Rle Requirement

RLE REQUIREMENT
Ms. Tasha Baliquig, RN
Rabago III, Roberto

Recimilla, Julia Andrea
Rizabal, Wenard Gabrille C.
Rojas, Christian Emmanuel
Ruiz, Luiza Paula
Sadangsal, Jewel
Samson, Ryan haze
Seraga, Mayldrid Angel
Sumud-ong, Eunice Mae
Tecbobolan, Quennie
Torrenueva, Kyrstine Kjell
Villorente, Erika Jane
Virgines, April Nicole
Yap, Randrylle
Zuno, Christian John
October 24, 2022

GENERAL OBJECTIVES
After 4 days of clinical exposure in the special area, specifically in the Intensive
Critical Care Unit (ICCU) and Neonatal Intensive Care Unit (NICU), in Southwestern
Medical Center being aided with the concept of “Care of patients in Labor and
Delivery; Intra and Post-operative Nursing Care”, we will be able to gain more
knowledge, develop our skills, professional attitudes, as well as our knowledge
towards the care of our patients.
SPECIFIC OBJECTIVES
1. To be able to apply our learnings and skills from our previous rotations.
2. To be able to gain knowledge in handling patients from being a student nurse
to a professional nurse.
3. To share my knowledge and skills relating to real life nursing practices.
4. To be confident in handling and delivering care to the patients.
5. To be prepared in dealing with our patients.
6. To add experiences for real life health situations and problems.
7. To be oriented to physical setup, rules, policies, and staffs in the hospital.
8. To display respect during all interaction with the patient and towards other
healthcare provider.
9. To be able to increase level of awareness and understanding towards the
condition of the patient.
10. To be able to establish rapport and provide health education to the
patient.
Cerebrovascular Disease
The word cerebrovascular is made up of two parts – "cerebro" which refers to

the large part of the brain, and "vascular" which means arteries and veins.
Together, the word cerebrovascular refers to blood flow in the brain. The term
cerebrovascular disease includes all disorders in which an area of the brain is
temporarily or permanently affected by ischemia or bleeding and one or more of
the cerebral blood vessels are involved in the pathological process. Cerebrovascular
disease includes stroke, carotid stenosis, vertebral stenosis and intracranial
stenosis, aneurysms, and vascular malformations.
Restrictions in blood flow may occur from vessel narrowing (stenosis), clot
formation (thrombosis), blockage (embolism) or blood vessel rupture
(hemorrhage). Lack of sufficient blood flow (ischemia) affects brain tissue and may
cause a stroke.
Blood Flow to the Brain
The heart pumps blood up to the brain through two sets of arteries, the
carotid arteries and the vertebral arteries. The carotid arteries are located in the
front of the neck and are what you feel when you take your pulse just under your
jaw. The carotid arteries split into the external and internal arteries near the top of
the neck with the external carotid arteries supplying blood to the face and the
internal carotid arteries going into the skull. Inside the skull, the internal carotid
arteries branch into two large arteries – the anterior cerebral and middle cerebral
arteries and several smaller arteries – the ophthalmic, posterior communicating and
anterior choroidal arteries. These arteries supply blood to the front two-thirds of the
brain.
The vertebral arteries extend alongside the spinal column and cannot be felt
from the outside. The vertebral arteries join to form a single basilar artery near the
brain stem, which is located near the base of the skull. The vertebrobasilar system
sends many small branches into the brain stem and branches off to form the
posterior cerebellar and posterior meningeal arteries, which supply the back third of
the brain. The jugular and other veins carry blood out of the brain.
Because the brain relies on only two sets of major arteries for its blood supply, it is
very important that these arteries are healthy. Often, the underlying cause of an
ischemic stroke is carotid arteries blocked with a fatty build-up, called plaque.
During a hemorrhagic stroke, an artery in or on the surface of the brain has
ruptured or leaks, causing bleeding and damage in or around the brain.
Whatever the underlying condition and cause are, it is crucial that proper blood flow
and oxygen be restored to the brain as soon as possible. Without oxygen and
important nutrients, the affected brain cells are either damaged or die within a few
minutes. Once brain cells die, they cannot regenerate, and devastating damage
may occur, sometimes resulting in physical, cognitive and mental disabilities.
Stroke
Stroke is an abrupt interruption of constant blood flow to the brain that

causes loss of neurological function. The interruption of blood flow can be caused by
a blockage, leading to the more common ischemic stroke, or by bleeding in the
brain, leading to the more deadly hemorrhagic stroke. Ischemic stroke constitutes
an estimated 80 percent of all stroke cases. Stroke may occur suddenly, sometimes
with little or no warning, and the results can be devastating.
Stroke Symptoms
Warning signs may include some or all of the following symptoms, which are
usually sudden:
 Dizziness, nausea, or vomiting

 Unusually severe headache
 Confusion, disorientation or memory loss
 Numbness, weakness in an arm, leg or the face, especially on one side
 Abnormal or slurred speech
 Difficulty with comprehension
 Loss of vision or difficulty seeing
 Loss of balance, coordination or the ability to walk
Types of Stroke and Treatment
Ischemic Stroke
Ischemic stroke is by far the most common type of stroke, accounting for a
large majority of strokes. There are two types of ischemic stroke: thrombotic and
embolic. A thrombotic stroke occurs when a blood clot, called a thrombus, blocks an
artery to the brain and stops blood flow. An embolic stroke occurs when a piece of
plaque or thrombus travels from its original site and blocks an artery downstream.
The material that has moved is called an embolus. How much of the brain is
damaged or affected depends on exactly how far downstream in the artery the
blockage occurs.
In most cases, the carotid or vertebral arteries do not become completely

blocked and a small stream of blood trickles to the brain. The reduced blood flow to
the brain starves the cells of nutrients and quickly leads to a malfunctioning of the
cells. As a part of the brain stops functioning, symptoms of a stroke occur. During a
stroke, there is a core area where blood is almost completely cut off and the cells
die within five minutes. However, there is a much larger area known as the
ischemic penumbra that surrounds the core of dead cells. The ischemic penumbra
consists of cells that are impaired and cannot function, but are still alive. These
cells are called idling cells, and they can survive in this state for about three hours.
Ischemic stroke is treated by removing the obstruction and restoring blood

flow to the brain. One treatment for ischemic stroke is the FDA-approved drug,
tissue plasminogen activator (tPA), which must be administered within a three-hour
window from the onset of symptoms to work best. Unfortunately, only 3 to 5
percent of those who suffer a stroke reach the hospital in time to be considered for
this treatment. This medication carries a risk for increased intracranial hemorrhage
and is not used for hemorrhagic stroke. For patients beyond the three-hour time
window, intrarterial thrombolysis with drugs or mechanical devices may be an
option. Carotid endarterctomy, and or stenting of the cervical and intracranial
vessels, may help reduce recurrent stroke in some cases.
The Merci Retriever, approved recently by the FDA, is a corkscrew-shaped

device used to help remove blood clots from the arteries of stroke patients. A small
incision is made in the patient’s groin, into which a small catheter is fed until it
reaches the arteries in the neck. At the neck, a small catheter inside the larger
catheter is guided through the arteries until it reaches the brain clot. The Merci
Retriever, a straight wire inside the small catheter pokes out beyond the clot and
automatically coils into a corkscrew shape. It is pulled back into the clot, the
corkscrew spinning and grabbing the clot. A balloon inflates in the neck artery,
cutting off blood flow, so the device can pull the clot out of the brain safely. The clot
is removed through the catheter with a syringe.
Hemorrhagic Stroke
A hemorrhagic stroke can be caused by hypertension, rupture of an

aneurysm or vascular malformation or as a complication of anticoagulation
medications. An intracerebral hemorrhage occurs when there is bleeding directly
into the brain tissue, which often forms a clot within the brain. A subarachnoid
hemorrhage occurs when the bleeding fills the cerebrospinal fluid spaces around the
brain. Both conditions are very serious.
Hemorrhagic stroke usually requires surgery to relieve intracranial (within

the skull) pressure caused by bleeding. Surgical treatment for hemorrhagic stroke
caused by an aneurysm or defective blood vessel can prevent additional strokes.
Surgery may be performed to seal off the defective blood vessel and redirect blood
flow to other vessels that supply blood to the same region of the brain.
Endovascular treatment involves inserting a long, thin, flexible tube

(catheter) into a major artery, usually in the thigh, guiding it to the aneurysm or
the defective blood vessel and inserting tiny platinum coils (called stents) into the
blood vessel through the catheter. Stents support the blood vessel to prevent
further damage and additional strokes.
Recovery and rehabilitation are important aspects of stroke treatment. In

some cases, undamaged areas of the brain may be able to perform functions that
were lost when the stroke occurred. Rehabilitation includes physical therapy,
speech therapy and occupational therapy.
Regardless of what type of stroke has been suffered, it is critical that victims
receive emergency medical treatment as soon as possible for the best possible
outcome to be realized. By learning the signs and symptoms of stroke and treating
risk factors preventively, it is possible to help avert the devastating results of this
disease.
Transient Ischemic Attack (TIA)
A TIA is a temporary cerebrovascular event that leaves no permanent

damage. Most likely an artery to the brain is temporarily blocked, causing stroke-
like symptoms, but the blockage dislodges before any permanent damage occurs.
Symptoms of a TIA may be similar to stroke, but they resolve quickly. In

fact, symptoms may be so vague and fleeting that people just "brush" them off,
especially when they last just a few minutes. The main symptoms of a stroke or TIA
can be remembered with the word FAST, which stands for:
 Face – the face may have drooped on one side, the person may be unable to
smile, or their mouth or eye may have dropped.
 Arms – the person may not be able to lift both arms and keep them there
because of arm weakness or numbness in one arm.
 Speech – their speech may be slurred or garbled, they may not be able to
talk at all or they may not be able to understand what you are saying to
them.
 Time – it's time to seek immediate care
While there is no treatment for the TIA itself, it is essential that the source of
the TIA be identified and appropriately treated before another attack occurs. If you
experience TIA symptoms, seek emergency medical help and notify your primary
care physician immediately. About 30 percent of all people who suffer a major
stroke experience a prior TIA, and 10 percent of all TIA victims suffer a stroke
within two weeks. The quicker you seek medical attention, the sooner a diagnosis
can be made and a course of treatment started. Early intervention is essential to
effectively preventing a major stroke. Treatment options for TIA patients focus on
treating carotid artery disease or cardiac problems.
Risk Factors
Although they are more common in older adults, strokes can occur at any age.
Stroke prevention can help reduce disability and death caused by the disease.
Controllable or treatable risk factors for stroke include:
 Smoking: Decrease risk by quitting smoking. Risk may be increased further

with the use some forms of oral contraceptives and are a smoker. There is
recent evidence that long-term secondhand smoke exposure may increase
the risk of stroke.
 High blood pressure: Blood pressure of 140/90 mm Hg or higher is the
most important risk factor for stroke. Controlling blood pressure is crucial to
stroke prevention.
 Carotid or other artery disease: The carotid arteries in the neck supply
blood to the brain. A carotid artery narrowed by fatty deposits from
atherosclerosis (plaque buildups in artery walls) may become blocked by a
blood clot.
 History of transient ischemic attacks (TIAs).
 Diabetes: It is crucial to control blood sugar levels, blood pressure and
cholesterol levels. Diabetes, especially when untreated, puts one at greater
risk of stroke and has many other serious health implications.
 High blood cholesterol: A high level of total cholesterol in the blood (240
mg/dL or higher) is a major risk factor for heart disease, which raises the risk
of stroke.
 Physical inactivity and obesity: Being inactive, obese or both can increase
the risk of high blood pressure, high blood cholesterol, diabetes, heart
disease and stroke.
Uncontrollable risk factors include:
 Age: People of all ages, including children, have strokes. But the older you
are, the greater your risk of stroke.
 Gender: Stroke is more common in men than in women.
 Heredity and race: There is a greater risk of stroke if a parent,
grandparent, sister or brother has had a stroke. Blacks have a much higher
risk of death from a stroke than Caucasians do, partly because they are more
prone to having high blood pressure, diabetes and obesity.
 Prior stroke or heart attack: Those who have had a stroke are at much
higher risk of having another one. Those who have had a heart attack are
also at higher risk of having a stroke.
GORDON’S 11 FUNCTIONAL HEALTH PATTERN
1. Health Perception and Health Management Pattern

- The patient is fully immunize. Patient is aware of his high blood and have a
maintenance.
2. Nutrition and Metabolism

- Patient is on Peptamen diet given by his doctor.
3. Elimination Pattern
- Pattern will urinate and defecate through diaper. Urine color is yellow and
stool is brown.
4. Activity and Exercise
- Patient is on bed rest. He was also scheduled for Physical Therapy to
correct his stroke on the right side of his body.
5. Cognition and Perception

- Patient can still understand and cooperate with the nurses. He knows that
he is admitted in the hospital. In terms to time and date he needs to be
reminded.
6. Sleep and Rest

- Sleeping pattern is good. He can sleep properly if his secretion was
suctioned well. Also, he can rest anytime if he feels tired.
7. Self-Perception and Self Concept

- NA
8. Roles and Relationship

- He is an outgoing person and easily to approached. Also, he is a provider.
9. Sexuality and Reproduction pattern

- NA
10. Coping and Stress Tolerance

- Patient tends to eat a lot to cope up with stress or travel somewhere else.
11. Values and Belief Pattern

- Patient is a Roman Catholic and does believe in God. Attend to church
every Sunday.
Course in the ward:
Upon admission patient was received intubated from other institution, GCS 7
(E1VTM6), follows commands he was immediately attached to MV. Additional
laboratories were requested. Patient was stabilized and then transferred to ICU. On
the first hospital day, was noted to have bloody secretions from ETT thus
Rivaroxaban was temporarily stopped but was resumed after 24 hours. On 3 rd HD,
patient was noted to have sudden onset of desaturation as low as 40%, mucus plug
was considered due to no breath sound bilaterally upon auscultation of the lungs,
patient was immediately reintubated and referred to a Pulmonologist and was
advised for early tracheostomy, Piperacillin + Tazobactam was shifted to
Meropenem due to pneumonia. On the 4 th HD, patient was noted to have bloated
abdomen ultrasound was unremarkable, x-ray of the abdomen showed non-specific
and non-obstructive bowel gas pattern. On the 5 th hospital day, patient had
tracheostomy. On the 6th HD, still noted to have bloated abdomen now associated
with loose to watery bowel movement was then referred to Gastroenterologist. On
8th HD, patient was weaned from MV now at T-piece noted no desaturation, no
tachypnea, no tachycardia. On 9th HD, noted watery stools, mucoid, stool exam was
done but was unrevealing was then started with Metronidazole, CT-scan of the
abdomen with contrast was done which showed distention at the rectum filled with
fluid and mild diffuse long segment wall thickening that may represent as
nonspecific inflammatory process flexible sigmoidoscopy was planned once patient
is more stable. On 11th HD, was referred for rehabilitation therapy. On 17 th HD,
patient was noted to have occ wheezing and tight airway was Salbutamol
nebulization and started with Salmeterol + Fluticasone inhaler. Meropenem was
completed for 14 days, other medication were continued.
V. ANATOMY AND PHYSIOLOGY
(Show and label the affected organ/system and provide a brief discussion of its
function/uses)
THE BRAIN
Image Reference:
 Sukel;, K. (2019, August 25). Anatomy of The Brain. Dana Foundation.
https://www.dana.org/wp-content/uploads/2019/08/anatomy-function-brain-
areas-basics-aug-2019-2024.jpg
1. Cerebral Cortex – responsible for speech, memory, logical and emotional

