DIABETES MELLITUS

Introduction
 Clinical syndrome/Chronic disease of absolute or relative insulin deficiency or resistance
characterized by hyperglycemia associated with disturbance in carbohydrate, protein, and
fat metabolism
 Two primary forms :
 Type 1, characterized by absolute insufficiency (5-10%), due to immune mediated
destruction of pancreatic beta cells. More common in childhood, adolescence, and
young adults. Causes ketoacidosis due to breakdown of fats
 Type 2, characterized by insulin resistance with varying degrees of insulin
secretory defects (90-95%). It results from genetic, environmental factors. More
common in adults above 40 year of age. It is non-ketotic since presence of insulin
prevents breakdown of fats
 Other forms of diabetes include
 Gestational diabetes mellitus ([GDM] 2-5 % of all pregnancies): glucose intolerance
with onset during pregnancy
 Pathologic/genetic /chemicals e.g. resulting from
o Exocrine Pancreatic diseases of: pancreatitis, neoplastic disease, cystic fibrosis,
pancreatectomy, haemocromatosis
o Medication/chemical induced e.g. corticosteroids, thiazide diuretics,
phenytoin
o Associated with genetic syndromes e.g. Turner’s syndrome, Down’s
syndrome, muscular dystrophies, Friedreich’s dystrophies
o Endocrine disorders: Excessive endogenous hormonal antagonistic to insulin
e.g. GH (Acromegaly), glucocorticoids (Cushing syndrome), thyroid hormone
(hyperthyroidism), catecholamines (pheochromocytoma), human placental
lactogen (pregnancy) and counter regulatory hormones (as in burns and
trauma)
o Infections: certain viruses that destroy the beta cells of pancreas
o Genetic defects in insulin action, ranging from hyperinsulinemia to severe
DM

Pathophysiology
 The effects of diabetes mellitus (DM) result from insulin deficiency or resistance to
endogenous insulin.
 Insulin allows glucose transport into the cells for use as energy or storage as glycogen.
 Insulin also stimulates protein synthesis and free fatty acids storage in the adipose
tissues.
  Insulin deficiency compromises the body tissues’ access to essential nutrients for fuel
storage.

Causes
 Genetic factors
 Autoimmune disease (type 1): islets cell autoantibodies and insulin autoantibodies
 Idiopathic: no known etiologic causes

Risk factors
 Viral infections (type 1)
 Obesity (type 2)
 Physiologic or emotional stress
 Sedentary lifestyle (type 2)
 Pregnancy
 Medication, such as thiazide diuretics, adrenal corticosteroids, and hormonal
contraceptives.

Incidence
 Type – usually occurs before age 30, although it may occur at any age
 More common in males
 Type 2 – usually occurs in obese adults after age, 30, although it may be seen in obese,
North American youths of African, American, Native American, or His-panic descent
and other races.
 Affects about 8% of United States.
 About one third of patients undiagnosed
 Increases with age (type 2)

Common characteristics
 Polyuria
 Polydipsia
 Polyphagia
 Weight loss
 Fatigue

Complications
 Ketoacidosis (type 1)
 Hyperosmolar hyperglycemic nonketotic syndrome (type 2)
 Cardiovascular disease
 Peripheral vascular disease
 Retinopathy, blindness
 Nephropathy
 Diabetic dermopathy
  Impaired resistance to infection
 Cognitive depression
 Hypoglycemia

Special population
Neonates of diabetic mothers have a two to three time’s greater incidence of congenital
malformations and fetal distress, unless the mothers’ blood glucose levels are well-controlled
before conception and during pregnancy.

Assessment
History
 Polyuria, nocturia
 Dehydration
 Polydipsia
 Dry mucous membranes
 Poor skin turgor
 Weight loss and hunger
 Weakness, fatigue
 Vision changes
 Frequent skin and urinary tract infections
 Dry, itchy skin
 Sexual problems
 Numbness or pain in the hands or feet
 Postprandial feeling of nausea or fullness
 Nocturnal diarrhea

Type 1
 Rapidly developing symptoms

Type 2
 Vague, long-standing symptoms that develop gradually
 Family history of DM
 Pregnancy
 Severe viral infection
 Other endocrine diseases
 Recent stress or trauma
 Use of drugs that increase blood glucose levels

Physical findings
 Retinopathy or cataract formation
 Skin changes, especially on the legs and feet
  Muscle wasting and loss of subcutaneous fat (type 1)
 Obesity, particularly in the abdominal area (type 2)
 Poor skin turgor
 Dry mucous membranes
 Decreases peripheral pulses
 Cool skin temperature
 Diminished deep tendon reflexes
 Orthostatic hypotension
 Characteristic “fruity” breath odor in ketoacidosis (type 2)
 Possible hypovolaemia and shock in ketoacidosis and hyperosmolar hyperglycemic
state.

Test results
Laboratory
 Fasting plasma glucose level is greater than or equal to 126mg/dL on at least two
occasions.
 Random blood sugar level is greater than or equal to 200mg/dl.
 A two-hour postprandial blood glucose level is greater than or equal to 200mg/dl.
 Glycosylated hemoglobin (Hb A1C) level is increased.
 Urinalysis may show acetone or glucose.

Diagnostic procedures
 Ophthalmologic examination may show diabetic retinopathy.

Treatment
General
 Exercise and diet control
 Tight glycemic for prevention of complications
 Modest caloric restriction for weight loss or maintenance
 American Diabetes Association recommendations to reach target glucose, Hb A12
lipid, and blood pressure levels
 Regular aerobic exercise

Medications
1) INSULIN
Exogenous insulin (type 1 or possibly type 2). They are categorized into four classifications:
 Rapid-acting (Lispro, Aspart, Glulisine), patient should be instructed to eat no more
than 5-15 min after injection. Onset 10-15 min; peak 1 hour; duration 2-4 hours.
 Short-acting (Regular), administered 20-30 minutes before a meal. Onset 30 min to 1
hour; peak 2-3 hour; duration 4-6 hour.
  Intermediate-acting (NPH, Lente insulin); act as basal insulin and are divided into 2
injections (morning and evening) to maintain 24-hour coverage. Onset 3-4 hours;
peak 4-12 hours; duration 16-20 hours.
 Very long-acting (Glargine, Detemir); these are peakless basal insulins that are
absorbed very slowly over 24 hours to provide constant levels of insulin. Given once a
day, usually in the morning. Should not be mixed with other insulins, because they
precipitate.

2) ORAL HYPOGLYCEMICS
Oral antidiabetics (for DM type 2), categorized into:
1. First-Generation Sulfonylureas: stimulate beta pancreatic cells to secrete insulin;
improve insulin binding its receptors or may increase insulin receptors. Side effects
include hypoglycemia and weight gain. They include:
 Acetohexamide (Dymelor)
 Chrorpropamide (Diabenese)
 Tolazamide (Tolinase)
 Tolbutamide (Orinase)
2. Second-Generation Sulfonylureas (more powerful than first generation): stimulate
beta pancreatic cells to secrete insulin; improves binding between insulin and insulin
receptor cells, or increase insulin receptor cells. Side effects include hypoglycemia,
weight gain and sulfa allergy. They include:
 Glipizide (Glucotrol)
 Glyburide (Micronase, Glynase)
 Glimepiride (Amaryl)
3. Beguanides: they inhibit production of glucose by the liver, increase body tissue’s
sensitivity to insulin, and decrease hepatic synthesis of cholesterol. Side effects
include lactic acidosis, hypoglycemia, GIT disturbance. They include:
 Metiformin (Glucophage)
 Metiformin with glyburide (Glucovance)
4. Alpha-Glucosidase Inbitors: they delay absorption of complex carbohydrates in the
guts and slow insulin entry into blood circulation. Side effects include hypoglycemia,
GIT disturbance, drug-drug interactions. They include:
 Acarbose (Precose)
 Miglitol (Glyset)
5. Non-Sulfonylurea Insulin Secretagogues (Meglitinides): they stimulate pancreas to
secrete insulin, thereby controlling blood glucose. Side effects include hypoglycemia,
drug interactions, weight gain, though less common. They include:
 Repaglinide (Prandin)
 Nateglinide (Starlix)
 6. Thiazolidinediones (or glitazones): they sensitize body tissue to insulin; stimulate
insulin receptor sites to lower blood glucose. Side effects include hypoglycemia,
weight gain, anaemia, edema, possible liver dysfunction, impaired platelet function.
They include:
 Pioglitazone (Actos)
 Rosiglitazone (Avandia)
7. Dipeptidyl Peptidase-4 Inhibitors: they increase/prolong incretin hormone that
increases insulin secretion, decreases glucagon levels to improve glucose control. Side
effects include URTI, stuffy-runny nose, sore throat, headache, stomach discomfort,
diarrhoea, and hypoglycemia. They include:
 Sitagliptin (Januvia)
 Viltagliptin (Galvus)

Surgery
 Pancreas transplantation

Diagnosis
Nursing Diagnoses
 Risk for fluid volume deficit related to polyuria and dehydration
 Imbalanced nutrition related to imbalance of insulin, food, and physical activity
 Deficient knowledge about diabetes self-care skills and information
 Potential self- care deficit related to physical impairments or social factors
 Anxiety related to loss of control, fear of inability to manage diabetes, misinformation
related to diabetes, and fear of diabetes c omplications.
 Risk for complications.

