
4. Persistent beyond the first 2 weeks of life
Unconjugated form: Breast milk jaundice, hypothyroidism, galactosaemia
5. Conjugated Hyperbilirubinaemia
- A high conjugated level, then an anatomical obstruction or neonatal hepatitis is
the most likely cause
DDx
Unconjugated Hyperbilirubinemia
Physiologic Increased Bilirubin Production
Blood Group Incompatibility: Rh
Congenital: G6PD deficiency, Hereditary Spherocytosis, Alpha-Thalassemia
Decreased bilirubin conjugation or excretion: Hypothyroidism, Gilbert
syndrome, Crigler-Najjar
- Increased Enterohepatic Circulation: Breast-milk jaundice, Bowel obstruction,
Pyloric stenosis
- Infection: Bacterial, Viral
Conjugated Hyperbilirubinemia
- Bile duct abnormalities: Biliary atresia, Choledochal cyst

- Infection: Toxoplasmosis, CMV, Herpes simplex, UTI, Sepsis
- Metabolic: Alpha-1 Antitrypsin deficiency
- Others: Neonatal hemochromatosis, Idiopathic neonatal hepatitis
Clinical Assessment of Jauundice
- Jaundice can be detected when the serum level about 80-90 umols/l
Kramers Rule
100
Limited to head and neck
150
Over upper trunk
200
Over lower trunk, thighs
>250
Over arms, legs, below knee
If the rate of rise is maintained investigations
Signs of extravascular blood: Ecchymosis, Cephalo-hematoma

Ascites, Pleural effusion, Hepatomegaly Rh, Alpha-thalassemia
Pallor, Hepatosplenomegaly Hemolysis
Fever, Temp., Lethargy, Respiratory distress, Vomiting, Seizures
Microcephaly, Petechiae, Hepatosplenomegaly, Chorioretinitis
TORCH infections
Abdominal Mass Choledochal cyst, Intestinal obstruction
Dark urine and acholic stool cholestasis
Management
Phototherapy
-
Convert unconjugated bilirubin to a more readily excretable form

Blue light
SE: Increase water loss, Retinal injury from UV light, Bronze-baby syndrome
(pigment causing is unknown, not a contraindication for phototherapy)
IV Fluid
- To compensate the water loss
Exchange Transfusion
Rapidly correct hyperbilirubinemia and remove antibodies in the setting of
isoimmune hemolytic disease
IV Immune Globulin for Isoimmune Hemolytic Hyperbilirubinemia
-
Treatment of Conjugated Hyperbilirubinemia

-
Lab
Coordinate with a gastroenterologist

Medical management is limited and is purely supportive
Kasai Portoenterostomy for biliary atresia
Conjugated and unconjugated bilirubin

Coombs test test for autoimmune hemolytic anemia
FBC, Blood film
Sepsis blood culture, urine culture, CFS
Serum albumin in assessing the risk of acute bilirubin
encephalopathy
Newborn screens: Hypothyroidism , G6PD deficiency, CF,
Galactosemia
Newborns-L1-Ambiguous Genitalia
Case 1
This newborn has an ambiguous genitalia.
Please take a history from the patient
Explain to the patient what is happening
How to manage/investigate?
Case 2
A newborn was born with ambiguous genitalia. Lab result indicates that she is genetically female with congenital adrenal hyperplasia.
Please explain to the mother.
Answer questions from the mother: What is it? What causes it? How is it treated? Can my baby have a baby in the future? Can it be outgrown? I want to have a baby
again, any screening tests?
1. What are the possible causes?
2. What is your approach to this patient?
Genotypic Females who are Virilized
Always history, physical examination and investigations
Congenital adrenal hyperplasia 21 hydroxylase deficiency
Use a team approach including endocrinology, genetics, urology and psychiatry
Exogenous androgen exposure
Advise the parents to delaying naming or announcing the birth until the definite
Genotypical Males who are Undermasculinized
gender is assigned, which will be determined within 48 to 72 hours
Androgen Insensitivity Syndrome
Remember karyotype should not be the only factor in gender determination
Other androgen synthesis defect
Females will CAH congenital adrenal hyperplasia
Problems of Gonadal Differentiation
History
Partial or mixed gonadal dysgenesis
Maternal: Focus on medications ingestion, exposure to teratogens or infections
Congenital Embryopathy
Fx: Similar situation
Palpable gonads
Length and diameter or the phallus, the position of the urethra, the degree of
fusion of the labioscrotal folds, existence of a vagina
Other dysmorphic features E.g. Urinary tract and anus
Investigations
Karyotyping using the blood and bone marrow samples, also include
AMH A marker for testicular tis
Serum level of 17-Hydroxy-progesterone, 17-Hydroxy-pregnenolone,
Testosterone, DHT, 11-Deoxycortisol, Androstenedione
Serum level of LH and maternal androgens
Biopsy samples
Imaging: Pelvic US can demonstration uterus
3. What is congenital adrenal hyperplasia?
4. What causes it?
The most common cause of virilization in genetic females
Genetic disorder, where there is a deficiency in 21-hydroxylase deficiency
21-hydroxylase deficiency represents 90% of cases
deficiency of cortisol increase in ACTH adrenal hyperplasia causes too
It is an autosomal recessive disorder, with the defect in cortisol synthesis
much androgen to be produced
21-hydroxylase deficiency deficiency of cortisol increase in ACTH
adrenal hyperplasia causes too much androgen to be produced
Clinical Features
External genitalia are virilized
Evaluation
Diagnosis: Measure steroid level following ACTH administration

5. How is it treated?
Cortisol and mineralocorticoid replacement life long
Cosmetic surgical repair
If without treatment
Too little cortisol: Tiredness, weight loss, low BP
Lack of aldosterone: Dehydration
Too much androgen: Grow too fast, early pubic hair and acne, stop growing too
soon causing short statue
7. Can it be outgrown?
No
6.
-
8.
-
Can my baby have a baby in the future?

Increased androgen may cause irregular period in female, make it harder to
conceive a baby
If she takes medications as directed, she can become pregnancy and have a
baby
I want to have a baby again, any screening tests?

Can be diagnosed by amniocentesis or chorionic villus sampling
Newborns-L1-Vomiting
This baby was born few hours ago. On first feeding, the baby vomited. Her first time mum was worried and asked for your help.
Please take a history from the mother
What do you think is happening?
What is your plan?
She turn out to have pyloric stenosis. Please explain to the mother.
1. Possible causes.
2. Explain hypertrophic pyloric stenosis.
Metabolic: Galactosemia, Other inborn errors of metabolism, DM
Causes
Congenital: Esophageal stricture/web/ring/atresia, Pyloric stenosis, MalMost common congenital abnormalities of children
rotation, Imperforate anus, Hirschsprung disease
Caused by the hypertrophy and hyperplasia of the smooth muscle
GIT: Reflux (remember if fails to respond to treatment, consider EE Eosinophilic
Clinical Features
esophagitis), Obstruction, Fistula
Symptoms usually begins between week 4 and 7 of age
Infectious: Viral, Bacterial
Progressive, forceful, non-bilious vomiting
Common Causes by Age
Dehydration, weight loss and FTT can develop
If left undiagnosed, metabolic alkalosis and jaundice in 5% of infants
- Infants: Anatomic obstruction, Metabolic disorder, Infection, Reflux,
Evaluation
Overfeeding, Bezoar
Palpable mass or visible peristaltic wave in the RUQ
- Toddler: Infection, Medication, Reflux, Intussusception, Foreign body,
Abdo US is the diagnosis of choice
Bezoar, Malrotation
Treatment
- Child: Reflux, Cyclic vomiting, Malrotation, Infection
Fluid resuscitation
- Adolescent: Pregnancy, Bulimia, Infection, Ulcer, Malrotation, Celiac
Pyloromyotomy
disease, Pseudo-obstruction, Drug abuse, Pancreatitis, Reflux, Cyclic

vomiting
PMH Guidelines
Background
Important Elements of the History
- Very common symptom in children

- Infection is the most common cause of vomiting in children
- But not all vomits is gastroenteritis
Some Points to Remember
The younger the child, the less specific vomiting is for the cause
In infants, reflux is normal, only a problem if they cause pain or FTT
Vomiting is rarely caused by constipation alone
Bilious vomiting (green) implies bowel obstruction distal to the ampulla
of Vater
Vomiting of fresh blood usually implies bleeding proximal to the gastric
cardia
Vomiting of coffee ground implies exposure of blood to gastric juice over
a period of time
Vomitus with a fecal odour is consistent with peritonitis or a low GIT
obstruction
Nature of vomiting: Color (blood/bile), Composition (food), Frequency,

Progression, Projectile (force), Relationship to feeding and position
Bowel Actions: Usual pattern, when was stool last passed, diarrhea
Abdominal Pain
Abdominal Distension Suggest lower bowel obstruction
Infectious contacts
Febrile? Indicates a more serious cause
Other symptoms E.g. UTI
Cough, grunting, respiratory distress Suggests pneumonia
Features of CNS
History of trauma
Possibility of accidental poisoning
Neonates Delayed passage of meconium following birth
Examinations
-
Full general examination
Abdomen, Groin in both sexes

Look for signs of raised intracranial pressure
Investigations
Management
Pre-school children with unexplained vomiting should have urinalysis

If abdominal trauma has occurred, presence of hematuria on urinalysis
may indicate renal or urinary tract trauma
FBC and blood culture
Septic child, Peritonitis
Stool microscopy + Culture
Septic, Bloody stools
U&E, Creatinine
Prolonged vomiting, Sever dehydration
1.
2.
3.
Blood gases
Acidotic, Profuse vomiting, Diabetic patients

with vomitin
Abdominal XR
Suspicion of bowel obstruction/Peritonitis
Abdominal US
Pyloric stenosis, Intussusception, Appendicitis
4.
5.
Use of anti-vomiting medications in children is not recommended

The suppression of vomiting may mask a more serious underlying cause
These drugs associate with significant risk of extra-pyramidal SE and
dystonic reactions in children
If shock correct with normal saline boluses IV
If gastroenteritis is the cause, manage according to the GE guidelines
Surgical consultation: Bile stained vomiting, Bloody stools, Abdominal
distension, Guarding, Rebound tenderness, Localized tenderness,
Palpable mass, Inguino-scrotal pain, Diagnosis unclear
Correct dehydration and electrolyte abnormalities
If bowel obstruction is present, keep fasted, insert a NGT and leave the
tube on open drainage
More Info
Reflux Disease
-
Etiology: Movement of the stomach contents into the esophagus,

commonly caused by a delay in the gastric emptying or transient
relaxation of the lower esophageal sphincter
Clinical Features: Many newborns, typically resolves by 3-6 months, in an
effortless manner, other symptoms E.g. heartburn, chest or epigastric
pain, dysphagia, globus
More severe cases E.g. Recurrent pneumonia from aspiration, esophagitis
If fail to respond to omeprazole likely to be eosinophilic esophagitis
due to food allergy
Evaluation: A clinical diagnosis, but contract studies, upper endoscopy,
milk scans, 24 hour pH probe can be done
Treatment: Improved positioning, Feeding thickened food, Eliminate
spicy food, caffeine and peppermint, Ranitidine, PPI, Antacids
Eosinophilic Esophagitis
-
Etiology: Allergic esophageal disorder

Clinical Features: In children symptoms similar to reflux, vomiting,
regurgitation, epigastric pain, poor feeding, FTT, Older children with
heartburn, water brash, nausea, dysphagia
Evaluation: Upper endoscopy with biopsy
Treatment: Dietary elimination, PPI, Corticosteroid
Achalasia Not common in children
Hypertrophic Pyloric Stenosis
Etiology: Abnormality in the smooth muscle ganglion cells of esophagus,

incomplete relaxation, esophagus become extremely dilated, serving a
reservoir foe food, which can be vomited hours or days after ingestion
- Clinical Features: Rarely develops before teenage years, vomiting and
dysphagia
- Evaluation: Upper gastrointestinal series (a dilated esophagua) or
esophageal manometry (abnormal function of the smooth muscle)
- Treatment: Balloon dilation of the lower esophageal sphincter
Malrotation
Etiology: Most common congenital abnormalities of children,

hypertrophy of the smooth muscle around the gastric pylorus protrude
into the pyloric channel
- Clinical Features: Symptoms usually between 4-7 years of age,
progressive forceful vomiting, dehydration, weight loss, FTT, metabolic
alkalosis
- Evaluation: Palpable stomach, abdominal US (thickened pyloric channel)
- Treatment: Fluid, Pyloromyotomy
Esophageal Atresia
Etiology: Failure of the fetal midgut to rotate to its normal position,

resulting in intestinal obstruction and ischemic bowel
Clinical Features: Signs and symptoms of intestinal obstruction E.g. Bile
stained emesis, abdominal pain, but symptoms can be delayed for many
years, older children present with intermittent vomiting and abdominal
pain
Evaluation: Contrast studies, position of the ligament of Treitz
Treatment: To prevent complication of mal-rotation
Galactosemia
Rare condition
Autosomal recessive condition
Absence of enzyme to digest galactose
Upon commencement of milk develop vomiting, diarrhea, jaundice,
FTT
Investigations
- Plasma concentration is raised
Newborns-L1-Diarrhea
Etiology: Esophagus ends as a blind tube, most commonly include a distal

tracheoesophageal fistula (>80%), not commonly isolated atresia or
fistula
Clinical Features: Diagnosed within hours of birth, the infant coughs,
chokes, and vomits, aspiration pneumonia can occur
Evaluation: Can be quickly diagnosed by passing a nasogastric tube, CXR,
Contrast studies
Treatment: Upright position, frequent nasopharyngeal suction, IV fluid,
Nil by mouth, Surgical correction, patients often require long term
omeprazole
Acute
Viruses: Rotavirus, Enterovirus, Enteric adenoviruses, Noroviruses

Bacteria: Salmonella, Shigella, Campylobacter, Pathogenic E. coli, Clostridium difficile
Parasite: Entamoeba histolytica, Giardia species
Other Infection: UTI, Otitis media, Sepsis
Toxic Causes: Medications, Household cleaners, Neonatal drug withdrawal
Others: Hyperthyroidism, Congenital adrenal hyperplasia
Inflammatory: Appendicitis, Inflammatory bowel disease
Anatomical: Intussusceptions, Partial obstruction
Also consider celiac, lactose intolerance
Chronic
Infection: E.g. Bacteria, Parasitic, Viral infection

Medications: Antibiotics, Mannitol, Chemotherapy agents
Metabolic: Lactose intolerance, Others (Congenital lipase deficiency, Congenital chloride diarrhoea, Congenial sodium diarrhoea, Congenital adrenal hype
Hyperthyroidism, Fat Mal-absorption, Carbohydrate Malabsorption, Protein Malabsorption = Celiac
Anatomic: Mal-rotation, Partial small bowel obstruction, Fistula, Short gut syndrome
Dietary: Overfeeding, Food allergy, Fructose intolerance
Inflammatory: IBD
Others: Irritable bowel syndrome
Neoplastic: VIPoma, Gastrinoma, Lymphoma
Newborns/Kids-L1-FTT Failure to Thrive

This 24 days infants have not been getting enough weight.
Take a history from the mother
What would you look for on physical examination
Work out DDx and investigation if any
Failure to Thrive
rd
Requirements for Normal Growth
Weight < 3 percentile

Definition: Deceleration from growth or falls below 3rd percentile, height
or weight
Taking a History
- Adequate Nutrition
- Normal Physiology
- Hormones
Examination
Thorough Dietary History
Wasting, Height, Head circumference (E.g. Microcephaly)

Look for signs of malnutrition / Dysmorphic features
Observe mother-infant interaction and feeding habits E.g. Position of
child during feeding, Does the mother overreact, Vigorous suck from
baby
- Growth Chart Most patients have normal head circumference but
weight reduced out of proportion to height
- Signs of dehydration,
- Childs Mental Status: Alertness, Interest, Interaction, Responses to
stimuli, Eye contact, Expression of emotion
Common Signs of Malnutrition
Caloric intake, Breast vs bottle, Duration, Dilution, Frequency,

Solid/Liquid
- Problems with feeding: Refusal, vomiting, diarrhea, constipation
- Typical meal for a baby 150ml/kg/day over 4-6 feeds
- Frequency of output
- Onset of weight loss/time period
Birth History
-
Gestational age, Birth weight, Head circumference, Body length, Growth

chart, Complications at birth
Psychological History
Family structure, Unsupportive mother/father, Alcoholic spouse,
Unwanted pregnancy, Unwanted sex of child, Parents with psy illness,
Poor finance, Cultural aspects
Medical History
-
- Genetic potential for normal growth

- Absence of disease
Low BMI, Oral symptoms (bleeding gum in scurvy, vit C), Musculo (muscle
loss, fragile bones, calcium, vit D), Decreased organ function (heart, renal,
lung, intestine, stomach), Abdominal (swollen abdomen, Kwashiorkor)
Major Categories of Causes of FTT
At a glance - Causes
Inadequate Intake
Environmental Non-Organic
Anatomic Cleft palate

Feeding Issues Poor technique, Improper formula preparation, Poor
knowledge of nutrition
- Psychosocial Poor mother-infant bonding, Child neglect, Emotional
deprivation, Maternal mental health, Anorexia
- Neurologic Lack of suck coordination, Hypotonia
Inadequate Absorption
-
Emesis Reflux, GI obstruction, Metabolic disorders

Malabsorption Chronic diarrhea, Celiac disease, Giardiasis, CF, Proteinlosing enteropathy, Excessive juice intake
- Chronic liver disease
Excessive Output
-
- Congenital HD
- Pulmonary D
- Hyperthyroidism
Genetics
Commonest, Eating difficulty, Maternal depression, Disturbed maternalinfant interaction

IUGR (Intrauterine Growth Restriction)
- Low birth weight
- TORCH Toxoplasmosis, Rubella, CMV, HSV, Other viruses
CF: with diarrhea, chest infections
Genetic Syndrome
- Low birth weight, Dysmorphic features
Celiac Disease
- Diarrhea, Irritability
Others: Reflux, Endocrine, Chronic illness
- Metabolic disorder, DM
- Immunodeficiency
- Recurrent Infection
Inborn errors of metabolism, Osteochrondrodysplasias, Chromosomal

abnormalities
Psychological Factors
- Parental depression
- Distractions at meal times
- Poverty
- Poor social support
- Neglect
Management
Types
- Diagnose and treat underlying diseases

- Ensure adequate nutrients
- May consider blood tests for current nutrient status: E.g. Iron studies
- Parental education about diet: Referral to a feeding services
Consider Hospitalization if
- Abuse or neglect is suspected

- Severe malnutrition
- Patient is not responding to outpatient management
Investigations
FFT due to Environmental or Psychosocial Issues
Blood count and ferritin study is useful

Other Examination bases on the clinical presentation
FBC, Iron
Iron deficiency is common, can cause anorexia
I: FTT without other symptoms or signs (E.g. good appetite, no diarrhea)

II: FTT with symptoms (E.g. vomiting in narrowing of the stomach
outflow)
III: FTT with physical abuse
IV: Primary organic disease complicated by FTT
Most common
Difficulties at home, limitations in the parents, maternal depression
Loss in weight, followed by height and head circumference
Developmental stages may delay
U&E
Renal failure
Stools
Low chymotryosin and presence of fat malabsorption
Celiac Ab
Celiac disease
Sweat test
CF
Thyroid, TSH
Congenital hypothyroidism
Karyotype
Chromosomal abnormalities
- Often due to eating difficulties, where meals become very stressful

Management
-
Nutritional advice
Feeding services
Social health services if neglect
Malabsorption
Chronic Illness
Important cause of FTT

Symptoms of diarrhea, colic
Commonest causes: Celic disease, CF
Celic disease: Weight loss coincident with introduction of gluten to the
diet
Newborns-L1-Prematurity
Not commonly grow poorly

Rarely present as FTT
This infants was born premature at 28 weeks.

- What are the signs of prematurity on physical examination?
- What are some medical problems of premature infants?
- How will you manage?
23-27 Weeks
31-41 Weeks
At 24 weeks, about 700g

Thin skin, Dark red color
Ears: Pinna soft, no recoil
No breast tissue palpable
Male: no testes in scrotum, Female: Prominent clitoris, labia majora
widely separated
Breathing: Need respiratory support, apnea common
No coordinated sucking, Usually needs total parental nutrition then tube
feeding
Faint cry
Eyelids may be fused, infrequent eye movement
Startles to loud noise
Limbs extended, jerky movements
Airway, Breathing
Examination
-
Respiratory Distress Tachypnea, Breathing with chest wall recession,

nasal flaring, expiratory grunting, cyanosis, Apnea
Management
At 40 weeks: 3.4 kg
Thick skin, Pale pink color
Pinna firm, Immediate recoil
One or both nodules >1cm
Male: Scrotum has rugae, testes in scrotum, Female: Labia minora and
clitoris covered
Rarely requires respiratory support
Coordinates sucking
Cry loudly
Makes eye contact
Follow faces
Turns head and eyes to sound
Flexed posture, smooth movements
Temperature Controls
Place in a plastic bag at birth to keep warm
Perform stabilization under a radiant warmer or in an incubator to avoid
hypothermia
Avoid hyperthermia, as may increase brain injury
- Clear the airway

- Oxygen
- CPAP
- Mechanical ventilation
Monitoring
-
Oxygen saturation, maintain 88-95% if preterm

HR, RR, Temp., BP, Glucose, Blood gases
Weight
Venous and Arterial Lines
Peripheral IV line
CXR +/- Abdominal XR

-
- Required for IV fluid, antibiotics or other drugs

- May be used for parenteral nutrition
Umbilical Venous Catheter
Assists in the diagnosis of respiratory disorders and to confirm the

postion of the tracheal tube and central lines
May be used for immediate IV access to obtain blood samples or to

administrate fluids or medications
Arterial Lines
-
Inserted if frequent blood gas analysis, blood tests and continuous blood
pressure monitoring
- Usually umbilical artery catheter, sometimes peripheral cannula of for
short period of time
Central Venous Line
-
For parenteral nutrition

Inserted peripherally when infant is stable
Investigations
Antibiotics
FBC, Hb, Neutrophil, Platelet

Blood urea, creatinine, electrolytes
Culture Blood/urine/CSF
Blood glucose
CRP
Coagulation if indicated
Minimal Handling
All procedures adversely affect oxygenation and the circulation

Analgesia should be provided to prevent pain
Infants require ICU care usually given broad-spectrum antibiotics
Parents
Time must be found for parents to allow them to see and touch their
baby
Newborns-L2-Murmur
Case 1
A baby was born yesterday. On newborn examination, you notice a cardiac murmur.
-
What is your approach?
What are the features of an innocent murmur?
How about pathological murmur?
What are some pathological causes of a murmur?
Case 2
6 months old comes to see you for his vaccination. You noted a cardiac murmur.
-
List 6 factors that will help you decide if this is pathological based on history or examination.
You think it is a small ventricular septal defect. What important information and advice will you give Ryans parents?
What are the contraindications of vaccination?
1. Approach.
- History, Physical Examination, Investigations
History
- Ask for symptoms of heart failure, tachycardia, tachypnea, edema
- Cyanosis
- Poor feeding
- Weight and height
- Fx of chromosomal disorder or congenital heart disease
- Also ante-partum, during labour and post-partum history
- Peripheral Signs: Dysmorphic features, Growth charts, Cyanosis, Clubbing,
BP, Peripheral pulses, Chest observation
- Palpation and Auscultation: Thrills, Heaves
- Listen to the characteristics of the murmur
Investigations
- Refer to an experienced cardiologist, who can differentiate innocent
murmur quite well
- ECG, CXR
- Echo required sedation, should only be ordered by the cardiologist who
have examined the kid, take about 45-60mins to complete
3. What are the features of a pathological murmur?
- Thrills
- Harsh
- Diastolic murmur
2. What are the features of an innocent murmur?

- Vary with position E.g. Softer on sitting or standing
- Louder with temperature or exercise
- Usually ejection systolic, apart from a venous hum
- Not harsh
- Quite localized
- Grade 1-3
- Never a thrill
- Never a diastolic murmur
Venous Hum
- Turbulent flow at the junction of the subclavian vein and head vessels
- Continuous murmur, which disappear when turning the head
4. Organic causes of a murmur.