responses, consciousness, the interpretation of sensation, and voluntary
movement. This is divided into the left and right hemispheres.
2. The Lobes - The cerebral hemispheres are further divided into four major
lobes: the occipital, located near the back of the brain; the parietal, located
just above the ear; the temporal, located just behind the forehead temples;
and the frontal, located just above the eyes at the very front of the cortex.
o Occipital lobe – responsible for processing and interpreting visual
information. It’s the seat of the primary visual cortex.
o Temporal lobe – t he major processing center of sound (including
language) and some forms of memory.
o Parietal lobe – the home of the somatosensory cortex, the area of the
brain responsible for processing sensation and touch information, as
well as some aspects of spatial processing.
o Frontal lobe - the largest brain lobe, is responsible for executive
function, with a hand in reasoning, decision-making, sensory
integration, planning, and execution of movement.
3. Brain stem – about the size of a thumb in diameter and approximately 3
inches long. Its structures include the mid brain, pons, and medulla
oblongata
o Mid brain –
o Pons – means “bridge”. Contains important nuclei involved in the
control of breathing
o Medulla Oblongata – contains many nuclei that regulate vital visceral
activities. It also contains centers that control heart rate, blood
pressure, breathing, swallowing, and vomiting.
Reference:
 Marieb, E., & Keller, S. (2017, January 5). Essentials of Human Anatomy &
Physiology (12th ed.). Pearson.
 Penttila, N. (2022, August 11). Neuroanatomy: The. . . Dana Foundation.
Retrieved October 22, 2022, from
https://www.dana.org/article/neuroanatomy-the-basics/
THE HEART
Reference:
 Michigan Medicine. (2019, February 27). Anatomy of The Heart. Michigan
Health.
https://healthblog.uofmhealth.org/sites/consumer/files/2020-01/heart_beati
ng_0.gif
1. Heart walls - Your heart walls are the muscles that contract (squeeze) and
relax to send blood throughout your body. A layer of muscular tissue called
the septum divides your heart walls into the left and right sides.
o Endocardium: Inner layer.
o Myocardium: Muscular middle layer.
o Epicardium: Protective outer layer.
2. Heart chambers - Your heart is divided into four chambers. You have two
chambers on the top (atrium, plural atria) and two on the bottom (ventricles),
one on each side of the heart.
o Right atrium: Two large veins deliver oxygen-poor blood to your right
atrium. The superior vena cava carries blood from your upper body.
The inferior vena cava brings blood from the lower body. Then the
right atrium pumps the blood to your right ventricle.
o Right ventricle: The lower right chamber pumps the oxygen-poor blood
to your lungs through the pulmonary artery. The lungs reload blood
with oxygen.
o Left atrium: After the lungs fill blood with oxygen, the pulmonary veins
carry the blood to the left atrium. This upper chamber pumps the
blood to your left ventricle.
o Left ventricle: The left ventricle is slightly larger than the right. It
pumps oxygen-rich blood to the rest of your body.
3. Heart valves - Your heart valves are like doors between your heart chambers.
They open and close to allow blood to flow through.
o The atrioventricular (AV) valves open between your upper and lower
heart chambers. They include:
 Tricuspid valve: Door between your right atrium and right
ventricle.
 Mitral valve: Door between your left atrium and left ventricle.
o Semilunar (SL) valves open when blood flows out of your ventricles.
They include:
 Aortic valve: Opens when blood flows out of your left ventricle to
your aorta (artery that carries oxygen-rich blood to your body).
 Pulmonary valve: Opens when blood flows from your right
ventricle to your pulmonary arteries (the only arteries that carry
oxygen-poor blood to your lungs).
4. Blood vessels
o Arteries - carry oxygen-rich blood from your heart to your body’s
tissues. The exception is your pulmonary arteries, which go to your
lungs.
o Veins - carry oxygen-poor blood back to your heart.
o Capillaries - are small blood vessels where your body exchanges
oxygen-rich and oxygen-poor blood.
5. Coronary arteries
o Left coronary artery - Divides into two branches (the circumflex artery
and the left anterior descending artery).
o Circumflex artery - Supplies blood to the left atrium and the side and
back of the left ventricle.
o Left anterior descending artery (LAD) - Supplies blood to the front and
bottom of the left ventricle and the front of the septum.
o Right coronary artery (RCA): Supplies blood to the right atrium, right
ventricle, bottom portion of the left ventricle and back of the septum.
6. Electrical conduction system
 Sinoatrial (SA) node: Sends the signals that make your heart
beat.
 Atrioventricular (AV) node: Carries electrical signals from your
heart’s upper chambers to its lower ones.
o Your heart also has a network of electrical bundles and fibers. This
network includes:
 Left bundle branch: Sends electric impulses to your left ventricle.
 Right bundle branch: Sends electric impulses to your right
ventricle.
 Bundle of His: Sends impulses from your AV node to the Purkinje
fibers.
 Purkinje fibers: Make your heart ventricles contract and pump out
blood.
Reference:
 Marieb, E., & Keller, S. (2017, January 5). Essentials of Human Anatomy &
Physiology (12th ed.). Pearson.
THE SMALL AND LARGE INTESTINES
Reference:
 Belleza, M. (2021, February 11). Anatomy of the Small and Large Intestines.
Nurselabs. https://nurseslabs.com/wp-content/uploads/2017/04/Small-and-
Large-Intestine-Digestive-System-Anatomy-and-Physiology.png.webp
Small Intestine
1. Duodenum - the first part of the small intestine that the stomach feeds into.
It’s a short, descending chute (about 10 inches long) that curves around the
pancreas in a “C” shape before connecting to the rest of the coiled intestines.
2. Jejunum - the remaining small intestine lays in many coils inside the lower
abdominal cavity. Its middle section, called the jejunum, makes up a little less
than half of this remaining length. The jejunum is characterized by many
blood vessels, which give it a deep red color.
3. Ileum - the ileum is the last and longest section of the small intestine. Here
the walls of the small intestine begin to thin and narrow, and blood supply is
reduced. Food spends the most time in the ileum, where the most water and
nutrients are absorbed.
Large Intestine
1. Cecum - the saclike cecum is the first part of the large intestine.
2. Appendix - hanging from the cecum is the wormlike appendix, a potential

trouble spot because it is an ideal location for bacteria to accumulate and
multiply.
3. Ascending colon - the ascending colon travels up the right side of the
abdominal cavity and makes a turn, the right colic (or hepatic) flexure, to
travel across the abdominal cavity.
4. Transverse colon - the ascending colon makes a turn and continuous to be

the transverse colon as it travels across the abdominal cavity.
5. Descending colon - it then turns again at the left colic (or splenic) flexure,
and continues down the left side as the descending colon.
6. Sigmoid colon - the intestine then enters the pelvis, where it becomes the S-
shaped sigmoid colon.
7. Anal canal - the anal canal ends at the anus which opens to the exterior.
Reference:
 Belleza, R. M. N. (2021, February 11). Digestive System Anatomy and
Physiology. Nurseslabs. Retrieved October 22, 2022, from
https://nurseslabs.com/digestive-system/?
fbclid=IwAR1T3FHRW0SQcXQG6M8mmT4LFrOIiybGKDozVDV_dzXPyCphPKyz
AT0Vh0w
VI. PATHOPHYSIOLOGY
(Trace the disease process of the patient’s diagnosed condition. Provide a brief
discussion after the tracing)
Reference:
 Yu, Y. (2015, October 28). Ischemic Stroke Pathophysiology. Calgary Guide.
https://calgaryguide.ucalgary.ca/wp-content/uploads/2015/10/Stroke-
Pathogenesis.png
A stroke occurs when blood flow to a specific area of the brain is disrupted,
resulting in permanent neurological damage. Ischemic stroke (lack of blood and
thus oxygen to an area of the brain) and hemorrhagic stroke (bleeding from a burst
or leaking blood vessel in the brain) are the two major types of strokes. In our
example, pt. We witnessed an ischemic stroke. The brain tissue requires continuous
perfusion; 20% of our cardiac output is directed toward the brain. It is critical that
the brain receives an adequate blood supply for both nutrient delivery and toxin
removal. Brain tissue can become dysfunctional if blood flow to the brain is
reduced. This CVD is most likely secondary to a cardio-embolic stroke, according to
the patient's diagnosis. Also, the pt. experienced a subacute (1-3 weeks) infarct on
both their thalamus and left midbrain. Your body's information relay station is the
thalamus. All information from the body's senses (except smell) and motor
functions must pass through the thalamus before being sent to the cerebral cortex
of your brain for interpretation. Damage to the thalamus caused difficulties with
attention, loss of alertness, difficulty processing sensory information, and impaired
movement in the patient. The infarct also affected the left midbrain, affecting its
functions. The left midbrain functions include right-side movement of the body and
head. As can be seen, suffers from hemiplegia. Damage to the midbrain can also
cause a wide range of movement disorders, vision and hearing problems, and
memory problems.
High blood pressure forces your heart to pump harder and harder. When your heart
is pushed to the limit for too long, the muscle doesn't get stronger, it gets thicker
and stiffer. Electrical signals can't move as easily through a less flexible, enlarged
heart muscle, and that could lead to A Fibrillation. For people with high blood
pressure, the force of blood pushing against the arteries as the heart pumps blood
is too high. That causes gradual damage to the arteries, including those to the
brain. A weakened blood vessel may rupture in or near the brain, or diseased
arteries may become blocked by a clot or plaque buildup. In atrial fibrillation, the
chaotic heart rhythm can cause blood to collect in the heart's upper chambers
(atria) and form clots. If a blood clot in the left upper chamber (left atrium) breaks
free from the heart area, it can travel to the brain and cause a stroke. Right bundle
branch block can be complete or incomplete. The patient has a complete right
bundle branch block in which it is a problem with your right bundle branch that
keeps your heart’s electrical signal from moving at the same time as the left bundle
branch. Instead of moving together on the left and right sides, the signal on the
right side is running behind. This creates an irregular heartbeat (atrial fibrillation).
The patient has a moderate ventricular response. But in some cases of A-fib involve
atrial fibrillation with rapid ventricular response (RVR). This is when the rapid
contractions of the atria make the ventricles beat too quickly. If the ventricles beat
too fast, they can't receive enough blood. So, they can't meet the body's need for
oxygenated blood.
Over time, excessive blood glucose can result in increased fatty deposits or clots in
blood vessels. These clots can narrow or block blood vessels in the brain or neck,
cutting off the blood supply, stopping oxygen from getting to the brain and causing
a stroke. Blood glucose is an important measure to assess for
hyperglycemia/hypoglycemia and must be collected on all suspected patients with
stroke symptoms. Transient hypoglycemia (blood glucose <60 mg/dL) may
manifest as a stroke mimic with acute mental status changes, seizure, loss of
consciousness, hemiplegia, and aphasia. The majority of acute stroke patients have
disorders of glucose metabolism, and in most cases this fact has been
unrecognized. High blood glucose levels are often present in patients with acute
stroke. Interestingly, almost half of these patients have no history of DM. These
high levels of blood glucose are either transient or persistent, reflecting previously
undiagnosed prediabetes or even DM. On the other hand, serious stress, like
stroke, can be a trigger for acute stress reaction that stimulates the hypothalamus–
pituitary–adrenal axis, which consequently leads to a significant release of
catecholamines, glucagon, and cortisol. This can lead to states of insulin resistance,
gluconeogenesis, and glycogenolysis presented by hyperglycemia.
Systemic inflammation seen in inflammatory bowel disease (IBD) may cause
electrophysiological changes in the atria leading to atrial fibrillation (AF). One of the
clinical manifestations on the patient that we had observed during our shift was the
patient seldom had a bowel movement or stool. The presence of continuous
chronic systemic inflammation in IBD patients is linked to numerous
pathophysiological processes within the cardiomyocytes leading to
electrophysiological and structural remodeling for the atria, promoting the
development and maintenance of atrial fibrillation (AF), according to an article
written by Asim Kichloo, MD, et. Al.
Reference:
 https:\/\/calgaryguide.ucalgary.ca\/author\/yanyu\/#author. (2017,
November 15). Ischemic Stroke: Pathogenesis | Calgary Guide. The Calgary
Guide to Understanding Disease. Retrieved October 22, 2022, from
https://calgaryguide.ucalgary.ca/ischemic-stroke-pathogenesis/?
fbclid=IwAR2ZVoGYfvftqLnTU-
 hMBZ5eYvUzs9jOe2sPKN0x9j7nyeDSASu2VTv5BM
Reference:
 Yu, Y. (2019, May 5). Inflammatory Bowel Disease Pathophysiology. Calgary
Guide.
https://calgaryguide.ucalgary.ca/wp-content/uploads/2017/11/Ischemic-
Stroke-Pathogenesis.png
The intestinal immune system is key to the pathogenesis of inflammatory bowel

disease (IBD). The intestinal epithelium prevents bacteria or antigen entry into the
circulation by sealed intercellular junctions. In IBD, these junctions are defective
from either a primary barrier function failure or as a result of severe inflammation.
Additional protective mechanisms include mucus production by goblet cells and
Paneth cells secretion of a-defensins with intrinsic antimicrobial activity. Excessive
inflammatory reactions lead to continued deterioration of the epithelium and further
exposure to intestinal microbes thereby furthering worsening the inflammation.
In ulcerative colitis, there is always mucosal inflammation that leads to edema,

ulcers, bleeding, and electrolyte losses. The inflammation in ulcerative colitis
usually starts in the rectum and progresses in an uninterrupted fashion to the
proximal colon. In Crohn disease, there are skip lesions. In close to 20% of patients
with UC, the disease remains confined to the rectum. Pancolitis is seen in about
15% of patients. As the disorder becomes chronic, the colon becomes more rigid
and short with a loss of the haustral markings leading to a 'lead-pipe appearance on
a barium enema.
Reference:
 McDowell C, Farooq U, Haseeb M. Inflammatory Bowel Disease. [Updated
2022 Jun 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls
Publishing; 2022 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK470312/
URINALYSIS
URINALYSIS PATIENT’S RESULT

ITEM NAME REFEREN 09/13/20 SIGNIFICANCE 09/15/20 SIGNIFICANCE 10/10/20 SIGNIFICANCE 10/16/20 SIGNIFICANCE
CE RANGE 22 / 22 / 22 / 22 /
INTERPRETATI INTERPRETATI INTERPRETATI INTERPRETATI
ON ON ON ON
Macroscopic
examination The patient’s Presence of A presence of Rare bacteria in
Color: PALE LIGHT- results are within DARK albumin in the DARK WBC in the urine YELLOW the urine means
YELLOW YELLOW normal values. It YELLOW urine indicates an YELLOW is an indication of that there is an
Volume: --- --- means there is 20 mL abnormal renal 40mL an infection. 45mL infection of the
CLEAR CLEAR no indication of HAZY function or HAZY Nitrite in the CLEAR urinary tract of
Transparency: abnormal renal kidney disease. urine means that the patient.
Specific 1.005- 1.015 function. 1.020 Blood in the urine 1.005 there is a 1.010
Gravity: 1.030 can be an bacterial infection
μmol/l indication of an in the urinary
Chemical infection, renal tract of the
Examination illness such as patient which is
Albumin: <30 mg/g --- 1+ renal calculi, a TRACE also TRACE
blood ailment, or characterized by
pH: 5.0-8.0 6.0 6.0 7.5 7.0
caused by certain the hazy urine
Ketone: NONE NEGATIVE NEGATIVE medications. A NEGATIVE and the few NEGATIVE
Blood: 0-9 NEGATIVE 2+ hazy urine means 1+ bacteria seen in NEGATIVE
Glucose: NONE NEGATIVE NEGATIVE a sign of infection NEGATIVE the urine. NEGATIVE
Nitrite: NONE NEGATIVE NEGATIVE or is caused by POSITIVE NEGATIVE
bacteria, WBC, or
Bilirubin: NONE NEGATIVE 1+ NEGATIVE NEGATIVE
RBC.
0-17 3.4 TRACE NORMAL NORMAL
Urobilinogen: μmol/l
Microscopic
Examination
WBC: ≤4cells/ 0 2-4/HPF TNTC/HPF 0-1/HPF
HPF
RBC: <3cells/ 0 5-12/HPF 10-15/HPF 0-1/HPF
HPF
Epithelial 0-28/μL 0 RARE RARE RARE
cells:
Mucus ≤ 15 – 0 --- RARE RARE
Threads: 20/HPF
Bacteria: NONE --- FEW FEW RARE
CULTURE/SENSITIVITY TEST
DATE TYPE OF EXAM SPECIMEN PATIENT’S RESULT SIGNIFICANCE/INTERPRETATION

09/15/2022 CULTURE/SENSITIVITY TEST TRACHEAL ASPIRATE NO GROWTH AFTER 48 HOURS OF The urine culture is regarded as negative
INCUBATION and the culture is complete when there is no
or little growth on the agar after 48 hours of
incubation, suggesting there isn't an
infection present.
09/19/2022 CULTURE/SENSITIVITY TEST TRACHEAL ASPIRATE NO GROWTH AFTER 3 DAYS OF This means that the patient doesn’t have an
INCUBATION infection.
10/10/2022 CULTURE/SENSITIVITY TEST TRACHEAL ASPIRATE SENSITIVE Patient will have therapeutic effect on these
Cefotaxime medications Cefotaxime, Ceftazidine, and
Ceftazidine Netilmicin.
Netilmicin
INTERMEDIATE Patient needs a higher dose of Azithromycin