Collaborative Problems/Potential Complications

 Fluid overload, pulmonary edema, congestive heart failure
 Hypokalemia
 Hyperglycemia and DKA
 Hypoglycemia
 Cerebral edema

Planning and Goals

The major goals of the patient may include attainment of fluid and electrolyte balance,
optimal control of blood glucose, regaining weight loss, ability to perform basic (survival)
diabetes skills and self-care activities, reduction in anxiety, and absence of complications.

Nursing Interventions

Nursing consideration
Key outcomes
The patient will:
 Maintain optimal body weight
 Remain optimal body weight
 Remain free from infection
 Avoid complications
 Verbalize understanding of the disorder and treatment
 Demonstrate adaptive coping behaviors

Nursing interventions
 Administer prescribed drugs
 Give rapidly absorbed carbohydrates for hypoglycemia or, if the patient is
unconscious, glucagon or L.V. dextrose, as ordered.
 Administer I.V. fluids and insulin replacement for hyperglycemic crisis, as ordered.
 Provide meticulous skin care, especially to the feet legs
 Treat all injuries, cuts and immediately
 Avoid constricting hose, slippers, or bed linens
 Encourage adequate fluid intake
 Encourage verbalization of feelings
 Encourage emotional support
 Help develop effective coping strategies

Monitoring
 Vital signs
 Intake and output
 Daily weight
 Serum glucose
 Urine acetone
 Renal status
 Cardiovascular status
 Signs and symptoms of:
 Hypoglycemia
 Hyperglycemia
 Hyperosmolar coma
 Urinary and virginal infections
 Diabetic neuropathy

Maintaining Fluid and Electrolyte Balance

 Measure intake and output
 Administer intravenous fluid and electrolytes as ordered
 Encourage fluid intake
 Measure serum electrolytes (sodium, potassium), and monitor closely.
  Monitor vital signs to detect dehydration: tachycardia, orthostatic hypotension.

Improving Nutritional Intake

 Plan the diet glucose control as the primary goal
 Take into consideration patient’s lifestyle, cultural background, activity level and food
preferences
 Encourage patient to eat full meals and snacks as per diabetic diet.
 Make arrangements for extra snacks before increased physical activity.
 Ensure that insulin orders are altered as needed for delays in eating due to diagnostic
and other procedures.

Reducg Anxiety
 Provide emotional support, set aside time to talk with patient
 Clear up misconceptions patient or family may have regarding diabetes
 Assist patients and family to focus on learning self-care behaviors.
 Encourage patient to perform the skills feared most self-injection or finger stick for
glucose monitoring
 Give positive reinforcement for self-care behaviors attempted

Monitoring and Managing Potential Complications

 Fluid overload: measure vital signs and monitor central venous pressure (CVP) and
total hemodynamic status at frequent intervals; assess cardiac rate and rhythm, breath
sounds, venous distention, skin turgor, and urine output; monitor intravenous fluid
and other fluid intake.
 Hypokalemia; replace potassium cautiously; ensure that kidneys are functioning
before administration; monitor cardiac rate, rhythm, electrocardiogram (ECG), and
serum potassium levels.
 Hyperglycemia And DKA; monitor blood Glucose levels and urine ketones;
administer medications (insulin, goal hypoglycemic agents); monitor for signs and
symptoms of impending hyperglycemia and DKA, administering insulin and
intravenous fluids to correct.
 Hypoglycemia: treat with juice or glucose tablets; encourage patient to eat full meals
or snacks as prescribed; review signs and symptoms, possible causes, and measures to
prevent or treat.
 Cerebral edema: prevent by gradual reduction in blood glucose level; monitor blood
glucose level, serum electrolyte levels, urine output, mental status, and neurologic
signs; minimize activities that increase intracranial pressure.
Teaching Patients about Self Care
 Teach preventive behaviours for long-term diabetic complications and patient
survival skills. Cover simple pathophysiology, treatment modalities, recognition and
 prevention of acute complications, and pragmatic information (where to obtain
supplies, when to call physician).
 Provide special equipment for instruction on diabetic survival skills (e.g. magnifying
glass for insulin preparation or injection aid device for insulin injection).
 Tailor information according to patient’s ability to understand.
 Instruct family so that they may assist in diabetes management
 Recommend follow-up education with outpatient diabetic specialist regarding
optimal equipment for patients physical impairment; recommend and arrange for
home care nurse, as indicated
 Assist in identifying community resource for education and supplies, giving
consideration for financial and physical limitations.

Nutrition
 Initial education addresses the importance of consistency in eating habits, the
relationship of food and insulin, and provision of individualized meal plan.
 Follow-up education focuses on more in-depth management skills, such as restaurant
eating, food labels, and adjusting meals for exercise, illness, and special occasions.

Be sure to cover:
 The disorder, diagnosis, and treatment
 Medications and possible adverse effects
 When to notify the practitioner
 Prescribed meal plan
 Prescribed exercise program
 Signs and symptoms of:
- Urinary tract and vaginal infection
- Hypoglycemia
- Hyperglycemia
- Diabetic neuropathy
 Self-monitoring of blood glucose
 Complications of hyperglycemia
 Foot care
 Annual regular ophthalmologic examinations
 Safety precautions

Discharge planning
 Refer the patient to a dietitian
 Refer the patient to a podiatrist, if indicated
 Refer the patient to an ophthalmologist.
 Refer the adult patient who is planning a family for preconception counseling.
  Refer the patient to Juvenile Diabetes Foundation, the American Association of
Diabetes Educators, and the American Association to obtain additional information

DIAGNOSTIC CRITERIA FOR DKA AND HHS

DKA
Mild DKA Moderate DKA Severe DKA HHS
 Plasma glucose (mg/dL) >250 >250 >250 >600
 Arterial pH 7.25 - 7.30 7.00 - 7.24 <7.00 >7.30
 Serum Bicarbonate (mEg/L) 15 - 18 10 - < 15 <10 >15
 Urine ketones positive positive positive small
 Serum ketones positive positive positive small
 Effective serum
Osmolarity (mOsm/kg) Variable Variable Variable >320
 Alteration in sensoria
Or mental obtundation Alert Alert/drowsy Stupor/coma Stupor/coma

TYPICAL TOTAL DEFICITS OF H2O AND ELECTOLYTES IN DKA AND HHS

DKA HHS
Total water (litres) 6 9
Water (ml/kg) 100 100-200
+
Na (mEq/kg) 7-10 5-13
-
Cl (mEq/kg) 3-5 5-15
K+ (mEq/kg) 3-5 4-6
PO4 (mmol/kg) 5-7 3-7
2+
Mg (mEq/kg) 1-2 1-2
2+
Ca (mEq/kg) 1-2 1-2

MANAGEMENT OF DIABETIC KETOACIDOSIS

SEVERE DEHYDRATION:
First priority is fluid replacement. IV infusion (isotonic (0.9%) or half isotonic (0.45) saline, 1
litre in the 1st hour, followed by 2 litres in 4hours, then 4 litres in the next 24hrs, watching
patient for signs of fluid overload.

NB: Fluid replacement causes a fall in blood glucose by dilution insulin administration in
severe ketoacidosis
Soluble insulin (regular) should be given by continuous IV infusion ideally by a pump in a
concentration of 0.1 unit/ml in isotonic saline, at a dose of 0.1 unit/kg/hour, that is, 7 units
per hour in a 70kg adult.

The dose is increased or lowered using a slide scale of blood sugar concentration as follows:

Blood glucose (mmol/L) Infusion rate

>15 --------------------------------------------- 8.0 u/hour
12-16------------------------------------------- 4.0 u/hour
8-12--------------------------------------------- 2.0 u/hour + change from saline to glucose 5%
if BS is < 10 mmol/L
5-8 --------------------------------------------- 1.5 u/hour.
3-5---------------------------------------------- 1.0 u/hour.
<3----------------------------------------------- 0.3 u/hour.

NB: If intravenous route is used, stat dose of 10-20 units should be given at the outset and
then 10 units hourly.
Progress: When BS has fallen to10 mmol/L 0.02 units/kg per hour until patient can eat and
drink, and subcutaneous insulin is restarted. Similar progression is used if the insulin is given
intramuscularly, e.g. lower doses 2 hourly.

NB: Doses are tailored to the clinical situation, which requires close monitoring.
Glucose administration
When BS falls to10 mmol/L the fluid infusion should be changed from normal saline to D5%
to prevent hypoglycemia, which can cause cerebral oedema, and coma.