- Cyanotic: TGA (Transposition of the great arteries), Tetralogy of fallot
- Non-Cyanotic: VSD, ASD, PDA, Coarctation, Aortic stenosis, Pulmonary
stenosis
- Radiation of the murmur to the back

- Absent femoral pulses
- Cyanosis
- FTT
- Signs of heart failure
4 types of innocent murmur
- Still murmur Musical, normal ECG and CXR
- Venous hum Continuous murmur, usually on right side, disappear on
lying
- Pulmonary flow murmur Loudest in the 2nd left intercostal space
- Physiological neonatal peripheral pulmonary stenosis Loudest in the 2nd
left intercostal space, radiate to back
Newborns-L2-Down Syndrome
This baby was born with Down Syndrome. The parents have just been informed about the diagnosis and know nothing about the condition.
- Please explain to the parents what Down Syndrome is and the implication of it on their baby.
- Answer questions from the parents.
1.
2.
Introduction
Medical Complications
- Greet parents, Introduce self
- Congenital Heart Diseases: 50% have a congenital heart disease
Diagnosis
- Malignancies: Leukemia are common, transient leukemia can affects up
to 20% - typically benign and resolve on its own
- Down Syndrome
- Thyroid: Hypothyroidism is common
Knowledge
- How much do they know about the condition?
- GIT: Risk of Hirschsprung disease (nerve controlling part of colon is absent
severe constipation)
Attitude
- Reassure and comfort the parents as necessary
- Neurology: Risk of epilepsy and Alzheimers disease
Etiology, Clinical Manifestations, Complications
- Eyes: Cataracts, Strabismus, Refractive errors are common
- A chromosomal abnormalities with the presence of an extra 21
- Hearing loss
chromosome causing:
- Physical Characteristics: Un-slanting eyes, Wide palpebral fissure,
Prominent tongue, Hypotonia, Flattened occiput, Single palmar creases,
Wide space between 1st and 2nd toes, Spots on the iris, Curved 5th finger
- Mental Characteristics: Intellectual disability IQ 50-70, Mental qualities
have been described to be unisexual, playful, affectionate, Commonly
have a speech, fine motor skills, gross motor skills delay, some will being
walking at around 2 years
3. How are we going to manage her?
4. Can she get married and have children?
- Multidisciplinary approach
Infertility
- Manage medical complications
- Both males and females are affected
- Regular follow-ups
5. My baby look weird, can plastic surgery help?

Plastic Surgery
-
Females: Often have miscarriage, premature birth, difficult labor
Males: Also all infertile, as defects in spermatogenesis
6. Can my daughter graduate from uni and work?

- Most graduate from high school and can do paid work
To reduce the facial features associated with Down Syndrome

decrease social stigma, better quality of life, but still uncommon and
continues to be controversial
7. How about the life expectancy?

- Shorter than normal people, mean about 60, but 87 is the oldest reported - But most develop Alzheimers disease like dementia in late 40s and 50s
Newborns-L2-Cerebral Palsy
-
What is cerebral palsy?
List 8 problems associated with cerebral palsy.
What are the causes?
What are the early features?
What are the types?
What is the management?
1.
-
2.
Disorder of the movement and posture due to lesion of the motor
pathways in the brain
The lesion is non-progressive, but symptoms emerge over time
Most common cause of motor impairment in children
4.
Learning difficulties
Epilepsy
Hearing impairment
Speech disorder
Visual impairment, Strabismus
Feeding problems
Behavioral disorder
Hip subluxation, Joint contractures, scoliosis
Antenatal: Congenital infection, Structural mal-development of brain,

Genetic syndromes
At Birth: Hypoxic ischemic injury
Postnatal: Meningitis, Encephalitis, Head trauma, Kernicterus
6.
Abnormal limb tone or posture, delayed motor milestones

Feeding difficulties Slow feeding, gagging, vomiting
Abnormal gait
Asymmetric hand function
Primitive reflexes may persist
3.
5.
Spastic: Most common form, 70-80% of individuals, injury UMN pathway,

limb tone is increased, brisk deep tendon reflexes, 3 types: Hemiplegia,
Quadriplegia, Diplegia (all 4 limbs affected, but legs affected more)
- Ataxic: Cerebellar injury, signs are relatively symmetrical, side based
unsteady gait, abnormalities of voluntary movement
- Dyskinetic: Injury to the basal ganglia, classically associated with
kernicterus, chorea
- Mixed
Kids-L1-Abuse (Came out in 2012)
-
Refer to central for cerebral palsy

Physio Walking aid, Strecthes
OT
Speech
Social working
Ophthalmology, ENT
Hearing services
Rehabilitation team
If you see a X-ray in any of the ped station, 99% it will be an abuse station. Usually there will be 2 x-rays. One really obvious to have a fracture, while the
other one is not obvious = a healed fracture. They wont show you a normal X-ray.
1. Interpret this X-Ray.
2. Take a history from mum.
The mum denied any abuse.
3. Discuss management.
4. What are the 4 features that would
make you think about child abuse?
5. What would you do in a case of
suspected child abuse?
2.
- Ask about how the accident occur? When? Where? Who was supervising
the child? Any delay in seeking treatment? Type of injury? Magnitude of
force? First time?
- Focus on the social history E.g. Divorced? Unplanned pregnancy?
Financial difficulty? Relationship with partner?
- Alcohol or drug abuse?
4.
- History from parents does not correlate with the signs and symptoms of
the child
- Delay in seeking medical attention
- Injury in pre-mobile infants
- Abnormal parent-child interaction
- Parents more interested in returning home than child
3.
- Explain to the mum, what she has been describing does not correlate
with the X-ray
- There is a possibility physical abuse may have occurred, and require more
investigations for confirmation E.g. Skeletal survey, Brain US/CT, more
detailed physical examination
5.
-
Skeletal survey, Brain US/CT, Check other sites for injury

Contact child protection unit
Discuss with a senior team member
Record accurately
Involve social worker
- Previous abuse in other children

- Domestic issues E.g. Alcohol, Drugs, Mental problems, Poverty, Violence
Kids-L1-6 weeks check, breast feeding issues
-
Basically, it is same for the newborn check (see also newborn check in neonatal section)
But also have to take a history from the mum E.g. Feeding issues, depression, recovery from pregnancy, contraception
General Inspection
- Distress, Breathing difficulty, Interaction with surrounding
- Color: Blue, Jaundice
- Skin: Rashes, Dermatitis, Salmon patches, Mongolian spots, Caf au lait
macules (brown macules, > 6 is suggestive of neurofibromatosis)
Eyes
- Check for red reflexes and exclude cataract
- Strabismus Should be diminished within the first 2-3 months of life, if
persists after age of 3 months ophthalmologist
- Features of Down Syndrome: Up-slanting eyes, Wide palpebral fissure,
Prominent tongue, Flattened occiput, Single palmar creases, Curved 5th
finger, Wide space between the 1st and 2nd toes, Spots on iris
Oral Cavity
- Teeth: Primary teeth typically occurs at the age of 6 months, Natal teeth
can present shortly after birth and may interfere with feeding
- Cleft palate
- Thrust
- Epsteins Pearl, Bohns Nodule, Dental Lamima Cyst
Abdomen
- Palpation: Enlarged liver, Spleen, Kidneys
- Umbilicus: Cord generally falls off 7-12 days, may take linger, presence of
oozing, a few drops of blood, a mild odor is normal, concern if significant
redness, discharge, bleeding continuously
- Umbilical Hernia (repaired is usually done if persists beyond 5 years),
Omphalitis, Umbilical granuloma, Patent omphalo-mesenteric duct
(connection between the ileum and umbilicus), Patent urachus
(connection between the urinary bladder and the abdominal wall)
- Femoral pulse
Genitalia - Girls
- Labial adhesion
Cranium
- Inspection: Swelling or asymmetry of the cranium caput succedaneum
(caused by fluid collection by the pressure of the presenting part, resolves
during the first few days of life), Cephalo-hematoma, Molding (positional
plagiocephaly)
- Palpation: Premature closure of a suture by feeling the fontanelles
Ear
- Hearing:
Chest
- Inspection: Movement of chest wall for respiratory distress
- Auscultation: Heart sounds, Murmur
- Breast hypertrophy , may result from passage of maternal hormones
across the placenta during gestation
- Galactorrhea
- Mastitis
Genitalia Boys
- Hypospadias Urethra opens on the ventral side
- Epispadias Urethra opens on the dorsum of penia
- Undescended testis Most descends during the first 3-6 months, if
undescended at 4-6 months refer to urologist, treatment can be
performed after 4 months to 1 year of age
- Inguinal hernia
- Hydrocele Persistence of the process vaginalis, allows fluid to pass into
the scrotal sac, transilluminate, if persists at the age of 6 months to 1 year
referral to a surgeon
Hip Screen for developmental dysplasia of the hip
Barlow Test
Vaginal discharge and bleeding (if happens in the first week, discharge
usually due to maternal estrogen in gestation, bleeding usually due to
withdrawal of maternal estrogen)
Detects a hip that can be dislocated posteriorly by gentle adduction and

posterior pressure
- Placing the middle finger on the greater trochanter with the knee bent,
then flex the hip gently pushing into the examination table
- The purpose is to dislocate unstable hip
- If the hip can be popped out of socket = +ve
Ortolani Test
- A dislocated femoral head that is reduced into the acetabulum
- Involves abducting the hip and palpating for a clunk as the hip joint
relocates
- If clunk can be heard and felt as the femoral head relocates anteriorly
into the acetabulum = +ve
If both are +ve referred to an orthopedist, or have a US, if >4 months
consider hip XR
- If uncertain E.g. Soft click check again in 2 weeks,
Last but no least
- Weight, Length, Head circumferences
-
Neurological
- Tone: Including head lag, assess by pulling baby to sit with his/her hands,
head lag will still be present, but the baby should then bring head to
upright position for a short time, When holding baby prone, baby should
raise head and legs above horizontal with back straight
- Turn the infant over and check spine (Check of bulges, Spina bifida,
Pigmentation)
- Check anus is patent
Reflexes:
- Grasping Gone by 3 months
- Rooting and Sucking Gone by 4-6 months
- Stepping reflex Gone by 6 weeks
- Moro reflex Gone by 4 months
- ATNR Asymmetrical Tonic Neck Reflex Gone by 6 months
- Landua Reflex Present at 4 months, gone by 2 years
- Parachute Reflex Present at 8 months and persists
Others
- Neck Righting Gone by 2 years
- Head Righting Present at 4-6 months and persists
Kids-L1-UTI
Zoey Smith, 20 months old patient has had a urinary tract infection confirmed on microscopy and culture on a clean catch urine specimen. Zoey is completing
an appropriate course of antibiotics and has turned with her mother for review. Please explain to Mrs smith what you management will be and why.
A brief history.
Management
When did you son has the UTI? Symptoms free now?
Has he been taking the antibiotics? Any side effects from the antibiotics?
Is this the first time that your son has been diagnosed with an UTI?
So he has never had any ultrasound scan done on his urinary tract?
Further Management
- Another thing I need to organize is further investigations of your sons
urinary tract.
- It is important for us to rule any structural abnormalities of the urinary
tract, because of potential long term complications E.g. Hypertension,
Renal failure
- When we talk about urinary tract, we are taking about 2 kidneys, 2
ureters, 1 bladder and 1 urethra. Let me draw you a little diagram.
Urination keeps the urinary tract free of bacteria by flushing them away.
If there are any abnormalities along the urinary tract, the flushing process
may be inhibited and increases risk of UTI.
- Renal US and Voiding cysto-urethro-gram
Renal US
So there are few things we need to do now for the urinary tract infection.
First of all, it is good to hear that your son is improving and is now
symptom free.
However, we do need to repeat the urine test to make sure that the
infection is cleared before we stop the antibiotics. Even though you son is
symptom free now, but the infection could still be there which can be
detected by analyzing the urine.
If ve, we can stop the antibiotics, If +ve, we need to continue the
antibiotics
1.
2.
3.
4.
This is not painful

Looks for structural abnormalities of the tract, Kidney size, Any scarring or
damage
Voiding cysto-urethro-gram
-
1.
-
A catheter (a plastic tube) will be inserted to empty the bladder

This is uncomfortable
Radiocontrast dye run through and fills the bladder, the movement of the
dye will be viewed by live x-ray while the patient micturates
But the only way to assess if the urine refluxes back up towards the
kidneys from bladder
Vesico-ureteric reflux = urine flow from the bladder into the ureter or
kidneys (causes: Short ureters, Increased bladder pressure E.g.
Obstruction)
If +ve for reflux prophylactic antibiotics
2.
Most of the time, the bacteria come from normal flora in the bowel E.g. E. coli
Yes
Where did the infection come from?

Are these tests really necessary?
What are you looking for?
Can you tell me how the test is done?
It is important for us to rule any structural abnormalities of the urinary

tract, because of potential long term complications E.g. Hypertension,
Renal failure
- Abnormal urinary tract is found in over 40% of children who have had a
UTI
Urine Sampling
3.
Abnormalities is found in over 40% of children who have a UTI
-
Urine bag samples are unreliable, should not be used

Clean catch samples are more reliable and preferred
If samples are required urgently (E.g. in order to give timely antibiotics in
infants), bladder catheterization is preferred, may consider supra-pubic
aspiration (pre-procedure to confirm a full bladder)
Samples for urinalysis, microscopy, culture
Vesico-ureteric reflux Flow of urine from bladder to kidneys

Posterior urethral valve Bladder outlet dysfunction buildup of
pressure
- Pelvico-ureteic junction obstruction Obstruction between the renal
pelvis and the ureter
- Vesico-ureteric obstruction O between the ureter and bladder
Kids-L1-Burns
18 month old brought in with burns on her face and chest after pulling a hot cup of coffee onto herself.
1.
2.
3.
4.
5.
1.
What further history would you ask from mother?

What features of the burns would you look at on examination? What other general examination would you do?
2 most important things you would do straight away? How to manage?
What are the indications for admission?
What would you tell the mother about preventing future accidents?
2.
What happened? How did it happen?

Time since burn?
Types of burns
Duration of burns
Was there an explosion associated inhalation burns
Any first aid? Running cool water for 20 mins?
Any delay in seeking medical treatment?
Vaccination up to date?
- Superficial: Pink, Erythema

- Partial: Painful, Erythema, Blister, Blanch with pressure
- Full: Black, Painless
- Distribution, Burns surface area %
Also
-
Vitals
Burns surface area %
Check for airway E.g. Inhalation
Check for concurrent injuries E.g. Fractures?
Px medical history, Allergies?

3.
-
4.
ABC
Analgesia
ABC
Airway: Consider early intubation with inhalation burns
Breathing: Give oxygen as required
Burns >8%, Chemical/electrical burns, Partial or full thickness burns,

Inhalation burns, Abuse, Social concerns, Special body area
- Circulation: Treat acute shock with 0.9% saline

First Aid (if this has not been done)
- Stop the burning process
- Cool the burn with cool running water for 20 min, do not use ice
- Remove clothing, cut around adhered clothing if required
- Remove jewellery
- Keep the patient warm
Analgesia
- Intranasal Fentanyl = 1st line
- With vascular access IV morphine
- Oral: Paracetamol, Ibuprofen
Assess for Concurrent Injuries
Dressing
At the burn clinic, apply an antibacterial cream (SSD Silver Sulfadiazine)
can be applied to the anywhere except the face
- SSD is ototoxic and must not get into the ear canal
- For facial burns, apply Chlorhexidine cream 4 hourly (this is available on
the burn units)
- Cover the SSD with gauze, then apply bandaging
Tetanus
-
5.
Prevention of Hot Tap water
-
Always test the water temperature before bathing a child (maximum

temp. = 38)
- Runs the cold water before hot water
- Always stay with the children when they are in the bathroom
Prevention of Hot Food and Drink
- Use non-slip placemats
- Put hot drink in the center of the table
- Keep children out of kitchen while cooking
Prevention of Contact Burns
- Keep children out of kitchen while preparing meals
- Supervise children at BBQ
Kids-L1-Anaphylaxis
Case
Jenny Smith is a 25 years old lady, who has a son recently diagnosed with Mars Bar Allergy. Explain to her about anaphylaxis and how to use an Epipen.
Explanation of Anaphylaxis
Presentations
Our body has an immune system that helps us fight against harmful
pathogens such as bacteria or parasites.
However, for some reasons, our body may mis-recognize non-harmful
substance (such as food or medications) as harmful substance and start
to attack them.
While attack them, it releases a lot of inflammatory mediators such as
histamines which causes a range of symptoms and signs of
anaphylaxis
Clinical Features
-
Skin: Rashes, Conjunctival erythema, Itch, Urticaria, Angioedmea

Resp: Dysphagia, Stridor, Chest tightness, Cough, Wheeze
Cardio: Palpitation, Tachycardia, ECG changes, Hypotension, Cardiac
arrest
Abdominal: V+N, Abdominal pain
Neurological: Dizziness, Collapse, Confusion, Incontinence
Prevention in Long Term

-
Identification and avoidance of triggers E.g. Skin prick test, RAST test
Strict elimination diet
Dietician referral
Review 1-3 yearly with repeat SPT/RAST +/- Oral challenge tests to
determine clinical tolerance
Difficulty breathing
Swelling of tongue
Tightness of chest
Difficulty talking or hoarse voice
Symptoms
- Coughing
- Wheezing
- Shortness of breath
- Vomiting
- Collapse
Management
Signs
-
Wheeze or persistent cough

Loss of consciousness
Pale and floppy
Collapse
Stridor
Aphonia
Bronchospasm
Shock
Cardiorespiratory arrest
In regard to the management plan, Epipen is designed to manage this kind

of situation.
- When your son showed any symptoms or signs of anaphylaxis, you need
to use an Epipen.
- Epipen is actually a pen looking needle which contains Adrenaline, which
is the medication we need to give in someone with anaphylaxis.
- When you son showed any symptoms or signs of anaphylaxis, you need to
lay your flat, do not stand or walk
- Remove the Epipen out of the carrier tube
- With your other hand, pull off the blue safety release
- Hold orange tip near outer thigh
- Firmly push against outer thigh until it clicks (so that it is perpendicular to
the thigh)
- Hold it for 10 seconds
- Remove it, and the orange cover will cover the needle (may massage the
area for 10s)
- Call ambulance to seek further treatment
- Take the used epi-pen with you to the ED
- If no response after 5 mins, give another dose is available
Dosage
-
0.3 mg for patients who weigh 30kg or more

Epipen Jr: 0.15mg for patients who weigh 15-30kg
Learn to recognize early warning signs, carry an EpiPen, also put one at
school, also give an action plan for school
- Anaphylaxis action plan
- Wear Medic Alert Bracelet
Kids-L1-Juvenile onset DM
You are a RMO working at the PMH ED. A mother brings in her 6 years old son who does not look so well. Take a focus history and explain to the mother what
is wrong with the child. What needs to be done?
History - PC
Px
-
Im one of the doctors working in the ED. Can I have you name please? I
understand that your son has not been feeling well. And I would like to
take a more detailed history and see what we can do about it.
- When did the vomiting start?
- Frequency? How often? How many times has he vomited?
- What is the color of the vomit? No blood?
- Could you describe the action of vomiting? For example projectile
vomiting? Effortless? Really exhausted?
- Anything makes it worse or better?
- Has he been recently sick or in contact with people who are sick?
- Has he been drinking enough water?
- When was stool last passed,
- Other symptoms: Diarrhea? Abdominal pain? Jaundice?
- General: Sleeping? Appetite? Loss of weight? Fever? Fatigue?
- Any skin rashes? Viral GN
Systemic Review
- Respiratory: Coryza, Cough, Breathing difficulties, Sweating at nights

- Cardio: Have he been blue? Swelling of limbs?
- Endo: Polyuria, Polyphagia, Hypo/Hyperthyroidism
- Genito-Urinary: Dysuria, Smelly urine
Medications and Allergies
Immunization
Fx
- Up to date
Developmental
Diabetes
Pregnancy History
- How was the pregnancy?
- Was it term?
- Complications?
- Low birth weight?
Birth History
-
What was the method of delivery? Why?

How long did it take?
Any complications during labour like prolonged labour, ruptured water
bag, fever
Newborn Hx
How was he at birth?

How much was his weight?
Any complications? E.g. Yellow, blue, fever, didnt cry immediately?
What/When/How long?
Physical: What is his weight and height now?

Millstones: Is he able to? (Gross motor, fine motor, speech, social) At
what age is he able to walk? Was he able to complete formboards by the
age of 2? How about his speech? Toilet training? Self-feeding using
cutlery?
Social
Kid
- How is he doing at school? Not missing out a lot of school?
Parents
- What is the occupation of parents?
- What is the height of the parents?
- Financial issues?
Environment
Social/School performance: How is his temper? Is he irritable, crying

frequently? What about sleep? What grade? Any problems at school? Any
failures or suspensions? What is his daily routine?
More History from the patient
-
Vomiting consistently for 3-4 days = Diabetes

Lost 7 kg over the past 6-7 weeks
Always tired
Going to toilet more often, Has been wetting the bed
- Similar problems in relatives, daycares, school?

- Who is usually taking care of him?
- How are the family relationships?
- How has this been affecting the family?
- Do you feel your mood down?
- Any lost workdays?
- How are you managing with the expenses?
Investigations
I would also like to examine you son. This is quite important as it helps
me to evaluate how sick your son it. Basically Im going to:
General Inspection: Responsive? Interacting? Distress? Jaundice? Skin
rashes? Pallor?
Vitals: HR, RR, Temperature, BP
Weight
Hands: Pallor? Diminished skin turgor? Capillaries refills?
Head: Pallor? Dry mucous? Sunken eyes?
Abdominal: Tenderness? Distension?
You son has been vomiting for the past 3-4 days. Common things are
common. The commonest causes are infection such as viral
gastroenteritis/infection of the gut or UTI.
- However, something that you told me in the history, for example, loss of
weight of 7 kg and going to toilet more often makes me think about other
possibilities such as diabetes. We do see kids with diabetes present with
vomiting, weight loss and passing water more often. What is more, you
son is quite sick.
Therefore, I would like to do initial investigations:
-
Management
At this moment, while waiting for the test results to come back, only
management is rehydration
Fluid hydration
Insulin if diabetic ketoacidosis
If DK, watch for K+, may need K+ replacement
Blood: FBC, U&E, CRP, ESR, Glucose, Ketone

Urinalysis (also check for glucose)
Others: Blood culture, Stools culture, Abdominal XR or US (Bowel
obstruction, Peritonitis, Pyloric stenosis, Intussusception, Appendicitis)
Kids-L1-Rehydration/Gastroenteritis
Simon is a 4 years old boy who presented with 8 hours history of being unwell with 3 non-bilious vomits and 2 loose stools. You feel that he looks well that is
not dehydrated and you can wait and see. What advices would you give to his patient regarding management for the next 24 hours?
Introduction
Causes
-
I am a one of the doctor working for the emergency department. Can I

have you name please?
- I understand that your 4 years old Simon has vomited 3 times and had 2
episodes of diarrhea over the past 8 hours.
- He looks well and is not dehydrated.
- So basically Im here to discuss to you what are the likely causes and how
we are going to manage your sons vomiting and diarrhea. There will be
time for you to ask me any questions.
Management
1.
In regard to the management, sometimes we do investigation such as

blood test or stool culture if the patient is really sick. However, you son
Simon looks well and hydrated. So those investigations are not
appropriate in his case.
The main management will be getting him hydrated. It is because
vomiting and diarrhea can lose quite a lot of fluid especially in children
and make you son really dehydrated.
(No anti-emetics or anti-diarrheals, risk of dystonic reaction in children)
To do that, we can give him water (small risk of hyponatremia) or oral
rehydrating solution (better, less vomiting, less diarrhea) in frequent and
small volumes by spoon or synringe. For example, 5ml for every 1-2
minutes. Less likely to vomit
Replacement in the first 4 hours: 100/ml x 10 weight (kg) = 1000 over 4
hours
In the next 24 hours: About the same E.g. 1000ml over 24 hours
Importantly, we should avoid sweets drinks or juices make the
diarrhea worse due to osmotic effects
Do you have any questions
1. I gave him a drink but he vomited it all back.
2. What is gastrolyte or oral rehydrating fluid?
3. I shouldnt give him any food or milk. Im worried about that he hasnt
eaten since last night.
4. What should I worry about?
5. Could this be anything else? What should I look for?
Vomiting and diarrhea in children can have a number of different causes.