Azithromycin to get its therapeutic effect.
RESISTANT Resistant means that the bacteria can

Amoxiclab proliferate even using these medications. It
Aztreonam suggest that the patient is unlikely to gain
Cefoxitin therapeutic effect. So these are considered
Ceftriaxone an ineffective antibiotic.
Cefuroxime
Imipinem
Meropenem
Pip/Tazobactam
Trim/Sulfa
VERY LIGHT GROWTH OF GRAM (-)
ORGANISM
(PRELIMINARY RESULT)
IDENTIFICATION OF BACTERIA TO
FOLLOW)
10/10/2022 CULTURE/SENSITIVITY TEST TRACHEAL ASPIRATE INTERMEDIATE Patient needs a higher dose of Cefipime to
Cefipime get its therapeutic effect.
SENSITIVE Patient will gain a therapeutic effect on these

Chloramphenicol medications Chloramphenicol, Ciprofloxacin
Ciprofloxacin and Levofloxacin.
Levofloxacin
VERY LIGHT GROWTH OF

STENOTROPHOMONAS
MALTOPHILIA
10/10/2022 CULTURE/SENSITIVITY TEST TRACHEAL ASPIRATE SENSITIVE Patient will gain a therapeutic effect by using
Ceftazidime Ceftazidime and Netilmicin.
Netilmicin
RESISTANT Patient will not be able to use these

Amoxiclab antibiotics because bacteria can still grow
Azithromycin even when using these.
Aztreonam
Cefotaxime
cefoxitin
Ceftriaxone
Cefuroxime
Imipinem
Meropenem
Pip/Tazobactam
Trim/Sulfa
LIGHT GROWTH OF
STENOTROPHOMONAS
MALTOPHILIA
10/10/2022 CULTURE/SENSITIVITY TEST BLOOD (TWO SITES) NO GROWTH AFTER 7 DAYS OF There is no blood infection.
INCUBATION
10/10/2022 CULTURE/SENSITIVITY TEST URINE NO GROWTH AFTER 48 HOURS OF There is no infection in the urine.
INCUBATION
HEMATOLOGY
HEMATOLOGY PATIENT’S RESULT

TEST REFERENCE 09/13/20 SIGNIFICAN 09/15/202 SIGNIFICAN 09/17/202 SIGNIFICAN 09/18/202 SIGNIFICAN
RANGE 22 CE/ 2 CE/ 2 CE/ 2 CE/
INTERPRET INTERPRET INTERPRET INTERPRET
ATION ATION ATION ATION
WBC 4.40 – 11.0 --- The patient’s 9.81 High 9.97 Low rbc, 10.28 Since the
x10^3/mm ^3 results are monocyte hemoglobin, patient has
NEUTROPHILS 37 – 80 % 71 within normal 72.7 may mean 73.8 hematocrit 78.8 an IBD, there
LYMPHOCYTES 10.00 – 50.00 % 16 values. 10.8 that there is 7.7 L and platelet 6.6 L is low rbc,
MONOCYTES 0.00 – 12.00 % 9 13.9 H an infection. 14.2 H count 12.9 H hemoglobin,
EOSINOPHILS 0.00 – 7.00 % 3 2.2 High MCV 3.6 indicates 1.2 hematocrit
and MCH may anemia, and platelet
BASOPHILS 0.00 – 2.50 % 1 0.4 0.7 0.5
indicate a infection, or count and
RBC COUNT 4.50 – 5.90 x10 4.67 3.98 L 3.65 L 3.46 L
macrocytic internal also high in
^6/uL
anemia bleeding monocytes,
HEMOGLOBIN 14.00 – 17.40 14.9 15 13.8 L 13.2 L
causing low which MCV, MCH,
g/dL
RBC. A low suggest IBD. and MCHC.
HEMATOCRIT 41.50 – 50.40 % 42.5 42 38.3 L 36.1 L
RBC count is High MCV
PLATELET 150.00 – 450.00 5, 250 115 L a sign of 128 L and MCH 124 L
COUNT x10 ^3/uL internal indicate a
MCV 80 – 96 um3 91 105.3 H bleeding 104.7 H macrocytic 104.2 H
MCH 27.50 – 33 pg 31.9 37.8 H suggesting 37.8 H anemia which 38 H
MCHC 32 – 36 g/dL 35.1 35.9 IBD. 36 is a common 36.5 H
RDW-CV 11.60 – 14.80 % 13 13.7 13.6 manifestation 13.4
MPV 6 – 11 um3 --- 10 10 in IBD 10.1
PDW 11 – 22 um3 --- 13.9 15.4 patients. 14.9
PCT 0.15 - 0.40 % --- 0.12 L 0.13 L 0.13 L
P-LCC 44 – 140 x10 --- 34 L 38 L 38 L
^3/uL
P-LCR 18 – 50 % --- 29.6 29.8 30.5

RANGE 22 CE/ 2 CE/ 2 CE/ 2 CE/
WBC 4.40 – 11.0 10.30 High 9.29 The results 8.01 The results 8.46 PLT are
x10^3/mm ^3 neutrophils is indicates still indicates known to
NEUTROPHILS 37 – 80 % 82.2 H a sign of 71.2 infection, 73 IBD. It is 71.3 change in
LYMPHOCYTES 10.00 – 50.00 % 5.1 L infection 9.1 L inflammation, 10.5 associated 12.2 quantity,
MONOCYTES 0.00 – 12.00 % 9.8 which 12 and bleeding 9.4 with several 10.7 shape, and
EOSINOPHILS 0.00 – 7.00 % 2.6 suggest IBD. 7.1 suggesting 6.8 alterations of 5.7 function in
This could IBD. PLT, including IBD patients,
BASOPHILS 0.00 – 2.50 % 0.3 0.6 0.3 0.1
also cause number, and these
RBC COUNT 4.50 – 5.90 x10 3.42 L 3.91 L 4.15 L 4.46 L
low rbc shape, and abnormalities
^6/uL
count, function, as are mostly
HEMOGLOBIN 14.00 – 17.40 11.4 L 13.4 L 13.8 L 15
hemoglobin, seen in the explained by
g/dL
hematocrit, increase MPV, the highly
HEMATOCRIT 41.50 – 50.40 % 33.8 L 38.8 L 40.9 L 43.8
PLT count PCT and P- active state
PLATELET 150.00 – 450.00 177 and as well 273 372 LCC. 393 of circulating
COUNT x10 ^3/uL as high MCV, PLT in these
MCV 80 – 96 um3 98.8 H MCH and 99.2 H 98.6 H 98.3 H patients.
MCH 27.50 – 33 pg 33.3 H MPV. 34.3 H 33.2 H 33.6 H
MCHC 32 – 36 g/dL 33.7 34.6 33.7 34.2
RDW-CV 11.60 – 14.80 % 14.2 13.7 13.9 13.7
MPV 6 – 11 um3 11.1 H 11.3 H 11.5 H 11.3 H
PDW 11 – 22 um3 17.2 18.9 19.2 18.1
PCT 0.15 - 0.40 % 0.20 0.31 0.43 H 0.44 H
P-LCC 44 – 140 x10 67 111 155 H 157 H
^3/uL
P-LCR 18 – 50 % 37.9 40.6 41.6 39.8
RANGE 2 CE/ CE/ 2 CE/ 2 CE/
WBC 4.40 – 11.0 10.50 PLT are 8.21 Certain 12.81 H PLT are 19.95 H Increased
x10^3/mm ^3 known to medical known to WBC and
NEUTROPHILS 37 – 80 % 75.3 change in 64.1 conditions 77.3 change in 82.7 H neutrophils
LYMPHOCYTES 10.00 – 50.00 % 10 quantity, 13.4 and 9.5 quantity, 6.5 L means there
MONOCYTES 0.00 – 12.00 % 8.7 shape, and 13.1 H medications 7.7 shape, and 8.6 is an
EOSINOPHILS 0.00 – 7.00 % 5.5 function in 9.2 H can cause 5.4 function in 2.0 infection.
IBD patients, high IBD patients, Increased
BASOPHILS 0.00 – 2.50 % 0.5 0.2 0.1 0.2
and these eosinophil and these lymphocytes
RBC COUNT 4.50 – 5.90 x10 4.30 L 4.73 4.64 4.71
abnormalities and abnormalities maybe due to
^6/uL
are mostly monocyte are mostly infections,
HEMOGLOBIN 14.00 – 17.40 14.2 15.6 15.4 15.5
explained by counts. explained by diseases, or
g/dL
the highly Increased the highly the patient’s
HEMATOCRIT 41.50 – 50.40 % 42.2 45.9 44.9 46
active state MCV, MPV, active state medicines.
PLATELET 150.00 – 450.00 343 of circulating 348 and P-LCC 265 of circulating 250
COUNT x10 ^3/uL PLT in these correlates to PLT in these
MCV 80 – 96 um3 98 H patients. 97 H IBD. 96.8 H patients. In 97.7 H
MCH 27.50 – 33 pg 33 33 33.2 H addition, 33
MCHC 32 – 36 g/dL 33.7 34 34.3 increased 33.8
RDW-CV 11.60 – 14.80 % 13.9 13.5 13.8 WBC 14.2
MPV 6 – 11 um3 11.6 H 11.5 H 11.5 H indicates 11.2 H
PDW 11 – 22 um3 19.1 19.3 19.8 infection. 18.1
PCT 0.15 - 0.40 % 0.40 0.40 0.31 0.28
P-LCC 44 – 140 x10 141 H 141 H 109 97
^3/uL
P-LCR 18 – 50 % 41.3 40.6 41.0 36.8
TEST REFERENCE RANGE 10/13/202 SIGNIFICAN 10/16/2022 SIGNIFICAN 10/19/2022 SIGNIFICANCE/INTERPRETATION
2 CE/ CE/
INTERPRETA INTERPRETA
TION TION
WBC 4.40 – 11.0 12.73 The result still 8.81 There is 6.95 The presence of infection and bleeding
x10^3/mm ^3 shows the infection and is a sign that the patient has IBD.
NEUTROPHILS 37 – 80 % 76.8 manifestation 57.1 bleeding which 62.2
LYMPHOCYTES 10.00 – 50.00 % 9.7 of IBD like 13.2 is indicative of 16.1
MONOCYTES 0.00 – 12.00 % 9.1 bleeding that 19 H IBD that the 13.9 H
cause low patient has.
EOSINOPHILS 0.00 – 7.00 % 4.3 10.3 H 7.5 H
RBC,
BASOPHILS 0.00 – 2.50 % 0.1 0.4 0.3
Hemoglobin,
RBC COUNT 4.50 – 5.90 x10 4.06 L and 3.92 L 3.89 L
^6/uL hematocrit.
HEMOGLOBIN 14.00 – 17.40 g/dL 13.3 L High MCV and 12.9 L 12.7 L
HEMATOCRIT 41.50 – 50.40 % 39.4 L MPV still 37.9 L 37.8 L
PLATELET 150.00 – 450.00 x10 240 indicates the 279 324
COUNT ^3/uL effects of IBD
MCV 80 – 96 um3 97 H on patient’s 96.7 H 97.2 H
MCH 27.50 – 33 pg 32.6 platelet. 32.8 32.8
MCHC 32 – 36 g/dL 33.6 33.9 33.7
RDW-CV 11.60 – 14.80 % 14.6 13.8 14.2
MPV 6 – 11 um3 11.3 H 10.6 11.4 H
PDW 11 – 22 um3 18.4 16.5 19.2
PCT 0.15 - 0.40 % 0.27 0.29 0.37
P-LCC 44 – 140 x10 ^3/uL 93 94 130
P-LCR 18 – 50 % 38.9 33.6 40
APTT, PT & TROPONIN
DATE TYPE OF EXAMINATION REFERENCE RANGE PATIENT’S RESULT SIGNIFICANCE/INTERPRETATION

9/13/2022 TROPONIN 1 0.00-0.08 ng/mL 0.01 Patient’s result is within normal range which means
(QUANTITATIVE) a heart attack is unlikely to happen.
9/14/2022 ACTIVATED PARTIAL 25.1- 36.5 secs 27.6 Patient’s result is normal and it means the blood
THROMBOPLASTIN TIME clotting of the patient is normal.
9/14/2022 PROTHROMBIN TIME (sys) 10.2-13.9 secs 10.2 secs A low INR means the patient’s anticoagulation dose
%Activity 80.5-109.3% 113.7%↑ is too low and their blood is clotting too quickly
INR 0.90-1.35 0.85↓ putting the patient at risk for blood clot.
9/15/2022 BLEEDING TIME 2-6mins 4mins & 21secs The patient’s bleeding and clotting time is normal.
CLOTTING TIME 5-15mins 8mins &15secs
9/15/2022 PROTHROMBIN TIME (sys) 9.2-13.2 secs 13.7↑ A high PT level means it takes more time than
%Activity 83-143% 93.43 % usual for the patient’s body to form clot.
INR 0.84-1.11 1.07
9/19/2022 BLOOD TYPE --- O+ The patient’s bleeding and clotting time is normal.
BLEEDING TIME 2-6mins 4mins & 12secs
CLOTTING TIME 5-15mins 9mins &5secs
9/20/2022 PROTHROMBIN TIME (sys) 9.2-13.2 secs 13.4 ↑ A high PT level means it takes more time than
%Activity 83-143% 1.05 usual for the patient’s body to form clot.
INR 0.84-1.11 95.52
ACTIVATED PARTIAL 25.4 – 38.4 secs 34.4 The aPTT is normal which means that the patient’s
THROMBOPLASTIN TIME blood clotting is normal.
BLOOD GLUCOSE
DATE TYPE OF EXAMINATION INTERPRETATION REMARKS: SIGNIFICANCE/INTERPRETATION

9/13/2022 HBA1C 5.1 4.30-6.40% The patient’s result is normal and suggest that the
patient is not diabetic.
9/14/2022 GLUCOSE (FBS) 139.0 ↑ 75-110 mg/dL A high blood glucose levels is an indication of an
CHOLESTEROL 138. 131.-239. mg/dL impaired fasting glucose or the patient is pre-
TRIGLYCERIDES 102.6 0-200 mg/dL diabetic.
DIRECT HDLC 39.9 ↓ 40.-60. mg/dL
LDL 78. 0.-150. mg/dL
VLDL 21 0.-40. mg/dL
9/15/2022 BLOOD GLUCOSE
HGT 152 mg/dL ↑ 70-99 mg/dL This indicates that the patient has diabetes.
DATE TYPE OF EXAMINATION PATIENT’S RESULT REFERENCE RANGE SIGNIFICANCE/INTERPRETATION