Administration of potassium
Plasma potassium falls with intravenous Normal saline (dilution) and insulin, which draws
potassium into cells within minutes. Potassium chloride (KCl) should be added to the 2 nd and
subsequent litres of fluid according to plasma K+ (only if passing urine) or per hour as follows:

 If <3.5 mmol/L, add 40 mmol/L of fluid

 If 3.5 – 5.0 mmol/L, add 20mmol/L of fluid
 If >5.0 mmol/L, no potassium should be given

Bicarbonate administration – should be given only of plasma pH is < 7.0 and peripheral
circulation in good, insulin corrects acidosis

Dose of Bicarbonate:
 If pH <6.9, dilute NaHCO3 (100 mmol) in 400ml H2O. Infuse at 200 ml/hour.
 If pH 6.9 – 7.0, dilute NaHCO3 (50 mmol) in 200 ml H2O and infuse at 200 ml/hour
 Repeat HCO3 administration every 3 hours until pH > 7.0. Monitor serum potassium
(K+) also.
  Antibiotics should be given in case of infection since it may not be possible to abolish
ketosis until they are controlled.

HYPEROSMOLAR HYPERGLYCEMIC (DIABETIC) COMA (SYNDROME): HHS

This occurs chiefly in Type II diabetics who fail to compensate for their continuing, osmotic
glucose diuresis. It’s characterized by:
 Severe dehydration
 A very high blood sugar (>33mmol/l:300mg per 100ml) ad
 Lack ketosis and acidosis

Treatment:
 Isotonic or hypotonic saline with less K + than in severe ketoacidosis, that is 0.9% NaCl
(1litre/hour) and/or plasma expander if in hypovolaemic shock)
 Insulin according to blood (glucose level; it may be lower than the amount used in
severe ketoacidosis because in this condition there is no acidosis that resists insulin).
 Regular insulin 0.15 u/kg as IV bolus followed by 0.1/kg/hour IV insulin infusion
 Check serum glucose hourly, if serum glucose does not fall by at least 50-70mg/dl in
first hour then, double insulin dose hourly until glucose falls at a steady hourly rate of
50-70mg/dl.
 After resolution of HHS, follow blood glucose (BG) every 4 hours and give sliding
scale regular insulin SC in 5units increments for every 50 mg/dl increase in BG above
150mg/dl increase in BG above 150mg/dl for up to 20 units for BG > 300 mg/dL
 Change to 5% Dextrose with 0.45% NaCl and decrease insulin to 0.05 - 0.1 u/kg/hour
to maintain serum glucose between 250-300 mg/dl until plasma osmolarity is >315
mosm/kg and patient is mentally alert.

Potassium replacements
 If serum K+ is < 3.3 mEq/L, hold insulin and give 40 mEq K + (2/3 as KCL and 1/3 KPO4
until K+ > 3.3 mEq/L)
 If serum K+ >5.5 mEq/l do not give K+ but check K+ every 2 hours
 If serum K+ >3.3 but <5.5mEq/l, give 20 mEq – 30 mEq K+ in each litre of IV fluids
(2/3 as KCl and 1/3 as KPO4) to keep K+ at 4-5 mEq/l.
 Check the blood chemistry (i.e. electrolytes) every 2-4 hours until stable. Look for
precipitating factors /causes and treat them.

Skin care:
 Provide meticulous slain care especially to the feet and legs
Pheochromocytoma
Description
 Catecholamine producing tumor, typically benign; usually derived from adrenal
medullary cells
 Most common cause of adrenal medullary hypersecretion
 Usually produces norepinephrine; large tumors secrete both epinephrine and
norepinephrine
 Potentially fatal, but with treatment carries a good prognosis.

Pathophysiology
 Pheochromocytoma causes excessive catecholamine production from autonomous
tumor functioning.
 The tumour stems from a chromaffin cell tumour of the adrenal medulla or
sympathetic ganglia (more commonly in the right adrenal gland than in the left).
 Extra- adrenal pheochromocytomas may occur in the association with the 9 th and 10th
cranial nerves.

Causes
 Rare; seen in about 0.5% of newly diagnosed hypertensive patients
 Seen in all races
 Affects both sexes equally
 Typically familial
 Most common in patients age 30 to 50

Common characteristics
 Paroxysmal or sustained hypertension
 Hypertensive crises triggered by condition that displace the abdominal contents or by
use of opiates , histamine, glucagon, or corticotrophin
 Headache
 Flashing
 Diaphoresis
 Tachycardia
 Retinal changes

Complications
 Stroke
 Retinopathy
 Irreversible kidney damage
 Acute pulmonary edema
  Cholelithiasis
 Cardiac arrhythmias
 Heart failure

Alert
Pheochromocytoma may occur during pregnancy when uterine pressure on the tumor causes
more frequent hypertensive crises. These crises carry a high risk for spontaneous abortion
and can be fatal for both the mother and fetus.
Assessment
History
 Unpredictable episodes of hypertensive crisis
 Paroxysmal symptoms suggesting a seizure disorder or anxiety attack
 Hypertension that responds poorly to conventional treatment
 Hypotension or shock after surgery or diagnostic procedures.

During paroxysms or crises

 Throbbing headache
 Palpitations
 Visual blurring
 Nausea and vomiting
 Severe diarrhoea
 Feeling of impending doom
 Precordial abdominal pain
 Moderate weight loss
 Dizziness or light-headache when moving to an upright position

Physical findings
During paroxysms or crises
 Hypertension
 Tachypnoea
 Pallor or flushing
 Profuse sweating
 Tremor
 Seizures
 Tachycardia

Test results
Laboratory
 Vanillylmandelic acid and metanephrine levels in a 24-hour urine specimen are
increased.
 Total plasma catecholamine levels are 10 to 50 times higher than normal on direct
assy.
Imaging
 Computed tomography (CT) scan or magnetic resonance imaging of adrenal glands
may show intra-adrenal lesions.
 CT scan, chest x-rays, or abdominal aortography may reveal extra –adrenal
pheochromocytoma

Treatment
General
 High – protein diet with adequate calories
 Rest during acute attacks

Medications
 Alpha-adrenergic blockers such as phenoxybenzamine
 Catecholamine-synthesis antagonists
 Beta-adrenergic blockers such as atenolol
 Calcium channel blockers
 I.V. phentolamine or Nitroprusside during paroxysms or crises

Alert
Because severe and occasionally fatal paroxysms have been induced by opiates, histamines,
and other drug, all medications should be considered carefully and administered cautiously in
patients with known or suspected pheochromocytoma.
Surgery
 Removal of pheochromocytoma

Nursing considerations
Key outcomes
The patient will:
 Maintain stable vital signs
 Maintain fluid balance
 Maintain normal cardiac output
 Express feelings of increases comfort
 Avoid complications

Nursing intervention
 Take orthostatic blood pressures
 Administer prescribed drugs
 Ensure the reliability of urine catecholamine measurements
 Provide comfort measures
 Consult a dietician, as needed
 Tell the patient to report symptoms of acute attack
 Encourage the patient to express his feelings
  Help the patient develop effective coping strategies

Alert
Be aware that postoperative hypertension is common because the stress of surgery and
adrenal gland manipulation stimulate catecholamine secretion.
Monitoring
 Vital signs, especially blood pressure
 Serum glucose level
 Daily weight
 Neurologic status
 Renal function
 Cardiovascular status
 Adverse to medications

After adrenalectomy
 Vital signs
 Bowel sounds
 Wound dressing
 Incision
 Signs and symptoms of haemorrhage
 Pain

Patient teaching
Be sure to cover:
 The disorder, diagnosis, and treatment
 Medication administration, dosage, and possible adverse effects
 When to notify the physician
 Way to prevent paroxysmal attacks
 Signs and symptoms of adrenal insufficiency
 Importance of wearing medical identification jewelry
 How to monitor his own blood pressure

Discharge planning
 Refer family members for genetic counseling of autosomal dominant transmission of
pheochromocytoma is suspected.
DIABETES INSIPIDUS
Definition: Diabetes insipidus is an endocrine disorder that develops when antidiuretic

hormone (ADH) from the neuro podiatrist hypophysis is insufficient.