But the most common causes are infection such as viral, bacterial or
sometimes parasitic infection. And viral gastroenteritis remains the
commonest cause.
Complications of Dehydrations
2.
Seizures
Shock with tachycardia
Shallow breathing
No urination Kidney failure
Coma
Death
Frequent and small volumes by spoon

If signs of dehydration + not drink consider NGT then IV fluid
But at this moment, he looks hydrated keep encouraging him to drink
frequent and small volumes
3.
-
They have the same concentration as the body fluid

Tolerated better, Rehydrated better
4.
He has the energy reserves to carry him through a period of fasting
Early introduction of diet promotes recover, as long as he is tolerating
- Poor fluid intake and still vomiting

- Large amount of vomiting and diarrhea
- Pallor, Lethargy, Drowsiness, Sunken eyes
- Poor urine output
- High fever, Headache, Urinary symptoms
- Bile-stained vomiting, Abdo pain
- New onset of symptoms
Others
5.
Enteric Infection: Viral (Rotavirus, Adenovirus, Astro virus), Bacterial
(Salmonella, Campylobacter, E. Coli, Shigella, Vibrio cholerae), Protozoa
(Giardia, Cryptosporidium, Entameba)
- Food Poisoning: Severe bacteria and bacterial toxins
- Systemic Infection: UTI, Septicemia, Pneumonia, Otitis media
- Surgical Conditions: Appendicitis, Intussusception, Partial bowel
obstruction
- Others: DM, Antibiotics, Congenital adrenal hyperplasia
What to Look for?
-
Careful hand-washing to avoid cross infection
- Bloody diarrhea
- Watch for reaction to food
- UTI passing urine, pain when passing urine
- Abdominal pain
- Thirsty, Loss of weight, Polyuria, Tired
Kids-L1-Ped resuscitation
Background Knowledge Adopted from Pediatric Hospital Life Support (August 2012)
Background
Estimated Weight in kg by Weight
Neonate Up to 28 days
Infant - <1 year
Child 1 year to puberty
Older children may be treated as adult, but they do not have the same
occurrence of ventricular fibrillation as adults
Anatomical Differences
0-12 months = (0.5 x age in months) +4

1-5 years = (2 x age in year) + 8
6-12 years = (3 x age in year) + 7
Vital Signs by Age
Airway: Neck in short, Head in large, Tongue is large (viewing of vocal

cords more difficult during intubation), Airway narrower (more easily
obstructed), Infants are obligate nose breathers (at risk of airway
obstruction if nose is blocked)
- Breathing: Immature thoracic features (at risk of respiratory fatigue) E.g.
immature intercostal muscles, weak accessory muscles, horizontal rib
position
- Circulation: Circulating blood volume is smaller (a small blood loss if
more significant)
- Psychological: Fear, Poor communication
Pathways Leading to a Cardiac Arrest
Recognition of Seriously Ill Child
Circulatory Failure
Effort of Breathing
- Fluid Loss: Blood loss, Burns, Gastroenteritis

- Fluid Misdistribution: Septic shock, Anaphylaxis, Cardiac disease
Respiratory Failure
- Respiratory rate
- Recession
- Accessory muscle use
- Flaring of the nares
- Stridor or wheezing
- Grunting (exhale against the glottis)
Circulation
- Respiratory Distress: Asthma, Croup, Foreign body, Bronchiectasis

- Respiratory Failure: Convulsion, Increased ICP, Drug induced
In Children
-
Most are secondary to a respiratory cause

Can also due to loss of fluid cardiac failure
Rarely from cardiac disease
- Alert, Respond to voice, Respond to pain, Unresponsive

Oropharyngeal Airway
Airway and Breathing Management

-
- Capillary refills (>2s = poor circulation)

- Weak pluses
- Cyanosis
- Hypotension
Neurological
Infant = Neutral Position
Child = Sniffing Position
Inspect the airway (before this, check for response and call for help)
-
Useful to maintain a patent airway
It is acceptable to use suction to remove secretions from the oropharynx

and nasopharynx
Breathing
-
Once a patent airway is achieved, spontaneous breathing should occur

If breathing is abnormal or not present 2 rescue breaths (mouth to
mouth or a bag and mask Connect to oxygen 10L/min)
Cardiac Arrest and Lethal Arrhythmias
-
Infant: Pulse rate <60 bpm Start chest compression

Children (1-8 years): Pulse rate < 40 Start chest compression
(30 compressions to 2 breaths) Attach a defibrillator (adults patches
for children > 10kg, Infant patches for children <10kg)
(ask for IV/IO access) Urgent blood sample may be taken at this point
(check for glucose)
Compression and breaths for 2 mins (about 5 cycles)?
ETT
Size = Determined by the distance between the center of the lip and the
angle of the mandible
Inserted under direct vision, using a tongue depressor
4 Cardiac Arrest Rhythms

Asystole
- Most common
- A flat line
- Make sure it is not caused by disconnected leads
- Treatments: Immediate CPR, Followed by administration of adrenaline
Pulseless electrical activity
- Treatments: Immediate CPR, Followed by administration of adrenaline
Ventricular fibrillation
- Uncommon in child
- Treatment: Defibrillation and CPR
Pulseless ventricular tachycardia
- Pharmacology and Fluid

Fluid Administration (given after the defibrillator)
-
Intraosseous Access
Intravenous or intraosseous access should be gained

Followed by a bolus of 20mL/kg of normal saline (except for those with
sign of heart failure)
- Urgent blood sample may be taken at this point
Adrenaline
- Indicated in asystole and pulseless electrical activity

- Also in VF and pulseless VT after the second shock
- Dose: 10mcg.kg (0.1ml/kg of 1 in 10,000) via IV or IO
- SE: HTN, Myocardial ischemia, Tachyarrhythmias
- (Adrenaline can be administrated via ETT)
Glucose
- Blood glucose should be check frequently

- 2ml/kg of 10% glucose
Calcium Gluconate
- Transiently increases myocardial contractility and excitability

- Seldom indicated in cardiac arrest
- Indicated for hyperkalemia, hypocalcemia, over-dose of Ca++ blockers
Post Resuscitation Care
Re-evaluate ABCDE
12 lead ECG
Treat precipitating causes
Re-evaluate oxygenation and ventilation
Temperature control
Extremely uncommon
Treatment: Defibrillation and CPR
Quicker than IV
Indicated if attempts to gain IV access take longer than 90s
Preferred insertion site: Medical surface of the proximal tibia
Amiodarone
Indicated in pulseless VT and VF after the 3rd shock
Sodium Bicarbonate
Indicated in hyperkalemia, may be considered for metabolic acidosis
Consider and correct

Hypoxia
Hypovolemia
Hyper/Hypokalemia/Metabolic disorders
Tension pneumothorax
Tamponade
Toxins
Thrombosis (Pulmonary/Coronary)
Case 1
You are a RMO on your first day of pediatric rotation at PMH. You walk into little Kims room and notice she is lying still on her bed. She is a 6 months old girl.
Her mother has gone out to get lunch and you are the first one on the scene.
1. Please take charge of this scenario.
2. A second person arrives Please delegate task
3. A third person arrives Please delegate task
Beginning
Check response:
The first person arrives
Touch the 6 months old baby. (Never shake the baby)

Verbal stimulation
(I would like to call for a pediatric code blue.)
Attach a defibrillator
(ask for IV/IO access) Urgent blood sample may be taken at this point
(check for glucose, Glucose, hyperkalemia, hypocalcemia)
The second person arrives
ABC: Airway, Listen for breathing
Followed by a bolus of 20mL/kg of normal saline (except for those with

sign of heart failure)
Adrenaline
-
Indicated in asystole and pulseless electrical activity

Also in VF and pulseless VT after the second shock
Dose: 10mcg.kg (0.1ml/kg of 1 in 10,000) via IV or IO
SE: HTN, Myocardial ischemia, Tachyarrhythmias
The first person help with the oxygen
Breathing
If breathing is abnormal or not present 2 rescue breaths (mouth to
mouth or a bag and mask Connect to oxygen 10L/min)
- After the 2 rescue breaths, check for circulation - Brachial pulse, Check
for breathing response or movement
Compression If no sign of life
-
- 30 chest compression and then 2 breaths, 1/3 depth of chest

- Continue for 2 mins
Case 2
- Baby with a history of acute diarrhea was found to be unresponsive.
(in this case, likely to be caused by circulatory shock)
DRSABCD
Airway
Breathing Remember to connect to the oxygen, at a flow rate of 10L/min,
95-100% oxygen
Defibrillator Mainly to monitor the airway
Exam Questions
-
What oxygen flow rate?

What are the shockable and non-shockable rhythm? Pulseless VT, VF
How to measure the size of the OPA oropharyngeal airway? From the
centre of the mouth to the angle of the jaw.
Resuscitation Fluid Given as interosseus route, 20mL/kg, normal saline,

consider blood if more than half of the circulating volume has been replaced
Drugs Adrenaline 0.1mL/kg, Sodium bicarbonate 1mmol/kg, Calcium
gluconate 20mg/kg
Exam Keep Silent, dont have to explain what you are doing
Case 3
- Child with anaphylaxis
- DRSABCD
- Breathing Resisting breathing, Use the mask instead of the bed
- Circulation
- No need for defibrillator, but could be useful with ECG monitoring
- Use of the epi pen. IM
Kids-L1-Immunization
Case
How to put the OPA and why? Insert the concave side over the tongue
under direct vision to avoid damage to palate.
What is the location of the interosseus insertion? What are the
contraindications? What can you do with the bone marrow?
What are the reversible causes of cardiac arrest? Hypoxia,
Hypovolemia, Hypo/Hyperkalemia, Hypo/Hyperthermia, Tension
pneumothorax, Tamponade, Toxins, Thromboembolism
What are you check in circulation? Capillary refill on sternum, BP,
Pulses, Color, Temperature
What would you like after the adrenaline administration? Re-assess
the patient, wait for 2 minutes
Discuss immunization with a concerned mother. Her child had a reaction to the 2 months schedule, missed the 4 month and is now 6 months old. What
should they do now?
- Answer questions from the mother.
History
-
Could you tell me about what happened last time you child received the
vaccination?
- Does he have the common reaction such as swelling or redness on the
injection site? Fever? Become irritable? Vomiting or diarrhea? Fainting?
- Seizure, how long did it last for?
- Does he have the uncommon reactions such difficulty breathing? Welling
of eyes and mouth? Sudden collapse? Blue? Pale color? Seizures?
- Did he develop any neurological disorder after the vaccination?
- What happened after? Did he get better?
At this moment
-
How is he?
No fever? Diarrhea or vomiting?
Does he have any past medical history? E.g. Autoimmune disease
Medications? Steroids?
Measure the temp.

Not able to do so as your son is not here
- Allergies?
- Feeding? Breast feeding? Weight gain?
Birth History
-
How was he at birth?

Any complications? Low birth weight?
Full term? Vaginal delivery?
Any complications with pregnancy
Fx? Social history (who liver with? Anyone smoking at home?)
Developmental history (Put everything in mouth? Single or double
syllables)
Management
In term of the management, what should we do now?

- First of all, I need to explain to you how important it is to have your child
vaccinated against the diseases because these diseases can be life
threatening in children. They also prevent the possible disability associated
with those diseases.
- Common side effects included: swelling or redness on the injection site?
Fever, can associate with seizure? Become irritable? Vomiting or diarrhea?
Fainting?
- I understand that your son has had a seizure and fever after the 2 months
vaccination. However, they are not the contraindications for vaccination.
They may happen in 1 in 10.
- Fever with simple seizure 1 in 1000
- Some rare side effects such as allergic reaction and anaphylaxis are the
contraindications. But they are very rare. 1 in 10,000 for allergic reactions,
0.6 in 100,000 for anaphylaxis
- Now, since your son is not sick and has no fever, we can give the 4 months
immunization today. And has the 6 months vaccination after 2 months.
- 2,4,6 months Pneumococcal, Rotavirus, Diphtheria, Tetanus, Pertusis,
Polio, Hepatitis B, Hemophilus influenzae type b
- Meanwhile, if you son once again had any seizure, seek medical attention.
If you have any concern, you can come to see me.
What are some rare reactions?
Seizures
- Some children predisposed to seizure when having a high fever
- Seizure lasts about 20s, rarely more than 2 mins
- Always see a doctor
Other Serious SE
What are some common side effects?

Local reactions
- Red swollen area around the site of injection
- Action: Give paracetamol, Place a cold damp cloth
Fever
-
Action: Monitor temperature, give extra fluid, Paracetamol may be

required
Irritability, Decreased Appetite, Sleepiness
-
Common, usually disappear over 24-48 hours and they do not usually
require treatment
Vomiting and Diarrhea
- Action: Continue to breast feed, give small frequent feeds
Small Lump at the Injection Site
- Usually disappear in a few weeks
Fainting
-
To lie down until symptoms subside
Are there any contraindications to vaccination?

Unwell, Acute febrile illness, Acute systemic illness
-
Action: Defer all vaccines until afebrile, but children with minor illness
without acute systemic signs/symptoms should be vaccinated
- Rationale: To avoid SE in an already unwell child
Had a disease/treatment which lowers immunity
Unable to breath, Collapse, Pale color, No breathing
- Seek expert advice, avoid live vaccines

Anaphylaxis following a previous dose of vaccine
- Do not vaccine
Pregnant
-
Live vaccines should be deferred until after delivery

Conception should be deferred at least 28 days after administration of live
viral vaccines, inactivated vaccines are generally not contraindicated
Born Preterm
- Preterm infants at 6 months require an extra dose of some vaccines

What does it mean by live vaccine? Will that cause disease since they are alive? What should I come back for further vaccination?
- Birth Hepatitis B
- 2,4,6 months Pneumococcal, Rotavirus, Diphtheria, Tetanus, Pertusis,
Polio, Hepatitis B, Hemophilus influenzae type b
- 6 months to y years Influenzae
- 12 months Measels, Mumps, Rubella, Hemophilus influenzae type b,
Meningococcal C
- 12-35 months Pneumococcal
- 18 months Varicella
- 3-4 years Pneumococcal
- 4 years Measles, Mumps, Rubella, Diphtheria, Tetanus, Pertussis, Polio
- Year 7 Hep B, HPV, Diphtheria, Tetanus, Pertussis, Varicella
Kids-L1-Febrile convulsion
Case
You are an RMO at PMH. A mother has brought her 8 months old son Jason into ED. Jason has recently been unwell with coryzal symptoms and has had a 4 min
fit. You have taken a thorough history and have decided is most likely a febrile convulsion due to a viral URTI.
- Explain this to the mother in clear lay-terms and answer any questions she may have.
Introduction
Explanation
-
Im one of the doctors working here today. Can I have you name please?
I understand that your 8 months old son Jason has recently been sick and
has had a seizure. Is that right?
So basically, Im here to explain to what have happened to Jason and what
are we going to do now.
So basically what happened to Jason is what we call a febrile convulsion.

Febrile means you son is having symptoms or signs of fever
While convulsion means seizure , which is the physical finding or change in
behaviors that occur after an episode of abnormal electrical activity in the
brain
First of all I need to tell you that it is a benign condition that is not
uncommon in children when they have a fever.
When children have a fever, it may trigger an episode of abnormal
electrical activity in the brain, which causes seizures.
It is commonly occur in children 6 months to 5 years old. (PMH guidelines)
It is self-limiting.
No evidence that simple febrile convulsions causes any lasting damage

30% will have a recurrence
So now we are going to observe Jason for a while, make sure he is fine
before discharging him home
- Do you have any questions?
- Febrile convulsion > 15 min, occur more than 1 in 24 hours, or are focal
Increased incidence of later epilepsy Require admission for observation
and investigations
Questions from examiner.
6. What is status epilepticus? What to do?
7. What is complex febrile seizure? What to do?
-
Questions from mother.

1. Does that mean my child has epilepsy?
2. What can I do to prevent this from happening again?
3. If I give him Panadol will it prevent it?
4. What should I do if it happens again?
5. Any dont?
1.
-
No
There are a number of causes of seizures and epilepsy is one of them.
Epilepsy is recurrent attack of seizures, usually without an identifiable
cause
While in Jason case, the seizure is very likely to be caused by the fever
Havent said, have a febrile convulsion dose slightly increases the chance of
developing epilepsy in the future. But not really significant.
Majority will grow out of this
2.
- Important to prevent your son getting infection.
- Most importantly, up to date vaccination
- Wash hands often
- No smoking at home
- Avoid contact with sick people
When you son is ill
-
Plenty of water and rest
3.
4.
- No
- But it is good for symptomatic relief
5.
- Seek medical attention

- May want to lay you son on one side, to prevent aspiration, but very rare
6.
Generalized tonic-clonic convulsion lasting more than 30 min

It can be life-threatening = a medical emergency Any seizure lasting more
than 5 min should be treated as status epilepticus
- Treatment for status epilepticus does not treat the underlying cause (E.g.
Derangement of blood sugar or electrolyte, CNS infection)
- Different children have different responses to various anticonvulsants
Management
Do not panic
Do not put anything into the mouth
Do not restrict convulsive movements may cause fracture, may injure
the helper
Do not give water until fully conscious
Initially: Airway, Breathing, High flow O2, Check blood sugar level, after 5
min:
With vascular access: Diazepam 0.25mg/kg or Midazolam 0.15mg/kg
Without vascular access: PR, IM
7.
- Febrile convulsion > 15 min, occur more than 1 in 24 hours, or are focal
- Increased incidence of later epilepsy
- Require admission for observation and investigations
Kids-L1-Otitis media
Case
Still Fitting: Repeat dose

Still Fitting: Load with Phenytoin 18mg/kg in normal saline over 30 mins or
Phenobarbitone 20mg/kg and give Paraldehyde 0.4ml/kg rectally
Still Fitting after 20 mins: Intubation with rapid sequence induction and
arrange transfer to ICU
An alternative anticonvulsants: Clonazepam
You are an ED resident at PMH and you receive a call from a country nurse regarding a patient. The patient is a 10 year old indigenous child who she suspects has
otitis media.
1. Please discuss with her how you may better diagnosis the patient?
2. What physical examinations?
3. Any possible DDx and how to rule out?
4. Any further investigation you think may be necessary?
5. Any treatment you think may be needed?
6. Any investigations you would prefer the patient for?
Introduction
-
1.
To diagnose someone with otitis media history and physical
examination
History Symptoms
-
Symptoms of otitis media: Painful ear, Abnormal discharge, Hearing loss,

Fever
Important to work out the duration of the symptoms, as we want to know
about if this is acute or chronic otitis media
Also has the patient recently had an acute otitis media, as a glue ear can
occur after acute otitis media
How long? Anything any it worse? Color of the discharge? Amount?
Hearing loss?
How does it affect their appetite and sleep?
Any trauma to the ear? Did the patient put anything into the ear? Recently
swimming? Contact of people who are sick?
Screening of different systems
Px: Gourmet put in? Any surgery? Medications? Allergies?
Social: Affect the school? Smoking?
2.
3.
4.
-
General Inspection: Does the kid look sick? Irritable? Ear redness?
Swelling? Discharge?
Vitals: Temperature, RR, PR, BP
Have a look with an otoscope. Look at the ear canal, and the tympanic
membrane, look at the good one then the affected one
Membrane: Look red, Bulging, Perforation, Pus
Foreign objects
Also examine the throat, nose eyes, neck lymph nodes
Assess hearing
5.
Investigation really depends on how sick the patient
If really sick E.g. High fever, malaise, I would do a septic screen
Urinalysis, routine
Also depends on the history, if more than 3 months hearing test
Ear swabs should not be done, usually do not influence management, only
indicated if ongoing otorrhea despite appropriate management
6.
- Audiology for tympanometry to assess for chronic or OM with effusion
More Info PMH Guildelines
Background
-
Otitis externae
Mastoiditis
Foreign objects
Cholesteatoma
Infection of the middle ear cavity

3 types: Acute otitis media, Otitis media with effusion or glue ear, Chronic
suppurative otitis media (Discharging otitis media)
Traditionally treated with antibiotics, buy evidence suggest that this at best
shortens the duration of pain by less than 1 day, and does not reduce
recurrence rate nor complication rate
Therefore, it is reasonable to consider supportive treatment in the first 48
hours of symptoms in low risk children
Antibiotics are indicated if the symptoms persists or the child becomes
worse
In high risk children E.g. infants, children of low socio-economic standing,
indigenous, immunocompromised treat with antibiotics
Complications E.g. Mastoiditis, Discharging otitis media
Generally Amoxycillin is indicated, if no response in 48 hours Augmentin
Analgesia is the most important, often paracetamol alone is not adequate,
Painstop-day and Painstop-night
Topical anesthetic oil (Auralgin) if there is no perforation
Acute Otitis Media
Common presentation to GP or ED
Child will usually present with a painful ear and fever
Often follow a prodrome of URTI
A younger child may present with fever, crying, screaming or even
vomiting
- Otoscopic examination red and bulging eardrum
- Note: The eardrum erythema can be due to fever or crying, beware
especially when there is no history of earache
Diagnosis
-
Acute onset
Middle ear effusion (bulging TM, limited TM mobility, Air-fluid level,
Otorrhea)
- Signs and symptoms of inflammation E.g. Distinct TM erythema, Otalgia
Treatment
-
Otitis Media with Effusion (Glue Ear)

-
Uncommon presenting complaint

Usually asymptomatic
Not readily diagnosed without tympanometry or pneumotoscopy
Largely self-resolving and needs no interventions
It is universally following acute otitis media
10% persist longer than 3 months
The commonest cause of imbalance in children
Important to see if hearing is affected before language development
Assessment by formal audiology is indicated if beyond 3 months or
parental concerns
Traditionally treated with antibiotics, buy evidence suggest that this at best
shortens the duration of pain by less than 1 day, and does not reduce
recurrence rate nor complication rate
- Therefore, it is reasonable to consider supportive treatment in the first 48
hours of symptoms in low risk children
- Antibiotics are indicated if the symptoms persists or the child becomes
worse
- In high risk children E.g. infants, children of low socio-economic standing,
indigenous, immunocompromised treat with antibiotics
- Complications E.g. Mastoiditis, Discharging otitis media
- Generally Amoxycillin is indicated, if no response in 48 hours Augmentin
- Analgesia is the most important, often paracetamol alone is not adequate,
Painstop-day and Painstop-night
- Topical anesthetic oil (Auralgin) if there is no perforation
Chronic Suppurative OM or Discharging OM
Treatment
-
Controversial
No evidence to support medical intervention
Wait for 3 months, if no improvements, 4 weeks of broad spectrum
antibiotics may be trialed
A history of atopy use of steroid nasal spray
Hearing loss with OM effusion insertion of grommets +/adenoidectomy
Less common complication of acute otitis media or in some children with

chronic perforation or a grommet
- Non-painful, white, yellow or green discharge, with no evidence of ear
canal inflammation
- Often difficult to treat
- If recent onset, usually contains multi-resistant organisms E.g.
Pseudomonas or proteus species
Treatment
-
Ear swabs should not be done, usually do not influence management, only
indicated if ongoing otorrhea despite appropriate management
Oral antibiotics are usually ineffective and are not recommended
Topical Antibiotics have been shown to be most effective, usually
Ciprofloxacin used
Dry ear with tissues spears can be used
Kids-L1-Developmental stage determination

1. Grossly describe the changes in gross motor, fine motor, social, hearing and speech from 4-6 weeks to 12 months.
2. List some red flag symptoms in gross motor, fine motor, speech and behaviors.
3. List 3 tests that can help to determine the developmental status.
Gross Motor
Fine Motor
Lying on front
Eyes
4-6 weeks: Momentarily lift chin
4-6 week: Fixes on mother when feeding
3-4 months: Lift head and chest
3 months: Follows through 180 degrees
6 months: Lift head, chest and supports with extended arms, rolls over
6 months: Full eye movements
Head lag
9 months: Visual attention to hear and far objects
Hand
5 months: Gone
Sitting, Standing and Walking
3 months: Hands held in midline
6 months: Sits with support, takes weight on legs when held
6 months: Palmar grasp
9 months: can sit alone, can stand holding
6-8 months: Transfer from one hand to the other
12 months: walks hand held
11 months: Pincer grip

12 months: Retain 3 cubes
Social
Hearing, Speech
6 weeks: Social smiles
4-6 weeks: Startled by sound
4 months: laughs
3 months: Cry appropriately
6 months: When toy fall forgets it
6 months: Babbles
9 months: Tell strangers, look for fallen toys
12 months: 2-3 words, understand simple commands
12 months: Play interactive with balls

2.
3.
Gross Motor: Delayed walking by 3 years, delay

running from 3-5 years, inability to kick a ball by 5-8
years
Fine Motor: Delayed pincer grip after 10 months,
difficulty with cutting from 3-5 years, avoid drawing
from 5-8 years
Speech: Absence of single word by 18 months, Use of
gestures more than words from 3-5 years, Speech
unclear to family from 5-8 years
Behavioral: excessive tantrum by 3 years, persistent
tantrums from 3-5 years, difficulty making friends
from 5-8 years
Kids-L1-Vomiting E.g. DKA