9/19//2022 HBsAg(Qualitative) NON-REACTIVE NEGATIVE OR NON- There is no hepatitis B surface antigen that was
REACTIVE found in the patient meaning the patient is not
infected with Hep. B virus.
DATE TYPE OF EXAMINATION PATIENT’S RESULT REMARKS SIGNIFICANCE/INTERPRETATION
9/13/2022 CHEST AP SUPINE PORTABLE AP supine view of the chest is Expiratory chest film The patient's heart is enlarged and he has
taken at a moderate study. osteoarthritis of the spine.
expiratory phase. Cardiomegaly.
The lung fields are clear. The Spondylosis of the
suprahilar vascular markings thoracic spine.
appear normal. Trachea is in
the midline, superior
mediastinum is not widened
and cardiac shadow is
enlarged. Diaphragm in both
sides are intact.
Osteophytic changes are seen
along the articulating margins
of the thoracic spine. The rest
of the Bony structures are
unremarkable.
Incidentally, an endotracheal
tube is inserted in place with
its tip seen at the level of T2
and T3.
9/15/2022 CHEST AP SUPINE PORTABLE Lung fields are clear. Heart is Clear lungs. Cardiomegaly and thoracic spondylosis are seen.
enlarged with a CT ratio of Cardiomegaly. The patient has a gradual buildup of plaque in his
0.6. There are calcifications in Atherosclerotic Aorta aorta but the ETT is still in place.
the aortic arch. The Thoracic Spondylosis
pulmonary vascular markings Endotracheal tube in
are within normal limits. Both place
hemidiaphragms and
costophrenic sulci are sharp
and distinct. The visualized
osseous structures show tiny
marginal spurs in the thoracic
spine. There is an
endotracheal tube with its tip
seen 5.8 cm from the carina.
9/17/2022 CHEST AP SUPINE PORTABLE Comparison with the previous No remarks seen on the The patient’s aorta may be twisted, curved,
study done 9/15/2022 shows lab test. enlarged or narrowed blood vessel of his heart. An
interval development of hazy underlying cause of the distorted shape may be due
and slightly confluent opacities to a build up of fatty tissue that collects on the
in both lower lung fields. walls of the vessels. In a neutral position, the EET
Heart remains magnified. should be at the lower border of the mandible
Aorta is tortuous. The should be projected over C5/C6.
pulmonary vascular markings
are within normal limits. The
previously noted endotracheal
tube is only partially visualized
seen at the level of C7/C6.
The rest of the findings are
stationary.
9/18/2022 CHEST AP SUPINE PORTABLE Follow-up with the previous 1. Minimal progression of Minimal progression of pneumonia in both lungs
study done 9/17/2022 shows pneumonia in both lower may progressed to double pneumonia in this case
minimal progression of the lung fields. since it affects both lower lung fields. Bilateral
hazy and confluent opacities in 2. Consider minimal pleural effusion is an abnormal accumulation of
both lower lung fields, development of minimal fluid in the pleural space -- the space between the
blunting both costophrenic bilateral pleural effusion. lungs and the chest wall. Repositioning the EET
sulci and rendering both 3. Interval repositioning happened on this day of examination. The rest of
hemidiaphragms ill defined. of an endotracheal tube in the findings are consistent.
There is interval repositioning place.
of the endotracheal tube, now 4. The rest of the findings
with its tip at the level of are stationary.
T2/T3. The rest of the findings
are stationary.
9/20/2022 CHEST AP SUPINE PORTABLE Comparison with the previous 1. Significant clearing of Pneumonia has been significantly cleared up in both
study done 9/18/2022 shows pneumonia in both lower lower lung fields. On this day of examination, the
significant clearing of the hazy lung fields. EET was replaced with a tracheostomy tube. The
and confluent opacities in both 2. Resorption of the endotracheal tube is only for providing generally
lower lung fields, rendering minimal bilateral pleural short-term mechanical ventilation.
both hemidiaphragms and effusion.
costophrenic sulci sharp and 3. Interval removal of an
distinct. The rest of the lungs endotracheal tube with
are clear. Heart remains placement of a
magnified. The pulmonary tracheostomy tube.
vascular markings are within 4. The rest of the findings
normal limits. There is interval are stationary.
removal of an endotracheal = magnified cardiac
tube with placement of a silhouette with no signs of
tracheostomy tube. The rest pulmonary congestion.
of the findings are stationary. = atherosclerosis of the
thoracic aorta.
= spondylosis of the
thoracic spine.
9/24/2022 CHEST AP SUPINE PORTABLE Follow-up examination to the 1. Development of Pneumonia in both lower lungs develops on this day
previous study dated pneumonia in both lower of examination. The rest of the findings are
9/20/2022 shows significant lungs consistent.
development of hazy opacities 2. The rest of the findings
in both lower lungs. are stationary:
The rest of the lungs are clear. = magnified cardiac
Heart remains magnified. The silhouette with no signs of
pulmonary vascular markings pulmonary congestion
are within normal limits. The = atherosclerosis of the
tracheostomy tube remain in thoracic aorta
place. The rest of the findings = spondylosis of the
are stationary. thoracic spine
= tracheostomy tube in
place
9/29/2022 CHEST AP SUPINE PORTABLE Comparison with the previous 1. Partial clearing of Pneumonia in both lower lung fields has somewhat
study done 9/24/2022 shows pneumonia in both lower cleared up. The rest of the findings are consistent.
partial clearing of the hazy lung fields.
opacities in both lower lung 2. The rest of the findings
fields. The rest of the lungs are stationary.
are clear. Heart remains = magnified cardiac
magnified. The pulmonary silhouette with no signs of
vascular markings are with pulmonary congestion.
normal limits. = tracheostomy tube in
The rest of the findings are place.
stationary. = tortuous aorta.
thoracic spine.
10/3/2022 CHEST AP SUPINE PORTABLE Comparison with the previous 1. Further clearing of Pneumonia in both lower lung fields are getting
study done 9-29-2022 shows pneumonia in both lower better. The rest of the findings are consistent.
further clearing of the lung fields
infiltrates in both lower lung 2. The rest of the findings
fields. The rest of the lungs are stationary:
are clear. Heart remains = magnified cardiac
magnified. The rest of the silhoutte.
findings are stationary. = tortuous and
atheromatous aorta.
thoracic spine.
10/4/2022 CHEST AP SUPINE PORTABLE Comparison with the previous 1. Re-progression of The patient’s pneumonia relapsed in both lower
study done 10-3-2022 shows pneumonia in both lower lung fields. It was also seen that the visualization
reprogression of the infiltrates lung fields. of the right apical area's minimal fibrosis improved.
in both lower lung fields. 2. Better delineation of The rest of the findings are consistent.
There is also better minimal fibrosis in the
delineation of a linear sharp right apical area.
density in the right apical 3. The rest of the findings
area. The rest of the lungs are are stationary:
clear. Heart remains = magnified cardiac
magnified. The rest of the silhouette.
findings are stationary = tortuous and
atheromatous aorta.
thoracic spine
10/7/2022 CHEST AP SUPINE PORTABLE Comparison with the prior 1. Significant clearing of Both lower lungs of the patient's pneumonia have
study done 10-4-2022 now pneumonia in both lower significantly cleared. The rest of the findings are
shows significant clearing of lungs consistent.
the infiltrates in both lower 2.The rest of the findings
lungs. The linear, sharp are stationary:
density in the right apical area = minimal fibrosis in the
is unchanged. The rest of the right apical area
lungs are clear. Heart remains = magnified cardiac
magnified. The rest of the silhouette
findings are stationary. = tracheostomy in place
= tortuous and
atheromatous aorta
thoracic spine
10/10/2022 CHEST AP SUPINE PORTABLE Comparison with the previous 1. Resolution of the
study done 10/7/2022 shows residual infiltrates in the
resolution of the residual left lung base.
infiltrates in the left lung base. 2. The rest of the findings
The fibrolinear opacity in the are stationary.
right apical area, is again = minimal fibrosis in the
appreciated. The rest of the right apical area.
lungs are clear. Heart remains = tracheostomy tube in
magnified. The rest of the place.
findings are stationary. = magnified cardiac
silhouette.
= atherosclerosis of the
thoracic aorta.
thoracic spine.
10/14/2022 CHEST AP SUPINE PORTABLE Follow-up examination to the 1. Further significant Patient’s pneumonia in both lower lung fields are
previous study dated 10-11- clearing of pneumonia in getting better was seen on this day of examination.
2022 shows further significant both lower lung fields The rest of the findings are consistent.
clearing of the infiltrates in 2. The rest of the findings
both lower lungs. The rest of are stationary:
the lungs are clear. Heart = magnified cardiac
remains magnified. The rest of silhoutte
the findings are stationary. = tortuous and
atheromatous aorta
thoracic spine
9/21/2022 ABDOMEN AP SUPINE The gas pattern of the Nonspecific and non- There is some gas found in the patient's bowel.
gastrointestinal tract is obstructive bowel gas The patient’s spondylosis arise in the region that
nonspecific and non- pattern. connects the flexible lumbar spine and the rigid
obstructive. There are no Spondylosis of the thoracic cage.
abnormally dilated bowel thoracolumbar spine.
loops. Negative for abnormal
calcification, mass lesion or
free air within the abdominal
cavity. Psoas shadows are
clear.
Flank stripes are intact.
Osteophytes are seen arising
in the lateral articulating
margins of the thoracolumbar
spine. The rest of the osseous
structures are unremarkable.
9/22/2022 ABDOMEN AP SUPINE The visualized small and large Non- specific and non- Small and large segments that are visualized are
segments are nonspecific obstructive bowel gas neither particular nor obstructive. The flank stripes
and non- obstructive. Psoas pattern and psoas shadows are unharmed. There isn't any
shadows and flank stripes are Lumbar spondylosis definite proof of a large lesion, free air, or an
intact. No definite evidence of unusual fluid buildup in the abdominal cavity. The
mass lesion, free air, or lumbar spine's marginal spurs are small and can be
abnormal fluid collection in the seen in the visible osseous structures.
abdominal cavity. The
visualized osseous structures
show tiny marginal spurs in
the lumbar spine.
10/11/2022 ABDOMEN AP SUPINE Comparison with the previous Interval development of Food and liquids cannot flow through the patient's
study done 9/22/2022 now adynamic ileus. stomach because a dynamic ileus is developing,
shows gas distended small Presence of a nasogastric which prevents this from happening. Some
and large bowel loops. There tube and rectal catheter. osteophytes are seen bridging the lateral
is placement of a nasogastric Spondylosis of the articulating margins of the thoracolumbar spine.
tube with its tip well within the thoracolumbar spine.
gastric fundus. A lead-lined
tube is also seen
superimposed on the left side
of the abdominopelvic cavity,
representing the rectal tube.
Negative for abnormal
calcification, mass lesion or
free air within the abdominal
cavity. Psoas shadows are
clear. Flank stripes are intact.
Osteophytes are seen arising
in the lateral articulating
margins of the thoracolumbar
spine, some showing bridging.
The rest of the visualized
osseous structures are
unremarkable
CT SCAN

9/13/2022 BRAIN PLAIN Unenhanced axial CT scan of No definite evidence of The patient's sinus mucosa is inflamed, and pus is
the brain shows the 4th, 3rd intra-cranial and bony subsiding, causing obstruction and pressure on the
and lateral ventricles are pathology. ethmoid sinus area.
normal in size, shape and Incidental finding of
location with the lateral bilateral acute ethmoid
ventricles noted to be sinusitis.
symmetrical. No focal hypo
nor hyperdense lesions seen
in the supra and infratentorial
brain parenchyma. The basal
and sylvian cisterns are intact
and symmetrical. Septum
pellucidum is in the midline.
Bone window setting shows
the demonstrated bony
structures are unremarkable.
However, most of the ethmoid
air cells show soft tissue
fullness. Likewise, the inferior
nasal turbinates in both sides
are hypertrophied.
9/14/2022 BRAIN PLAIN COMPLETION This is a follow-up Sub-acute infarction now Subacute infarction is now being examined in both
unenhanced axial CT scan of considered in the sides of the thalamus, as well as the left side of the
the brain and compared to the thalamus of both sides, as midbrain. Previously suspected bilateral ethmoid
previous scan performed well as in the left side of sinusitis was confirmed. There have been no other
approximately 17 hours the midbrain. significant findings.
earlier. Previously considered
Small hypodense lesions, with bilateral ethmoid sinusitis
poorly defined borders, are again noted.
now seen in the thalamus of
both sides, as well as in the
left side of the midbrain.
No other new significant
findings seen.
9/15/2022 BRAIN/CRANIAL PLAIN Axial slices of the whole brain 1. CONSIDER ARTERY OF The patient has a possibility to have an abnormal
were done without PERCHERON INFARCT variant of the arterial supply of the thalamus.
intravenous contrast. 2. CHRONIC INFARCT IN Because of his age, the patient's brain volume
There is no evidence of acute THE LEFT CEREBELLAR shrinks overall, but his frontal lobe and
territorial infarct and HEMISPHERE hippocampus are responsible for cognitive functions
intracranial hemorrhage. 3. AGE-RELATED and they shrink more than other areas. It was also
There is no focal mass lesion. CEREBRO-CEREBELLAR found that plaque grew in the patient's carotid
There is hypodensity in both VOLUME LOSS arteries.
thalamus and left side of the 4. ARTERIOSCLEROSIS
midbrain. OF BOTH INTERNAL
A CSF-density lesion is seen in CAROTID ARTERIES
the left cerebellar hemisphere. 5. BILATERAL ETHMOID,
The ventricles, cisterns and MAXILLARY AND
sulci are widened. SPHENOID SINUSITIS
Midline structures are in place.
The cavernous sinuses are
symmetrical. The sella and
suprasellar regions are intact.
There are calcifications in both
internal carotid arteries.
The brainstem and cerebellum
are preserved.
There is mucosal wall
thickening in both ethmoid,
maxillary and sphenoid
sinuses.
The rest of the visualized
paranasal sinuses and
petromastoids are adequately
aerated.
The osseous structures are
intact.
WHOLE ABDOMEN Axial slices of the whole No remarks seen on the

abdomen were done before lab test.
and after administration of
nonionic intravenous contrast.
There is minimal bilateral
pleural effusion, more on the
right, associated with passive
atelectasis in both lung bases.
No pulmonary nodules seen.
The imaged heart is enlarged.
The liver is normal in size. The
hepatic contours are smooth
with no distortion of the
internal architecture. The
intrahepatic and extrahepatic
bile ducts are not dilated. The
gallbladder is distended with
fluid. There is no calcified
gallstone. The gallbladder wall
is not thickened. The portal
and splenic veins show
homogeneous enhancement.
The spleen is normal in size
and show homogeneous
enhancement after
intravenous contrast.
The pancreas display normal
lobulated contour. The
pancreatic duct is not dilated.
There is no focal mass lesion.
The adrenal glands are normal
in configuration and not
enlarged.
The kidneys are normal in
shape and position. The
outlines are smooth. The renal
cortices are of normal
thickness and show
homogeneous enhancement.
Both renal arteries are normal
in caliber. There good
pacification of both renal
veins. The perinephric fat is
preserved. There are no
calcifications within both
kidneys. The renal calyces,
pelves and ureters are not
dilated. There is excretion of
the contrast medium into both
upper urinary tracts.
The urinary bladder is
suboptimally distended with a
balloon catheter in place.
There is no calcified stones
within the urinary bladder.
Minimal stranding of
perivesical fat is noted.
The seminal vesicles are
symmetrical. The prostate
gland is not enlarged. The
pre-prostatic fat planes and
ischio-rectal fat are preserved.
The stomach is undistended
with nasogastric tube in place.
There is no focal mass lesion
detected. The small and large
bowel loops are normal in
caliber. The bowel walls are
not thickened. The mesentery
and omentum are normal.
The rectum is physiologically
distended and filled with fluid.
There is milld diffuse long
segment wall thickening
associated with minimal
stranding of the adjacent soft
tissues.
There are no enlarged lymph
nodes in the intra-abdominal,
retroperitoneal or pelvic side
walls.
The abdominal aorta is normal
in caliber with calcific plaques
lining its walls. There is no
focal dilatation or narrowing.
The superior and inferior
mesenteric and celiac arteries
are normal in caliber.
The lumbar lordosis is smooth.
There is no segmental
malalignment. The vertebral
bodies and intervertebral discs
are of normal height.
Osteophytes are seen in the
articulating margins of the
thoracolumbar spine. The
vertebral endplates are also
smooth. The pedicles are
intact.
The apophyseal joints are
normal. There is no evidence
of bone destruction. The
sacro-iliac joints and
symphysis pubis are normal.
Both hip joints are also
normal.
ULTRASOUND