Causes
 Head trauma that damages the pituitary
 Primary or metastatic brain tumours
 Surgical causes (hypophysectomy- removal of the pituitary)
Pathophysiology
Anti- diuretic hormone secreted by the posterior pituitary regulates reabsorption of water in
the kidney tubules. Lack of this hormone (ADH) secretion causes the client (between 20-40
litres per day). This rapidly causes hypovolaemic shock and electrolyte imbalance, which can
lead to death, if prompt intervention is not provided.
Clinical features:
 High urine out-put 20-40 litres/24 hrs
 Dilute urine with specific gravity less than 1.002
 Urine excretion continues even with fluid intake limitations
 Excessive and constant thirsty due to fluid volume deficit (polydipsia)
 Limited activities related to need for frequent drinking and voiding which is frequent.
Diagnostic evaluation:
 Failure to concentrate urine during the period of fluid deprivation test (when fluid
withheld for 8-12 hours) (characteristic of the disorder)
 Urinalysis reveals virtually colourless urine of low specific gravity
 The 24- hour urine output is abnormally large
Medical management:
 Administration of Desmopressin (DDAVP) nasal solution and nasal spray (Lypressin
[Diapid]) synthetic drugs with ADH activities to reduce urine output to 2-3 L/day.
 Intravenous fluids given to replace excessive fluid volume loss and correct electrolyte
imbalances.
  Intramuscular ADH (vasopressin tannate in oil)- given if intranasal route is
impossible. Given after every 24-96 hours and it is given in the evenings so as to give
its maximum effect during the night.
 Clofibrate (hypolipidemic agent) provides antidiuretic effects in patients with residual
hypothalamic vasopressin (ADH).
 Chlorpropamide (diabenese) and thiazide diuretics provide synergistic effect (i.e.
potentiate) on the action of vasopressin.
 For the diabetes insipidus which originates from renal problems, vasopressin is
ineffective. For that case, the problem may be relieved with the administration
thiazide diuretics, prostaglandins and slight depletion of salt.

NURSING MANAGEMENT
 The nurse provides support to the patient while undergoing through studies for
possible cranial lesion.
 There should be continuous assessment and close monitoring of the following
observations:
o Vital signs

o Daily weights

o Hydration status

o Electrolyte status

o Input and output record of fluids

o Urine specific gravity between doses

 Provide protective measures to the patient if feeling dizzy or has muscle weakness by
raising the side rails up and by assisting and supporting the patient to walk.
 Provide meticulous skin and mouth care; applying petroleum jelly, as necessary, to
cracked or sore lips.
 Psychological support is providing to the patient and family to allay anxiety related to
the condition.
 Specific verbal and written instructions on home care and medications are shared
with the patient and family.
  Demonstrations on drug administration are given by the nurse with feedback (return
demonstration) from the client and family.
 The patient is instructed to wear a medical identification bracelet and to carry
medication and the information about his/ her disorder daily.
 Precautions should be taken in a patient with coronary artery disease when giving
vasopressin because it causes vasoconstriction.
 The patient with diabetes insipidus may be referred for counseling and psychosocial
adjustments or coping or support groups.

COMPLICATIONS
 Electrolyte imbalance
 Fluid volume deficit (dehydration)
 Hypovolaemic shock
 Cardiovascular collapse
 Renal failure
SIMMOND’S DISEASE (PANHYPOPITUITARISM)
Definition: Panhypopituitarism (Simmond’s disease) is an endocrine disease resulting from
undersecretion (hyposecretion) of all the anterior pituitary hormones
Causes:
 Destruction of anterior pituitary gland
 Sheehan’s syndrome ( postpartum pituitary necrosis) – related to severe
haemorrhage, hypovolaernia and hypotension following delivery
 Pituitary tumours and hypothalamic tumours
 Inflammatory process ( meningitis, pituitary abscesses)

Pathophysiology
Simmond’s disease results into atrophy of the thyroid gland, the adrenal cortex, and the
gonads due to loss of the trophic- stimulating hormones (i.e. ACT, FSH, LH, TSH). Thus
patient would present with clinical syndromes of hypothyroidism, adrenal insufficiency,
sexual problems, etc. When it occurs in children, they would have retarded growth and
delayed puberty. Total loss of all hormones from adenohypophysis is fatal unless treated.
Clinical features
 Amenorrhoea, regression of secondary sexual characteristics and infertility in women
related to lack of LH and FSH.
 Impotence, testicular atrophy, regression of secondary sexual characteristic, decreased
spermatogenesis, infertility in men.
 ACTH deficiency results into fatigue, hypotension and intolerance of stress and
infection.
 Extreme weight loss and hair loss, emaciation related to adrenal insufficiency and
polyuria
 Hypometabolism
 Hypoglycemia
 Coma
 Diabetes insipidus (polyuria)
  Mental and physiologic abnormalities e.g. lethargy, psychosis, hypostatic hypotension
bradycardia, anaemia, anorexia.
 Clinical features related with pituitary tamours include: headache, bilateral temporal
(hemianopia, loss visual acuity, and possible blindness).
 Death may result from renal insufficiency, hypotension, organ failures (e.g. heart
failure, renal failure), and electrolyte imbalances.
Management of Panhypopituitarism
 Replacement of hormones secreted by the target glands is the most effective treatment
for Simmond’s disease. The hormones administered include:
i) Levothyroxine to correct hypothyroidism
ii) Glucocorticoids (e.g. cortisol) to correct adrenal insufficiency.
iii) LH and FSH; Oestrogens and progesterone (for women) are given to correct
hypogonadotrophic hypogonadism.
iv) Mineralocorticoids (e.g. Aldosterone) to correct electrolyte imbalance (esp.
Na+)
v) Biosynthetic growth hormone for children to promote growth.
 Surgical intervention – if hypopituitarism was due to pituitary tumour,
transsphenoidal resection or hypophysectomy is done and postoperative care is
provided s as appropriate.
 Monitor the patient’s vital observation closely to identify any deviation from normal
and establish interventions as necessary ( TPR, BP) - 4 hourly
 During therapeutic hormonal replacements, the patient should closely be
monitored for the following serum levels of GH, free T4, cortisol, Na+, Kt, glucose.
 Electrolyte imbalances and fluid volume deficit are corrected by appropriate fluids-
intravenously and orally.
 Meticulous skin care is provided to avoid infection and pressure sores
 All measures of infection prevention should be provided since the patient has severe
low immunity.
  Watch for anorexia which is common in a patient with panhypopituitarism and plan
with the patient a menu that contains his/her favourite foods –especially high-caloric
foods
 In acute / severe cases, the patients are managed in complete bedrest, turned two
hourly and given daily bed baths including 4 hourly oral care.
 If patient presents with severe anaemia, he/she is given blood transfusion.
 If patient’s body temperature is subnormal related hypothyroidism, provide additional
clothing and covers, as needed, to keep him / her warm.
 The patient should be managed in a darkened room if he presents with severe
headache and visual disturbances associated with pituitary tumour
 Hypoglycemia is corrected with 50% glucose (dextrose) intravenously. Patient and
family are supported psychologically to as to allay anxiety. Children with dwarfism
and their parents may be referred for special counseling services.
 The patient and family are given full explanations and instructions on the therapeutic
regimens, medication adherence, side effects, and clinical checkup appointments,
infection prevention, diet and signs indicating worsening of the disease.

COMPLICATIONS
 Mental confusion
 Electrolyte imbalance
 Dehydration
 Heart failure
 Renal failure
 Anaemia
 Mental and growth retardation
 Infertility
 Hypoglycemia
 Coma
 Death
DWARFISM
Definition: Dwarfism is an endocrine disorder characterized by short stature (hypopituitary
dwarfism) resulting from deficient production of human growth hormone during infancy
and childhood.
N.B: - Height is less than the 3rd percentile
- Growth rate (velocity) is less than or equal to 4 cm per year.
- Bone age is greater than or equal to 2 years behind chronologic age.
Etiologic factors:
1) Decreased GH secretion due to:
i) Hypothalamic causes such as
 Decreased secretion of GRH
 Organic lesion ( tumours)
ii) Pituitary cause such as
 Decreased secretion of GH alone or with other pituitary hormones
 Pituitary tumour
 Functional GH deficiency ( emotion deprivation)
2) Defective growth hormone (GH) Action resulting from:
 Defective growth hormone (GH) receptors ( Loran dwarfism)
 Secretion of abnormal forms of GH
 Nutritional impairment of GH- induced sometomedin formation ( e.g. in
Kwashiorkor)
3. Impaired skeletal response to somatodin (GH) as occurs in:
 Constitutional short stature
 Gonadal dysgenesis s( Turner’s syndrome)
 Primary cartilaginous or bone disease
 Chronic renal disease ( e.g. renal failure)
 Chronic inflammatory disease
 Excess corticosteroids ( pituitary and adrenal disorders; therapeutic use of
corticosteroids)
4) Hypothyroidism (primary or secondary)
5) Precocious puberty (CNS – “true precocious puberty”) with early epiphyseal closure.
6) Diabetes mellitus (type 1)
7) Adrenocortical insufficiency
Clinical features;
 Growth retardation with normal proportions
 Delayed pubertal development ( delayed sexual maturation)
 Excessive subcutaneous fat and poor muscle development; immature facial features;
immature voice;
Diagnosis
o Reduced response to provocative stimuli to GH release (i.e. decreased levels of GH)
o Clinical manifestations.