- see Newborns
Kids-L1-Diarrhea Acute + Chronic
- see Newborns
Kids-L1-FFT, Celiac disease
- Make sure you know celiac disease well
Kids-L1-Rash
DDx Rashes with a Fever
- Bacterial Causes: Scarlet fever, Staphylococcal scalded skin syndrome =
Bullous impetigo, Toxic shock syndrome, Acute meningo-coccemia,
Rocky mountain spotted fever
- Viral Causes: Herpes simplex, Varicella, Roseola infantum (Sixth
Disease), Erythema infectiosum (Fifth Disease), Enteroviruses, Measles,
Rubella, Lyme disease
- Others: JIA, Kawasaki disease
Scarlet Fever
- Usually in children 2-10 years of age
- Etiology: Caused by hemolytic Streptococcus
- Clinical Features: Begins with fever and pharyngitis, followed in 24 to 48
hours by enanthem (small spots on the mucous membrane) and
exanthema (rash on body), face appears flushed, but circumoral pallor
(skin around the mouth pale), white strawberry tongue (has a white
coating) the progresses to a red strawberry tongue, cervical and
submandibular lymphadenopathy, Rash (sand paper like, diffuse
erythema), rash resolves in 4-5 days with fine peeling of skin starting on
face
- Evaluation: Culture or rapid test of a pharyngeal swab
- Treatment: Penicillin, Amoxicillin, Erythromycin if allergic to penicillin
Rash in a Neonate Yellow = Pustular

- Erythema toxicum, Transient pustular melanosis, Miliaria, Seborrheic
dermatitis, Candidiasis, Neonatal acne, Acropustulosis of infancy
- Eczematous Dermatitis: Atopic/Contact/Nummular/Asteatotic
Dermatitis
- Papulosquamous Disease: Psoriasis, Lichen planus, Seborrheric
dermatitis, Tinea infection, Tinea versicolor, Pityriasis rosea, Secondary
syphilis, Pityriasis lichenoides, Acrodermatitis enteropathica, Exfoliative
dermatitis
- Vesiculobullous Disease: Herpes simplex, Herpes zoster, Varicella, Rhus
dermatitis (poison ivy), Contact dermatitis, Insect bite, Urticaria
pigmentosa
- Annular Erythema: Lyme disease, Erythema multiforme
- Papular Eruptions: Scabies, Papular acrodermatitis of childhood, Papular
urticaria, Molluscum contagiosum, Warts
- Others: Milia
Staphylococcal Scalded Skin Syndrome / Bullous Impetigo
- Etiology: Caused by toxin produced by some strains of Staphylococcus
aureus
- Clinical Features: Typically in children <5 years of age, begins with
fever/irritability after conjunctivitis/rhinitis/URTI, the rash is most
prominent in the flexures, can involve hands and feet, initially
erythematous and tender, begins around the nose and mouth then
spread to the trunk, after 1-2 days bullae (large vesicles containing fluid)
develops and begins peeling, after 2 days skin become crusted and begin
to develop scaling
- Evaluation: Sometimes isolated by bacterial culture of the nose,
nasopharynx, throat, conjunctiva, perinanl areas
Circumoral Pallor
Sand Paper like

Pastia Lines in Scarlet Fever
-
Petechiae in lines
Petechiae may occur on
Mainly affects infants and children younger than 2 years of age

Skin around usually itchy but not sore
Causes: Staphylococcus aureus, sometimes by Streptococcus pyogenes
Treatment: Diflucloxacillin orally or IV
the soft palate or uvula
Meningococcemia
Toxic Shock Syndrome
- Etiology: A multisystem disease caused by exotoxin producing stains of S.
aureus (TSS) or Streptococcus pyogenes (STSS)
- TSS is seen in association with menstruation, but non-menstrual TSS is
now more common
- STSS is usually a complication of a wound infection
- Clinical Features: Fever, Rash, Hypotension are the hallmark,
involvement of other organs myalgias, acute renal failure,
encephalopathy, DIC, diarrhea, metabolic acidosis, hepatitis, rash may
appear morbiliform or erythroderma (Erythema and scaling affects
nearly the entire cutaneous skin), can involve palms and soles, late
desquamation, strawberry tongue
- Evaluation: Blood cultures should be sent, culture of cutaneous wounds,
FBC, U&E, LFT, Urinalysis, CK, Coagulation studies
- Treatment: Vancomycin
Herpes simplex
Meningococcemia
- Etiology: Caused by Neisseria meningitidis, asymptomatic nasopharygeal
carriage occurs and transmission occurs via respiratory droplets
- Clinical Features: Begins with symptoms of URTI, followed by fever,
malaise, headache, petechial eruption, can have erythematous macules,
papules and urticarial lesions, in severe cases the purpura can involve
large areas that eventually necrose
- Always think of meningococcemia when a patient presents with fever and
petechiae
- Evaluation: Cultures of blood, CFS or skin lesions, gram stain
- Treatment: Penicillin, Ceftriaxone, Cefotaxime
Varicella (chickenpox)
Rare but serious condition

Usually caused by vertical transmission, 85% occur during birth when the
baby comes in contact with the infected birth canal
- Most common with mothers that have newly been exposed to the virus
- Treatments: E.g. Acyclovir, but morbidity and mortality remain high
Roseola Infantum
- Etiology: Caused by Human Herpes Virus 6
- Clinical Features: 3 days of high fever, febrile seizures, after the fever a
diffuse, faint, blanchable, erythematous reticulated rash appears and
last for several days, an enanthem on soft palate and uvula may also
develop
- The child is usually well looking
- Evaluation: Usually made clinical, serology or serum PCR for HHV6 if
diagnosis not clear
- Treatment: Self-limiting
Pearls
- Rashes during the febrile course of an illness are not roseola
- The patient is no longer contagious with appearance of the rash
- Most frequent complications = Febrile seizures
Erythema Infectiosum
- Etiology: Caused by Parvovirus B19, Transmission via respiratory droplets
- Clinical Features: Seen mainly in school age children, between 4 and 10
years of age, prodromal symptoms of fever, pharyngitis, malaise, coryza
followed by slapped cheek, a reticulated erythematous exanthema can
develop on the extremities, older children may complain of arthralgias or
arthritis
- Evaluation: Diagnosis usually made clinically, serologic test and serum
PCR for parvovirus B19 may be performed if the diagnosis is unclear
- Treatment: Self-limiting
A cause of hydrops fetalis or fetal

deaths early in pregnancy
- Issue of aplastic crisis in patients with
hematological problems E.g. Sickle cell
disease, hereditary spherocytosis,
hemolytic anemias
Pearls
-
Enteroviruses
- Etiology: Some entero-viruses can have cutaneous manifestation E.g.
Cox-Sackie-Virus A1-10, 16, 22 are common causes of Herpangina, CoxSackie-Virus B 16 is the most common cause of hand-foot-mouth disease
- Clinical Features: Prodromal symptoms of Fever, Malaise, Headache,
Pharyngitis, Diarrhea, Herpangina presents with small gray-white vesicles
and erosions of the hard palate, buccal mucosa, tongue and gingiva,
Papules and vesicles may also be seen on the buttocks
- Note: Many patients have significant oral pain and decreased oral intake
young infants are at risk of dehydration
- Evaluation: Diagnosis is usually clinical
- Treatments: Self-limiting, Hydration + Analgesics
Can reappear with exercise,

overheating, emotional upset, sun
exposure
Parvovirus B19 is the most common
cause of hydrops fetalis
In young adults, causes popular
purpuric gloves and socks syndrome
Kawasaki Disease
- Etiology: Unknown
- Clinical Features: 5 out of 6 criteria: Fever for at least 5 days, Bilateral
non-purulent conjunctivitis, Erythema and crusting of the lips, Edema
with subsequent desqumation, Rash, Cervical adenopathy
- Rash: Generalized erythema, Erythema multiforme, pustular lesions
- An important cutaneous finding is the desquamation of the perineal area
early in the disease
- Evaluation: Thrombocytosis in 2nd week, Hyponatremia,
Hypoalbuminemia, Elevated ESR, Anemia, Leukycytosis, Echo should be
performed to look for coronary artery aneurysmal dilation
- Treatment: IV gamma globulin, Aspirin
Herpangina
Erythema Toxicum
- Etiology: unknown, Develop 3-4 days of birth, Rash anywhere except for
palms and soles, few to several hundred lesions
- Evaluation: A smear of a pustule reveals clusters of eosinophils
- Treatment: Resolve by 2 weeks of age
Transient Neonatal Pustular Melanosis

- Etiology: Unknown, more commonly seen in African American infants
- Clinical Features: Pustules, Vesicles, Hyperpigmented macules, present at
birth, the pustules rupture leaving a fine white scale, the eruption
resolves within several days
- Treatment: No treatment
Diffuse macular rash

Found in up to 70% of newborns
Disappearing within 2 or 3 days
New lesions may occur during first 2 weeks of life
The neonate should appear well and lack of systemic signs (except
occasional peripheral eosinophilia)
Pearls
- Erythema toxicum is the most common rash of the newborn
- Rash tends to spare the palms and soles
- Lab evaluation is usually unnecessary
Miliaria
- Rash most commonly seen in flexor regions
- Treatment: Avoid excessive heat, humidity,friction
Small blister quickly rupture and leaves a typical superficial scale

processes
The cause of this condition is not known, and it resolves within 10 days
No treatment is required
Seborrheic Dermatitis
- Etiology: Unknown, May be related to maternal hormonal stimulation
- Clinical Features: Begins during the first 12 weeks of life, with scaling of
the scalp, generally cleared by 1 years of age, Characterized by greasy
yellow scales associated with patches of erythema, fissuring and

occasional oozing of the scalp, face, ears, trunk, and inter-triginous areas
(two skin areas that run on each other E.g. Axilla)
Treatment: Gently loosen the scale with a soft comb or brush, Application
of baby oil to scalp prior to shampooing, A low-potency topical steroids
Occurs when the sweat is

retained in the pores of the
skin, producing itchy tiny
blisters that break easily
No associated inflammation
Common in hot and humid
conditions
Common in children and infants
due to their underdeveloped
sweat glands
Candidiasis
- Etiology: Common in neonates and infants, commonly caused by Candida
albicans, transmission usually occurs during or after delivery
- Clinical Features: Superficial erythematous papules and pustules,
involvement of diaper area and other intertriginous areas
- Evaluation: Microscopic examination demonstrate budding yeast, A
fungal culture can be performed if diagnosis unclear
- Treatment: Antifungal cream or ointment, Affected area should be kept
dry, Frequent diaper changes
Neonatal Acne
- Etiology: Unknown, probably due to stimulation of sebaceous gland by
maternal and infant androgens
- More common in boys, Closed comedones (whiteheads) are most
common, Open comedones, inflammatory papules and pustules also be
noted
- No treatment is necessary
- Refer to a dermatologist in moderate to severe cases
Atopic Dermatitis
- Etiology: One of the most common causes of pruritus in children, poorly
understood, characterized by inflammatory hyper-reactivity, believed to
be caused by abnormal T cell function with IgE overproduction
- Clinical Features: Most with Fx of asthma, hay fever, dermatitis, Many
children later develop asthma or hay fever, Rash usually appear on the
face/neck/trunk in the first year of life, Eruption with erythematous,
poorly demarcated patches and initially is exudative and later forming
crusts, There may be associated papules or vesicles, with scratching
lesion become thickened or lichenified, Pigmentation changes are
common complications
- Has a chronic and recurrent nature
It may be difficult to differentiate between seborrheic dermatitis from
atopic dermatitis in infants
- Seborrheic Dermatitis: Appears in the first 2 months of life, Scale is
yellow and greasy, Often seen behind the ears
- Diagnosis of atopic dermatitis may be delayed until repeated outbreaks
occur
- Treatment: Moisturize, Eliminate possible irritants, Topical steroid (1%
hydrocortisone cream), Secondary skin infection with staphylococci or
herpes can occur
Contact Dermatitis
- Etiology: Primary Irritant Dermatitis (response of skin to an irritant E.g.
Soaps, Bubble baths, Saliva, Urine, Feces, Citrus juice, Chemicals, Wool,
Perspiration = sweat) Allergic Contact Dermatitis (Characterized by a
delayed hypersensitivity E.g. Poison ivy, poison oak, poison sumac,
cosmetics, nail polish, shoe material, clothing material latex)
- Clinical Features: Most prominent in the areas of direct contact
- Treatment: removal of offending agents, topical steroids, failure to
respond indicates possible misdiagnosis
Nummular Dermatitis
- Manifestation of dry skin and ichthyosis (rough and scaly skin), Rash is
coin-shaped with vesicle, papules, erythema, scaling
- It may be confused with impetigo or tinea corporis
Psoriasis
- Etiology: Unknown, An immune defect may be a primary or secondary
- Clinical Features: Erythematous plaques with silvery scale, located
symmetrically on the elbows, knees, extensors surfaces of the wrist,
genitalia and scalp, Nail changes include pitting and onycholysis
- Evaluation: A clinical diagnosis, Skin biopsy if in doubt
- Treatment: Mid-potency topical steroid, topical retinoids, Topical
calcipotriene, Anti-seborrheic shampoos, in severe cases UV light therapy
or systemic medication
Lichen Planus
- Clinical Features: 5P = Pruritic, Polygonal, Purple, Planar, Papules located
on the flexor surfaces, genitalia, mucous membrane, scalp, nails
- Cause is unknown
- Disease eventually lead to scarring of the scalp and nails
- Evaluation: A skin biopsy confirms the diagnosis when clinically in doubt
- Treatment: Topical steroids, some may require oral corticosteroids or
phototherapy
Tinea (Dermatophyte) Infections

- Etiology: Superficial cutaneous infection with dermatophyte molds
- Clinical Features: May involve body (tinea corporis), face (tinea facie),
hands (tinea manuum), feet (tinea pedis), groin (tinea cruris), scalp (tinea
capitis), nail (onychomycosis), Usually present with pruritus and scaly
erythematous papules and annular plaques, Cervical lymphadenopathy
may be prominent in tinea capitis
- Evaluation: Microscopic examination demonstrate fungal hyphae, Fungal
culture
Tinea Versicolor
- Etiology: Caused by superficial infection with Malassezia furfur
- Clinical Features: Hypopigmented or hyperpigmented round oval
coalescent macules, with superficial scale on the chest, back, abdomen,
proximal extremities, usually asymptomatic
- Evaluation: Diagnosis made clinically, Microscopic examination with a
potassium hydroxide preparation demonstrate fungal spores and hyphae
with a spaghetti and meatballs appearance
- Treatment: Topical antifungal cream E.g. Ketoconazole
-
Treatment: Topical antifungal agents (Clotrimazole, Ketoconazole),

treatment of tinea capitis requires the use of systemic antifungal,
treatment of onychomyosis requires the use of systemic antifungal
Tinea corporis
Tinea capitis
Pityriasis Rosea
- Etiology: Cause is unknown
- Clinical Features: Acute, self-limiting, most cases start with a single, large,
oval, scaling plaque known as herald patch, then within one week small
pink scaled plaques develop on the trunk, have a tendency to follow skin
cleavage lines creating a Christmas tree pattern, Usually spares the face
except in children, May associate with moderate pruritus
Herald Patch
Can mimic secondary syphilis, should be considered in sexually active
adolescents
Erythema Multiforme
- Etiology: Reactive inflammatory dermatosis (skin disease), usually as a
response to infection/medication, most common cause is herpes simplex
virus
- Clinical Features: Target lesion, dusky erythema, surround by a ring of
pallor and a peripheral ring of erythema, common sites palms and
extremities, some patients complain of pruritus or burning, associate
with fever, fatigue, pharyngitis, Stevens-Johnson syndrome is a more
severe form with mucosal involvement
- Evaluation: Diagnosis usually made clinically
- Treatment: Use of topical steroids or systemic antihistamines may be
helpful, systemic steroid for severe cases, this condition is self-limited
Often include symptoms fever, itching, general malaise, aching joints

Eye involvement may occur
3 Zones of Color Changes: A peripheral rim of erythema with an inner rim
of relative pallor and a central erythematous macule
Blister when present, form centrally in most cases, but a peripheral
pattern also occur
Urticaria Multiforme
- A relatively new term to describe extreme hives
- It is different from Erythema Multiforme because the raised areas move
- Also less likely to have necrotic centers like Erythema Multiforme
- Can be misdiagnosed as Erythema Multiforme
- Treatment: Using H1 and H2 antihistamine is the best treatment, Steroid
is considered in extreme cases
From the Emergency Book
- Acute urticarial is a common condition, associate with an infection, insect
bite, ingestion of food or medications
- Sudden onset of pruritic, transient, erythematous, well-circumscribed
wheals scattered over the body
- The lesions blanch with pressure
- Have a central clearing or associated tense edema
- Most reactions last 24-48 hours, rarely take weeks to resolve
- May be reactions such as wheezing, stridor, angioedema
- DDx: Erythema multiforme, HSP, Contact dermatitis, Reactive erythema,
Allergic vasculitis
ED Treatment
- Antihistamine
- Steroid or adrenaline may be considered in systemic reaction
- Unless there is evidence of acute angioedema, most cases can be
discharged home on oral antihistamines
The disease is self-limited but often recurrent

Major = Stevens-Johnson Syndrome
Common Causes: Herpes simplex virus infection, medication,
Mycoplasma pneumonia
- Use of steroid uncertain
Scabies
- Etiology: Caused by Sarcoptes scabiei, the mites burrow into the stratum
corneum and deposits eggs and feces which causes itching
- Clinical Features: Papules, pustules, vesicles, rash distribution on infants
(neck, face, scalp, axilla, groin), older children (wrists, axilla, interdigital
webs, belt line)
- Evaluation: Skin scrapings from an unscratched burrow in immersion oil
under 10x magnification should reveal the female mite and her eggs and
feces
- Treatment: Permethrin 5% cream to entire body and left on for 12 hours,
may by repeated in 2 weeks if necessary, highly contagious, household
contacts should also be treated, bedding and clothing should be
laundered
Molluscum Contagiosum
Pearls: A lesion must change or resolve within 24 hours
Bedbugs
- Etiology: It emerges at night, after feeding returns to dark, not known to
transmit disease
- Clinical Features: Macules that become popular, erythematous,
indurated, young patients may develop popular urticarial, when healed
the lesions maybe hypo-pigmented
- Evaluation: Small dark brown stains on the bedding, Recent travel, a
careful search of the bedroom, turning the mattress over
- Treatment: Clean and application of topical antibiotic ointment,
Eradication of insect from house requires an exterminator
Lyme Disease
Etiology: Caused by molluscum virus, may be spread by close physical

contact, sharing towel
Clinical Features: Most commonly seen in school-age children, small
pearly umbilicated papules, involvement of the face is common, an
intense inflammatory reaction with surrounding erythema may develop,
self-limiting and generally resolves 9-15 months
Evaluation: Diagnosis made clinically
Treatment: No treatment
Salmon Patches (Nevus Simplex)

- Most common vascular lesion in infancy, 40% of newborns
- Pink to purple macule on the nape of neck, glabella, mid-forehand, upper
eyelids
- Lesions generally fade over the first 2 years of life
- Can become more prominent with crying or straining
ED Management
- No therapy
- Parental education
- Laser may be considered for persistent lesions
Pearls
- Salmon patches are composed of dermal capillaries
- Appear symmetrically and cross the midline
- Stork bite = Nape of back
- Angels kiss = Forehead
Etiology: Tick borne illness, Caused by Borrelia Burgdorferi, Most

commonly seen northeastern US
Clinical Features: Early symptoms fever, myalgias, arthralgias, headache,
fatigue, late with arthritis, carditis, neurologic abnormalities E.g.
meningitis, bell palsy
Evaluation: Serology
Treatment: Doxycyline
Measles
- Acute febrile illness, with 3-4 days prodromal period of dry cough, coryza,
conjunctivitis, malaise
- Kopliks spots, red papules with white centers on the buccal mucosa,
usually present 1-2 days before the development of the rash
- Rash: Begins as dark red to purple macules and papules on the forehead
spread body and extermities
- Most cases recover without complications
- Complications: Otitis media, croup, pneumonia, encephalitis, myocarditis
ED Management
- Supportive: Bed rest, antipyretics, fluid balance
- Treat complications
- Post-exposure prophylaxis administration of the measles mumps rubella
vaccine within 72 hours of exposure to a patient with active measles
HSP
Milia
Systemic vasculitis of small vessels

Erythematous hemorrhagic papules in a symmetric distribution, usually
involves the buttocks and extremities
- A disease of children (3-12 years of age) and young adults
- Often associate with abdominal pain (caused by edema and hemorrhage
of the intestinal wall) and arthritis
- GI symptoms (abdominal pain, occult and gross bleeding,
intussusception) may precede the rash
- Renal involvement is the most frequent and serious complications,
usually occurs during the first month microscopic hematuria and may
progresses to glomerulonephritis
- Lab tests are usually normal except for urinalysis
- Prognosis is excellent, full recovery in most instances
- Remission in 50% of patients
ED Management
- Supportive
- Corticosteroid may be used to treat severe abdominal pain
- If intussusception is suspected surgical consultation and diagnostic US
or air-contrast enema
Pearls
- All children presenting to the ED with suspected HSP should have a stool
occult blood test if they have abdominal pain and a urinalysis for
nephritis
- Intussusception with HSP is seen in 2% of patients, most commonly in
boys, particularly those about 6 years of age
- Joint symptoms may precede the rash in 25% of patients, ankles and
knees are the most commonly affected joints
- Monthly urinalysis should be performed for 3 months following diagnosis
to screen for delayed renal involvement
Acropustulosis of Infancy
Keratin filled cyst, usually around the nose and eyes

Often disappear within 2-4 weeks
In adults may require removal by a physician
History
Intensely itchy vesico-pustular eruption of the hands and fret

Papules and vesicles are similar to those found in scabies, but there is
absence of the typical burrows on skin
Ask about associated symptoms E.g. fever, pharyngitis, malaise,

Important to ascertain how the rash has developed
Any topical or systemic treatment
Medication and Immunization history
Case
You are a GP. Catherine has brought her 7 years old son because he has developed a rash on his hands and body.
Please take a history to exclude possible causes. Provide a differential. Discuss further investigation and management.
Introduction
- My name is Anthony. Im a doctor working here today. I understand that
your 7 years old son has developed a rash on his hands and body. And I
have been asked to come to take a history and see what we can do about
it.
History
- When did it first start?
- What part of body was affected? Does it spread? Does it affect the nail?
- Does it affect the elbow or knee?
- Could you describe the rash to me? What is it like? Color? Red? Pus?
Bleeding? Flatten or raised? Has it been oozing? Any discharge?
- Anything may have triggered it? For example food?
- Itchy? Painful?
- How does it affect his appetite and sleep?
- It is the first time you son has had this kind of rash?
- Recent travelling?
- Have you son been sick recently?
- Apart from the rash, other symptoms? E.g. Fever? Neck stiffness?
Photophobia? Difficulty breathing? Watery/red eyes? Abdominal pain
- General inspection
- Take the vitals
- General examination: Neurological, Lungs (allergic reaction)
Eczema
- Chronic relapsing pruritic inflammatory skin disease
- Occurs mostly in children
- Associated with serum IgE level, allergic rhinitis and asthma
Treatment
- Avoid irritants: Synthetic clothing, soaps, detergents, chemical reagents
- Contact allergens: Latex, Metals, Perfumes
- Dietary factors: Cows milk, eggs, peanuts, tree nuts, wheat, soy, fish,
sheelfish
- Inhalant: House dust mites, trees
- Environmental: Hard water, humidity, temperaures
- Complications: Skin infection, scarring, sleep disturbances, psy
- Associated condition: Asthma, allergic rhinitis, acute bronchitis
Management
- Avoid triggers
- Moisturizers
- Topical steroids used on flaring as first line
- Dietary exclusions
- If moderate dermatitis, use moderate potency
- Watch for potent steroids on face cataract risk
Kids-L1-Abdo Pain
-
Kids-L1-Asthma - Management in PMH ED
Mild
Moderate
Px: History of asthma? Hay fever? How was he at birth? Pregnancy

normal?
- Medications?
- Allergies?
- Fx: Eczema? Asthma?
- Immunization up to day?
- Social: Live with who? Anyone sick in the family?
DDx
- Eczema
- Viruses: HHV-6, Hand foot and mouth disease (coxsackie), Enteroviruses,
Parovirus B18, Rubella/measles, Roseola infantum
- Parasite: Scabies
- Autoimmune: HSP, Allergies
Investigations
- Food allergies Food challenges, Skin prick testing
- Blood: IgE level, FBC Eosinophilia
- However, it is likely to be eczema and because you son is not very sick, we
can do these investigation later E.g. Food challenges
- If you son is not responsive to treatment, we may consider other
possibilities
Severe
Critical
Wheeze
Wheeze
Wheeze
Marked reduced air entry, silent
Normal air entry
Reduced air entry
Decreased air entry
chest
Minimal use of accessory muscle
Use of accessory muscles
Marked use of accessory muscles
Exhausted, Cyanosis
SaO2 >95%
SaO2 92-95%
SaO2 85-92%
SaO2 <85%
Management
< 6 years: 6 puffs Salbutamol
< 6 years: 6 puffs of Salbutamol, 4
Oxygen 8L/min if SaO2 < 92%
Oxygen
> 6 years: 12 puffs
puffs of Ipratropium
Salbutamol and Ipratropium see left
Continuous nebulized Salbutamol
Consider Oral steroid
Double if > 6 years
Oral or IV Steroid
and Ipratropium
IV steroid
Oral steroids
Then
Discharge
Then
Observation Ward or Discharge
Then
Admission
Consider IV Magnesium SO4 /