9/17/2022 Whole abdomen Right hepatic lobe: 13.7 cm 1. Hepatosteatosis The patient has a fatty liver, which is a buildup of
Spleen: 4.6 cm 2. Low-density fat in the liver and is sometimes referred to as
Right kidney: 10.5 x 6.2 x 1.7 (matrix/oxalate/uric hepatic steatosis or hepatosteatosis. Patient has
cm (L x W x Parenchyma) acid/xanthine) calculi in also a low density kidney stones.
Left kidney: 10.5 x 6.6 x 1.9 both kidneys*
cm (Lx W x Parenchyma) 3. Normal gallbladder,
Prostate gland: 3.1 x 2.7 x 3.2 pancreas, abdominal
cm; 13.6 grams aorta, spleen, urinary
The liver is not enlarged with bladder and prostate
normal lobar proportions and gland sonogram.
exhibits homogenous *These may not always
echopattern. Parenchymal be seen on CT scan
echogenicity is increased. No
evident solid or cystic lesions.
The portal vein and hepatic
vessels shows normal course
and caliber. Intrahepatic ducts
not dilated.
The gallbladder is contracted,
precluding evaluation. The
common duct is not dilated.
The pancreas and spleen are
normal in size with
homogeneous echopattern. No
frank parenchymal lesion. The
abdominal aorta is
unremarkable.
Both kidneys are normal in
size, shape and echogenecity.
The parenchymal thickness is
normal. The sinus-
parenchymal and
corticomedullary demarcations
are distinct. The collecting
system is not dilated. There
are tiny (0.1-0.2 cm) medium
to high level echoes in the
central echo complex of both
kidneys.
The urinary bladder is
distended, echo free, with
smooth contours. The bladder
wall is not thickened.
The prostate gland is not
enlarged. No evident mass nor
calcifications noted. No
indentation along the floor of
the urinary bladder
FLEXI – SIGMOIDOSCOPY Patient was placed on the left 1. Non-specific colitis, The patient has an inflammatory condition of the
lateral position under mild recto-sigmoid R/O colon that microscopically lacks the characteristic
sedation. The scope was = IBD features of any specific form of colitis on the last
inserted up to the splenic section of his bowel.
2. Internal
flexure and slowly withdrawn Grade I hemorrhoids are seen as small bulges into
while inspecting the following Hemorrhoids, the lumen.
segments closely. Grade 1
RECTUM: Non-engorged
hemorrhoidal vessels above
the dental line.
SIGMOID: Edematous
mucosa, no mass lesions
DESCENDING: Edematous
mucosa, no mass lesions
9/16/2022 Echocardiographic Report Study done with patient in Normal left ventricular Patient’s results are normal.
atrial fibrillation geometry with normal
Normal left ventricular systolic function
dimension with adequate wall Normal right ventricular
motion and contractility geometry with normal
Dilated left atrium systolic function
Normal right ventricular Normal pulmonary artery
dimension with adequate wall systolic pressure
motion and contractility
Normal right atrial size
Structurally normal mitral,
tricuspid and pulmonic valves
with good opening and closing
motion
Structurally normal aortic
cusps with good opening and
closing motion; Aortic annular
calcification
Normal main pulmonary artery
and aortic root dimension
No intracardiac mass
No pericardial effusion
DOPPLER STUDY:
Tricuspid regurgitation, mild
Normal pulmonary artery
systolic pressure of 37mmHg
by TR jet
ECG
CLINICAL CHEMISTRY
TEST UNIT NORMA 09-13-22 09-15-22 09-17-22 09-18-22 09-19- 09-21-22 09-22-22 09-24- 09-25- 09-26- 09-29-
L 22 2022 22 22 22
RANGE
Creatinine mg/dL 0.51 – 1.04 H 1.02 H 0.98 H 1.04 H 0.61 H 0.88 H 0.76 H 0.77 H
0.95
Sodium mmol/ 137.0 136.1 144 144 147 H 141 140 141
L –
145.0
Potassium mmol/ 3.60 – 3.48 L 3.70 3.10 L 3.80 2.9 L 4.00 3.30 L 3.80 3.70 3.90
L 5.00
Urea Nitrogen mg/dL 9.0 – 14.9
20.0
ALT/SGPT U/L 0. – 30. 24
50.
Blood urea mg/dL 6.0 - 8.3
nitrogen 20.00
Blood uric acid mg/dL 2.4 – 3.90 3.70
5.7
Albumin g/dL 3.97 – 3.36 L
4.94
Magnesium mg/dL 1.7 – 2.08
2.4
INTERPRETATI Patient has Patient’s Creatinin Patient’s Potassiu Creatinine Potassium Creatinin Potassiu Creatinin Creatinin
ON hyponatrem albumin e levels result has m level levels are and e and m level e levels e levels
ia as well as levels are are the same is within consistent. magnesiu potassiu is within are are
increased decrease consisten levels normal Sodium m are m levels normal consiste consiste
creatinine d. This t. compared range. blood test within are range. nt nt
level. This can be a to the first results that normal consisten
may be a sign of examinatio are higher range t.
sign that liver or n. than normal
the kidneys kidney Increased may be a
are not disease creatinine sign of a
filtering the or level and condition,
blood another decreased such as:
effectively. medical potassium Dehydration
condition level. , which may
. be caused
Creatinin by not
e levels drinking
are enough,
consisten diarrhea, or
t. Other taking
tests are diuretics.
within Hyponatrem
normal ia is also
range. present.
TEST UNIT NORMAL RANGE 10-01-22 10-04-22 10-07-22 10-10-22 10-14-22 10-13-22 10-16-22 10-19-22
Creatinine mg/dL 0.51 – 0.95 0.73 H 0.84 H 0.76 H 0.83 H 0.71 H 0.71 H 0.70 H
Sodium mmol/L 137.0 – 145.0 139.00 141.00 141.00 137.00 138.00 141.00 143.00
Potassium mmol/L 3.60 – 5.00 4.00 3.50 L 4.00 4.50 4.30 4.40 4.00
Urea Nitrogen mg/dL 9.0 – 20.0
ALT/SGPT U/L 0. – 50.
Blood urea nitrogen mg/dL 6.0 - 20.00
Blood uric acid mg/dL 2.4 – 5.7 3.46
Albumin g/dL 3.97 – 4.94
Magnesium mg/dL 1.7 – 2.4
INTERPRETATION Creatinine Creatinin Creatinine Creatinine Blood uric Creatinin Creatinine Creatinine
levels are e and levels are levels are acid level e levels levels are levels are
consistent potassiu consistent consistent is within are consistent consistent
m levels normal consisten
are range. t
consisten
t.
STOOL EXAMINATION
MACROSCOPIC 09-24-22 09-25-22 09-25-22 10-01-22

EXAMINATION
Color: Brown Yellow Yellow Light Brown
Consistency: Mucoid Mucoid Soft Mucoid
PARASITE EXAMINATION
WBC 0-2/HPF 0-1/HPF 0-1/HPF 2-3/HPF
RBC 0-1/HPF 0-1/HPF 0-1/HPF 0-1/HPF
REMARKS NO NO NO NO
OVA/PARASIT OVA/PARASITE OVA/PARASIT OVA/PARASITE
E SEEN SEEN E SEEN SEEN
YEAST CELL - YEAST CELL -
FEW RARE
INTERPRETATION Normal Few amount of Few amount of WBC in stool,
findings. candida are candida are can be a sign
seen on this seen on this of a bacterial
day of day of infection that
examination. examination. affects the
digestive
system.
THYROID STUDIES
TEST UNIT NORMAL 09-16-

RANGE 22
TSH uIU/mL 0.3 – 4.5 0.145 L
FT3 pg/mL 2.0 – 4.2 2.14
FT4 pg/mL 8.9 – 17.2 11.80
INTERPRETATION Decreased TSH levels are most
likely that the patient’s thyroid
gland is making excess thyroid
hormone.
Name of the Drug Mechanism Of Indication/s Side Nursing
Action Effects Responsibilities
Generic Name: Binds to an Erosive Stomach Before:
ESOMEPRAZOLE enzyme on esophagitis. pain 1. Consider
gastric parietal Hypersecretory 10 rights
Classification: cells in the conditions, of
GASTROINTESTI presence of including
medicatio
NAL AGENT; acidic gastric Zollinger-
PROTON PUMP pH, preventing Ellison ns.
INHIBITOR the final syndrome. 2. Check
transport of With amoxicillin hypersen
hydrogen ions and sitivity to
Dosage: 40 mg 1 into the gastric clarithromycin any
TAB lumen. to eradicate proton
Route: NGT Therapeutic Helicobacter
pump
Frequency: Effects: pylori in
Before meals Diminished duodenal ulcer inhibitor
accumulation disease or or hepatic
Timing: 8am- of acid in the history of impairme
1pm-6pm gastric lumen duodenal ulcer nt.
with lessened disease. 3. Lab tests:
gastroesophag Decrease risk Periodic
eal reflux. of gastric ulcer
liver
Healing of during
duodenal continuous function
ulcers. NSAID therapy. tests,
Decreased Contraindicatio Adverse CBC,
incidence of n/s Reactions Hematocr
gastric ulcer Use Cautiously CNS: it &
during in: Severe Headache. Hemoglob
continuous hepatic GI:
NSAID in,
impairment Nausea,
therapy. (daily dose vomiting, urinalysis
should not diarrhea, for
exceed 20 constipatio hematuri
mg); Geri: n, a and
Increased risk abdominal proteinuri
of hip fractures pain,
a.
in patients flatulence,
4. Educate
using high dry mouth.
doses for >1 patient
year; about the
Pedi: Children medicatio
<1 yr (safety n
not administe
established).
red the
side
effects of
the
medicatio
n.
During:
1. Monitor
for Signs
and
symptom
s of
adverse
CNS
effects
(vertigo,
agitation,
depressio
n)
especiall
y in
severely
ill
patients.
2. Monitor
phenytoi
n levels
with
concurre
nt use.
3. Monitor
INR/PT
with
concurre
nt
warfarin
use.
After:
1. Report
any
changes
in urinary
eliminatio
n such as
pain or
discomfor
t
associate
d with
urination
to
physician.
2. Report
severe
diarrhea.
Drug may
need to
be
discontinu
ed.
Reference: NCBI - WWW Error Blocked Diagnostic. (n.d.). Retrieved October 21,
2022, from https://www.ncbi.nlm.nih.gov/books/NBK507910
Name of the Mechanism Indication/s Side Effects Nursing

Drug Of Action Responsibiliti
es
Generic Name: Racecadotril Racecadotril Before:
RACECADROTR is a prodrug (acetorphan) is 1. Check the
IL HIPRASEC that needs to an oral label of
be enkephalinase medication
Classification: hydrolyzed to inhibitor for use 2. Use
Antidiarrheal its active in the treatment hygiene
metabolite of acute measures to
thiorphan, diarrhoea. By prevent
Dosage: 100 which is an preventing the reinfection or
mg 1 tab inhibitor of degradation of spread of
enkephalinas endogenous infection.
e, a cell enkephalins, 3. Crushed
membrane racecadotril medication
Route: NGT peptidase reduces before
located in hypersecretion administering
various of water and 3. Assess
tissues, electrolytes into abdomen,
Frequency: TID notably the the intestinal bowel
epithelium of lumen. movement
Timing: 8am- the small Treatment with and sound
1pm-6pm intestine. racecadotril 4. Assess if
This enzyme reduces the they have a
contributes incidence and high
both to the duration of temperature
hydrolysis of acute diarrhoea (fever) and
exogenous and reduces there has
peptides and diarrhoea- been blood or
to the associated pus in their
breakdown of symptoms stools.
endogenous compared with 5. Educate
peptides such placebo in patient about
as adults. the side
enkephalins. Contraindication Adverse effects of the
Consequently /s Reactions medication.
, racecadotril Diarrhea  Nervous After:
protects associated with system 1.
endogenous fever and/or disorders: Administered
enkephalins bloody or Headache. medication
that are purulent stools; before NGT
physiologicall antibiotic-  Respiratory feeding.
y active at associated , thoracic 2.
digestive diarrhea. and Administered
tract level, Patients who mediastinal Racecadotril
prolonging have disorders: via NGT.
their experienced Tonsillitis During:
antisecretory angioedema (particularl 1. Monitor
effect. with ACE y in infants carefully for
inhibitors. or side/adverse
children). effects.
2. Inform
 Skin and physician of
subcutaneo all
us tissue medications
disorders: being taken.
Rash, 3. Record the
erythema administratio
nodosum, n of the
erythema prescribed
multiforme, drug.
urticaria, 4. Notify the
papular physician for
rash, any allergic
prurigo, reactions.
pruritus. 5. Document
the
 Potentially medications
Fatal: administered.
Rarely,
severe skin
reactions
Reference: Stewart, M. (2020, January 17). Racecadotril for acute diarrhoea in
children (Hidrasec). Retrieved October 21, 2022, from
https://patient.info/medicine/racecadotril-for-acute-diarrhoea-in-children-hidrasec
Name of the Mechanism Of Indication/s Side Effects Nursing

Drug Action Responsibili
ties
Generic Itopride HCl Treatment of Before:
Name: is rapidly and chronic 1. Consider
GANATON almost gastritis or 10 rights of
completely non-ulcer medication.
absorbed dyspepsia ie, 2. Check
Classification: from the feeling of the label of
Gastroprokine gastrointestin abdominal medications
tics al tract. bloatedness, 3. Crushed
Relative upper medications
bioavailability abdominal before
Dosage: 50 is calculated pain, administere
mg 1 tab to be 60% heartburn, d
due to liver nausea and 4. Use
first-pass vomiting. hygiene
metabolism. Contraindicati Adverse Reactions measures to
Route: NGT There is no on/s prevent
effect of food Hypersensitivit  Blood and transmissio
on y to itopride Lymphatic n of
bioavailability hydrochloride System microorgani
Frequency: . Peak plasma or any of the Disorders: sm
TID levels excipients of Leukopenia
(Cmax=0.28 Ganaton. and During:
Timing: 8am- mcg/mL) are Patients in thrombocytop 1. Monitor
1pm-6pm reached after whom an enia. dizziness or
0.5-0.75 hrs increase in any adverse
after itopride gastrointestina  Immune reaction.
HCl 50 mg. l motility could System 2.
Following be harmful eg, Disorders: Administere
multiple oral gastrointestina Anaphylactoid d
doses ranging l hemorrhage, reaction. medication
from 50-200 mechanical before NGT
mg 3 times obstruction or  Endocrine feeding
daily, itopride perforation. Disorders: 3.
HCl and its Increased Administere
metabolites prolactin level d ganaton
showed linear and via NG tube
pharmacokine gynecomastia
tics over a . After:
treatment 1.Monitor
period of 7  Nervous the venous
days, with System access after
minimal Disorders: administrati
accumulation. Dizziness, on
headache and 2.Inform
tremor. physician
medications
 Gastrointestin being taken
al Disorders: 3. Check
Diarrhea, patient's BP
constipation, after giving
abdominal the
pain, medications
increased
saliva and
nausea.
 Hepatobiliary
Disorders:
Jaundice.
Skin and
Subcutaneous
Tissue
Disorders:
Rash, redness
and itching.
Reference: 1mg.com. (n.d.). Ganaton Tablet: View Uses, Side Effects, Price and
Substitutes. 1mg. Retrieved October 21, 2022, from
https://www.1mg.com/drugs/ganaton-tablet-33275

Drug Action Responsibilitie
s
Generic Rebamipide is Acute gastritis & Before:
Name: a mucosal acute 1. Consider 10
REBAMIPIDE protective exacerbation of rights of
agent and is chronic gastritis. medication.
postulated to Gastric ulcer. 2. Use
Classification increase Prevention of hygiene
: gastric blood NSAID-induced measures to
Antiulcerant, flow, gastropathy. prevent
Antacids prostaglandin transmission
biosynthesis Contraindication/ Adverse of
Acute gastritis s Reactions microorganism
Dosage: 100 & acute Is  Skin: .
mg 1 tab exacerbation contraindicated Rash, 3. Crushed
of chronic in elderly and Pruritus, drug- medications
gastritis. children and eruption, like before
Gastric ulcer. adult patients eczema. administered
Route: NGT Prevention of with chronic
NSAID- illness including  Gastro: During:
induced cancer. 1.
gastropathy. Rebamipide Constipation, Monitor/watch
Frequency: and decrease should not be Bloating, out for
TID free oxygen prescribed to diarrhea, abdominal
radicals. patients allergic Nausea, distention.
Timing: Helps in to synthetic Vomiting 2. Monitor for
8am-1pm- replacement formulations, Stomach upset, any adverse
6am of lost tissue dye and heartburn, reactions.
by increasing chemicals. Also abdominal pain, 3.
Skin: Rash, contraindicated belching, taste Administered
Pruritus, for pregnancy abnormality. medication
drug-eruption, and lactation. before NGT
like eczema.  Others: feeding
Gastro: Cold 4.
Constipation, sweat, Difficulty Administered
Bloating, breathing Rebamipide
diarrhea, via NG tube
Nausea,
Vomiting After:
Stomach 1. Check
upset, patient's BP
heartburn, after giving
abdominal the
pain, medications.
belching, 2. Inform
taste physician
abnormality. medications
Others: Cold being taken
sweat, 3. Notify the
Difficulty physician for
breathing any allergic
the expression reactions.
of epidermal 4. Document
growth factor the
(EGF) and medications
EGF administered.
receptors.
These EGF
causes
contr
raindication/s
Adverse
Reactions
angiogenesis,
increased
production of
granulation
Is
contraindicate
d in elderly
and Dizziness,
drowsiness,
dry
tissue and
epithelization
of children
and adult
patients with
mouth,
constipation,
diarrhoea,
ulcer healing.
chronic illness
including
cancer.
abdominal
distention,
nausea,
Reference: J.Rebamipide Drug study, retrieved April 21,2021 from

https://www.scribd.com/d0c/120728060/drug-study
Name Mechanism Indication/s Side Nursing Responsibilities
of the Of Action Effects/Adverse
Drug Reactions
Generic Citicoline Supportive