TREATMENT OF DWARFISMS
 Replacement therapy with human GH stature related to GH deficiency e.g.
biosynthetic GH 0.1 mg / kg (0.2 IU/kg) intramuscularly 3 times a week (is effective –
increases height up to 15 cm in the first year of treatment, but may slow down in
subsequent years).
 Replacement of cortisol and thyroid may be needed but excess administration of these
should be avoided because they may impair the response to GH.
 After normal puberty has been reached and pubertal changes have occurred, growth
hormone will have little effects and therefore should be stopped.
 If GH is not effective, small closes of androgen may be given to stimulate growth, but
great caution to be taken to prevent premature closure of epiphyses.
 The nurse’s role is to monitor the growth of the child (height, weight) development of
sexual organs and secondary sexual characteristics.
 The nurse provides psychosocial support to the child and parents as necessary
 The nurse provides adequate explanation and instructions about the specific
treatment and the expected results (effects) to include increased general well-being,
physical endurance and improvement in body composition and bone mineral density.
ADDISON’S DISEASE (ADRENOCORTICAL INSUFFICIENCY)
Definition: It is an endocrine disorder resulting from adrenocortical insufficiency, which
occurs where adrenal cortex function is inadequate to meet the patient’s need for cortical
hormones. The condition develops insidiously and usually, progressively.

Causes (etiology)
o Autoimmune or idiopathic atrophy of the adrenal glands (responsible for 80-90% of
all cases).
o Surgical removal of both adrenal glands ( bilateral adrenectomy)

o Infection of the adrenal glands (tuberculosis, histoplasmosis)

o Inadequate secretion of ACTH from adenohypophysis (decrease stimulation to

adrenal glands) – Hypopituitarism
o Therapeutic use of corticosteroids ( which interferes with the normal negative feed
back mechanism)
o Sudden stoppage of use of corticosteroid (suppresses normal body’s response to stress
with normal feedback mechanism.
o Congenital adrenal hypoplasia

o Metastic cancer

o HIV

o Chemotherapy

Pathophysiology
The principal hormones synthesized by the adrenal cortex are cortisol (20mg), aldosterone
0.2mg and gonadocorticosteroid (dehydroisoandrosterone, which is converted into
testosterone, which is converted into testosterone.
In Addison’s disease, there is increased secretion of sodium (Na) and decreased secretion of
potassium (K) chiefly in the urine, which is dilute, and also in the sweat, saliva, and GIT.
Thus, there are low concentrations of Na, Cl and high serum K. This results into the kidneys’
inability to concentrate urine, in combination with electrolyte imbalance, thereby
producing severe dehydration, increased plasma concentration, decreased circulatory
volume, hypotension and circulatory collapse. Cortisol deficiency causes hypotension,
disturbance in metabolism of carbohydrate, proteins and fats. More so, cortisol inadequacy
results into severe insulin resistance. All these will cause inadequate gluconeogesis ( from
proteins), hypoglycemia and diminished resistance to infection, trauma, and stress, more so,
myocardial weakness, and dehydration cause low cardiac output and circulatory failure.
Progressive dehydration can lead to adrenal crisis (Addisonian crisis) with shock, kidney
failure and death. Glucocorticoid deficiency may also lead to dysphoria, apathy, or depression
(emotional instability).

Clinical features;
o Increased urinary excretion of Na and retention of K

o Dehydration and reduced blood Plasma volume

o Weakness, fatigue, dizziness, light headedness, due to hypogluconeogenesis

o Hypotension, postural hypotension, hypothermia, tachycardia.

o Vascular collapse because of poor myocardial tone decreased cardiac output, weak and
irregular pulse.
o Weight loss, anaemia, anorexia and gastrointestinal symptoms

o Emotional instability, nervousness, period of depression, apathy and confusion

o Hypoglycemia from a deficiency of the hormones that facilitate the conversion of

proteins into glucose; episodes of hypoglycemia may occur 5 - 6 hours after eating
(the period before breakfast is especially dangerous).
o Abnormally dark pigmentation, especially of exposed areas of the skin and mucous

membranes; and decreased hair growth (due to primary adrenal insufficiency)

o Profound shock and kidney failure that may lead to death.

Diagnostic tests
 Early morning cortisol measurement of blood serum reveals low levels of cortisol
(Less than 165 nmol/L)
 Plasma ACTH in primary adrenal insufficiency is greatly increased (>22.0 pmoI/L)
  Decreased levels of blood glucose (hypoglycemia)
 Decreased levels of Na (hyponatraemia)
 Increased levels of K the serum ( hyperkalemia)
 Abdominal CT may reveal atrophy of the suprarenals
 Increased BUN
 MRI
 Urinalysis – low volume, proteinuria, casts

Medical/Nursing Management
 Emergency management include combating circulatory shock by restoring blood
circulation through IV fluids preferably D5% in normal saline.
 Administration of corticosteroids: such as IV hydrocortisone to correct cortisol
deficiency. Administration of antibiotics to combat and prevent infection since
patient has an extremely low immunity.
 The patient is assessed closely to identify any other factor which could have caused
acute episode of adrenal insufficiency, e.g. stressors, infections/illnesses
 For chronic adrenal insufficiency, life- long replacement of corticosteroids and
mineralocorticoids will be essential e.g. cortisol and aldosterone.
 Administer glucose intravenously to treat or correct life threatening hypoglycemia.
 The nurses must monitor closely for signs of fluid deficit and electrolyte imbalances
and correct them with appropriate fluid
 The nurse’s assessments should include checking for weight changes, muscle
weakness and fatigue and provide remedial measures for the anomalies.
 The nurse should closely monitor the patient for signs of Addisonian crisis
manifested by shock – hypotension; rapid, thready pulse; bradypnoea, pallor; and
lethargy or profound weakness.
 The patient should be prevented from exposure to cold, overexertion, infection and
emotional stress to prevent circulatory collapse and shock, which are the common
complications of addisonian crisis.
 Addisonian crisis is corrected with the administration of IV fluids, glucose,
electrolytes (Na+), corticosteroids, and vasopressors.
 During the acute crisis, the nurse maintains a quiet, non- stressful environment and
performs all activities (e.g. daily bed baths, turning 2 hourly) for the patient.
 All procedures performed are explained to the patient and family members to reduce
their anxiety and minimize stress during acute crisis.
 The patient is assisted to resume activities gradually as he/she improves from a crisis
 Promotion of home care and community-based care are enhanced by:
 Teaching the patient on self-care, for he/she will be on long-term (lifelong)
replacement of corticosteroids to prevent Addison crisis.
 Giving the patient and family explicit explanation and instructions on the importance
of drug adherence and proper dosages
MYXOEDEMA
Definition: Myxoedema is an endocrine disorder resulting from severe hypothyroidism,
which, if untreated, may progressively advance to Myxoedema coma (Life-threatening
myxedema coma). Myxoedema implies the accumulation of mucopolyccharides in
subcutaneous and other interstitial tissues.

Causative factors:
 Inadequate production of thyroid hormone due to thyroidectomy, radiotherapy,
inflammation, chronic autoimmune thyroiditis (Hashimoto’s disease)
 Failure of pituitary gland to produce thyroid stimulating hormone
 Hypothalamic failure to produce thyrotropin-hormone
 Inborn errors of thyroid hormone synthesis (cretinism)
 Iodine deficiency leading to inability to synthesize thyroid hormone
 Use of drugs, such as propylthiouracil
 Atrophy of thyroid glands.
Conditions which precipitates Hypothyroidism to progress to myxoedema coma:
 Infection
 Trauma
 Exposure to excessive chills
 Taking narcotics (opioid analgesics)
 Using sedatives
 Using tranquilizers

Diagnostic evaluation
o Radioimmunoassay confirms low thyroid hormone (T3, T4 )

o In thyroid insufficiency, there is increased TSH levels

o In hypothalamic or pituitary insufficiency, TSH levels are decreased

o Serum cholesterols, alkaline phosphates, and triglycerides are elevated.

o Anaemia ( Normocytic, normochromic)

 o In Myxoedema coma; Low serum sodium, levels decreased pH, increased pCO 2

indicating respiratory acidosis

Clinical features of myxoedema
 Decreasing mental stability
 Dry, flaky, inelastic skin
 Puffy face, hands and feet
 Periorbital oedema
 Upper eyelid droop
 Dry sparse hair (hair loss)
 Thick, brittle nails
 Anorexia
 Abdominal distension with constipation
 Infertility
 Ataxia
 Nystagmus
 Delayed reflex relaxation time (esp. Achilles tendon)
 Cardiovascular involvement manifestations include:
o Decreased cardiac output

o Slow pulse rate

o Signs of poor peripheral circulation (cyanosis)

o Enlarged heart

Myxoedema coma is characterized by:

o Gradual progressive deterioration of condition, though may develop rapidly incase of