Aminophylline / Salbutamol
Then ICU
Kids-L2-Septic arthritis
Case
You are a rural GP talking a call from a nurse. A 5 years old girl with a swollen knee.
Take history, DDx and Management.
Important
-
Rule out rheumatic fever
Investigations
-
Temperature, Vitals
Blood: FBC, CRP, ESR, blood culture
Consider X-ray +/- US
Joint aspirate
If relevant, bone scan, bone biopsy, (check RA, ANA, HLA-B27)
More Info
Child with 1 Swollen Joint Not sick
DDX
-
Septic Arthritis Red, Painful joint, Occasionally not too unwell

Trauma
Coagulopathy Hemarthrosis = bleeding into joint space, look for bruising
Viral or Post-Vital Arthropathy Transient swelling
JIA Swelling for more than 6 weeks, look for overgrowth of limb, most
common form of persistent arthritis in children
OA Tender painful bone, sterile effusion in joint
Bone tumor (The child may be well)
Thorn synovitis (Thorns can penetrate very deeply)
Synovial hemangioma and pigmented villnodular synovitis (rare in
children)
Actions
- Take careful history
- Examine joint for bruises, redness, evidence of trauma, swelling
Investigations
-
Blood: FBC, ESR, CRP, if considering JIA (check RA, ANA, HLA-B27)
X-ray if bone tumors
Aspirate joint and culture
If relevant do bone scan
If <2 weeks, keep child under careful view
If >2 weeks, refer
Child with 1 Swollen Joint - Sick

DDx
-
Osteomyelitis (Tender, painful bone, redness, sterile effusion)

Septic Arthritis (Red, painful joint)
Viral Arthritis (Usually not very sick)
Rheumatic Fever (Constant fever E.g. Non-spiking, Migratory joint
swelling)
Juvenile Idiopathic Arthritis (subgroup: systemic arthritis)
Reactive Arthritis (Follow recent proven bacterial infection)
Actions
-
Take history, examine

Check EBC, ESR, blood culture, streptococcal serology
Aspirate and culture joint fluid, If relevant bone scan
If septic arthritis or osteomyelitis suspected IV antibiotics after blood
culture taken
A sick child with a swollen joints is best in hospital, if not possible start
IV antibiotics with phone guidance
Septic Arthritis of a hip is an emergency and the joint should be aspirated
or opened if suspected
More than 1 joint, Not sick

DDx
Actions
Viral or Post Viral Arthropathy (Usually not very sick)

Henoch-Schonlein Purpura A disease of skin and other organs most
commonly affects children, it is a systemic vasculitis with deposition of
immune complexes containing the antibody IgA, cause unknown (Transient
joint welling, purpura) Small amount of blood or protein may present in
urine
- Juvenile Idiopathic Arthritis (Swelling lasts for at least 6 weeks)
- Reactive Arthritis (Follow recent proven bacterial infection)
More than 1 Joint, Sick
Take careful history, Examine

Check FBC, ESR, ANA, HLA B27, RF which will usually be negative in JIA
Check urine is HSP considered
If duration of welling more than 2 weeks refer
Rheumatic Fever (Constant fever, migratory joint swelling)

Leukemia (Hepatosplenomegaly, bone pain, misery)
Henoch-Schonlein Purpura (Transient joint swelling, purpura)
Septicemia (Joints infected or have sterile effusion, usually very sick)
Septic arthritis (Occasionally multiple joints may be septic: infants,
toddlers, immune-suppressed)
Viral or Post Viral Arthropathy (Involved joints may change every few
days)
Serum Sickness (Target lesion, Hives)
Juvenile Idiopathic Arthritis: Systemic Arthritis (Spiking fever, rash,
hepatosplenomegaly)
Reactive Arthritis (Follows recent proven bacterial infection)
Rheumatic Fever (Constant fever, migratory joint swelling)
Leukemia (Hepatosplenomegaly, bone pain, misery)
Henoch-Schonlein Purpura (Transient joint swelling, purpura)
Septicemia (Joints infected or have sterile effusion, usually very sick)
Take history
Examine for joints, rashes, cardiovascular abnormalities
Check FBC, ESR, CRP, blood culture, streptococcal serology
Treat with antibiotics if septicemia possible, after blood culture taken
If systemic arthritis is possible, check for pericarditis
If leukemia is possible refer immediately
If HSP possible check urine for blood
A sick child with swollen joints is best in hospital whatever the cause
Take history
Examine for joints, rashes, cardiovascular abnormalities
Check FBC, ESR, CRP, blood culture, streptococcal serology
Treat with antibiotics if septicemia possible, after blood culture taken
Septic arthritis (Occasionally multiple joints may be septic: infants,

toddlers, immune-suppressed)
- Viral or Post Viral Arthropathy (Involved joints may change every few
days)
- Serum Sickness (Target lesion, Hives)
- Juvenile Idiopathic Arthritis: Systemic Arthritis (Spiking fever, rash,
hepatosplenomegaly)
- Reactive Arthritis (Follows recent proven bacterial infection)
Kids-L2-Limping
A 4 years old girl presents with a 2 days history of limp.
-
1.
2.
3.
4.
5.
If systemic arthritis is possible, check for pericarditis

If leukemia is possible refer immediately
If HSP possible check urine for blood
A sick child with swollen joints is best in hospital whatever the cause
Take a history
Explain examination
What are your ddx?
What are the investigations?
What are some causes of painless and painful limping?
1.
-
2.
Duration, onset, pattern
Trauma, history of trauma
New shoes
Well/Unwell
Site of maximum pain
Pain when not weight bearing, worsening
Pain at night
Stiffness in the morning
Locking of the knee
Joint involvement
General
- Temperature
- Rashes
- Unwell child poor perfusion, tachycardia
Gait
Gait, Joints, Skin, Muscles (power, wasting, swelling, tenderness), Lymph glands in
groin, Evidence of trauma
3.
4.
All age: Trauma, Infection (septic arthritis, OA, discitis), Tumors,

Cellulitis, Regional lymphadenitis, Non-accidental injury
Child 4-10 years
Transient synovitis = Transient Arthritis, can affect hip, knee or

other joints
Blood: FBC, ESR, CRP, blood culture

X-ray
Bone scan infection, tumors
Others: ANA, RF, HLA-B27
5.
DDx
Common Conditions Causing Painful Limp
Painless
Neurological: Cerebral palsy, Hemiplegia, Poliomyelitis

Unequal leg length: Multiple causes
Deformity: Congenital, Past trauma, Past infection, Long standing
inflammation, Malignancy
Painful
-
Infections: OA, Septic arthritis, Discitis

Inflammation: Transient arthritis of Hip (irritable hip), JIA
Tumor/Malignancy
Trauma, Toddlers fracture
Mechanical (Osteochondroses = a group of disorder that share certain features):
Freibergs, Kohlers, Perthes, Esteochondritis dissecans knee, Scheuermanns
Mechanical (Apophysitis): Osgood-Schlatter disease, Severs disease
Others: Slipped upper femoral epiphysis, Reflex sympathetic dystrophy,
Psychosomatic limp, Patello-femoral pain
Infection, inflammation, Trauma, Tumor, Mechanical problems (E.g.

Osteochondroses, Aponphysitis) of the back, pelvis, hip, thigh, calf,
knee, ankle or foot
More Info PMH Guildeines
Background
- Lumping is common in children
- Caused by a wide range of problems
- Can be secondary to pain, muscle weakness or structural changes, or combinations of above
DDx
All age: Trauma, Infection (septic arthritis, OA, discitis), Tumors,

Cellulitis, Regional lymphadenitis, Non-accidental injury
1-3 years
Toddlers Fracture
DDH developmental dysplasia of the hip
Muscular dystrophy
Congenital scoliosis
JIA
Cerebral palsy
Rickets
Hemophilia
Discitis
HPS
Child 4-10 years

- Transient synovitis = Transient Arthritis, can affect hip, knee or other joints
- Perthes disease
- Kohlers disease
- Leg length discrepancy
- Ricketts
- Hemophilia
- HPS
Adolescent 10-16
-
Slipped upper femoral epiphysis

Spondylolysis
Osgood-Sclatter
Chondromalacia
Frieberg Disease
DDx
Common Conditions Causing Painful Limp
Painless
Neurological: Cerebral palsy, Hemiplegia, Poliomyelitis

Unequal leg length: Multiple causes
Deformity: Congenital, Past trauma, Past infection, Long standing
inflammation, Malignancy
Painful
-
Infection, inflammation, Trauma, Tumor, Mechanical problems (E.g.

Osteochondroses, Aponphysitis) of the back, pelvis, hip, thigh, calf,
knee, ankle or foot
Initial Investigations
OA
Blood: FBC, ESR, CRP, blood culture

X-ray
Bone scan infection, tumors
Others: ANA, RF, HLA-B27
Infections: OA, Septic arthritis, Discitis

Inflammation: Transient arthritis of Hip (irritable hip), JIA
Tumor/Malignancy
Trauma, Toddlers fracture
Mechanical (Osteochondroses = a group of disorder that share certain
features): Freibergs, Kohlers, Perthes, Esteochondritis dissecans knee,
Scheuermanns
Mechanical (Apophysitis): Osgood-Schlatter disease, Severs disease
Others: Slipped upper femoral epiphysis, Reflex sympathetic dystrophy,
Psychosomatic limp, Patello-femoral pain
Septic Arthritis
Generally unwell, febrile, significant pain

Redness and diffuse swelling
May be a sterile effusion in the adjacent joint
Initial Investigations: FBC, ESR, Blood culture, X-ray (normal for the
first 7 days), Bone scan (hot spots)
Discitis
Usually sick, has a stiff back
Transient Arthritis of Hip
JIA
Usually well, may have a recent viral illness

More common in boy, with pain in the groin or referred knee pain
Refuse to take weight on the leg
Hip movement is restricted
Age: 3-10 years
Initial investigations: FBC, ESR, X-ray of hip (to exclude other conditions E.g.
Perthes)
- Management: Rest in bed, Anti-inflammatory medications optional
Tumors
- For more than 6 weeks

Trauma
- Pain usually worse at night

Toddlers Fracture
- A spiral fracture of the tibia from documented trauma

- Investigation: X-ray sometimes useful, bone scan more reliable
Kohlers
Freibergs
The second metatarsal head becomes deformed, and is associated

with tenderness, until gradual regeneration occurs
Perthes
- Femoral head becomes deformed
- Gradual onset of pain around one hip, referred pain to the knee
- Limited movement
Osgood-Schlatter Disease
The navicular bone becomes compressed, gradual regeneration over 1-2 years
Tenderness and swelling around the navicular bone, associated with x-ray
changes
Osteochondritis Dissecans Knee
-
Locking of the knee inability to bend or straighten their knee
Slipped Upper Femoral Epiphysis
Tenderness of the tibial tubercle, pain on resisted extension of the

- Classically in obese adolescent boys
knee
- Bilateral in 2-%
- Discomfort is particularly noted after running and sport
- Hip pain or referred knee pain, External rotation of the leg
Kids-L2-Developmental Delay
3 years old boy brought it by his mother who concerned that he is only speaking in single words. Day care teachers find it difficult to understand him when he
speaks.
1.
2.
3.
4.
Take a history.
What to look for on examination.
What investigations?
1.
Hearing problems
Symptoms of autism: Stereotypes behaviors, Mannerism, Not seem to be
listening when spoken to
- Symptoms of sensory processing disorder: Over sensitive to
touch/noises/smells
- Symptoms of epilepsy
- Sleeping ok? Bed wetting?
- Weight loss?
- Fx history of epilepsy, or symptoms suggestive of epilepsy
- Social history: Parents separation? Change in routine?
Developmental history
Speech: Absence of single word by 18? Not using simple sentences by 2.5
years? Use of gesture more than words by 3-5 years?
Other Developmental Delay?
Pregnancy, Birth history
Px, Vaccination
3.
General Inspection: Dark circles, Conscious level (E.g. Hypoglycemia,

Seizure), Dysmorphic features
Weight and height: Plot it on growth chart
Inattentive Symptoms: Easily distracted, Difficulty focusing on one task,
Not seen to listen when spoken to, Daydream, Struggle to follow
instructions
Symptoms of Autism: Poor eye contact, Socially passive, Lack of use of
gestures or facial expression, Repeated motor mannerisms, Persistent
preoccupation with parts of objects
Signs of Hypothyroidism: Bradycardia, Dry skin, Cold hands, Non-pitting
edema, Pleural effusion, Round puffy face
Signs of Heart Problems: Murmur, Edema
Signs of Anemia: Pallor
Signs of Asthma: Wheezing
- Check Ears
-
Depends on the history and physical examination

Blood: FBC, Glucose, ESR, CRP, TFT, screen for nutritional deficiency
Urinalysis
Heart: ECG, 24 hours holter, Echo
EEG if suspects seizures
Psychological Referral to social workers
Sensory Process Disorders: Sensory profile (screening)
ADHD: Strength and weakness attention and normal behavior scale
SWAN, WISC Wechsler Intelligence scale for children, Diagnosis base on
DSM IV criteria
- Autism: Autism Spectrum Screening Questionnaire ASSQ (for children 716), Modified checklist for autism in toddlers M-CHAT (16-30 months),
Diagnosis base on DSM IV criteria
- Developmental and Behavioural Screening Tools: Age and stages
questionnaires (1-66 months), Children development inventory (0-6 years)
- MDT: OT, Social worker, Pediatrician, Neurologist, Psychologist,
Psychiatrist
Kids-L2-Delayed Puberty
Mum brings in his 14 years old son. She complains that her son is the shortest in his class and request for growth hormones.
1.
2.
3.
4.
5.
6.
1.
Take a history
Examination
DDx
Investigations
What are the causes of growth hormone deficiency?
What are the indications of growth hormone replacement therapy?
2.
-
Measure the parents height and estimate mid-parental height (If child
below 3rd height centile, is this appropriate for mid-parental height)
- Take serial height measurements at least 6 months apart (is child growing
slow down?)
- Calculate height velocity
- Assessment of pubertal status (in older children)
- General features of chronic disease, nutritional state and dysmorphic
features
- Look for signs of hypothyroidism
Male
-
(Maternal height + Paternal height + 13)/2 = Ans +/- 6.5
Females
- (Maternal height + Paternal height - 13)/2 = Ans +/- 6.5
4.
3.
-
Familial short stature

Constitutional delay of growth/puberty
Psychosocial causes of short stature
Isolated growth hormone deficiency
Chromosomal disorder E.g. Turners syndrome
Nutritional E.g. Celiac disease
Autoimmune
Chronic disease
Skeletal disorders
General Investigations: FBC, U&E, Creatinine, Urea, Urinalysis

Karyotype: All girls with unexplained short stature should have a
karyotype performed to exclude Turners syndrome
- Celiac disease:
- TFT
- IGF1 Insulin-like growth factor-1
- GF Stimulation test E.g. Insulin stimulate the release of GH, to test for
pituitary function
X-ray of the left wrist to ascertain bone age: This is delayed in growth
hormone deficiency, hypothyroidism and celiac disease
5.
6.
- Mutation of genes producing GH

- Genetic syndromes: Prader willi syndrome, Turner
- Chronic renal insufficiency
- Intracranial tumors
- Autoimmune
- Sheehan syndrome
Kids-L2-Precocious Puberty
1.
2.
3.
4.
5.
2.
Growth spurt
Maturation of primary sexual characteristics E.g. Gonads, Genitals
Appearance of secondary sexual characteristics
Menstruation and spermatogenesis
Precocious <9years (8 if girls)

Delayed = no signs by 14 years
4.
Central Caused by FSH and LH

-
Turners syndrome
Prader willi syndrome
Chronic renal insufficiency
Idiopathic short stature
List 4 manifestation of puberty.

How to define precocious and delayed puberty?
What are the 2 main classification of precocious puberty?
Tell me more about central precocious puberty.
Tell me more about peripheral precocious puberty.
1.
3.
Infectious: Meningitis, Encephalitis, TB, Sarcoidosis

Brain tumors
Brain injury
Idiopathic
Most cases no cause is found, especially in female

In boys, almost always serious CNS tumor
Evaluation: FSH, LH high
Treatment: Synthetic GnRH agonist
Peripheral Caused by elevation of sex steroids

5.
Exogenous estrogen E.g. Pills, Vaginal creams

Anabolic steroid
Neoplastic: Leydig cells tumors, Ovarian tumors
Congenital adrenal hyperplasia
Possible sources: Gonads, Adrenal glands, Exogenous

Evaluation: FSH, LH should be low, Measure HCG level in boys to rule out
secreting tumoes
Treatment: Tamoxifen, Spironolactone
6. What are the causes of delayed puberty?

-
Constitutional delay in growth and puberty

Systemic disease
Anorexia
Syndromes E.g. Kallmann syndrome, Prader willi syndrome, Turners
syndrome
Hypothyroidism
Congenital adrenal hyperplasia
Notes: Neonatal Station = Neonatal Resus or Newborn check

KEMH Guideline - Neonatal Resuscitation
Neonatal Resuscitation (For Infants up to 28 days post due day)
- 70% of infants requiring resuscitation at birth can be predicted from the
presence of some condition of pregnancy or labour
- Up to 10% of newborn infants require some form of resuscitation after
birth
- 1% need extensive resuscitation to survive
- Premature infants have anatomical and physiological differences that
place them at a higher risk of problems at birth (E.g. Surfactant
deficiency, inadequate thermoregulation, fragile cerebral capillaries,
higher incidence of congenital infection)
Newborn Resuscitation Aligorithm
Birth 30s
- Term Gestation? Breathing or crying? Good tone?
30s 60s
- On 30s, check HR and assess colors
- If HR below 100 but >60? Gasping? Apnea?
60s Onwards
- HE below 100 but >60?
- HR below 60?
Neopuff
Targeted SpO2 After Birth

1 min 60-65%
5 min 80-85%
10min 85-95%
Yes Provide warmth, Clear airway if necessary, Dry, Ongoing evaluation

No Warm, Clear airway if necessary, dry, stimulate until 30s
Yes SpO2 monitoring, PPV Positive Pressure Ventilation for 30s then
reassess the HR
No (E.g. HR>100) Labored breathing or persistent cyanosis? If yes Clear
airway, SpO2 monitoring, Consider CPAP
Yes Continue PPV
Yes Chest compression with PPV (ratio of 3 to 1, for 30s, then recheck HR),
if still below 60, give IV Adrenaline
If still not improving, consider hypovolemia and pneumothorax
Laerdal Bag
It has a theoretical advantage over the Laerdal bag (self-inflating bag)

that it provides an efficient PEEP (Positive end expiratory pressure)
- >34 weeks 30cm H2O
- <34 weeks 25cm H2O
Air or Oxygen
- Remain controversial
- Where a blender is available, the initial setting should be 30%
- A saturation monitor should be attached as sson as possible
Administration of Drugs and Fluids
Adrenaline
- If HR remains <60/min despite adequate ventilation and 30 seconds of
compression give
Does
- >34 weeks or >2.0kg give 1 mL of 1:10,000 solution
- <34 weeks or <2.0kg give 0.5mL or 1:10,000 solution
Route
- The quickest effective route of administration is via the ETT
- If unsuccessful Umbilical vein catheter
- Other routes of administration are not acceptable
Naloxone
- A second line resuscitation, only indicated in specific circumstances and
after other resuscitative measures
Criteria
- The mother has received narcotics within 4 hours of delivery
- The mother has is not and illicit user of narcotics
- There is a continued respiratory depression after +ve pressure ventilation
has restored normal heart rate and color
(Naloxone should not be used in the first 5 misn of life)
Dose
- 100 micrograms/kg
Route
- IV, dose may be repeated, but Naloxone has been traditionally given IM
When to cease resuscitation attempts
- Decision to cease resuscitation should only be made by a neonatal
consultant or senior registrar
- A decision to cease will be made generally after failure to obtain cardiac
activity 15 mins
Volume Expansion
- Given to infants who is not responding to an initial dose of Adrenaline
receive a 10ml/kg bolus of normal saline via a UVC (umbilical vein
catheter)
- This is based on the possibility of covert blood loss
Fluid
- Normal saline, the most convenient and safest volume replacement
- O ve blood is ideal, but this may take time to obtain
Route
- Umbilical venous catheter
Volume
- 10mL/kg given as bolus over 1-2 mintues, may be repeated
Sodium Bicarbonate
- May be given if an arrest is going more than 10-15 mins, or if the infant is
not responding to adrenaline and volume
Dose
- 1-2 mmol/kg of 4.2 soIn (8.4% diluted 1:1 with sterile water)
Route
- UVC
Post-Resuscitation Care
- After the vitals has returned to normal admit to NICU Neonatal
Intensive Care Unit
Newborn Babies Check (also see 6 weeks check of kid)

Well-Newborn Care
Newborn Screening Tests
- Capillary blood from a heel-stick is obtained after 24 hours of age and prior to discharge from the hospital, with the ideal age being 2-4 days of age
- Sent for newborn screening tests, look for a variety of metabolic and genetic disorders
- Common tests: Congenial hypothyroidism, PKU (amino acid metabolism disorder), Galactosemia, CF, Congenital adrenal hyperplasia, Fatty acid
oxidation defects
- Limitations: Accuracy of the tests (the way specimen is collection, birth weight, gestational age, co-existing illness)
Skin
- Rashes: See note Rashes
- Diaper Dermatitis: Multiple factors E.g. Sensitive skin, Moisture trapped by a diaper, Acidity of the stool and urine, Prevention is the best cure
diaper area should be kept as dry as possible E.g. frequent diaper change, leave the perineal area open to air, apply a barrier cream
- Diaper Dermatitis: Irritant Contact Dermatitis (erythema with shallow ulcerations, sparing the creases), Candida Diaper Dermatitis (beefy red, scaly
plaques, papules, pustules, a KOH preparation would demonstrate the presence of yeast, treatment with a topical antifungal agent)
- Mongolian Spots (Congenital Dermal Melanocytosis): Blue-Gray macules, typically disappear by 7 to 13 years of age, but some persist into adulthood
- Salmon Patches: Smooth pink or red macular lesions, on the glabellar region or upper eyelids usually disappear by 1 year of age, those behind the
neck 50% persist
- Caf-au-Lait Macules: Pale brown macules with irregular margins, isolated macule occur in 10-20% of the normal population, presence of 6 or more >
5mm is very suggestive of neurofibromatosis, especially in combination with axillary or inguinal freckling, optic glioma, lisches nodules, Fx
Mongolian Spots
Caf-au-Lait Macules
Cranium
- Frontanelles: Anterior and posterior fontanelle, anterior closes by 6-18 months, the posterior is generally smaller and closes by 4 months of age
- Caput Succedaneum: A diffuse swelling of the soft tissue of the scalp, if uncomplicated no treatment is needed and the swelling resolves during the
first few days of life, rare instances a hemorrhagic caput may occur and cause shock
- Cephalo-hematoma: Subperiosteal hemorrhage, the swelling does not cross suture lines, a slow process, may not be evident until several hours after
birth, most are resorbed between age of 2 weeks and 3 months, sometimes calcification can occur, but yet no treatment is recommended
- Molding (Positional Plagiocephaly): Asymmetry in the appearance of the cranium results from gentle application of pressure, Occurs when an infant
spends a significant portion of time in the same position, Should be examined for torticollis, Molding can be managed by repositioning, if severe a
cranial molding helmet can be used, Passive stretching is recommended for torticollis
Cranio-synostosis (Premature Closure of a Suture): Because the skill cannot expand to the fused suture, it grows in the direction parallel to the closed
sutures
Caput Succedaneum
Caput Succedaneum
Plagiocephaly
Craniosynostosis
Eyes
- Eye Color: Eye color is usually formed by 3-6 months of age, additional iris pigmentation continues during the first year
- Strabismus: Should be diminished within the first 2-3 months of life, if persist after age of 3 months ophthalmologist
- Nasolacrimal Duct Obstruction: Lacrimal system develops fully over the first 3-4 years of life, Lacrimal glands begin to produce tears by week 3 or 4 of
life, 6% of newborns has one or both lacrimal ducts blocked, Affected children appear to have excessive tearing, therapy with gentle massage of the
duct in a downward direction, Most blocked lacrimal ducts open spontaneously by 6 months of age, If still blocked at 1 year of age <1% will open
spontaneously, if persistent from 6-12 months ophthalmologist
Ear
- Hearing: Auditory stimulation during the first 6 months of life is very important for the development of speech and language skills, hearing screening
should be done prior to discharge
Oral Cavity
- Teeth: Primary teeth eruption typically occurs at the age of 6 months (range from 3-16 months), Natal teeth are teeth present at or shortly after birth,
these teeth are generally poorly formed, they are the primary teeth that have erupted early, removal of the natal teeth is recommended only if they
cause significant irritant to the teeth, also present a danger of aspiration due to poor attachment, they may interfere with feedin
- Dental Lumina Cysts, Bohn Nodules, Epstein Pearls: Dental Lumina Cysts (Generally not painful), Bohn Nodules (yellowish nodules), Epstein Pearls, All
disappear within a few weeks
Thrush: White patches of the mouth, Fairly common, Caused by Candida albicans, Unlike residual milk candida patches cant be easily wiped off,
When removed the exposed mucosa is red and raw and may bleed, Treatment with a topical antifungal agents, Care should be taken to avoid reinfection from nipples and other items
Cleft palate
Chest
- Murmur
- Breast Hypertrophy: Brest buds are present in most infants (both males and females) born after 36 weeks of gestation, Result from the passage of
maternal hormones across the placenta during gestation
- Galactorrhea: Occurs in up to 6% of normal-term infants, the thin milky discharge may be caused by maternal estrogen or neonatal prolactin
- Both condition resolve within several weeks, but occasionally persist for months
- Mastitis: Can manifest as cellulitis or an abscess, Staphylococcus aureus is the most frequently involved, 5-10% caused by Gram ve enteric bacteria,
Purulent drainage, Infants usually appear well, 25% with fever or ill, treat with IV antibiotics
Umbilicus
- Normal Umbilicus: 2 arteries and 1 vein, which are surrounded by Whartons Jelly, After birth the cord is clamped and cut, the trend of dry cord care
without application of antimicrobial agents is the common practice, The cord generally falls off in 7-21 days, but may take longer, Parents should be
reassured that the presence of oozing, a few drops of blood, a mild odor are normal, Concern if significant redness, discharge, bleeding not stopped by
gentle pressure
- Umbilical Hernia: Presents as a bulge at the umbilicus, common in African American infants, premature infants, Down, Ehlers-Danlos, Hypothyroidism,
Most close spontaneously by the age of 5, Strangulation rarely occurs, The likelihood of closure is inversely related to the size of the hernia, Repair is
usually done if the hernia persists beyond 5 years
- Omphalitis: Infection of the umbilical cord or surrounding tissue, Now rare in developed countries, Systemic signs may present, Complication included
sepsis, hepatic abscess, peritonitis, portal vein thrombosis, Appropriate cultures of discharge, blood, CFS should be obtained, Treat with IV antibiotics
- Umbilical Granuloma: Results when an excessive amount of granulation tissue accumulates, A small pink mass is found at the base of the umbilicus,
(It is important to differentiate this from a more common and benign condition of patent omphalo-mesenteric duct and urachal remnant), Treatment
of application of silver nitrate to the granulation tissue 1-2 times a week for several weeks, generally few drops are required, care to be taken to avoid
the normal surrounding skin which can be burned by the silver nitrate, if it does not disappear after silver nitrate consider Omphalo-mesenteric
cyst
- Patent Omphalo-mesenteric Duct and Patent Urachus: The omphalo-mesenteric duct is a connection between the intestinal tract and the yolk sac
during fetal development, Normally regresses by 9th week of gestation, If it remains patent it persists as an attachment between the ileum and the
umbilicus which intestinal contents can drain, Varying degrees of patencies may result in umbilical polyp, Meckels diverticulum or omphalomesenteric duct cyst, These require further evaluation and surgical referral
Patent Urachus: A free connection between the urinary bladder and the abdominal wall through which urine may pass, The patient may present with
a constantly wet umbilicus or UTI, Incomplete patency may result an umbilical polyps, bladder diverticulum or urachal cyst, these require further
investigation and surgical referral
Umbilical Hernia
Omphalitis
Umbilical Granuloma
Patent Urachus
Genitalia - Boy
- Normal Care of the Penis: In uncircumcised boys, the foreskin is generally not retractable at birth, Avoid attempts to forcible retraction which may
result in scarring and phimosis, In circumcised boys the exposed glans should be coated with petroleum jelly with each diaper change
- Hypospadias and Epispadias: Hypospadias, the urethral meatus is abnormally located ventral to the tip of the glans, Classification of the type of
hypospadias anatomic location, also frequently associate with abnormality of the foreskin and chordee, circumcision should be deferred as the
foreskin facilities the subsequent repair of hypospadias
- Espispadias: The urethra opens on the dorsum of penis
- Cryptorchidism (Undescended Testicles): 3-6% of full term boys, unilateral or bilateral, most descend during the first 3-6 months, few tests descend
after this time, Treatment in Orchiopexy, which can be performed any age after 4 months, is optimally before 1 year of age to decrease risk of
infertility and testicular torsion, if undescended at 4-6 month refer to an urologist
- Inguinal Hernia and Hydrocele: Inguinal hernia occur in 1-5%of children, 10 times more common in boys than in girls, up to 30% of premature infants
before 36 weeks of gestation
- Hydrocele: Persistence of the process vaginalis, allows fluid to pass into the scrotal sac, transillumainates, may be communicating or noncommunicating, Most infant with isolated hydrocele undergo spontaneous closure of processus vaginalis with resolution of the hydrocele, If persists
at the age of 6 months to 1 year referral to a surgeon
Genitalia Girls
- Vaginal Discharge and Bleeding: Have well estrogenized vaginal mucosa because of the transplacental passage, therefore a thick vaginal discharge is a
normal finding, many also have a small amount of vaginal bleeding in the first week due to the withdrawal of maternal estrogen, parents should be
reassured that both findings are normal
Hip
All infants are examined for the developmental dysplasia of the hip (DDH) unstable, subluxed, dislocated hip, incidence is higher in girls, Ortolani
and Barlow maneuvers are used to assess hip stability in the newborn, Ortolani maneuver detects a dislocated femoral head that is reduced into the
acetabulum, Barlow maneuver detects a hip that can be dislocated posteriorly by gentle adduction and posterior pressure, they are only present for
the first 2-3 months of age, Other sign suggestive of hip dislocation are asymmetry of thigh folds or buttock creases, a +ve Galeazzi sign (relative
shortness of the femur with hips and knees flexed), discrepancy of leg lengths and limited hip abduction
- If a true +ve Ortolani or Barlow Sign is found refer to an orthopedist, infants with a soft click should have a follow-up examination in 2 weeks, if
findings persist have a US of hip by 3 weeks of age, XR if >4 months of age
Urination and Defecation
- Urate Crystals (Pink Diaper Syndrome): Parents may notice a pink crystalline substance in the diaper or a salmon-pink residue on the surface of the
diaper, resulting from the deposition of urate crystals, usually easily distinguished from blood on the basis of appearance, but occult blood test can be
performed, Urate crystals usually found in the setting of concentrated urine and may indicate dehydration, so assess for dehydration
- Meconium, Transitional Stool and Typical Stool: Passage of meconium usually occurs within the first 12 hours of life in 99% of full term infants and
95% of preterm infants, Transitional stools follow the passage of meconium before typical stool comes, Failure to pass meconium can occur as a result
of imperforate anus, functional intestinal obstruction (Hirschsprung disease), hypotonia, any infants who fail to progress to passing typical stools
should be evaluated in a timely fashion
- Establishment of a Bowel Pattern and Constipation: Initially the typical breast-fed baby passes a bowel movement after each feeding, but the age of
1 month this occur once every 1-7 days, typical formula-fed baby has a bowel movement every 1-3 days
- Constipation: Infrequent passage of hard or painful bowel movements, Contact the physician if the infant develops abdominal distention, vomiting,
refusal to eat, bloody stools or extremely hard stools
Reflexes
- Moro reflex, Sucking and rooting reflexes
Common Concerns
- Recommended Sleeping Position: Sleeping supine confers the lowest risk of sudden infant death syndrome, also not to put infants on waterbeds,
sofa, soft mattress, should not place any soft objects (E.g. Pillows, Toys) in infants sleeping environment
- Hiccups: The precise cause in unknown, persists for 5-10 mins are distressing to those caring of the baby, a few sucks on a bottle of sugar water may
relieve the hiccups
- Sneezing and Coughing: Can be a protective mechanism to clear material, if persistent may require further evaluation
- Chin Quivering: A babys chi may intermittently quiver, this motion is a reflection of an immature nervous system, the quivering stops as the nervous
system matures
-
Notes/Make-up scenarios: Oncology

Oncology
Level 1
Lung Cancer
Breast Cancer
Anti-emesis
Side Effects of Chemotherapy
Oncology Emergency x6
ECOG
TMN Stages
Skin Cancers
Pain Management / Constipation Management
Multiple Myeloma
Tumor Markers
Level 2
Skin Cancer
Colorectal Cancer
Prostate Cancer
Neck Lumps / Thyroid Cancer
Lymphoma
Leukemia
Level 3
Pancreatic Cancer
Hepatocellular Carcinoma
Myeloproliferative Disorder
Carcinoid Tumors
Onco-L1-Breast Cancer
Breast Cancer
This lady has found a breast lump. Please ans her questions.
1. How would you assess the risk of breast cancer?
2. When would you recommend screening programs?
3. What is the screening program in Australia?
4. What are the pros and cons of mammogram?
5. What happens if I have an abnormal mammogram?
6. What are the risk factors?
9. What is the staging?
1. How would you assess the risk of breast cancer?
Low Risk
- One first degree from either side of the family, diagnosed with breast
cancer over age of 50
- One second degree relative diagnosed with breast cancer at any age
- 2 close relatives diagnosed with breast cancer >50, but on different sides
of the family
Moderate Risk
- 1 or 2 first degree relatives diagnosed with breast cancer under the age
of 50
2. When would you recommend screening programs?

Low Risk Management
- Reassure
- Advise on breast awareness
- Advise to report any persistent symptoms of breast disease or a change in
family history
- Annual clinical breast examination
- Encourage women >50 for screening program
Moderate Risk Management
family history
2 close relative on the same side of family diagnosed with breast cancer
or ovarian cancer
High Risk
- 3 close relative on the same side of family diagnosed with breast cancer
or ovarian cancer
- Breast cancer diagnosed before age of 40
- Ovarian cancer diagnosed before age of 50
- Bilateral breast cancer
- Breast and ovarian cancer in the same woman
- Male breast cancer
3. What is the screening program in Australia?
- Age between 50-69 years
- Once every 2 years
- If moderate to high risk start 40-49
5. What happens if I have an abnormal mammogram?

- Further investigations
- US, FNA, Core biopsy cytology
- Blood: CEA, CA15-3, CA17-29 (CA = cancer antigen)
- Tumor expression E.g. Estrogen receptor, Progesterone receptor, HER-2
receptor
- In lack of ER, PR, HER-2 chemotherapy is the only option
- Tumors lack expression of HER-2 (Herceptin = Trastuzumab), ER
(Tamoxifen), PR have a higher risk of recurrence and metastases, and are
associated with a poorer survival
- MTD: Radiologist, Surgeon, Pathologist, Breast physician, Nurse
Annual clinical breast examination

Refer for screening when >40 for an annual screening
If women wants a more detailed risk assessment breast/genetics
clinics
Management
family history
- Refer to genetics for a detailed risk assessment
- Clinical examination every 6 months
- Annual breast screening
- Prophylactic surgery
- Participation in approved clinical research trials
4. What are the pros and cons of mammogram?
Pros
- Relatively cheap compared to other tests E.g. US, MRI
- Widely acceptable by women, Simple and quick
- High specificity 94%
- Can identify slowing growing cancer at least 2 years before reaching a
size that is detectable by palpation
Cons
- Low sensitivity 70-80%, require further investigations
- Pain and discomfort often reported by women
- Exposure to radiation
- False positive unnecessary stress
- False negative miss early treatment
6. What are the risk factors?
- Age
- Being female
- Fx
- Personal history
- Genetic: BRCA mutations
- OCP, HRT
- Pregnancy after age of 30
- Endometrial cancer
70% with breast cancer present with a lump (usually painless), most are
- Descending order of frequency
discovered by the patient
- Fibrocystic breast changes > Fibroadenoma > Intraductal papilloma >
- Less frequently: Breast pain, nipple discharge, Erosion, Retraction,
Lipoma > fat necrosis
Enlargement, Hardness, Shrinking of the breast
- Rarely: An axillary mass
- Systemic Metastases: Back or bone pain, Jaundice, Weight loss
- Frequency of carcinoma in various anatomic sites
9. What is the staging?
- Overall: Confirm the diagnosis, Staging and Grading, Identify spreading
- Surgery: Wide local excision or mastectomy +/- Breast reconstruction +
Spread
axillary node clearance
- Chest XR with CT for pulmonary metastases
- Radiotherapy: Reduce local recurrence, SE (pneumonitis, pericardiris,
- Abdominal CT and US for liver metastases
lymphadenopathy, Brachial plexopathy, ribs)
- Bone scan
- Chemotherapy:
- PET scan alone or combined with CT
- Endocrine Therapy: Aims to decease estrogen activity, and is used in all
Staging
estrogen or progesterone receptor +ve disease, E.g. ER estrogen receptor
- T1 - <2cm
blocker
- T2 2-5cm
- +ve for HER-2 Herceptin
- T3 - >5cm
- Distant disease: LFT, Ca++, CXR, Skeletal survey, bone scan, liver US
- T4 Fixed to chest wall, or orange peel skin
- Bisphosphonate and radiotherapy for bone disease
- N1 Mobile ipsilateral nodes
- Support Psychological support, support group
- N2 Fixed nodes
- Information Cancer council Australia
- M1 Distant mets
Possible Scenario: 42 years old women with moderate-poor prognosis of breast cancer. Please discuss management plan. Include SE of chemotherapy.
Treatment
Choice and Timing
Surgical Resection
- Staging, Tumor grade, Hormone receptors, HER-2
Breast-Conserving Therapy
- Stage 1-3: Standard care is surgical resection followed by adjuvant
- Lumpectomy
radiation or systemic therapy or both, which start when the breast has
- In stage I and II
adequately healed, usually 4-8 weeks after surgery
Mastectomy
- Neo-adjuvant therapy is becoming more popular since large tumors may
- Standard therapy for most patients with early-stage breast cancer
be shrunk by chemotherapy prior to therapy
Radiotherapy
Adjuvant Systemic Therapy
- After mastectomy may improve recurrence rates and survival
- Hormone modulating drugs
- HER-2 targeted Trastuzumab
- Cytotoxic chemotherapy
- Improves survival
Chemotherapy
Palliative Treatment
- Adjuvant chemotherapy reduces the risk of recurrence
- Breast cancer most commonly metastasize to liver, lungs, bone
Follow-up Care
- Local and distant recurrences occurs most frequently within the first 2-5
years
- Edema of the arm: Occurs in 10-30% of patients after axillary resection
without or without mastectomy, late edema may develop years after the
treatment, careful examination of the axilla for recurrence or infection, a
mild diuretic may be useful, if no improvement compressor pump and
then elastic glove or sleeve
- Breast Reconstruction: Should be discussed prior to mastectomy as it
offers important psychological relief, it is not an obstacle to the diagnosis
of recurrent cancer
Palliative radiotherapy, bisphosphonates, Endocrine therapy if hormone

receptor +ve breast cancer
Onco-L1-Colorectal Cancer
Colorectal Cancer
This patient has a poly. Please ans his questions,
1. What are polyps?
3. Risk Factors?
4. How to investigate?
5. DDx
6. Management
7. Treatment for Rectal Cancer
8. Follow-up after Surgery
9. Screening for Colorectal Cancer
10. Screening Tests
1. What are polyps?
- Majority of colorectal cancers develop from transformation of
adenomatous polyps
- They are finger like hyperplasia
- 2 types of polyps: Adenomatous polyps (85%), Serrated polyps (10-20%)
and are predominantly in proximal colon with a more favorable prognosis

- Asymptomatic: As adenocarcinoma grow slowly, may be present for
years before symptoms appear
- If asymptomatic, may be detected by fecal occult blood
Symptoms depends on the location
- Right Sided: Chronic blood loss, Anemia, Fatigue, Weakness, Uncommon
obstruction
- Left Sided: Left colon has a smaller diameter and the fecal matter is solid
obstructive symptoms may develop with colicky abdominal pain, a
change in bowel behaviours, constipation may alternate periods of loose
stools
Rectal Cancer: Feeling need to pass stools constantly, urgency, recurrent

hematochezia
- Liver should be felt for metastases
- PR examination
Investigation
- FBC for anemia
- LFT for metastatic disease
- CEA tumor marker, levels should normalize after complete surgical
resection
Colonoscopy
- Diagnostic procedure
- Permits biopsy for pathologic confirmation of malignancy
- Other Investigations: Barium enema, CT colongraphy
Then need to stage
-
Risk Factors
- 75% of all cases occur in people with no known predisposing factors
- Age: rises after age 45 years, 90% of cases occur in persons over the age
of 50 years
- Fx: Fx history of colorectal cancer is present in 20% of patients, or a family
history of adenomatous polyps, this risk is significantly increased (4 folds)
if the family member was diagnosed <45 years of age
- Inflammatory Bowel Diseases: Risk begins to rise 7-10 years after disease
onset in patients with ulcerative colitis and crohn colitis
- Dietary Factors: Diets rich in fats and red meats associated with increased
risk, diet high in fruits and vegetables decreased risk,
- Medications: Regular use of aspirin and NSAIDs decreased risk
- Others: Higher in blacks than in whites
DDx
- Irritable bowel syndrome
- Diverticular diseases
- Ischemic colitis
- IBD
- Infectious colitis
- Hemorrhoids
- Neoplasms must be excluded in any patients over age of 40 with a change
in bowel habits or hematochezia or who has an unexplained iron
deficiency anemia or occult blood in the stools
Treatment for Rectal Cancer

- Has a lower long term survival rates and higher rates of recurrence than
colon cancer, due to difficulty in achieving adequate surgical resection
margins
- Surgery +/- Radiotherapy (but has long been controversial)
Screening for Colorectal Cancer
Average risk individuals >50 years
- Annual fecal occult blood testing: Fecal immunochemical test
- Fecal DNA test
- Flexible sigmoidoscopy every 5 years
Management
- Adjuvant chemotherapy and radiotherapy improve overall survival
- Stage I No adjuvant therapy is needed
- Stage II Node ve disease, adjuvant therapy have not demonstrated any
survival benefit, may have some benefit in high risk stage II patients
- Stage III Node +ve, post-operative adjuvant chemotherapy significant
increase disease free survival
- Stage IV Metastatic disease, limited disease may be curable with
surgical resection of isolated liver or lung metastases
- For those with unresectable hepatic metastases (majority), local
cryosurgery, radio frequency or microwave coagulation, hepatic
chemotherapy may provide long term tumor control
Follow-up after Surgery
- Patients should be evaluated every 3-6 months for 3-5 years with history,
physical examination and CEA determinations
- Another colonoscopy 1 year after surgical resection, then every 3-5 years
Screening Tests
- Fecal Occult Blood: Fecal immunochemical tests that detect human globin
- Multi-target DNA assay: Analyzes fecal DNA for 22 gene mutations and
DNA integrity, high cost, not yet practical for population based screening
- Colonoscopy every 10 years

- CT colonography every 5 years
First degree Fx of colorectal cancer diagnosed >60
- Screening at age of 40
First degree Fx of colorectal cancer diagnosed <60
- Screening at age of 40 or 10 years younger than age of diagnosis of the
relative, whichever is first in time
Flexible Sigmoidoscopy: Visualization of the rectosigmoid and descending

colon, requires no sedation, chief disadvantage is that it does not
examine the proximal colon
Colonoscopy: Requires aggressive bowl cleansing prior to the
examination, IV sedation is used for most patients, however rate of
colorectal cancer within 3 years of a screening colonoscopy is 0.9%, that
means it may sometimes overlooked an adenomatous polyps
CT Colonography: CT to regenerate colon lumen, requires similar bowel
regimen as colonoscopy
Barium Enema: It is more time consuming compared to CT colonography,
also less accurate
Onco-L1-Lung Cancer
Lung Cancer
Right upper lobe nodule shows peripheral calcification

0.
1.
2.
3.
4.
5.
6.
Describe your findings.

What is DDx of a pulmonary nodule?
What are the symptoms?
Tell me some risk factors
Give 5 types of lung cancer.
What is para-neoplastic syndrome?
7. What are your investigations?

8. Can you tell me about the staging of lung cancer?
9. What is the management of lung cancer?
10. Palliative Therapy
1. What is DDx of a pulmonary nodule?
- Small lung cell carcinoma
- Aspergillosis
- Cyst
- RA
- Sarcoidosis
- TB
- Scar tissue
3. What are the symptoms?

- New cough or change in pattern of chronic cough
- Dyspnea, Hemoptysis, Anorexia, Weight loss
- Pain
- Endobronchial obstruction atelectasis
- Horner syndrome
- Symptoms of metastases E.g. Brain metastases Headache, N+V,
Seizures, Dizziness, Altered mental state
- Symptoms of para-neoplastic syndromes
- Clubbing
- Pleural effusion
- Persistent opacity
- Cytological or histological findings of lung cancer in sputum, pleural fluid
or biopsy specimen
5. Give 5 types of lung cancer.
- Small cell lung cancer
- Non-small cell lung cancer
- Adenocarcinoma
- Squamous cell carcinoma
- Bronchioloalveolar carcinoma
6. What are your investigations?

We need to make a diagnosis

- In a young non-smoking patient, can be monitor with serial imaging to
assess changes in size
Fleischner Recommendation
Low Risk Patient
- 4-6 mm CT scan at 12 months
- 6-8 mm CT scan at 6-12 months and 18-24 months
- > 8mm CT at 3, 9, 24 months, consider PET scan, +/-biopsy
High Risk Patient
- Similar to above, but more frequent
4. Tell me some risk factors
- Personal or family history of lung cancer or other cancers
- Smoking, Active or passive
- Miner, Industrial carcinogen
- Chronic lung diseases E.g. Pulmonary fibrosis, COPD, Sarcoidosis
6. What is para-neoplastic syndrome?

- They are the symptoms or signs that are not directly due to the presence
of tumors
- E.g. Mediated by hormonal factors, or Immune response to the tumor
- Most commonly with lung, breast, ovarian cancer
Examples
- Endocrine: Cushing syndrome, Hypercalcemia
- Neurological: Peripheral neuropathy, Myasthenia syndrome
- Dermatomyositis, Acanthosis nigricans
7. Can you tell me about the staging of lung cancer?
Non-small cell lung carcinoma
Sputum cytology is highly specific but not sensitive enough

Malignancy pleural effusion
FNA of the palpable lymph nodes
Bronchoscopy with brushing of the lesions, direct biopsy, FNA of the
mediastinal lymph nodes
- Transthoracic needle aspiration
Check for Metastasis
- PET scan
- CT/MRI
- Abdominal US
-
8. What is the management of lung cancer?

- Cure is unlikely without resection, has to consider if technically feasible
(E.g. impossible if tumor involving the heart, great vessels), is the
patient able to tolerate the surgery
- Stage I and II are treated with surgical resection where possible
- Stage II: Additionally recommended to receive adjuvant chemotherapy
- Stage IIIA: Poor outcomes when treated with resection alone so chemo
+/- radiotherapy
- Stage IIIB: May resection
- Stage IV: Chemotherapy or palliative therapy
Patient with small early stage lung cancer who are not candidates for surgery
because of surgical contraindications
- Stereotactic radiosurgery: Delivery of a large dose of radiation to a small
well defined target
- Also used in stages IIIA and IIIB
Neoadjuvant Chemotherapy
- Giving anti-neoplastic drugs in advance of surgery or radiation therapy
- More widely used in selected patients with stage IIIA and IIIB
- Some studies suggest a survival advantage, but remains an area of active
research
Adjuvant Chemotherapy
- Anti-neoplastic drugs following surgery or radiation therapy
- Staging guide treatment and give prognosis

TNM International Staging System
- T: Size and location of the primary tumor
- N: Presence and location of nodal metastases
- M: Presence or absence of distant metastases
- These stages are grouped into prognostic categories 1-4
- Many patients with stage 1 and 2 are cured through surgery
- Patients with stage IIIB and 4 do not benefit from surgery
- Patient with stage IIIA may benefit from surgery in certain circumstances
Small Cell Lung Cancer
- Not staged using the TNM system because micro-metastases are
assumed to be present at diagnosis
- Limited disease (30%) when the tumor is limited to the unilateral hemithorax or
- Extensive disease (70%) when the tumor extends beyond the hemithorax
(including pleural effusion)
- Patients with limited SCLC benefit from thoracic radiation therapy in
addition to chemotherapy
- Response rate to Cisplatin and Etoposide are excellent, 80-90% response
rate in limited stage disease
- However, response rate tend to be short-lived with a median of 6-8
months
- Once the disease has recurred, median survival is about 3-4 months
- Thoracic radiation therapy in limited small cell lung carcinoma, and is
given with chemotherapy
- Thoracic radiation is not beneficial for patients with extensive disease,
and they should receive chemotherapy alone
- There is a high rate for brain metastasis in SCLC prophylactic cranial
irradiation
Cisplatin-containing regimens have been shown to have an overall

survival benefit in at least stage II disease
- Although not curative, chemotherapy has been shown to provide a
modest increase in overall survival
Palliative Therapy
- Laser is sometimes performed on central tumors to relieve endobronchial
obstruction, improve dyspnea and control hemoptysis
- Also radiotherapy
- Removal of a solitary brain metastasis improves quality of life
Onco-L1-Tumor Markers
Tumor Markers
1. What is a tumor marker?
- A substance found in blood, urine or body tissue that can be elevated in
cancer
- Helps to detect the presence of cacner
- They are produced by the cancer or in response to the presence of cancer
- Types: Most are cancer antigen, can be proteins
2. Give some examples.