stress, infection or prolonged hypothyroidism

o Progressive stupor

o Hypoventilation

o Hypoglycemia

o Hyponatraemia

o Hypotension

o Hypothermia
Management of Myxoedema
 Replacement of thyroid hormone with the administration of levothyroxine (T4) and
sometimes liothyronine (T3). These are given through the IV line.
 In myxedema coma, management should be aimed at restoring the vital functions
while restoring euthyroidism.
 Blood pressure and pulse rate are supported by the administration of IV
levothyroxine and glucocorticoids e.g. hydrocortisone ( Cortisol) to correct pituitary
or adrenal insufficiency
 IV fluids are administered for fluid and electrolyte balance as part of the supportive
measures
 Antibiotics are given as prescribed to control infections.
 Provide a high-bulk, low calorie diet, and encourage activity to prevent constipation
and promote weight loss.
 Give cathartics and stool softeners as prescribed to relieve constipation.
 Monitor for symptoms of hypothyroidism related to administration of levothyroxine (
e.g. sweating, restlessness, excessive weight loss)
 Inform the client to report to the physician if he/she experience chest pain and
tachycardia which are signs / symptoms cardiac disease
 Client should adhere to drug regimens to avoid the possibility of developing
myxoedema coma.
 All possible measures should be put in place to prevent infection and any sign of
infection should be reported immediately for intervention
 For very severe form of hypothyroidism (myxedema coma) the following
management should be provided:
Check frequently for signs of decreasing heart output e.g. decreased urine output.
Monitor vital signs and especially temperature, which is usually subnormal and provide extra
blankets to keep the patient warm. Avoid rapid rewarming since it causes vasodilatation
leading to cardiovascular collapse. Monitor and record input and out put record daily and
report any abnormality.
Take the weight of the patient daily to note if body weight is decreasing.
Turn the client 2 hourly since he/she is bedridden and provide skin care (e.g. massaging) to
prevent pressure sores.
Drugs such as sedatives should be avoided since hypothyroidism delays there metabolism,
which can result into toxicity.
Intravenous fluid will be maintained for fluid and electrolyte balance
Serum electrolytes should be closely monitored when administering fluids to avoid
imbalances (overload)
Vital signs should be monitored continuously since the administration of levothyroxine can
cause tachycardia which may lead to cardiac failure.
Watch for signs of hypertension and heart failure in elderly patients during the
administration levothyroxine.
Blood gases (arterial) should be monitored to rule out hypoxia and respiratory acidosis and if
severe, the patient may be put on ventilatory supportive machines or oxygen be administered.
Administration of antibiotics to clear infection should be continued until the patient
improves and gets out myxedema coma
Sputum and urine should be tested regularly for the identification of infection
Patient may need insulin to reduce hyperglycemia associated with the administration of
levothyroxine.
Provide bed bath for a patient with myxoedema, oral care should be performed every 4 hours
to prevent oral-dental infections.
Upon improvement, patient will be assisted to perform the daily activities to prevent
complications.
Client will be helped to cope with severe emotional reactions related to change in appearance
and body image. Family members are also emotionally supported.
When client improves and is allowed home provide health education to patient and family

members on: .The course of the disease

 Drug adherence
 Monitoring of complications and drug side effect
 Follow – up for check up/ monitoring of the client.
  Exercise and diet.

ACROMEGALY/GIGANTISM
Definition: Gigantism is an overgrowth (excessive tallness) resulting from excess secretion of
growth hormone (GH) before puberty (i.e. before ossification of the long bones).
Definition: Acromegaly is an endocrine disorder, chronic in nature, which affects adults (after
bone ossification) and is characterized by gradual enlargement of the hands, feet and bones of
the head and chest; resulting from hypersecretion of growth hormone.
Definition: Acromegaly and Gigantism are syndromes of excessive secretion of growth
hormone (GH), nearly always due to pituitary adenoma of Somatotrophs (growth hormone
secreting cells).

Etiological factors:
 Pituitary tumour (general a macro-adenoma)- it is the commonest cause
 An ectopic growth hormone producing tumour (e.g. in the pancreas)- rare
 GH- releasing hormone (GHRH) producing tumour - rare
Diagnostic evaluations include:
 Obvious clinical manifestations
 Confirmation is achieved by assessment of growth hormone secretion (above 400
ng/ml)
 Elevated postprandial plasma glucose
 Elevated serum phosphates.
 Hypercalcemia/hypercalciuria.
 Radiographs show enlargement of the frontal and maxillary sinuses and thickening of
soft tissues.

Management of Gigantism/Acromegaly
Medical management
 Bromocriptine mesylate (an antiparkinsonian drug) to inhibit GH
 Octreotide (a somatostatin analog) to inhibit secretion of GH
Surgical treatment
Ablative therapy:
 Transsphenoidal resection of the tumour (hypophysectomy).
 Radiation to pituitary gland with subsequent destruction of the pituitary.
Nursing care:
 Priorities include:
 Correcting fluid volume excess or deficit.
 Relieving pain.
 Improving nutrition.
 Careful measurement of:
o Fluid intake and output

o Weighing of client daily

o Signs of fluid volume excess or deficit

 Notify to the physician if there is abrupt weight loss of gain

 Evaluate pain, noting type and location related to musculoskeletal changes.
 Give analgesics as ordered and note whether the client reports relief from the pain
 Support the client psychologically to cope up with the prominent physical changes,
erectile dysfunction (men) and decreased libido. Refer the client to sex therapist if
necessary.
 On discharge, provide health education on home care to include:
o The cause of the disease, its course and effects in the body

o Drug compliance and adherence

o Monitoring for possible side effects and steps to be taken

o Observe for complications that may arise from the condition

o Regular checkups for monitoring the disease process and response to treatment

o Psychological support.
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
SECRETION (SIADH)
Definition: SIADH is an endocrine disorder characterized by renal reabsorption of water
(water retention) rather than its normal excretion related to hypersecretion of antidiuretic
hormone.
Etiology (causative factors)
o Pulmonary disorders: malignant neoplasms (small cell carcinoma – most common cause

– 80% of all cases), tuberculosis, ventilator patients receiving positive pressure, lung
abscess.
o Other malignancies: duodenum, pancreas, prostate lymphoma, sarcoma, leukemia,
Hodgkin’s lymphoma, non-hodgkin’s lymphoma.
o CNS disorders: Tumours, infection, head trauma, cerebrovascular accident, surgery

o Drugs such as: Clofibrate, vasopressin, oral hypoglycemics ( e.g. Chlorpropamide),

thiazides, vincristine, cyclophosphamide, general anaesthetic agent, opioids, tricyclic

antidepressants, carbamazepine
o Stressors: Fear, acute infections, pain, anxiety, trauma, surgery

Pathophysiology
Inappropriate water retention (increased water volume) causes hypo-osmolar state with a
dilutional hyponatraemia. Though it causes expansion in intracellular volume, it never causes
oedema. However, this volume expression causes enhanced glomerular filtration and
decreased proximal tubular sodium reabsorption resulting in natriuresis (i.e. urinary sodium
excretion). Plasma hypoosmolarity creates an osmotic gradient across the cell membranes
(including the blood brain-barrier) causing flow of water into all cells.
A rapid fall in serum sodium (Na) levels can result in rapid–onset cerebral oedema and death,
whereas a gradual fall over several weeks may only cause lethargy. Features correlated with
Na levels are as follows: serum Na level equal or less than 125 mEq/L: nausea and malaise.
Serum Na levels 115-120 mEq/L: headache, lethargy, obtundation. Serum Na levels 110-114
mEq /L: seizures and coma.

CLINICAL MANIFESTATIONS:
 Early signs/symptoms:
 Anorexia
 Nausea
 Vomiting
 Weight gain
 Muscle weakness
 Irritability
 Late signs/symptoms
 Lethargy
 Headache
 Decreased deep tendon reflexes
 Mild disorientation
 Malaise
 Anger
 Anxiety
 Uncooperativeness
 Coma
 Seizures (muscle twitchings)
Fluid and electrolyte changes
 Decreased sodium in plasma
 Decreased plasma osmolality
 Increased urinary sodium and urinary osmolality
 Absence of oedema
 Decreased urinary volume
 Low normal/subnormal uric acid levels
MANAGEMENT OF SIADH
Medical management:
Treatment objectives include
i) To eliminate the underlying cause
ii) To correct water retention and electrolyte imbalance
Drugs used in the management:
Drugs used to correct water retention and increase diuresis are:
i) Osmotic diuretics e.g. mannitol
ii) Loop diuretics e.g. Frusemide (Lasix)
Severe Hyponatraemia is treated by IV 3% hypertonic sodium chloride solution to
replenish the lost sodium.
Surgical Intervention:
 If the cause of SIADH is due to a tumour, surgical resection is done to correct the
anormally.
 Other treatment provided include: radiation and chemotherapy to eradicate the
tumour’s cells.