- Hepatocellular cancer Alpha-Fetoprotein
- Breast Cancer: CA15-3, CA27-29
- Pancreatitis cancer: CA19-9
- Colorectal cancer: CA19-9
- MM: Bence Jones Protein
- CEA: Colorectal, Pancreatic, Lung, Breast
Onco-L1-MM
MM
1. What is multiple myeloma?
- Cancer of the plasma cells, which is derived from B lymphocytes
3. How do you diagnose it?

Criteria
- Protein band of electrophoresis
- Hypercalcemia
- Renal insufficiency
- Anemia
- Back pain
Tests
- FBC, Ca++, U&E, ESR,
- Screening test: Serum and urine electrophoresis
2. What are the symptoms?

- Osteocytes lesions: Back pain, Pathological fracture, Vertebral collapse
- Hypercalcemia: Bones, Stones, Groans (abdo pain, N+V, Constipation),
Psy
- Anemia, Neutropenia, Thrombocytopenia
- Recurrent bacterial infection
- Renal impairement due to light chain deposition E.g. Dysuria, Oliguria
4. Treatment?
General
- Analgesics
- Bisphosphonate to reduce fracture rate and bone pain
- Anemia with transfusion and erythropoietin
- Renal failure adequate fluid hydration (3L a day), dialysis may be
needed
- Infections: Antibiotics
Treatment
- Chemotherapy - Lenalidomide
Imaging: XR shows lytic lesions, fracture or osteoporosis
Autologous stem cell transplantation

Allogeneic transplantation
Onco-L1-Pain Relief
Pain Relief
Possible Scenario: This palliative cancer patient has been experiencing pain. Please take a history and state your management plan.
History
1. What are different types of pain?
- Type of cancer
- Neuropathic Pain
- Management
- Nociceptive Pain
- Pain severity
- Mixed
- Pain pattern: Breakthrough pain (acute pain), Pain in general (chronic
pain)
- Previous pain management and respond
- Type of pain E.g. Neuropathic? Nociceptive?
2. Discuss management of nociceptive Pain.
3. What can you tell me about Oxycodone?
Non-Pharmacological
- More potent than morphine orally
- Palliative radiotherapy
- Different people have different rate of metabolism of Oxycodone
- Heat or cold packs
- Work out the dose for the chronic pain and for the breakthrough pain
- OT, Physio, Massage
- Start with 2.5-5mg immediate release formulation every 4 hours until the
Pharmacological
pain is under control E.g. 2.5mg 4 times a day = 10mg for the extended
- Mild: Paracetamol or NSIADs
release
- Moderate: Tramadol, Low dose Oxycodone
- Breakthrough pain = 1/6 of the total daily maintenance dose
- Severe Pain: Potent opioids, Morphine is opioids of choive
Common Side Effects
- Constipation
- N+V, Drowsiness, Orthostatic hypotension, Urinary retention
- May cause respiratory depression in the newborn
4. The patient develops constipation with Oxycodone. What would you do?
Pharmacological Management of Constipation
- See below
- Can add Naloxone if regular laxatives are inadequate
- Tramadol: Less risk of constipation, also useful for neuropathic pain
Onco-L1-Constipation
Constipation
1. Diet and lifestyles.
- Dietary fibers
- Fluid intake
- Physical activity and exercise
2. Different types of Laxatives

- Bulk-forming: Increases the moisture in the stool, take 2-3 days to
achieve full effect (not recommended for opioid induced constipation)
E.g. Benefiber
Inappropriate habits E.g. Ignoring the urge to defecate
Osmotic: Draws water into the colon, effect occurs 2-48 hours E.g.
Lactulose syrup, Magnesium sulfate
Stimulant: Stimulate the intestinal motility, Can cause cramps, effects
occurs 6-12 hours, may be sold in combination with stool softeners E.g.
Senna
Stool Softening: If used as monotherapy = not effective
Onco-L1-Steroid
Steroid Side Effects
1. Acute
- Leukocytosis: Due with the migration of the leukocytes, less to the
vessels
- Cardiovascular: Water retention Can worsen hypertension and heart
failure, Hypokalemia
- GIT: Peptic Ulcers Increase the risk of peptic ulcers
- Endo: Diabetes Hyperglycemia and worsen diabetes control
- Skeletal: Muscle weakness and wasting Worsen myasthenia gravis
- Psy: Exacerbate psychiatric disorder
3. Mode of action
- Glucocorticoid Effects: Suppression of inflammation and immune
responses
- Mineralocorticoid Effects: Water retention, Potassium loss
Onco-L1-Emergency
Emergency
Possible Scenario:
2. Chronic
- Susceptibility to infection Latent TB may be reactivated, consider
Isoniazid
- Mask signs of infection
- Osteoporosis
- Muscular wasting
- Glaucoma OIP may increase
- Adrenal suppression
4. Adrenal suppression
- Chronic use of corticosteroid can cause adrenal suppression
- Consider withdrawing treatment gradually as abrupt withdrawal can
result in adrenal crisis
- Doses <7.5mg daily for prednisolone <3 weeks are unlikely to cause
adrenal suppression
- Minimize the risk of adrenal suppression by giving corticosteroid doses in
the morning
- Adrenal response may be depressed for >1 year after corticosteroids are
stopped corticosteroid may be needed during period of stress E.g.
Infection, trauma, surgery, blood loss
1.
-
Outline 6 Oncological Emergencies.

SVC obstruction
Spinal cord compression
Hypercalcemia
Febrile neutropenia
Tumor lysis syndrome
Also malignant effusion
Interpret this CT, what emergency would this man present?

2. Explain SVC obstruction.
- 70% due to lung cancer
Symptoms
- Dyspnea, Cough
- Facial swelling, Head fullness
- Arm swelling, Chest pain
- Dysphagia
Signs
- Venous distension of the neck and chest wall
- Facial edema, Facial flushing
- Cyanosis
- Arm swelling
Lung Cancer Subtype causing SVCO
- Small cell cancer > squamous cell cancer > adenocarcinoma > large cell
cancer
Investigations
- CT, MRI
- CXR Right hilar mass, Superior mediastinal widening, Pleural effusion
(malignancy), Bilateral diffuse infiltrates
- Accurate histological diagnosis of the cancer E.g. Effusion, Bronchoscopy
for small cell, FNA
Management
- Acute Management: Bed rest, Head elevated, Oxygen, Corticosteroid,
Diuretics (limited values)
Long Term: Chemotherapy for small cell carcinoma or non-Hodgkins

lymphoma
- Radiotherapy for NSCLC
- If fails stenting or bypass
4. Explain febrile neutropenia.
- That means the patient is febrile and neutropenic
- Detailsplease look it up..not so hard right
-
3. Explain spinal cord compression.

- Complication of lymphoma, MM, Metastases to the spine physical
damage, hemorrhage, pressure induced ischemia
- Back pain is the most common presenting symptom
- Treatment may reverse or prevent urinary and bowel incontinence
Symptoms and Signs
- Back pain 80%, worse by lying down, weight bearing, sneezing, coughing
- Development of neurological symptoms or signs
- Progressive weakness and sensory changes
- Late findings: Bowel and bladder incontinence
Imaging
- MRI
- Bone scan
Treatment
- Corticosteroid immediately
- Patient with a single area of compression are best treated with surgical
decompression followed by radiation therapy
- If multiple vertebral body levels are involved with cancer, radiation
therapy is the preferred treatment option
5. Explain tumor lysis syndrome.
- Complications of treatment associated tumor lysis of hematological
malignancy or rapidly proliferating malignancies
- May be worsen by thiazide diuretic use
- Rapid increase in the uric acid level acute urate nephropathy
- Reducing pre-chemotherapy serum uric acid is important
Clinical Findings
- N+V, Seizures
- Hyperkalemia Cardiac arrhythmias, Sudden death
- Seen commonly following treatment of hematological emergency
- Can also develop from any tumor highly sensitive to chemotherapy
- Caused by massive release of cellular maternal development of high
uric acid, high K+, high phosphate
- Acute renal injury from crystallization of uric acid and calcium phosphate
Treatment
- Prevention: Hydration before chemotherapy +/- Allopurinol
- Others: Rasburicase, contraindicated in G6PD deficiency
- Management: General measures
Onco-L1-Ecog
Ecog
1. What is Ecog score?
2. Briefly talk about the score.
Performance status to assess a patients general well-being and activities

of daily living
0
1
2
3
4
5
Completely normal
Symptomatic, but fully ambulatory
Symptomatic, Confined to bed <50% of waking hours
Symptomatic, Confined to bed >50% of waking hours
Bed bound
Death
Onco-L1-Chemotherapy
Chemotherapy
1. What are the different types of chemotherapy?
- Adjuvant Chemotherapy: Given after surgery, Used to eliminate micrometastatic disease that not visible on imaging
- Neo-Adjuvant Chemotherapy: Before local therapy
- Sensitizing Chemotherapy: Using chemotherapy to make radiotherapy to
work better
- Palliative
- Prevention?
2. What are the side effects of chemotherapy?

- Not all patient have side effects
- Not all drugs cause hair loss
- Not all drugs cause nausea
Skin
- Hair loss
- Hair always grow back, usually thicker
- Hand foot syndrome (reddening, swelling, numbness, desquamation of
palms and soles)
GIT
- N+V (acute, delayed, anticipatory)
- Can be controlled by anti-emetics
- Diarrhea, Constipation
- Changes in taste and smell
Cyclical Neutropenia
- Infection, Febrile
- Mouth ulcers
- Cystitis
Bone
- Neutropenia
- Thrombocytopenia risk of bleeding
- Anemia Need of blood transfusion
Others
- Individuals Drugs: Neuropathy, Sore eyes
- Fatigue
- Cardio toxicity
- Pulmonary toxicity
- Infertile
Onco-L2-Neck Lump
Neck Lump = Thyroid cancer
1. What is your DDx?
- Midline: Thyroid adenoma, Carcinoma, Thryroglossal cyst, Chondroma,
Dermoid cyst
- Anterior Triangle: Lymph nodes, Brachial cyst, Carotid aneurysm,
Laryngocele, Pharyngeal pouch
- Submandibular: Submandibular gland, Lymph nodes, Neoplasms, Salivary
stones
- Posterior Triangle: Cervical ribs, Subclavian artery aneurysm, Cystic
hydromas, Lymph nodes
2. What are the types of thyroid tumors?

Adenoma
- It is a benign tumor of the thyroid gland
- They are solitary
- Usually non-functioning, do not take up radioactive iodine, but can be hot
and producing hormones
- Examination: FNA, Radioactive scan
- Management: Most can be managed with watchful waiting E.g. Size,
Symptoms
- Some choose surgery
Carcinoma
- 4 major types: Papillary (70%), Follicular (20%), Medullary (5%),
Anaplastic (rare)
- Papillary: Lymph node spread in the neck is not common, If well
differentiated with a good prognosis
- Follicular: Typically cold nodules, 10 years survival rate about 30%
- Medullary: A tumor of C cells, produce calcitonin,
- Anaplastic: Prognosis very poor, usually die within first year of diagnosis
Onco-L2-Leukemia
Leukemia
Acute Lymphoblastic Leukemia
- The malignancy of the lymphoid cells, affecting B or T lymphocyte lines
proliferation of uncontrolled blast cells
- With bone marrow infiltration and failure
- The commonest cancer of children, rare in adults
- Downs syndrome is an important association
- CNS involvement is common
Classification
- Morphological into L1, 2 and 3
- Immunological into T cell ALL or B cell ALL
- Cytogenetic: Detect chromosome translocation E.g. Philadelphia
translocation
Signs and Symptoms
- Anemia, Neutropenia, Thrombocytopenia
- Hepatomegaly, Splenomegaly, Lymphadenopathy, Orchidomegaly
(testes), CNS involvement E.g. Cranial nerve palsies
Acute Myeloid Leukemia

- Malignancy of the myeloblasts (which will form basophils, neutrophils,
monocytes, Eosinophils)
- The commonest leukemia in adults
- Downs syndrome is an important association
- AML can be a long term complication from chemotherapy E.g. for
lymphoma
Symptoms
- Marrow Failure: Anemia, Infection, Bleeding,
- Infiltration: Hepatomegaly, Spelnomegaly, Gum hypertrophy, Skin
involvement
Diagnosis
- WCC is often up, but can be down or normal
- Blast cells can be present in the peripheral blood
- So diagnosis depends on bone marrow biopsy
- Cytogenetic analysis affects prognosis
Common infections: Chest, mouth, perianal and skin, Bacterial

septicemia, zoster, CMV, measles, candidiasis, Pneumocystic pneumonia
Tests
- Blast cells on blood film and bone marrow
- CXR or CT scan to look for mediastinal and abdominal lymphadenopathy
- Lumbar puncture to look for CNS involvement
Treatment
- Support: Blood or platelets transfusion, IV fluid, Allopurinol to prevent
tumor lysis syndrome
- Infection: Immediate IV antibiotics, prophylactic antivirals, prophylactic
antifungal
- Chemotherapy: Induction, Consolidation, CNS prophylaxis, Maintenance
- Adults are treated with DVPA (Doxorubucin = Adriamycin, Vincristine,
Prednisone, Asparaginas), with remission in 90% of patients
- If with Philadelphia translocation or bcr-abl, Dasatinib should be added
- Once 1st remission, allogenic stem cell transplantation is the best option
Prognosis
- Cure rate for children 70-90%, adults 40%
- Poor prognosis if: Adults, male, Philadelphia translocation, BCR-ABL gene
fusion, WCC >100x109/L
Chronic Myeloid Leukemia
- Uncontrolled clonal proliferation of myeloid cells
- Signs: Splenomegaly
- Male predominant, typically between 40-60 years of age
- Philadelphia chromosome present in >80% of cases, translocation
between chromosome 9 and 22, which has a tyrosine kinase activity
- Those without Philadelphia translocation has a worse prognosis
- Symptoms: Weight loss, Tiredness, Fever, Sweats, Bleeding
- Signs: Splenomegaly, Hepatomegaly
- History: Chronic phase lasting for months to years, Accelerated phase
(increase in symptoms and counts), Blast transformation (feature of acute
leukemia)
Treatment
- Glivec = Imatinib, prevention of disease progression
- More potent ones: Dasatinib
- Chemotherapy
- Stem cell transplantation
Complications
- Infection is a major problem
- Bacterial, viral and fugal prophylaxis is given during treatment
- Pitfalls: ALM itself causes fever
Treatment
- Most patients are treated with a combination of Daunorubicin or
Idarubicin + Cytarabine, produces 80-90% complete remission in patients
under age 60
- Once patients enter remission, autologous or allogeneic transplantation
should be given
Prognosis
- 70-80% of adults with AML under age of 60 achieve complete remission
- Allogeneic bone marrow transplantation is curative in 50-60%
- Cure rate for older patients only 10-15%
Chronic Lymphocytic Leukemia

- Mature B cells arrested in G0/G1 phase
- Commonest leukemia
- Pneumonia may be a triggering event
- Symptoms: Often none, as a surprise finding on a routine FBC, May be
anemia or infection prone, if severe LOW, sweats, anorexia
- Signs: Splenomegaly, Hepatomegaly, Lymphadenopathy
- Test: Increased lymphocytes, later autoimmune hemolysis, marrow
infiltration, anemia, thrombocytopenia
- Natural History: Some remain the same for years, may even regress,
usually nodes slowly enlarge, death is often due to infection or
transformation to aggressive lymphoma
- Treatment: Indicated if symptomatic, chemo, radiotherapy, stem cell
- Prognosis: 1/3 never progress, 1/3 progress in time, 1/3 actively
progressing
Notes: Eyes
Eyes Station 1 = Always visual acuity, fundoscopy + Imaging questions
Level 1
Visual Acuity Assessment (remember to use
Aged Related Macular Degeneration
pinhole)
Diabetes
Fundoscopy
Central/Branch Retinal Artery/Vein Occlusion
Retinal Detachment
Relative Afferent Pupillary Defect
Papilledema
Optic Neuritis
Glaucoma
Uveitis
Hyphaema
Level 2
Infectious Corneal Ulcer
Marginal Keratitis
Herpes Simplex Keratitis
Viral/Bacterial Conjunctivitis
Pre-septal Cellulitis
Endophthalmitis
Scleritis
Episceritis
Cataracts
Level 3
Entropion
Ectropion
Ptosis
Visual Field Defects
Dry eyes / Epiphora
Temporal Arteritis
Presbyopia
Knowing Level 1 topcis is safe enough.

Remember there is always visual acuity, fundoscopy
For visual acuity, they dont use 6m chart cos the room is too small and the examiner will pretend she/he cant see until 1-2m away from the chart.
Make sure you know how to report visual acuity correctly.
Make sure you use the pinhole.
Eyes-L1-Age-Related Macular Degeneration
- Progressive degeneration of the macula in the elderly
- Most common cause of blindness in patients >65
- Symptoms and Signs: A gradual loss of vision, may be followed by sudden
loss of vision, only central vision is lost, peripheral vision is maintained (so
patients usually can maintain an independent lifestyle), Metamorphopsia
(Straight lines appearing wavy)
- Classifications:
- Non Exudative (Dry): 90% of cases, slowly progressive loss of vision,
Drusen (tiny yellow accumulation Bruchs membrane, natural byproduct
of ageing), Retinal pigment epithelium atrophy (clumps of hyper or
hypopigmentation), May progress to wet ARMD (Neovascular)
Eyes-L1-Diabetic Retinopathy
- Major cause of poor vision in the working population in the developed
world
- Patient generally asymptomatic for a long time, in late stages may be
sudden loss of vision
- Signs: Vitreous hemorrhage, Diabetic macular edema
- Pathology: Micro-vascular changes causing ischemia (BM thickening,
endothelial cell damage ischemia, which manifests as cotton wool
spots, deep retinal hemorrhage, venous bleeding and
neovascularization), Macro-vascular changes causing leaking vessels
(results in blot and dot hemorrhage, hard exudates and diffuse edema)
Classification
Exudative (Wet): 10%, but 80% of the 10% result in severe visual loss,
Choroidal neovasvularization, May cause detachment of overlying retinal
pigment epithelium and retina Hemorrhage and lipid precipitates into
subretinal space, Disciform scarring and severe central vision loss
Risk Factors: Female, Old age, Fx, Smoking, Blue iris, Other associations
(Sun, cholesterol, HTN, Lack of exercise)
Investigations: Amsler Grid, Fluorescein Angiography (assess the degree
of neovascularization, injection of a dye into the systemic circulation),
Optical coherence tomography OCT
Management: Dry (No effective treatment, Monitor, Use Amlser Grid to
check for metamorphopsia, stop smoking, Sunglasses, Antioxidant, Vit
C/E/A), Wet (Intra-Vitreal injection of anti-antiogenesis growth factor =
anti-VEFG antibodies E.g. Ranibizumb, Bevacizumab), Laser
photocoagulation for neovascularization, Refer to blind association,
Register for visual impairment assistance
Non-Proliferative Diabetic Retinopathy: Mild (Micro-Aneurysm only),

Moderate (Micro-Aneurysm, Hard exudates, Macular edema, Dot/blot
hemorrhage, Cotton wool spots = Ischemic areas), Severe (Extensive
intraretinal hemorrhage in all 4 quadrant, venous bleeding in 2
quandrants, prominent microvascular anomalies E.g. Dilated, Leaky, No
signs of proliferative DR)
Proliferative: 5% of patients with diabetes, Neovascularization (new
vessles) of iris (rubeosis iridis, which can lead to glaucoma, commonly
associated with diabetes, but also CRVO, Chronic retinal detachment)
/disc/retina/vitreous, Fragile new vessels lead to vitreous hemorrhage
Diabetic Maculopathy (Clinically significant macula edema): Hard
exduates, retinal thickening, can occur at any stage of diabetic
retinopathy
Management: BP, Lipid and glucose control, Retinal laser (for patients
with severe NPDR and all PDR, also Macular Edema), Intravitreal
injection (Anti-VEGF, Steroid), Vitrectomy for advanced PDR
The best treatment is prevention
Drusen
Micro-Aneurysm only, Mild NPDR
Moderate NPDR
Drusen = Hyaline material, mainly in

peri-macular region
Hard/Soft Exudate = Lipid deposits in
the retina, associate with diabetic
retinopathy and hypertension
Metamorphopsia
Moderate NPDR
Moderate NPDR
Severe NPDR
Proliferative DR
Eyes-L1-Central Retinal Artery Occlusion

- Less common than vein occlusion
- Blood Supply: CRA Central Retinal Artery, PCA Posterior Ciliary Artery
- CRA obstruction causes ischemia of the inner retinal layers
- Blood flow must be restored in 100 mins, otherwise irreversible damage
occur at its narrowest point the lamina cribrosia
- A blockage peripherally gives rise to a branch artery occlusion
- Causes: Emboli, Vasculitis, exclude giant cell arteritis in elderly
- Signs and Symptoms: Sudden painless unilateral blindness in CRAO,
Sudden painless field loss or decrease in visual acuity in BRAO (branch
retinal artery occlusion)
- Clinical Features: Sudden, painless (except in temporal arteritis), Relative
afferent pupillary defect, patient will often experience amaurosis fugax,
Fundoscopy (cherry-red spot at the center of macula, retinal pallor,
narrowed arterioles, cotton-wool spots, cholesterol emboli)
- Investigations: Investigate the source of amboli, FBC, CRP, ESR,
Thrombophilia screen, BSL, cholesterol, carotid US, ECG, Echo
Proliferative DR
Macular Disease
rubeosis iridis
Eyes-L1-Central Retinal Vein Occlusion
- Second most frequent vascular retinal disorder after diabetic retinopathy
- Risk Factors: HTN, DM, Glaucoma, Vasculitis
- Clinical Features: Patients notice sudden loss of visual acuity if the
macula is involved, +/- Relative afferent pupillary defect (RAPD),
Fundoscopy (Blood and thunder appearance, diffuse retinal
hemorrhage, venous engorgement, swollen optic disc, macular edema)
- Investigations: Thrombus, Vasculitis
- Treatment: No treatment to restore vision, Treat risk factors,
Hemodilution, Laser therapy if neovascularization
Treatment: Emergency, Restore blood flow in 2 hours, Ocular massage,

Aspirin, Ocular antihypertensives, Calcium antagonists, Hemodilution,
Paracentesis
CRVO
BRVO
Eyes-L1-Retinal Detachement
Definition: Separation of the neural retina from the retinal pigment epitheium
Clinical Features: Gradual or sudden loss of vision, Flashes of light (due to mechanism stimulation of the retinal photoreceptors), Floaters (due to drops
of blood In the vitreous), Peripheral field loss, Loss of central vision, Decreased OIP (usually 4-5 mmHg lower), Ophthalmoscopy (detached retina is grey,
loss of red reflex), +/- relative afferent pupillary defect
Classification
- Rhegmatogenous Type: Most common, caused by a tear of hole in the neural retina fluid passes into sub-retinal space, Tears may be caused by
posterior vitreous detachment The vitreous humor separates from the retina, degenerative retinal changes, trauma, Incidence increases with
advanced age or after ocular surgery
- Tractional: Caused by vitreal traction (due to inflammation/fibrous tissue contraction), seen in DR (Diabetic), CRVO, Sickle cell disease, Retinopathy of
prematurity, Ocular trauma
- Exudative: Caused by damage to the RPE resulting in fluid accumulation in the subretinal space, main causes are intraocular tumors, posterior uveitis,
central serous retinopathy
- Management: Urgent Referral, Rhegmatougenous (Surgery), Tractional (Surgery), Exudative (Treat underlying cause)
- Vitrectomy, Laser, Cryotherapy, Scleral Buckle, Retinal tamponade
-
From Clinical Ophthalmology

Definitions
- Separation of the neurosensory retina from the retinal pigment epithelium accumulation of the subretinal fluid
- Rhegmatogenous: Full thickness defect, fluid gets to the subretinal space
- Tractional: Caused by contracting vitreo-retinal membranes in the absence of a retinal break
- Exudative: Subretinal fluid is derived from fluid in the vessels of the neurosensory retina or choroid
- Combined Tractional-Rhegmatogenous: A combination of retinal break and traction, most commonly seen in proliferative diabetic retinopathy
Rhegmatogenous:
- Causes: Dymanic vitreoretinal traction + Weakness in the peripheral retina
- Dymanic vitreoretinal traction: Syneresis (Liquefaction of the vitreous gel) Posterior vitreous detachment Retina not protected by the stable
vitreous cortex and directly affected by the dynamic forces Risk of retinal tears
- Weakness in the peripheral retina: Lattice degeneration, Snailtrack degeneration, Retinoschisis

Posteroir Viterous Detachment
Retinal Detachment
Lattice Degeneration
Snailtracks Degeneration
Retinoschisis
- Symptoms: Photopsua (flashing lights), Floaters, Visual field defects
- Signs: Marcus Gunn Pupil, Intraocular pressure (lowerd by 5 mmHg), Iritis, Retinal breaks
Fresh Retinal Detachment, U-Tear in A, Bullous retinal detachment in B, Shallow detachment in C
Long Standing Retinal Detachment

Proliferative Vitreo-Retinopathy in Rhegmatogenous
Retinal Detachment
Management
- Prophylaxis for a Retinal Breaks: Laser Photocoagulation, Cryotherapy (using a cryoprobe)
- Surgery: Scleral buckling, Drainage of subretinal fluid
- Fresh retinal detachment: Crytherapy and buckle

- Long standing detachment: Drainage of the subretinal fluid
Tractional Retinal Detachment
- Pathogenesis: Contraction of fibro-vascular membranes (thought to be caused by leakage of plasma constituents into the gel)
- Symptoms: Photopsia and Floater ar usually absent,
- Signs: Retinal breaks are absent (may develop in later stages)
Tractional Retinal Detachment in Severe Prolifeartive Diabetic Retinopathy

Exudative Retinal Detachment
- Accumation of subretinal fluid in the absence of retinal breaks or traction, it may occur in a variety of vascular inflammatory disease
- Main Causes: Chorodial tumors, Inflammation (E.g. Posterior Scleritis), Hypertensive Choroidopathy, Iatrogenic, Subretinal neovascularation, Idiopathic
- Symptoms: Photopsia is absent, Floater may bt present, Visual field defect may develop
Exudative Retinal Detachment caused by a choroidal melanoma
Eyes-L1-Relative Afferent Pupillary Defect / Marcus Gunn Pupil

- A medical sign during the swinging-flashlight test, demonstrate a
decreased pupillary response to light in the affected eye
- Sign = Patients pupils constrict less (therefore appearing to dilate) when
a bright light is swung from the unaffected eye to the affected eye
- The affected eye still sense light, but produced a diminished response
- Common Causes: Lesion of the optic nerve, severe retinal disease,
Examples = Retinal detachment, Optic neuritis, Optic nerve atrophy,
CRAO (E.g. By embolism or temporal arteritis)/CRVO
- Other causes: Ischemic optic neuropathy, Glaucoma, Optic nerve tumor
(glioma, meningioma, pituitary gland lesions), Compression damage to the
optic nerve, Optic atrophy
- New RAPD required urgent ophthalmology referral
Examination
- A normal response = Equal constriction of both pupils, regardless of which
eye the light is directed at which indicates an intact direct and
consensual pupillary light reflex
- When the test is performed in an eye with afferent pupillary defect
only mild constriction of both pupils
- When the test is performed in an normal eye normal constriction of
both pupils
Eyes-L1-Papillodema
- Bilateral optic disc edema secondary to raised intracranial pressure
- Causes: Tumor, Hydrocephalus, meningitis, Brain abscess, Encephalitis,
Malignant hypertension, Intracranial hemorrhage
- Optic disc changes: Blurring of the optic margins, elevation of the optic
disc, hemorrhage over or next to the disc, venous engorgement, Patons
lines radial retinal lines
- Investigation: CT/MRI as soon as possible
Patons Lines
Eyes-L1-Optic Neuritis
- Definition: Inflammation of the optic nerve,
- Papillitis A specific type of optic neuritis, where inflammation restricted to the optic nerve head
- Retrobulbar ON Behind the globe
- Women are more affected, 20-40% develop MS
- Etiology: Idiopathic, MS/Demyelination, Viral infection (measles, mumps, VZV, EBV), Meningitis/Sinusitis/Orbital Cellulitis, Granulomatous inflammation
(TB, Syphilis, Sarcoid, Cryptococcus)
- Clinical Features: Color vision loss, painful eye movement, deteriorating vision over a few days, Ophthalmoscopy (blurred disc margin, hyperaemia of
disc, no or few hemorrhage), +/- RAPD, Central scotoma
- Treatment: Treat underlying cause, if idiopathic will resolve spontaneously, high dose steroid can reduce duration (usually 6 weeks)
From Books Clinical Ophthalmology

Classifications - Locations
- Retrobular Neuritis: Optic nerve head is normal, frequently with MS
- Papillitis: Most common in children, hyperaemia and edema of the optic disc
- Neuroretinitis: Papillitis + inflammation of the retinal layer, rare

Classifications Causes
- Demyelinating Optic Neuritis: most common
- Parainfectious: after a viral infection or immunization
- Infectious: Sinusitis, Cat-scratch fever, Syphilis, Lyme disease
- Non-Infectious: Sarcoidosis, SLE, PAN
Eyes-L1-Glaucoma
-
nd
2 most common cause of blindness in developing countries

Classification: Primary/Secondary, Open/Close, Acute/Chronic, Congenital/Juvenile/Adult, !Normal IOP 10-21 mmHg/Ocular hypertension
Risk Factors: Most importantly IOP, Increased contact between lens and pupils (small eye, large lens, miosis), Increased viscosity of aqueous humour
(inflammation, blood)
- Open-Angle Glaucoma: Asymptomatic or painless gradual loss of vision, can be seen on gonioscopy
- Acute-Angle Glaucoma: Sudden onset intense pain, blurred and gradual loss of vision, headache, N+V, red eye, halos, Signs (Corneal edema, Fixed/Middilated pupil, Conjunctival injection)
Medications
Miotics
Old line treatment, increase the fluid outflow
E.g. Pilocarpine (have to take several times a day)
Beta-Blocker
Eye drops medications, Reduce the production of fluid
E.g. Timolol, Betaxolol
Carbonic
Decrease the fluid production, Eye drops medication, Add on to Beta-Blocker
Anhydrase
E.g. Brinzolamide, Dorzolamide
Inhibitor
Alpha-2
Decrease the fluid production, Increase the fluid outflow
Agonists
E.g. Brimonidine (some doctors use as 1st line)
Prostaglandin
Extremely Effective, promote fluid removal, but does not reduce its production
Agonist
E.g. Latanoprost
Procedure
Laser
Burning 80-100 holes in the drainage, takes about 15 mins, on an outpatient basis, little or no pain
Still need the eyedrops
60% success, lasts 2 years
Trabeculectomy Done if eyedrops and laser have failed, creates a new channel E.g. Putting a silicone tubes
Generally permanent
Lifestyle
Aerobic
May lower IOP by 20%
Exercise
Restricted fluid Not too much coffee
Introduction
- Aqueous secretion (ciliary epithelium) vs Aqueous outflow (trabecular meshwork 90% + Schlemm canal aqueous humor ciliary veins blood stream)
- IOP is determined by the balance between the aqueous secretion and outflow
- Normal IOP = 11-12mmHg, varies within the time of day, HR, BP, respiration, variation of 5mmHg, peak between 8am to noon
- Definition of Glaucoma: Difficult to define, commonly defined as damage to the optic nerve in a particular pattern
- Affects 2% over age of 40, 10% over age of 80, 50% may be undiagnosed
- Classification: Congenital vs acquired, Open-angle vs close-angle, Primary vs secondary
Tonometry
- Principles: Pressure = Force necessary to flatten a surface area
- Technique: Topical anesthetics and fluorescein are instilled, blue filter
- Sources of Errors: Excessive fluorescein, Pressure on the globe from the examiners finger, Central corneal thickness, Corneal edema, Incorrect calibration,
Astigmatism, Repeated readings over short period of time
Gonioscopy
- Evaluating the anterior chamber angle to provide information about the type of glaucoma
Evaluation of the Optic Nerve Head
- Neuroretinal Rim (broadest by the inferior > superior rim > Nasal rim > Temporal rim)
- Optic Disc size
- Cup-Disc Ratio
Changes in Glaucoma: Most of the time difficult to determine

1. Optic Nerve Head (A: Focal ischemia, B: myopic, C: Senile sclerotic, D: Concentrically enlarging)
2. Peripapillary Changes surrounding the optic nerve head
3. Retinal Nerve Fiber Layer
Risk Factors for Glaucoma

- High IOP, Old age, Low central corneal thickness, High cup-disc ratio, Heart disease, African-American race
Management of Ocular Hypertension
- Treatment aimed to reduce IOP to 24mmHg or less, most practitioners would treat every patient with an IOP of 30mmHg or more, but decision also
depends on risk profile, untreated ocular hypertension has 9.5% risk of developing POAG in 5 years
Primary Open-Angle Glaucoma
- Definition: Chronic simple glaucoma,
- Generally bilateral, IOP >21mmHg at some stages, optic nerve damage, open anterior chamber angle, visual field loss as damage progresses
- Most common type of glaucoma in European and African ethnic origin
- Some individuals may develop an elevation in IOP in response to topical steroid
- Optic Neuropathy mainly caused by direct mechanical damage and ischemic damage
- Screening: Age >40 with a family history of glaucoma
- Diagnosis: Visual symptoms usually absent unless advanced stage, previous history (ocular trauma, inflammation, eye surgery), Fx, Current medications
- Examination: Visual acuity likely to be normal ,Exclude RAPD, Color vision (optic neuropathy rather than glaucoma), slit-lamp, Tonometry, Gonioscopy,
Optic disc examination
Minimal Cupping
Moderate Cupping
Severe Cupping
- Management: Target pressure, Monitoring optic nerve and visual fields
Very severe, Gross cupping
Medical Therapy: Beta-blockers, Postaglandin analogue, Review usually 4-8 weeks initially then 3-6 months, Gonioscopy should be performed annually in
most patients as the anterior chamber angle tends to narrow with age
- Laser Traberculoplasty: Indicated in treatment failure, intolerance of topical medications
- Trabeculectomy
- Prognosis: If left untreated, 20 years before blindness
Normal Pressure Glaucoma
- A variant of POAG, IOP <21mmHg, Signs of optic nerve damage, Visual field loss
- Pathogenesis: No completely determined, ? low central corneal thickness
- Diagnosis: History, IOP, Optic nerve head, Visual field defects, others (BP, Vit B12, Folate, FBC, ESR, ACE, Autoantiboides, Treponemal serology, Lyme
disease)
- Treatments: Further lowering IOP is effective, Betaxolol (improve optic nerve blood flow, also lower IOP), Laser trabeculoplasty, Trabeculectomy
Primary Angle Closure Glaucoma
- Occlusion of the trabecular meshwork by the peripheral iris
- Classifications: Primary angle-closure suspect (normal IOP, intermittent angle-closure), Primary angle closure (raised IOP), Primary angle-closure glaucoma
(optic neuropathy)
- Symptoms: Most are asymptomatic, some present acutely (halos due to corneal edema, ocular pain, headache), others (mild blurring)
- Signs: Acute (IOP very high, anterior chamber is shallow, Corneal edema, Unreactive pupil), Chronic (Anterior chamber is shallow)
-
Corneal Epithelial Edema

Mid-dilated vertically oval pupil
Treatment
- Primary angle-closure suspect: Prophylatic laser iridotomy
- Chronic Presentation: Prophylatic laser iridotomy
- Acute and Subacute Presentation: Initial treatment (Oral Acetazolamide, Topical Prednisolone, Topical Pilocarpine, Analgesia), Subsequent treatment
(Topical steroid + Pilocarpine), If fails Laser iridotomy or iridoplasty
Eyes-L1-Uveitis
- Inflammation along the uveal tract (Comprising choroid, cilliary body, iris)
- Causes: Thought to be an immune-mediated process
- Classified anterior, intermediate, posterior, panuveitis
Anterior Uveitis
- Inflammation affects the iris +/- ciliary body
- Symptoms: Sudden onset of pain, blurred vision, photophobia, conjunctival injection
Signs: Ciliary injection, anterior chamber cells, aqueous flare due to presence of protein, keratic precipitates, posterior synechiae (iris-lens adhesions)
Causes: Idiopathic, Systemic inflammatory disease (Seronegative arthropathies, IBD, Psoriatic arthritis, Reiters), Autoimmune (sarcoidosis, Bechets),
Infections (Shingles, Toxoplasmosis, TB, Syphilis, HIV)
Managements: Topical steroid drops, Cycloplegic drops for pain and to prevent formation of posterior synechiae, blood test of HLA B27 to exclude
inflammatory diseases, infections, Immunosuppressives for systemic diseases

Definition
- Anterior Uveitis: Subdivided into Iritis (inflammation of the iris) and Iridocyclitis (Inflammation of the iris and the pars plicata of the ciliary body)
Anterior uveitis (most common) >

Posterior > intermediate > Pan
- Intermediate Uveitis: Inflammation of pars plana, the peripheral retina and the vitreous
- Posterior Uveitis: Retinitis, Choroiditis, Vasculitis
- Panuveitis: All the uveal tract
Clinical Features
- Acute Anterior Uveitis (Duration 3 months or less): Sudden onset of unilateral pain, photophobia, redness, may associate with lacrimation, occasionally
with a few days prodrome of mild ocular discomfort, Ciliary injection, Miosis, Anterior vitreous cells, Hypopyon, Posterior synechiae, Low Ocular pressure
A: Ciliary Injection B: Miosis C: Endothelial dusting D: Aqueous flare and cells E: Fibrinous exudate F: Hypopyon
A: Early Posterior Synechiae B: Extensive Posterior Synechiae

- Chronic Anterior Uveitis: Persistent relapses in less than 3 months after treatment
All: Keratic Precipitates
Nodules in Granulomatous Uveitis

Posterior Uveitis
A = Retinitis: Whitish retinal opacities, with not well defined borders

B = Choroiditis: Round yellow nodules
C = Vasculitis: Yellowish, or grey-white perivascular cuffing
Investigations: Tuberculin skin tests, Syphilis serology, Toxoplasmosis, HLA-B27
Principles of Treatment: Anti-inflammatory and immunosuppressive agents, Antibiotics if linked to syphilis or TB
Mydriatics: To promote comfort by relieving spasm of the ciliary muscle, To break down posterior synechiae, To prevent formation of posterior synechiae
Topical Steroids, Periocular steroid injection, Intraocular steroid injection, Systemic steroids
Others: Azathioprine, Methotrexate, Infliximab
Notes: Aboriginals
What are some cultural factors you might have to take into account
when caring for an Aboriginal person?
Kinship system/Skin groups (Based on respect and sharing)
Complex system of relationships that varies between communities
Obligations/responsibilities are applied to many of people within the
community
Terms brother/sister/aunt/uncle may have different meaning
Skin group determines who can marry
Avoidance relationships exist
Historical context
Taking away their land (native titles)
Stolen generation
Mistrust of Western medicine
What resources are currently available for Indigenous people?

Health services initiated, planned & managed by local Aboriginal
people and communities
Metropolitan
Derbarl Yerrigan (East Perth) - Aboriginal Community Controlled
organisation which involves Aboriginal Health Workers, Registered
Nurses, Doctors, Podiatrist, Physiotherapist, Dental
Aboriginal Liaison Officers
Provides emotional, social and cultural support to patients

and their families.
Advocate and liaise on behalf of patient and families
Provide information about hospital services
Arrange accommodation and transport for Aboriginal
people being discharged to hostels who have further
appointments.
Provide health education to patients relative to their
medical condition.
Assist with referrals to Aboriginal and non-Aboriginal
organizations.
Arrange transfer of Aboriginal cadavers to their homeland
for burial.
Coordination of support services for patients travelling to
Perth for specialist treatment under the Patient Assisted
Travel Scheme (PATS).
Arrangement of travel for patients returning home from
hospital and participate in discharge planning.
Rural: Kimberley Aboriginal Medical Services Council (KAMSC), South
West Aboriginal Medical Service (SWAMS) for Nyoongar People
State: Aboriginal health council of WA
National: National Aboriginal Community Controlled Health
Organisation (NACCHO) is the national peak Aboriginal health body
representing Aboriginal Community Controlled Health Services
Discuss the barriers for Aboriginal women to access regular screening

and if necessary, follow up and treatment for abnormal screening
Access
o Isolation location of service in relation to pt and
availability/ease of transport
o Language barriers
o Social issues may want to go but unable to leave children /
other family obligations; as main provider/caregiver for family
screening will often get pushed aside for other more pressing
priorities.
o Not aware of support services accommodation / PATS etc
Education/awareness/understanding
o Not understanding why procedure is necessary or need to
follow up / do regular pap smears
o May have recently had a vaginal swab for other reasons (eg
STI) and not realized that this was different to a pap smear
(ie: thought already had one)
o May not understand the options available in terms of follow
up / treatment and the implications of each.
o Fear of medical system / procedure / Dx / follow up having
to leave community and country
Previous bad experience with health service personally
Witness of previous experience where someone who
seemed well went to screening and then died in
hospital ie: had +ve test, ended up having to leave
community because of advanced cancer, travelled to
Perth, and eventually died
Communication/Contact
throughout Australia. Aboriginal communities operate over 140 AMSs

across Australia.
Accommodation:
Aboriginal Hostels Limited: Allawah Grove Hostel (South Guildford),
Derbarl Bidjar Hostel (Maylands)
Benefits include; acceptability, reduced racism, culturally secure
service, flexibility, holistic approach, training and education
Discuss possible strategies for overcoming these barriers as an
individual practitioner.
Access
o Outreach clinics form relationship with community
o Set up other support services eg creche so mothers can
attend
o Be opportunistic if pt has attended clinic for one thing see if
can also do pap smear , breast exam, mammogram, STI
screen etc
Education
o Both for patients and practitioners
o Elders and respected members of the community (help
advocate positive messages about womens health to
the wider community)
Communication
o Unsure pts understand what is being said to them; get
them to summarize what has been conveyed / feedback
so know that pt has understood concepts.
Culture/Trust
o Utilize the resources available ALO/AHW (female if possible)
o Form relationship with community maintain continuity of
care
o Encourage pts to attend clinics through incentives food and
fun (eg a womens/childrens health weekend)
o Realize that just because its womens business you dont have
to walk on eggshells. There will be a range of responses some
pts will be hesitant, others will be very happy to discuss
womens health issues with you even if you are male each
o Difficult to contact people who may move between

communities/locations for regular screening
o May be screened at one place when visiting family and then
unable to follow up if have since returned home.
o May be in communities that need to move periodically eg: if
seasonal flooding
Culture/Trust
o Difficulty in establishing and maintaining trust made
harder if there is a lack of continuity of care
o Womens business pts may not feel comfortable if service
is provided by male practitioners
o Concerns about confidentiality, especially problematic if in
small towns and if using AHWs or ALOs as they may
personally know pts and this may cause reticence to attend
clinic
Discuss possible systemic strategies for reducing these barriers
Setting up infrastructure for accessing care
o Clinics and support services (as mentioned above)
o Increasing capacity of workforce both Aboriginal and non
Aboriginal. Bit of a difficult negotiation as it comes down to a
constant funding struggle have to prove that there is a need
and also that there are people to fill positions should they
become available. Problem at the moment is that there are not
enough trained Aboriginal people to fill positions for AHW, but
also no incentive to train as an AHW as there are no positions
currently available chicken or egg problem hope that makes
sense)
o Staff education, training
Education
o One initiative would be to target schools and talk to
young aboriginal people about health issues so they are
aware of them, and also about considering the health
workforce as a career possibility helping to boost
capacity.
o Also could focus on increasing ongoing and more regular
education opportunities for the non-Aboriginal
doc/pt relationship will be different learn how to negotiate

those differences.
workforce so practitioners are more confident and

willing to tackle these issues and to take an active and
collaborative role in working with AHWs and ALOs and
not just handballing cases. This can often be a big
problem as such cases can be complex and sometimes
the AHW / ALO doesnt have the
time/knowledge/experience to deal with all the various
aspects of eth case. Collaborative Care is the key.
o Education for pts / community need to make materials
accessible and appropriate for audience
Communication
o Incorporate marketing of education and health services
in a way that creates an interest in and an incentive for
participation in health interventions - ensuring cultural
relevance and appropriateness
Summary
Cultural Factors
Complex family system E.g. Kinship
Obligation or responsibilities to the
community
Sister, brother, aunt, uncle may have
different meaning
Groups determine who can marry
History: Stolen generation
Mistrust western medicine
Lands are taken away
Resources
Metropolitan Areas
Debral Yerrigan (East Perth):
Abdominal community organization,
with aboriginal health worker,
registered nurse, doctors, OT, Physio,
Dental
Aboriginal Liaison Officers:
Emotional, social and cultural
support, Arrange accommodation
and transport, Health education,
Referrals to aboriginal and nonaboriginal organizations
Rural: Kimberley Aboriginal Medical
Services Council, South West
Aboriginal Medical Service
State: Aboriginal health council of
WA
Barriers
Access: Isolation, Language, Social
issues
Education: Not understanding why
the procedure/followings/meaning of
test result (CIN2) is needed, Not
understand the options, Also vaginal
swab vs pap smear
Discrimination
Communication: Difficult to contact
people who live far away, Letters not
delivered
Trust: Difficulty in establishing and
maintaining trust made harder if
there is a lack of continuity of care,
Obligations to community
Strategies
Access: Outreach clinics, Be
opportunistic if pt has attended
clinic for one thing see if can also do
pap smear , breast exam,
mammogram, STI screen etc
Education: For both doctors and
patients
Communication
Trust
Set up more organization, liaison
officer, public education
Good Luck for your OSCE.

Can anyone send me a copy of last year 4th year OSCE? (hiuhunglam@hotmail.com) Greatly appreciated.
Also please send me a copy of 2013 OSCE end of this year.

R 5th Year OSCE - Part 2

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R 5th Year OSCE - Part 2

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The H Book for 5th Year OSCE 2012-2013 Part 2

Chapter 3 Notes/Make-up scenarios

Table of Topics of Past OSCE

Notes/Make-up scenarios: Medicine

Chapter 1 Past OSCE (from 2002 to 2012)

Notes/Make-up scenarios: Peds

Notes/Make-up scenarios: Oncology

Notes/Make-up scenarios: Eyes

Notes/Make-up scenarios: Aboriginal

Chapter 2 Real Marking Guides

List of topics to know (Important)

Notes/Make-up scenarios: O&G

Notes/Make-up scenarios: Medicine

Station 2 - Lab Interpretation

Hypertension Primary + Secondary

- Acute renal failure

Knowing level 1 stuff should be safe enough to pass

(ECG 99% +/- CXR will come out in 2013 OSCE)

QRS duration > - 0.12s

Causes - The right bundle branch is vulnerable to stretch and trauma

1. The beat is ventricular in origin

Amplitude increased in cardiac hypertrophy

Note: VAT = Ventricular activation time, and is

Axis Deviation Determined by the QRS complex

Q Wave, Normal <0.04s

QT Interval, Represents the depolarization and the repolarization of ventricles

3. What is the above ECG showing you?

4. What is the below ECG showing you?

Acute Anterior MI ST elevation in anterior lead V3 and V4

1. Explain the ECG changes you can see in a MI.

2. How can you decide the location of MI?

Normal ECG prior to MI

Hyperacute T wave changes - increased T wave amplitude and

Marked ST elevation with hyperacute T wave changes

Pathologic Q waves, less ST elevation, terminal T wave

5. What is myocardial ischemia?

changes may occur following stress (physical or emotional) or even spontaneously.

(Pathologic Q waves are usually defined as duration

Pathologic Q waves, T wave inversion (necrosis and fibrosis)

Pathologic Q waves, upright T waves (fibrosis)

Ischemic changes with exercise

2. What is below ECG?

More common than LBBB

It does not interfere with ECG diagnosis of ventricular hypertrophy or Q wave

Chronically increased right ventricular pressure E.g. Cor pulmonale

2. What are the causes of 1st degree heart block?

3. How would you investigate?

History, Physical examination, Investigation

2. What are the causes of Type I Wenckebach?

Similar to the 1st degree heart block

Similar to the 1st degree heart block

2. What are the causes of Type 2?

3. How would you investigate?

History, Physical examination, Investigation

More likely to progress to complete HB treatment almost always

2. What are the causes of complete?

3. How would they present?