Nursing management:
 Patient’s fluid intake is restricted to 500 to 1000 m/s day. If with severe water
intoxication, fluid intake is restricted to 200 to 300 per day.
 Fluid intake and output should be closely monitored and record kept.
 Vital signs (observations) are monitored to defect any abnormality, such as, heart
problems related to fluid overload.
 Monitor daily weight, urine chemistry, blood chemistry and neurologic status.
 Careful assessment of the level of consciousness (LOC) is maintained and reported
to the physician as necessary.
 The nurse monitors for signs of fluid overload, to include confusion, dyspnoea,
pulmonary congestion and hypertension.
  The nurse should check for signs of hyponatraemia to include: weakness, muscle
cramps, anorexia, nausea, diarrhoea, irritability, headache, and weight gain
without oedema.
 The client and family should be supported psychologically to allay anxiety.
 Full explanations about the disease process and specific treatment approaches to
relieve the condition should be provided to client and family.
 Provide complete information on medication adherence and compliance and the
possible side effects and what to do if they occur.
 To prevent water intoxication, explain duly to the patient and family why he/she
must restrict fluid intake.

Complications
 Hypertension
 Heart failure
 Cerebral oedema
 Coma
 Electrolyte imbalance (hyponatraemia)
 Death
CUSHING SYNDROME

This is a condition resulting from hypersecretion of cortisol from the adrenal cortex (zona
fasculata).

Endocrine disorders resulting from excessive secretions of hormones by the adrenal cortex

Causes

Disorders of the hypothalamic pituitary adrenal axis

 CRH excess-from hypothalamic/ectopic

 ACTH excess-from pituitary adenomas/ectopic e.g. cricoids or lung cancer (15%)
 Adrenal cortex excess-from primary adrenal tumours, benign/malignant
 Glucocorticoids excess-from endogenous two degrees to any of the above and from
exogenous (therapeutic use) - hydrocortisone, dexamethasone, etc.

Incidence

More common in women ages 20-40 years than men

Approximate incident is 5 to 25 cases/1 million persons per year

Pathophysiology

The first discernible abnormality is the loss of diurnal variation in cortisol secretion. The
morning secretions is at its highest end of the normal range, whereas the evening show
no normal decline cortisol is at its highest normal end (25 ug/dl) in the morning (6-8am)
and lowest normal end (less than 10ug/l) in the evening (6pm).

The pathophysiology sequelae of cortisol excess involve multiple systems. It may present as
secondary metabolic dysfunction (e.g. DM) or hypertension before it is diagnosed as Cushing
syndrome. The client may be liable to emotional (ability) changes and psychiatric changes.

Adenohypophysis dysfunction is common which alters secretion of gonadotropin and

other hormones resulting into secondary organ dysfunction e.g. amenorrhoea,
overproduction of both adrenal androgens and cortisol is common, resulting into hirsutism
and acne.

Diagnosis

 Salivary free cortisol level is elevated

  Urinary free cortisol level is elevated: Confirmation of excess glucocorticoid
production i.e. 24 hours urine cortisol (best single test for the diagnosis)
 The 1 mg overnight dexamethasone suppression test is a useful screening test
 In ACTH – independent Cushing syndrome, the ACTH is low/subnormal secondary
to pituitary suppression
 In ACTH dependent Cushing syndrome, the ACTH is high normal/frankly elevated
 Evaluation of pituitary Cushing syndrome by administration of dexamethasone 8
mg at 11 pm and fasting serum measured at 8 am reveals 50% reduction of
cortisol.
 Iv bolus CRH will reveal a rise in ACTH levels in pituitary dependent Cushing
syndrome
 Magnetic resonance imaging for identification of pituitary lesion
 Adrenal computed tomography (CT) for identifying adrenal lesion/tumour
 Chest CT/abdominal CT for diagnosis of ectopic ACTH (but CT may give false
negative)

Clinical features

 Overproduction of adrenal cortisol may cause

 Arrest growth
 Obesity with a fatty “buffalo hump” neck and upper trunk/central obesity
 Musculoskeletal changes (relatively thin limbs)
 Glucose intolerance or overt clinical features of DM
 Skin is usually thin, fragile and easily traumatized, echymosis, bruises
 Patient complains of fatigue and lassitude (faintness, sluggish, lack of energy)
 Muscle wastage and osteoporosis due to excessive protein catabolism
 Kyphosis
 Backache
 Compression fracture of the vertebrae
 Moon-face appearance with increased oiliness of the skin and acne
 Increased susceptibility to infections
 Hyperglycemia
 Retention of NaH2O resulting from increased fluid and Na retention
hypertension/heart failure resulting from increased fluid retention
 Virilization characterized by masculine features in female due to increased
production of androgens characterized by
 Clitoris enlargement
 Excessive growth of hair (hirsutism)
  Breast atrophy
 Cessation of menses
 Deepening of the voice
 Loss of libido
 Infertility
 Sleep disturbance associated with altered diurnal secretion of cortisol.
 Mood and mental changes to include psychosis, distress and depression
 Visual disturbance possibly resulting from pressure on the optic chiasm due to
pituitary tumour.

Management

Medical management

Used when surgical interventions are not feasible or when radiotherapy is still pending.

Therapies revolve around inhibition of cortisol production in adrenal gland.

Drugs used are

 Ketoconazole
 Metyrapone
 Aminoglutethemide
 Mitotane

If the condition results from exogenous corticosteroids the drug should be tapered to
minimum level or use alternative therapy for the treatment of underlying disease.

Surgical management

The definitive management of Cushing syndrome is after identifying the cause (with
possible cure)

Transsphenoidal surgery results in 80-90% cure rate (with low morbidity and 1% mortality
rate).

Complications following transsphenoidal include:

 Permanent diabetes insipidus

 Panhypopituitarism
Adrenectomy done to remove adrenal tumours which may be done laparoscopically in
selected patients (choice of treatment)

Patients who have failed transsphenoidal surgery for pituitary Cushing syndrome,
bilateral adrenectomy is done as a second line of treatment

After surgery patients with unilateral solitary adrenal tumour, ACTH–producing

pituitary tumour or ectopic ACTH producing tumours experience suppression of the
normal ACTH–adrenal axis and require cortisol replacement for 6-24 months. But
bilateral adrenectomy require lifelong glucocorticoids and mineralocorticoids replacements.

Other management

Diet-modified according to individual and calories, sodium lipids and cholesterol are
commonly restricted.

If patients develop DM, dietary management to reduce and manage high blood glucose
levels is indicated

Activity: - usually patient is obese and fatigued with muscle atrophy and or pathologic bone
conditions. Thus, activities are maintained but restricted to particular complications.

Referrals: patients need to be referred for physiotherapy for muscle strength and
conditioning. He/she may be referred to social services or psychologist if indicated, e.g. in
case of psychosis, mental confusion or depression.

Nursing management

Assess (through health history/physical examination) for identifying problems for

management. Nursing diagnoses may include:

 Disturbed body image (changes in body characteristics and functioning)

 Risk of infection related to immunosuppression secondary to hypercortisolism
 Risk for injury (immunosuppressed from increased hypercortisolism, muscle
weakness, decreased bone mass, increased risk pathologic fractures)
 Deficient knowledge (lack of information regarding treatment plan)

Promotion of positive body image (discuss the impact it caused in his/her body, self-
concept and relationship with others will be modified by treatment and diet, symptoms
may subside with treatment)

Prevention of infection (avoids exposure to any known infectious source, assess for signs of
infection)
Promotion of skin care should include meticulous skin care to avoid injury to fragile
skin, and avoiding adhesive tape use.

Prevention of injuries (protective environment, assist in ambulation to avoid falls, give

food high in proteins, calcium, vitamin D to prevent muscle atrophy and osteoporosis)

Family and patient teaching include: diet restriction, prevention of infection, disease
process, planned treatment and specific care of complications, weight reduction, drug
compliance, side effects of drugs.

Health promotion - eliminate smoking, screening for secondary prevention and tertiary
prevention.

Improving thought process (by explaining to patient and family the cause of emotional
disturbance, coping mechanisms for mood swings, depression, etc.). Encourage
verbalization of feeling from patient and family, refer for treatment any psychotic behavior
or episodes

Promote rest and activity (moderate activity to prevent complications of immobility and
enhance self-esteem). Patient should be helped to plan rest periods for each day and
promote rest relaxation and sleep.

Assessing and management of complications - such as adrenal dysfunction and addisonian

crisis (low BP, weak elevated pulse, increased pulse rate, extreme fatigue, pallor etc.).

Correct fluid deficit and electrolyte imbalances through appropriate intravenous fluids

Administer drugs as indicated by the doctor e.g. Corticosteroids following surgery

Monitor vital signs (TPR and BP) closely to rule out/in circulatory collapse and shock in
Addison crisis

Monitor blood glucose levels, record, and report to the physician for any abnormality for
appropriate interventions e.g. management of DM if present.

On Client’s Teaching:

 Provide information verbally and written on the disease

 Provide health messages on self-care to prevent injuries and infections
 Emphasize on drug adherence/compliance
 Emphasize on diet modification and importance
 Educate the client monitoring for drug side effects

Complications of Cushing syndrome

 Corticosteroid induced osteoporosis and pathologic fractures
 Avascular necrosis, necessitating total joint replacement
 Panhypopituitarism/pituitary dysfunction (from radiation or chemotherapy)
 Hyperpituitarism from transsphenoid resection
 Dyslipidemia
 Peptic ulcer disease
 Impaired glucose tolerance
 Diabetes mellitus
 Slow-wound healing
 Suppressed inflammatory response
 Hypertension
 Ischemic heart disease
 Frequent infections
SIMPLE GOITRE
It is a condition characterized by enlargement of the thyroid gland without any dysfunction
of the gland.

Causes
 physiological : –puberty
-pregnancy
 Iodine deficiency

Signs and symptoms

 Uniform smooth enlargement of the thyroid gland
 Swelling on either side of the trachea or neck
 It moves up and down during swallowing
 Respiratory difficulty if goiter is very large

Management
 Iodine supplements
 In pregnancy/puberty thyroid supplements are given
 Thyroidectomy

MALINGNANT GOITRE
It is a condition characterized by enlargement of the thyroid gland due to carcinoma.
Causes/predisposing factors
 Age-elderly
 Sex male have reduced chance than female
 Radioiodine therapy in the past
 Toxic goiter

Signs and symptoms

 Irregular enlargement of the thyroid
 Swelling on the either side of the trachea in the neck
 Swelling moves up and down when swallowing
 Fixed swelling cannot move easily
 It is hard to move and feel
 Respiratory difficulty
 Cervical lymph nodes may be enlarged, they are hard and fixed
 Features of thyrotoxicosis include-irritability, restlessness, excessive appetite, loss of
weight with eye protrusion, tremors of finger and tongue, excessive vomiting, palms
are warm and moist, nausea with diarrhea.
 Investigations
 Thyroid scan-nodules seen
 Fine needle aspiration-malignant cells visible
 Cervical lymph nodes biopsy-cancer tissues visible

Management
 Radioiodine therapy
 Thyroidectomy

THYROTOXICOSIS
Severe hyperthyroidism, usually of abrupt onset. Also known as thyroid storm, grave’s
disease. Arises as the body tissue gets exposed to low levels of T3 and T4. The main effect will
be in the increased basal metabolic rate.

Causes
 Graves’s disease
 Toxic nodular goitre
 Bengin adenomas

Signs and symptoms

 High fever
 Extreme tachycardia
 Weight loss
 Diarrhea
 Abdominal pain
 Edema
 Chest pain
 Dyspnea
 Palpitation
 Altered mental state
 Delirium
 Psychosi

Precipitating factors
 Stress
 Infection
 Thyroid and non-thyroid surgery
 Tooth extraction
 Insulin reaction
 Diabetes mellitus acidosis
 Pregnancy
 Antithyroid drugs withdrawal
 Emotional stress

Diagnosis
 History
 Physical examination
 Serum T4 levels are elevated

Management
 Temperature reducing
 Administer oxygen after checking the blood gas levels and doing oximetry
 Infuse normal saline and alternate with glucose
 Give antithyroid drugs like carbimazole
 In case of shock, give hydrocortisone
 In cardiac symptoms, give propanolol and digitalis
 Administer iodine to reduce output of T4 from thyroid glands
HYPOPARATHYROIDISM (TETANY)

Hypoparathyroidism is inadequate secretion of parathyroid hormone after:-

 interruption of the blood supply to parathyroid gland
 surgical removal of parathyroid gland tissue during thyroidectomy,
 Parathyroidectomy or radical neck dissection.
 Atrophy of the parathyroid glands of unknown cause is a less common

Incidence
 Idiopathic and reversible forms most common in children
 Acquired form most common in older patients who have undergone thyroid gland
surgery

Pathophysiology
Causes
 Low secretion of parathyroid hormone by parathyroid gland
 Accidental removal of the parathyroid gland during thyroidectomy
 Vitamin D deficiency
 Acute pancreatitis
 Alkalosis-lowers calcium levels
 Autoimmune genetic disorder
 Congenital absence or malformation of parathyroid glands
 Haemochromatosis
 Neoplasms
 Massive thyroid irradiation
 Suppression of normal gland function due to hypercalcemia
 Tuberculosis
 Amyloidosis
 Delayed maturation of parathyroid glands
 Sarcoidosis
 Hypomagnesemia-induced impairment of hormone secretion
 Trauma

Symptoms of hypoparathyroidism are caused by a deficiency of parathormone that results in

elevated blood phosphate (hyperphosphatemia) and decreased blood calcium (hypocalcaemia)
levels.

In the absence of parathormone, there is decreased intestinal absorption of dietary calcium

and decreased reabsorption of calcium from bone and through the renal tubules.
Decreased renal excretion of phosphate causes hypophosphaturia, and low serum calcium
levels result in hypocalciuria.

Clinical Manifestations

 Irritability of the neuromuscular system

 Tetany (general muscle hypertonia, with tremor and spasmodic or uncoordinated
contractions occurring with or without efforts to make voluntary movements).

Symptoms of latent tetany are

 Numbness
 tingling, and cramps in the extremities
 Stiffness in the hands and feet.
 Constipation or diarrhoea

In overt tetany, the signs include

 bronchospasm,
 laryngeal spasm,
 carpopedal spasm (flexion of the elbows and wrists and extension of the carpophalangeal
joints),
 dysphagia,
 photophobia,
 cardiac dysrhythmias,
 Seizures (muscle tension and spasms)
 Difficulty in walking and tendency to fall.

Other symptoms include:-

 Anxiety
 Irritability
 Depression and delirium.
 ECG changes and hypotension

Assessment and Diagnostic Findings

A positive Trousseau’s sign or a positive Chvostek’s sign suggests latent tetany.

Trousseau’s sign is positive when carpopedal spasm is induced by occluding the blood flow to
the arm for 3 minutes with a blood pressure cuff.

Chvostek’s sign is positive when a sharp tapping over the facial nerve just in front of the
parotid gland and anterior to the ear causes spasm or twitching of the mouth, nose, and eye
Laboratory studies
 Tetany develops at serum calcium levels of 5 to 6 mg/dL (1.2 to 1.5 mmol/L) or lower.
 Serum phosphate levels are increased, and x-rays of bone show increased density.
 X-rays of the subcutaneous or paraspinal basal ganglia of the brain calcification is
detected.

Medical Management

 The goal of therapy is to:-

 raise the serum calcium level to 9 to10 mg/dL (2.2 to 2.5 mmol/L)
 to eliminate the symptoms of hypoparathyroidism and hypocalcemia

 Administer calcium gluconate intravenously. If does not decrease neuromuscular

irritability and seizure activity immediately, administer sedative like phenobarbital
 Parenteral parathormone can be administered to treat acute hypoparathyroidism with
tetany.
 Monitor closely for allergic reactions and changes in serum calcium levels.
 Hypocalcemia and tetany requires an environment that is free of noise, drafts, bright
lights, or sudden movement.
 Tracheostomy or mechanical ventilation may become necessary
 Bronchodilating medications, if the patient develops respiratory distress.
 A diet high in calcium and low in phosphorus is prescribed. Although milk, milk
products, and egg yolk are high in calcium, they are restricted because they also contain
high levels of phosphorus.
 Oral tablets of calcium salts, such as calcium gluconate, may be used to supplement the
diet.
 Aluminum hydroxide gel or aluminum carbonate (Gelusil) administered after meals to
bind phosphate and promote its excretion through the gastrointestinal tract.
 Variable dosages of a vitamin D preparation are required to enhance calcium absorption
from the gastrointestinal tract.

Nursing Management

Nursing management of the patient with possible acute hypoparathyroidism includes the
following:

o Care of postoperative patients having thyroidectomy, parathyroidectomy, and radical

neck dissection is directed toward detecting early signs of hypocalcaemia and
anticipating signs of tetany, seizures, and respiratory difficulties.
o Calcium gluconate is kept at the bedside, with equipment necessary for intravenous
administration. If the patient has a cardiac disorder, is subject to dysrhythmias, or is
receiving digitalis, calcium gluconate is administered slowly and cautiously.
o Maintain a patent IV line for medications
o Cardiac patient requires continuous cardiac monitoring and careful assessment.
o Teach the patient about medications and diet therapy.
o Teach patient reason for high calcium and low phosphate intake and the symptoms of
hypocalcemia and hypercalcemia
o Monitor the vital signs 4 hourly
o Administer the prescribed medications
o Monitor intake and output record
o Institute safety precautions
o Maintain seizure precautions
o Provide meticulous skin care
o Encourage patient to express his feelings
o Monitor electrocardiogram for QT interval changes and arrhythmias
o Monitor for signs and symptoms of decreased cardiac output
o Monitor Chvostek’s sign
o Monitor Trousseau’s sign
o Offer emotional support
o Instruct the patient about the need for lifelong treatment and follow-up care including
monitoring of calcium levels
o Help the patient develop effective coping strategies

Patient’s teaching
Teach patient on:
 The disorder, diagnosis and treatment
 Prescribed medication and side effects
 When to notify the physician
 Follow-up care
 Complications
 Period checks of serum calcium levels

Discharge planning:
 Refer the patient to an alcoholism treatment program for additional counseling, if
necessary.