Name: has treatment in Cardiac Before:
Citicolin beneficial combination disorders:
Bradycardia, ● Check patient CT
e effects on with other
tachycardia. scan report
Brand neurological medicines
Name: functions; it for Gastrointestinal ● Monitor
acts by improvemen disorders:
effectiveness of
Classific increasing t of Diarrhoea,
epigastric drugs in relieving
ation: the symptoms pain in arthritic
discomfort,
Psychos synthesis of in brain joints.
stomach pain.
timulan phosphatidy disorders
ts and lcholine, the such as General ● Assess for signs of
Nootrop primary thinking and disorders and bleeding,
ics neuronal memory admin site especially in
Dosage phospholipi problems conditions: patients on
Fatigue.
: d and due to anticoagulant
1 enhancing vascular Nervous system therapy.
gram/ the dementia disorders:
tab production Dizziness, ● Somasize must not
Route: of headache. be administered
NGT acetylcholin along with
Injury or Skin and medicaments
Freque e. Brain death of subcutaneous
ncy: phospholipi containing
brain cells tissue disorders:
TID d synthesis meclophenoxate
due to Rashes.
Timing: is impaired stroke
Vascular During:
following
8pm – disorders:
stroke and ● Report any of the
12am – Hypotension.
8:00pm ischemic Age related
events. Oral brain following to
citicoline damage and physician: tinnitus,
administrati loss of persistent gastric
on function that irritation,
increases affects epigastric pain,
the plasma memory and unexplained
levels of other bruising or
choline and essential bleeding.
cytidine, mental
● Avoid concurrent
building functions, or
use of other drugs
blocks used cause
containing aspirin
to restore tremors and
or salicylates
neuronal unintentiona
unless otherwise
membrane l
advised by
integrity movements
physician
A condition
● Watch out for
causing
hypotensive
difficulty in
effects
concentratio
n and After:
controlling
impulsive ● Contact the
behavior, physician
restlessness immediately if
(Attention allergic reactions
Deficit such as hives,
Hyperactive rash, or itching,
Disorder) swelling in your
face or hands,
Glaucoma mouth or throat,
(elevated chest tightness or
pressure in trouble breathing
the eye can are experienced.
damage
nerves and ● Keep all medicine
structures in locked up and
the eye away from
causing children.
blindness)
Citicoline
can reduce ● Store medicine
and prevent away from heat
this and direct
complication sunlight.
● Do not store
Contraindica medicine in the
tion/s bathroom, near
the kitchen sink,
or in other damp
If you are places.
allergic to
Citicoline or
any
components
of this
medicine
Conditions
causing
increased
muscle tone
or stiffness
(rigidity,
spasticity,
or dystonia)
Reference/Source: Availability. CHOLINE SALICYLATE. (n.d.). Retrieved November

8, 2021, from
http://www.robholland.com/Nursing/Drug_Guide/data/monographframes/
C075.html.
Name Mechanis Indication/s Side Nursing
of the m Of Effects/Advers Responsibilities
Drug Action e Reactions
Generic ● Reduce
Name: the risk Significant: Before:
Atorvas Atorvastat of Myopathy,
in is a myalgia, DM, ● Lab tests:
tatin myocard
statin persistent Monitor
Brand ial
medicatio serum lipid levels
Name: infarctio
n and a transaminase within 2–4
n
wk after
Classific competitiv ● Reduce elevations.
e inhibitor Rarely, initiation of
ation: the risk
of the immune- therapy or
HMG- of
enzyme mediated upon
CoA stroke
change in
reducta HMG-CoA ● Reduce necrotising
(3- myopathy dosage;
se the risk
monitor
inhibito hydroxy- for (IMNM),
3- interstitial lung liver
rs revascul
functions at
(statins methylglu arization disease.
taryl 6 and 12
) procedu
Hema: wk after
Dosage coenzyme res and
A) Thrombocytop initiation or
: angina
enia. elevation of
80 mg/ reductase, ● Reduce
which dose, and
tab the risk Hepatobiliary
catalyzes periodically
Route: of disorders:
the thereafter.
NGT myocard Cholestasis. ● Assess for
Frequen conversio ial
n of HMG- muscle
cy: infarctio Investigations:
CoA to pain,
OD n Abnormal LFT,
mevalonat tenderness,
Timing: ● Reduce elevated
e, an or
the risk serum creatine
8pm early rate- weakness;
of kinase, WBC
limiting and, if
stroke urine positive.
step in present,
● Reduce
cholestero Metabolism monitor
the risk
l and nutrition CPK level
of non-
biosynthe disorders: (discontinu
fatal
sis. Hyperglycaemi e drug with
myocard
Atorvastat a. marked
ial
in acts infarctio elevations
primarily n Nervous of CPK or if
in the ● Reduce system myopathy
liver, the risk disorders: is
where of fatal Headache, suspected).
decreased and dizziness, ● History:
hepatic non- paraesthesia, Allergy to
cholestero fatal amnesia. clopidogrel,
l stroke pregnancy,
Psychiatric
concentrat ● Reduce lactation,
disorders:
ions the risk bleeding
Insomnia,
stimulate for disorders,
nightmares.
the revascul recent
upregulati arization Renal and surgery,
on of procedu urinary hepatic
hepatic res disorders: UTI. impairment
low- ● Reduce , peptic
density the risk Reproductive ulcer
lipoprotein of system and
(LDL) hospitali breast During:
receptors, zation disorders:
● Report
which for CHF Rarely,
promptly
increases ● Reduce gynaecomastia
any of the
hepatic the risk .
following:
uptake of of
Skin and Unexplaine
LDL. angina
subcutaneous d muscle
tissue pain,
disorders: tenderness,
Alopecia, skin or
weakness,
Contraindicatio rash, pruritus, especially
urticaria.
n/s with fever
Vascular or malaise;
Hypersensitivit disorders: yellowing of
y to Epistaxis. skin or
atorvastatin, eyes;
Potentially stomach
myopathy,
Fatal: Severe pain with
active liver
rhabdomyolysi nausea,
disease,
s with acute vomiting,
unexplained
persistent
transaminase renal failure, or loss of
elevations, hepatitis, appetite;
pregnancy hepatic skin rash
(category X), failure. or hives.
lactation. Rarely, ● Administer
Stevens- as a single
Johnson dose any
syndrome, time of
anaphylaxis, day,
toxic without
epidermal regard to
necrolysis. food.
Swallow
tablets
whole, do
not crush,
break,
dissolve or
chew.
After:
● Advise
patient
that this
medication
should be
used in
conjunctio
n with diet
restrictions
(fat,
cholesterol
,
carbohydra
tes, and
alcohol),
exercise,
and
cessation
of
smoking.
Atorvastati
n/ezetimib
e does not
assist with
weight
loss.
● Assess for
muscle
pain,
tenderness
, or
weakness.
● Provide
comfort
measures
and
arrange for
analgesics
if
headache
occurs.
Reference/Source: Atorvastatin. Uses, Interactions, Mechanism of Action |

DrugBank Online. (n.d.). Retrieved November 8, 2021, from
https://go.drugbank.com/drugs/DB01076.
Name Mechanis Indication/s Side Nursing
of the m Of Effects/Adverse Responsibilities
Drug Action Reactions
Generic Carvedilo
Name: l inhibits Bradycardia, AV Before:
Carvedil exercise ● Hyperte block,
nsion, anginapectoris, ● Shake the drug
ol induce
alone hypervolemia,le before administration
Brand tachycard
Name: ia or with ucopenia,hypot
other ● Use only minimal
through ension,peripher
oral dose for minimal
Classific its al edema,
drugs, periods.
ation: • inhibition allergy,
of beta especia malaise, fluid ● Do not exceed its
Alpha- adrenoce lly overload,melen recommended dose.
and ptors. diuretic a,periodontitis,
beta- Carvedilo s hyperuricemia, ● Educate the patient
adrener l’s action ● Treatm hyponatremia,i and family about the
gic on alpha- ent of ncreased uses and
blocker 1 mild to alkaline recommended dose
severe phosphatase, of the drug.
•Antihy adrenergi CHF of glycosuria,prot
pertensi c ischemi
receptors hrombintime, ● Educate the patient
ve c or SGPT and and family about the
Dosage relaxes cardio
smooth SGOT possible side effects
: myopat levels,purpura,s of the medication.
6.2 mg muscle in hicorigi
vasculatu omnolence,imp
½ Tab n with ● Encourage family
re, otence,albumin
Route: digital to report unusual
leading uria,hypokinesi
NGT is,diure effects and changes
a,nervousness,
Frequen to tics, of the patient’s
reduced sleep disorder,
cy: ACE condition upon
periphera skin reaction,
(OD) inhibito administration.
tinnitus, dry
Timing: l vascular rs
resistanc mouth, anemia,
During:
8 AM e and an ● Left sweating
overall ventric
● Monitor BP and
reduction ular
pulse frequently
in blood dysfunc
during dose
pressure. tion
adjustment period
(LVD)af
At higher ter MI
doses, and periodically
calcium Contraindicati during therapy.
channel on/s
● Monitor the patient
blocking
for unusual effects
and
Hypersensitivi from the drug
antioxida
ty; severe
nt ● Administer the
chronic heart
activity drug within 30
failure,
can also minutes after
bronchial
be seen. opening the
asthma or
The container/ampule.
related
antioxida
bronchospasti
nt ● Assess for
c conditions;
activity orthostatic
severe
of hypotension when
hepatic
carvedilol assisting patient up
impairment.
prevents from supine position.
Patients with
oxidation
NYHA class IV ● If heart rate
of low
cardiac decreases below 55
density
failure, 2nd or beats/min, decrease
lipoprotei
3rd ° AV dose. Monitor intake
n and its
block, sick and output ratios and
uptake
sinus daily weight.
into
syndrome
coronary
(unless a After:
circulatio
permanent
n.
pacemaker is ● Report difficulty
in place), breathing, swelling of
cardiogenic extremities, changes
shock or in color of stool or
severe urine, very slow
bradycardia. heart rate, continued
Lactation. dizziness.
Reference/Source: https://www.scribd.com/doc/62250558/Carvedilol-Drug-Study-
www-RNpedia-com
DRUG STUDY

Drug Of Action Responsibilities
Generic Produces Fever Minimal GI Before:
Name: analgesia by reduction. upset. 1. Do not
PARACETAM unknown Temporary Thrombocytope exceed
OL mechanism, relief of mild to nia 4gm/24hr.
perhaps by moderate pain. Urticaria In adults
Brand Name: action on Generally as CNS stimulation and
peripheral substitute for Liver Damage 75mg/kg/
nervous aspirin when day in
system. the latter is not children.
Classification Reduces tolerated or is 2. Do not
: fever by contraindicated take for
NONNARCOT direct action . >5days for
IC on pain in
ANALGESIC, hypothalamu Contraindicatio Adverse children,
ANTIPYRETI s heat- n/s Reactions ten days
C regulating Hypersensitivity Body as a for pain in
center with to Whole: adults, or
consequent acetaminophen Negligible with more than
Dosage: peripheral or phenacetin; recommended three days
500 MG vasodilation, use with dosage; rash. for fever in
sweating, alcohol. Acute adults.
and poisoning: 3. Extended-
Route: dissipation of Anorexia, Release
PO: NGT heat. Unlike nausea, tablets are
aspirin, vomiting, not to be
acetaminoph dizziness, chewed.
Frequency: en has little lethargy, During:
Q4H PRN effect on diaphoresis, 4. Monitor
FOR >38’C platelet chills, epigastric CBC, liver,
aggregation, or abdominal and renal
Timing: does not pain, diarrhea; functions.
4-8-12 affect onset of 5. Assess for
bleeding hepatotoxicity— fecal
time, and elevation of occult
generally serum blood and
produces no transaminases nephritis.
gastric (ALT, AST) and 6. Avoid
bleeding. bilirubin; using OTC
hypoglycemia, drugs with
hepatic coma, Acetamino
acute renal phen.
failure (rare). 7. Take with
Chronic food or
ingestion: milk to
Neutropenia, minimize
pancytopenia, GI upset.
leukopenia, After:
thrombocytope 8. Report
nic purpura, N&V.
hepatotoxicity cyanosis,
in alcoholics, shortness
renal damage. of breath,
and
abdominal
pain as
these are
signs of
toxicity.
9. Report
paleness,
weakness,
and
heartbeat
skips
10. Rep
ort
abdominal
pain,
jaundice,
dark urine,
itchiness,
or clay-
colored
stools.
11. Rep
ort pain
that
persists
for more
than 3-5
days
Name of Mechanis Indication/s Side Effects Nursing

the Drug m Of Responsibilities
Action
Generic The 1. Symptom anxiety, Before:

Name: mode of atic relief nervousness,
orphenad action of of mild to agitation, 1. Check
irregular heartbeats, 10 rights
rine orphenad moderate
easy bruising
citrate rine has pain of unusual tiredness, to
with not been acute medicati
aspirin clearly musculos on
and identified keletal 2. Assess
caffeine , but disorders. the need
may be for
Brand 2. The medicati
related
Name: orphenad on
to its
rine administ
Norgesic analgesic
compone ration
forte propertie
nt is such as
s. pain
Classificat Norgesic indicated
level
ion: and as an
3. Assess
Norgesic adjunct to
vital
Analgesic rest, phys
Forte signs
Tablets ical especiall
do not therapy, y
directly and other respirato
relax measures ry rate
tense for the 4. Assess
skeletal relief of for
Dosage:
discomfor irregular
muscles
t heartbea
in man.
associate ts, easy
d with bruising
acute which
painful prevents
continua
musculos
tion of
keletal
Route: the drug
conditions
NGT During:
Contraindication Adverse Reactions 1. Assess
/s for level
of pain
Because of the CNS: Headache, relief
mild anti- dizziness, light- and
cholinergic headedness, anxiety, administ
effect of
Frequenc emotional lability, er prn
orphenadrine,
y: Norgesic and fatigue, malaise, dose as
Norgesic Forte drowsiness, anxiety, needed
8-4-12 confusion, depression, but not
Tablets should
not be used in aseptic meningitis. to
patients with exceed
glaucoma, CV: Hypertension, the
pyloric or palpitation, congestive recomm
duodenal heart failure (patient ended
obstruction, total
Timing: with marginal cardiac
achalasia, daily
prostatic function); peripheral
edema. dose.
hypertrophy, or
obstructions at 2. Monitor
the bladder Special
vital
neck. Norgesic Senses: Amblyopia
signs
and Norgesic (blurred vision,
and
Forte Tablets decreased visual acuity,
are also assess
scotomas, changes in
contraindicated for
color vision);
in patients with orthosta
nystagmus, visual-field
myasthenia tic
gravis and in defects; tinnitus,
hypoten
patients known impaired
sion or
to be sensitive hearing. GI: Dry mouth,
signs of
to aspirin or gingival ulcerations,
caffeine. CNS
dyspepsia, heartburn,
depressi
nausea, vomiting,
The drug is on.
anorexia, diarrhea,
contraindicated
constipation, bloating, 3. Disconti
in patients who
flatulence, epigastric or nue drug
have
abdominal discomfort or and
demonstrated a
pain, GI notify
previous
ulceration, occult blood physicia
hypersensitivity
loss. n if S&S
to the drug.
of
Hematologic: Thromboc
hyperse
ytopenia, neutropenia,
nsitivity
hemolytic or aplastic
occur.
anemia, leukopenia;
decreased Hgb, Hct; 4. Assess
transitory rise in AST, bowel
ALT, serum alkaline and
phosphatase; rise in bladder
(Ivy) bleeding function;
time. GU: Acute renal report
failure, polyuria, urinary
azotemia, cystitis, frequenc
hematuria, y or
nephrotoxicity, retention
decreased creatinine .
clearance.
5. Use
Skin: Maculopapular seizure
and vesicobullous skin precauti
eruptions, erythema ons for
multiforme, pruritus, patients
rectal itching, acne. who
have a
Body as a Whole: Fluid
history
retention with edema, of
Stevens-Johnson
seizures
syndrome, toxic or who
hepatitis,
are
hypersensitivity concurre
reactions, anaphylaxis,
ntly
bronchospasm, serum using
sickness, SLE,
drugs
angioedema. that
lower
the
seizure
threshol
d.
After:
6. Monitor
ambulati
on and
take
appropri
ate
safety
precauti
ons.
Name of Mechanism Indication/s Side Effects Nursing
the Drug Of Action Responsibilities
Generic Bacteriosta Prevention of Change in taste Before:
Name: tic or dental caries 1. Assess the need
Chlorhexidi bactericidal Other Oral staining of for chlorhexidine
ne in action, Complications in teeth, mouth, administration
depending Individuals with tooth fillings, 2. Assess for side
Brand on Altered and dentures or effects and
Name: concentrati Immunocompete other mouth adverse effects
on attained nce appliances before
Classificatio at site and l continuation of
n: susceptibili Decontamination tongue tip chlorhexidine
Anti- ty of in Critically Ill irritation administration and
infectives, organism. Patients provide specific
Miscellaneo supportive or
us Cationic palliative oral
compound; mouth care
antibacteri 3. Assess for any
Route: al activity obstructions or
Mouth results foreign objects in
from the mouth or
attraction suction secretions
between as needed
Frequency: positively
TID charged Contraindication/ Adverse During:
chlorhexidi s Reactions 4. maintain
ne and Hypersensitivity Increased aseptic technique
Timing: negatively Reactions staining of 5.Advise patients
8-4-12 charged teeth, esthetic that the solution
bacterial restorations, may cause some
cell and other oral tooth discoloration
surfaces. surfaces; or increase in
Becomes increased tartar (calculus)
adsorbed calculus formation. Import
onto cell formation; ance of contacting
surfaces of alteration of dental health-care
susceptible taste perception. provider for
organisms Subgingival removal of any
and inserts: Toothac stain or tartar at
disrupts he, upper least every 6
cell respiratory months or more
membrane infection, heada frequently if
integrity che. needed.
resulting in 6.Advise patients
increased that the solution
permeabilit may taste bitter
y. and can affect how
foods and
beverages taste;
this usually
becomes less
noticeable with
continued
use. Using the
solution after
meals may avoid
taste interference.
7.Subgingival
insert: Advise
patients that some
mild to moderate
sensitivity is
normal during first
week after insert
placement;
importance of
promptly notifying
dental health-care
provider if pain,
swelling, or other
problems occur.
8. observe for
effectiveness by
assessment of oral
mucous
membranes turgor
and appearance
9. observe for
signs of infection
and inflammation
10. if signs of
infection are
present, initiate
culture and
sensitivity to
address the
infection
After:
11. Importance of
informing
clinicians of
existing or
contemplated
concomitant
therapy, including
prescription and
OTC drugs, and
any concomitant
illnesses.
12. evaluate
effectiveness of
the medication by
assessment of oral
anatomy and
status
13. evaluate if
aseptic techniques
were done
Name of the Mechanis Indication/s Side Nursing

Drug m Of Effects Responsibilities
Action
Generic Name: Expands Temporary Frequent: Before:

intestinal relief of acute Some
BISACODYL fluid constipation degree of 1.Determine number
volume by and for abdominal of bowel movements
Brand Name: before administration
increasing evacuation of discomfort
Dulcolax epithelial colon before , nausea, 2.Assess patency of
permeabili flexible mild nasogastric tube
ty sigmoidoscopy cramps, before administration
Classification: without biopsy. faintness..
Induces 3. Ensure the drug is
GASTROINTESTI peristaltic used to cleanse well crushed to
NAL AGENT; contractio colon before prevent clogging in
ns by delivery and to the nasogastric tube
STIMULANT direct relieve while administration
LAXATIVE stimulatio constipation in
n of patients with
Dosage:
sensory brain injury
During:
1 tab nerve
endings in 1.Assess bowel
Contraindicatio Adverse
the sounds for
n/s Reactions
colonic peristalsis.
Route: NGT
wall. Acute surgical Systemic
abdomen, effects not 2.Monitor daily
nausea, reported. pattern of bowel
Frequency: qHS vomiting, Mild activity, stool
( Hold if >2 BM) abdominal cramping, consistency; record
cramps, nausea, time of evacuation.
intestinal diarrhea,
obstruction, fluid and 3.Assess for
Timing: 8 pm abdominal
fecal electrolyte
impaction; use disturbanc disturbances.
of rectal es 4.Institute measures
suppository in (especially to promote
presence of potassium defecation
anal or rectal and 5.Do not take
fissures, calcium antacids, milk, or
ulcerated other medication
hemorrhoids, within 1 hr of taking
proctitis. medication
(decreased
effectiveness).
After:
1.Report unrelieved
constipation, rectal
bleeding, muscle
pain or cramps,
dizziness, weakness.
2.Evaluate
periodically patient's
need for continued
use of drug;
bisacodyl usually
produces 1 or 2 soft
formed stools daily.
3.Monitor patients
receiving
concomitant
anticoagulants.
(Apixaban)Indiscrimi
nate use of laxatives
results in decreased
absorption of vitamin
K.
4. Evaluate signs of
hypokalemia and
metabolic acidosis
5. If bowel
movements become
frequent, provide
perianal care also
maintaining aseptic
technique

Stimulates Treatment of Frequent Before:
Generic Name: alpha2 - hypertension (40%– 1. Obtain B/P
Clonidine adrenergic alone or in 10%): Dry immediately
receptors, combination with mouth, before each
reducing other constipation. dose is
Classification: sympathetic antihypertensive Occasional administered, in
Alpha2 - CNS agents. (5%–1%): addition to
adrenergic response. Tablets, regular
agonist. Epidural: Injection: monitoring (be
Antihypertensive Prevents pedal alert to B/P
. pain signal edema, loss fluctuations).
transmissio of appetite, 2. Verify MAR
n to brain decreased and doctor’s
Dosage: and sexual orders
75 mg 1 tab produces function, 3.Assess for
analgesia at itching eyes, signs of
pre- and Contraindication/ Adverse hypotension if
Route: NGT post-alpha- s Reactions present withhold
adrenergic Contraindications Overdose 4. Determine
receptors in : produces history of allergy
spinal cord. Hypersensitivity profound to clonidine or
Frequency: Therapeutic to cloNIDine. hypotension, its similar
Effect: Severe coronary irritability, constituents
Q6h prn for BP Reduces insufficiency, bradycardia, 5. Determine
>(greater than peripheral recent MI, respiratory concurrent use
or equal to) 140 resistance; cerebrovascular depression, of other
mmHg decreases disease, chronic hypothermia antihypertensive
B/P, heart renal , miosis s
Timing: rate. impairment, (pupillary
6-12-2-12 Produces preexisting constriction) During:
analgesia. bradycardia, , 1.Monitor B/P,
sinus node arrhythmias, pulse, mental
dysfunction, apnea. status.
conduction Abrupt 2.Monitor daily
disturbances; withdrawal pattern of bowel
concurrent use may result activity, stool
with digoxin, in rebound consistency. If
diltiaZEM, hypertensio cloNIDine is to
metoprolol, n associated be withdrawn,
verapamil. with discontinue
nervousness concurrent
, agitation, betablocker
anxiety, therapy several
insomnia, days before
paresthesia, discontinuing
tremor, cloNIDine
flushing, (prevents
diaphoresis. cloNIDine
May produce withdrawal
sedation in hypertensive
pts with crisis).
acute CVA. 3. Assess for
MAP which
indicates the
perfusion or
tissues and
organs in the
body
4.Determine
electrical
conduction of
the heart by
interpreting ECG
findings
5. Provide
comfort
measures such
as emotional
support, hygiene
and on-time
institution of
certain
procedures
6. Provide
opthalmological
hygiene by
cleansing OD
and OS with
saline solution or
prescribed
cleansing
solution
After:
1.Avoid tasks
that require
alertness, motor
skills until
response to drug
is established.
2.To reduce
hypotensive
effect, rise
slowly from lying
to standing.
3. Evaluate for
constipation and
anticipate
administration of
laxatives or
increase in the
rate of IV fluids
4. Evaluate for
respiratory rate
which is a
priority ABC

Generic Stimulates maintenance Frequent Before:

Name: beta2 - treatment of (28%):
adrenergic asthma and Headache. 1. Screen for
Salbutamol concomitant
receptors in prevention of
Occasional medications
Brand lungs, bronchospasm
(7%–3%): known to
Name: resulting in in pts with
Cough, prolong QT
relaxation reversible interval.
of bronchial obstructive dizziness,
2. Assess lung
smooth airway disease vertigo, throat
sounds, vital
Classificatio dryness/irritat
muscle. signs.
n: ion,
Intervention/e
Therapeutic
Beta2 - Rare (Less valuation
Effect: 3. Assess first
adrenergic Than 3%):
agonist Relieves Palpitations, heart rate to
(long- bronchospa tachycardia, determine for
acting). sm, nausea, tachycardia
CLINICAL: reducing heartburn, GI which can be
Bronchodilat airway distress, exacerbated by
or. resistance. diarrhea. the drug
4. Gather
baseline ECG
findings
Dosage: 1
neb During
5. Monitor rate,
depth, rhythm,
Contraindicati Adverse type of
on/s Reactions respiration;
quality/rate of
Contraindicati May prolong pulse, B/P.
ons: QT interval Assess lungs
Route: Hypersensitivit (can for wheezing,
Tracheosto y to precipitate rales, rhonchi.
my salmeterol. ventricular 6. Periodically
Treatment of arrhythmias). evaluate serum
status Hypokalemia, potassium
asthmaticus, hyperglycemia levels.
acute episodes may occur. 7. Keep canister
of asthma or at room
COPD. Use as temperature
Frequency: (cold
q8h prn for monotherapy
decreases
dyspnea in treatment
effects).
of asthma
8. Do not stop
without medication or
concomitant exceed
long-term recommended
asthma dosage.
control
Timing: After:
medication
1. Report chest
(e.g., inhaled
8-4-12 pain, dizziness.
corticosteroids 2. Monitor for
). Cautions: signs of
Not for acute infection
symptoms; 3. Institute
may cause aseptic
paradoxical techniques and
maintain
bronchospasm
, severe sterility
asthma. 4. Monitor
Cardiovascular hyperglycemia
5. Evaluate lung
disorders
sounds and
(coronary
respiratory
insufficiency, rate
arrhythmias,
hypertension),
seizure
disorders,
diabetes,
hyperthyroidis
m, hepatic
impairment,
hypokalemia

Drug Action Responsibiliti
es
Generic Name: is an alkaloid Temporary gas, stomach Before:

derived from relief of pain pain,
Vi-gel cream plants and is from gouty constipation; 1.Assess
the active arthritis itching, skin and
Brand Name: joint area for
ingredient in increased
sweating; any lesions
hot peppers. or scaling
It is used as skin redness,
Classification: itching,
a topical 2.Record
dryness,
SKIN AND analgesic. Its estimate
scaling, or
precise pain baseline
MUCOUS peeling where
mechanism is rate by facial
MEMBRANE the medicine
grimace
AGENT; TOPICAL not fully was applied.
ANALGESIC understood. 3.Check Mar
Substance P and doctor’s
is thought to order
act as a
Dosage: 4. Position
principal
patient in a
neurotransmi
tter of pain comfortable
Route:integumen sensations Contraindicatio Adverse position for
tary from the n/s Reactions better
exposure of
peripheral Hypersensitivit CNS: Concentra the affected
neurons to y to vigel tion >1%: joints
Frequency: BID the CNS. cream or any neurotoxicity,
ingredient in hyperalgesia. During:
It is thought
that the drug the cream.
Skin: Burning, 1.Maintain
Timing:6 am-6
renders skin Patients on stinging, aseptic
pm technique
and joints ACE inhibitors. redness, itching
insensitive to Safety and .
pain by 2.Ensure
efficacy in gentle
preventing children <2 y Other: Cough.
manipulation
the have not been while
reaccumulatio established. applying the
n of cream
substance P
in peripheral 3. Provide
sensory comfort
measures
neurons.
such as
Thus it is an applying cold
effective compress if
peripheral pain persists
analgesic.
4. Assist in
joint mobility
by passive
flexion and
extension of
the affected
extremities
After:
1.Monitor for
significant
pain relief,
which may
require 4–6
wk of
application
three or four
times daily.
2.Monitor for
and report
signs of skin
breakdown
as these
generally
indicate
need for
drug
discontinuati
on.
3.Report
local
discomfort at
site of
application if
discomfort is
distressing
or persists
beyond the
first 3–4 d of
use.
4.Notify
physician if
symptoms
do not
improve or
condition
worsens
within 14–28
d.
Name of Mechanism Indication/s Side Nursing
the Drug Of Action Effects/Adverse Responsibilities
Reactions
Generic Acute herpes Before:

Name: zoster CNS: headache,
Potassium Inhibits viral infections dizziness, 1. Verify patient's
Citrate DNA (shingles). fatigue. identity
synthesis in Treatment/su
herpes- GI: diarrhea, 2. Assess for patient's
ppression of allergic reaction to
Brand infected nausea,
recurrent drug
Name: cells only. vomiting.
herpes
TASCIT genitalis in 3. Assess patient's
immunocomp history for
Classificati Therapeutic etent contraindications to d-
on: Effects: patients. rug
AUTONOM Decreased Treatment of
duration of 4. Verify any
IC recurrent
herpes medication order and
NERVOUS mucocutaneo
zoster make sure it’s
SYSTEM us herpes
infection complete. The order
AGENT; simplex virus
with should include the
ALPHA- (HSV)
decreased drug name, dosage,
AND infection in
duration of frequency and route of
BETA- HIV-infected
viral administration.
ADRENER patients.
GIC shedding. 5. Confirm
ANTAGONI Decreased appropriateness of the
lesion Contraindicati
ST; dose using a current
formation on/s
ANTIHYPE drug reference.
RTENSIVE and
improved Hyperkalaemi
healing in a; severe 1 During:
Dosage: recurrent renal
10 MEQS HSV 1.Assess for signs and
2 mg/tab infection. impairement; symptoms of
untreated hyperkalemia and
hypokalemia.
Route:
PO 2. Monitor pulse,
Addison's BP,and ECG
Frequenc disease; periodically during IV
y: severe tissue therapy.
TID trauma;
hyperkalemic 3.Determine serum
familial magnesium level if
Timing: periodic patient has refractory
paralysis hypokalemia;
8 am hypomagnesemia
should be corrected to
facilitate effectiveness
of potassium
replacement. Instruct
patient to avoid salt
substitutes or low salt
milk or food unless
approved by health
care professional.
4. Assess for
symptoms of
hyperkalemia toxicity.
5.Emphasize correct
method of
administration. GI
irritation or ulceration
may result from
chewing-enteric
coated tablets or
insufficient dilution of
liquid or powder
forms.
After:
1. Check the affected

person's movements
and reflexes, and
response.
2. Observing
breathing patterns
3.Test reflective eye

movement
4.Check if there are

adverse effect of the
patient after
administering the
drug.
5.Make sure that the

patient is well before
leaving
Reference/Source: Gervacio, J. M. (n.d.). K pota. Scribd. Retrieved October 21,

2022, from https://www.scribd.com/document/346948654/K-pota
Name of Mechanism Indication/s Side Effects/Adverse Nursing Responsibilities

the Drug Of Action Reactions
 Acute diarrhea Before:

Brand lasting 14 days Side Effects:
Name: It aids in 1. Verify patient's
caused by
the ●Immune System identity
Erceflora illness,
restoration Disorders
+respule medicines, or 2. Assess for patient's
of the toxins. ●Hypersensitivity allergic reaction to drug
intestinal
Classific microbial Reactions
 Chronic or 3. Assess patient's
ation: flora, recurrent history for
Antidiarr which has diarrhea (rashes,urticaria,ang contraindications to
heals been lasting more ioedema) drug
altered as than 14 days.
Adverse Effects:● No 4. Verify any
a result of
Dosage: adverse effects medication order and
a Contraindication
variety
were noted make sure it’s
of /s
Route: inclinical trials of complete. The order
microbial
B.clausii or in should include the drug
disorders.
Frequenc ● the product name, dosage,
y: Hypersensitivity information frequency and route of
BID to B.clausii or administration.
It to any of
produces a the product 5. Confirm
Timing: variety of excipients appropriateness of the
vitamins, dose using a current
particularl drug reference.
y group B
● Not for use in
vitamins,
immunocompro
and thus During:
mised persons
helps to
(cancer patients
correct 1. Shake the drug
on
vitamin before administration
chemotherapy,
deficiencie
patients taking 2. Use only a minimal
s caused
immunosuppres dose for minimal
by
sant meds) periods.
antibiotics
and 3. Do not exceed its
chemother recommended dose.
apeutic
agents. 4. Monitor the patient
Normalizat for unusual effects from
ion of the drug.
intestinal
5. Administer the drug
flora is
within 30 minutes
promoted.
After:
1. Check the affected
person's movements
and reflexes, and
response.
2. Observing breathing
patterns
3.Test reflective eye

movement

adverse effect of the
patient after
administering the
drug.
5.Make sure that the

patient is well before
leaving.
References: Bacillus Clausii Uses, Benefits & Dosage - Drugs.com Herbal Database.
(n.d.). Drugs.com. https://www.drugs.com/npp/bacillus-clausii.htmlDrugs.com
(2020). Bacillus Clausii. Drugs.com. https://www.drugs.com/npp/bacillus-
clausii.html Using Erceflora Against Intestinal Bacteria. (2020, May 2). Hello
Doctor. https://hellodoctor.com.ph/drugs-supplements/erceflora/
Name of the Mechanism Of Indication/s Side Nursing

Drug Action Effects/Advers Responsibilities
e Reactions
Generic Decreases Treatment of

Name: viscosity of respiratory Nausea,
acetylcystei respiratory affections Vomiting , & Before:
ne tract characterized other GI
1. Verify patient's
secretions by thick & symptoms,
identity
and promote viscous generalized
Brand their removal hypersecretion 2. Assess for
Name: breaking s; acute urticaria patient's allergic
Acetadote disulfide &chronic accompaniedb reaction to drug
bonds. In bronchitis & its y mild fever,
acetaminonhe exacerbation, hypotension, 3. Assess patient's
Classificatio n overdose, it pulmonary wheezing, history for
n: protects the emphysema, dyspnea,and contraindications to
Antidiarrheal liver from mucoviscidosis stomatitis. drug
s injury by & 4. Verify any
restoring medication order
glutathione bronchiectasis.
Dosage: Antidote in and make sure it’s
200mg/Sach acting as poisoning complete. The order
et 1 sachet alternate caused by should include the
in ½ glass substrate for paracetamol, drug name, dosage,
acetaminophe carbon frequency and route
Route: n metabolism tetrachloride,a of administration.
rsenic, metallic 5. Confirm
Frequency: mercury
TID appropriateness of
inhalation, the dose using a
yellow current drug
Timing: 8am
– 2pm – phosphorus & reference.
6pm for
cyclophospha
mide induced During:
hemorrhagic
1. Monitor signs of
cystitis
angioedema,
including rashes,
Contraindicatio raised patches of
n/s red or white skin
(welts),
burning/itching skin,
Hypersensitivit
swelling in the face,
y.
and difficulty
Phenylketonuri breathing.
a (contain
2.Monitor other
aspartate
signs of allergic
reactions and
anaphylaxis,
especially after IV
administration.
Signs include
pulmonary
symptoms
(tightness in the
throat and chest,
wheezing, cough,
dyspnea) and skin
reactions (rash,
pruritus, urticaria).
3.Monitor signs of
bronchospasm and
respiratory
irritation, including
wheezing, cough,
dyspnea, increased
secretions, and
tightness in the
chest and throat.
4. When used as a
mucolytic, assess
the quantity and
consistency of
sputum to help
document whether
this drug is
successful in
reducing the
viscosity of
respiratory
secretions.
5. Notify physician
of these signs
immediately.
After:
1. Check the
affected person's
movements and
reflexes, and
response.
2. Observing
breathing patterns
3.Test reflective
eye movement

adverse effect of
the patient after
administering the
drug.
5.Make sure that

the patient is well
before leaving.
Reference: Sinsuat, J. (n.d.). Drug Study(N Acetylcysteine. Scribd. Retrieved

October 21, 2022, from https://www.scribd.com/document/78591839/Drug-Study-
N-Acetylcysteine
PROBLEM LIST
1. Ineffective airway clearance related to presence of artificial

airway
2. Risk for ineffective cerebral tissue perfusion
3. Risk for infection

4. Risk for Impaired Skin Integrity
5. Impaired Physical mobility
6. Impaired Verbal Communication
DEFINING NURSING SCIENTIFIC PLAN OF CARE NURSING RATIONALE

CHARACTE DIAGNOSIS ANALYSIS INTERVENTIO
RISTICS NS
Ineffective Ineffective INDEPENDENT INDEPENDEN
SUBJECTIV airway airway SHORT TERM: T
E: clearance clearance is
related to the inability to After 1- 2hours
presence of maintain a of Intervention: 1. Suction
airway, as 1.To clear
artificial patent airway.
needed secretions
airway: Usually,
tracheostom protective
y as mechanisms Patient's
evidence by such as respiration will 2. Elevate the 2. To
mucus microscopic improve and head of the promote
OBJECTIVE difficulty of bed as
secretions organisms or physiological
: breathing will appropriate
coughing and
keep the be relieved psychological
respiratory ease of
Temp: 36.0 tract free of maximal
obstructions inspiration.
RR: 14 and
secretions.
PR: 73 However, if 3. Monitor
3. To verify
any of these pulse
maintenance
O2: 95 mechanisms oximetry, as
/improvemen
are impaired, LONG TERM: indicated
- attached t in O2
there is a risk
to 02 saturation.
for a
compromised
- After 2 or 3
airway.
production days of 4. Reposition
interventions, 4. Encourage a
of mucus the client
patient will position of
secretions frequently if
maintain a comfort.
immobility is
patent airway a factor.
5. Auscultate 5.
lung sounds Diminished
lung sounds
or
adventitious
lung sounds
such as
rhonchi, or
crackles can
result from
an
accumulation
of secretions
or a blocked
airway.
DEPENDENT
DEPENDENT
1.for
1. administer management
oxygen as of underlying
ordered pulmonary
condition,
respiratory
distress, or
cyanosis
2. give 2.works by
respiratory relaxing and
medication as opening air
ordered passages in
(salmeterol + the lungs,
fluticasone) making it
easier to
breathe.

CHARACTE DIAGNOSIS ANALYSIS INTERVENTIONS
RISTICS
INDEPENDENT
SUBJECTIV Risk for Tracheostomy is SHORT TERM:
E: infection a surgical
related to procedure in The patient will
excessive which an opening not experience 1. perform hand 1.in order to
pooling of is done into the aspiration hygiene and reduce the
secretions trachea to during his wear clean risk of
and prevent or hospitalization. gloves infection
bypassing of relieve the
upper airway
respiratory obstruction 2. Assess the 2. Fever
defenses as and/or to serve patient's vital may be a
evidence by as access for signs, especially manifestation
patient suctioning and the client's of an
having a for mechanical temperature infection or
OBJECTIVE: tracheostom ventilation and inflammatory
y and other modes of . process.
LONG TERM:
increased oxygen delivery
secretions. (tracheostomy 3.Assess skin 3. This is a
Client will
Temp: 36.0 collar, T-piece). integrity under common site
remain free of
tracheal ties. for infection
infection, as
RR: 14 A patient with a and skin
evidenced by
tracheostomy normal breakdown.
PR: 73 “breathes” temperature, 4. Suction
through an normal sputum 4. Suctioning
O2: 95 opening that a secretions clears mucus
culture, normal
surgeon through white blood cell from the
BP: 130/80 a procedure tracheostomy
(WBC) count,
called a absence of tube and is
-Under
tracheotomy purulent essential for
tracheosto
created through drainage proper
my
the trachea around the breathing.
compared to how stoma, and Also,
the average clear breath secretions
person who sounds. left in the
breathes through tube could
their nose. The become
nose in an contaminated
average person and infection
acts as a filter could
(which filters out develop.
bacteria, virus,
and debris from 5. perform 5.
entering the tracheostomy Tracheostom
lungs). care y care is
However, this is done to keep
not the case for a the trach
person who has a
“trach”. A tube clean.
person with a This helps
tracheostomy is prevent a
at risk for many clogged tube
different medical and
issues due to the decreases
in ability to clear the risk for
secretions and infection.
the amount of
care it takes to DEPENDENT
care for a
tracheostomy 1.Administer
etc. medication as 1. to treat
ordered the
underlying
condition and
promote
optimal
health

CHARACTE DIAGNOSIS ANALYSIS INTERVENTIONS
RISTICS
Risk for INDEPENDENT INDEPENDENT
SUBJECTIV ineffective Ineffective SHORT TERM:
E: cerebral cerebral
tissue perfusion After the 8
results in poor hours of shift: 1. Assess 1. Any
perfusion
cellular patient will patient’s changes
secondary to
nourishment demonstrate mental in LOC,
stroke
and stable vital status orientatio
oxygenation; it signs and no n, GCS
might be brief, signs of score, or
with little or no increased other
implications for intracranial neurologi
the patient’s pressure cal
health, or it can monitori
be more ng
chronic or methods
acute, with might
potentially indicate
OBJECTIVE
harmful a
: decrease
consequences.
LONG TERM: d
Temp: When
ineffective cerebral
36.0 Patient will
cerebral perfusion
maintain usual .
RR: 14 perfusion or improved
becomes LOC, cognition,
PR: 73 chronic, it can 2. Monitor
and motor or
cause cell and sensory the
O2: 95 tissue damage patient’s 2. Blood
function.
or death. vital pressure
BP: signs. within
130/80 the
normal
-Extreme
range
weakness
promotes
- right adequate
hemiparesi cerebral
s perfusion
.
- Hypotens
ion may
lead to
inadequa
3. Elevate te
the Head perfusion
of Bed of the
brain.
3. If a
patient
has
intracrani
al
pressure
(ICP) the
HOB
should
be
elevated
to 30
degrees
and their
neck
4. Assess kept in a
motor neutral
response position
to simple to
command promote
s circulatio
n and
lower
pressure.
4. Measures
5. Evaluate
overall
pupils,
awarenes
noting
s and
size,
ability to
shape,
respond
equality,
to
and light
external
reactivity.
stimuli.
5. Pupil
reactions
are
regulated
by the
oculomot
or (III)
cranial
nerve
and are
DEPENDENT useful in
determini
ng
whether
1. Administe
the
r
medicatio brainste
ns as m is
ordered intact.
(norgesic
forte)
2. Administe
r O2 as
ordered
1. Reduces
or
controls
fever and
its
deleterio
us effect
on
cerebral
metaboli
sm and
oxygen
needs
and
insensibl
e fluid
losses
2. Reduces
hypoxem
ia, which
is known
to
increase
cerebral
vasodilati
on and
blood
volume,
elevating
ICP.
XI. DISCHARGE PLANNING
General Case of the Patient:
Diagnosed with the following:
1. Cerebrovascular Disease: Subacute infarct on both thalamus and left
midbrain probably secondary to cardio-embolic stroke
2. Hypertensive cerebrovascular disease, atrial fibrillation in moderate
ventricular response with complete right bundle branch block
3. Impaired fasting glucose
4. T/C IBD vs colonic mass
Subjective Data Patient stated “Sugod karon, bantayan na nako ang
mga pagkaon nga akong gikaon ug mga kalihokan
nga akong gihimo aron malikayan nako ang ma-
stroke.”
Objective Data Patient portrays improvement with vital signs within
normal limits. Seen packed bags and ready for
discharge.
Assessment/Nursing Patient may go home as ordered by the physician.
Diagnosis Patient shows no unusualities upon assessment.
Planning After 10 minutes of patient health teaching, patient
will be able to understand the importance of following
treatment in order to prevent another stroke.
Intervention
Activity  Encouraged to ambulate and make sure home
is safe.
 Continue rehabilitation exercises to maintain
strength.
 Avoid vigorous activity until your doctor says it
is safe to do so.
 Ask your doctor when you will be able to return
to work.
 Do not drive unless your doctor has said it is
okay to do so.
Medication  Apixaban 2.5mg/tab 1 tab q12h
 Atorvastatin 80 mg 1 tab OD qHS
 Carvedilol 6.25 mg ½ tab OD
Environment The client is aware and understood the importance of

having a clean, comfortable and stress-free
environment. This can contribute to the improvement
of the client’s condition. Do not let anybody smoke in
your home.
Treatment The client and SO knows the purpose and action of
any treatment. Take home medications are vital for
the improvement of the client’s condition.
Health Teachings  Take medicines exactly as directed. Don’t skip
doses.
 Ask what side effects could occur. Report them
to your doctor.
 Talk to your doctor before you stop taking any
prescription medication.
 Do not share your prescription medication.
 Limit alcohol intake
 Control cholesterol level
 Learn stress management methods
 Instructed SO to check every day for pressure
sores at the heels, ankles, knees, hips,
tailbone, and elbows.
 Advised patient to avoid salty and fatty foods
and stay away from fast food restaurants to
make the heart and blood vessels healthier.
 Do not smoke.
 Maintain a healthy weight.
 Check blood pressure frequently.
Outpatient Referral Follow up check-up with Dr. Español after 1-week
discharge.
Diet  Reduce fat and cholesterol intake.
 Reduce the amount of sodium (salt) in diet
 Eat more fruits and vegetables
 Limit sweets and processed foods.
Evaluation Patient understood and cooperated with the teachings
and instructions provided.

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RLE REQUIREMENT

Ms. Tasha Baliquig, RN

Rabago III, Roberto

October 24, 2022

The word cerebrovascular is made up of two parts – "cerebro" which refers to

Blood Flow to the Brain

Stroke is an abrupt interruption of constant blood flow to the brain that

 Dizziness, nausea, or vomiting

Types of Stroke and Treatment

In most cases, the carotid or vertebral arteries do not become completely

Ischemic stroke is treated by removing the obstruction and restoring blood

The Merci Retriever, approved recently by the FDA, is a corkscrew-shaped

A hemorrhagic stroke can be caused by hypertension, rupture of an

Hemorrhagic stroke usually requires surgery to relieve intracranial (within

Endovascular treatment involves inserting a long, thin, flexible tube

Recovery and rehabilitation are important aspects of stroke treatment. In

A TIA is a temporary cerebrovascular event that leaves no permanent

Symptoms of a TIA may be similar to stroke, but they resolve quickly. In

 Smoking: Decrease risk by quitting smoking. Risk may be increased further

GORDON’S 11 FUNCTIONAL HEALTH PATTERN

1. Health Perception and Health Management Pattern

2. Nutrition and Metabolism

5. Cognition and Perception

6. Sleep and Rest

7. Self-Perception and Self Concept

8. Roles and Relationship

9. Sexuality and Reproduction pattern

10. Coping and Stress Tolerance

11. Values and Belief Pattern

1. Cerebral Cortex – responsible for speech, memory, logical and emotional

2. Appendix - hanging from the cecum is the wormlike appendix, a potential

4. Transverse colon - the ascending colon makes a turn and continuous to be

The intestinal immune system is key to the pathogenesis of inflammatory bowel

In ulcerative colitis, there is always mucosal inflammation that leads to edema,

URINALYSIS PATIENT’S RESULT

DATE TYPE OF EXAM SPECIMEN PATIENT’S RESULT SIGNIFICANCE/INTERPRETATION

INTERMEDIATE Patient needs a higher dose of Azithromycin

RESISTANT Resistant means that the bacteria can

SENSITIVE Patient will gain a therapeutic effect on these

VERY LIGHT GROWTH OF

RESISTANT Patient will not be able to use these

HEMATOLOGY PATIENT’S RESULT

HEMATOLOGY PATIENT’S RESULT

DATE TYPE OF EXAMINATION REFERENCE RANGE PATIENT’S RESULT SIGNIFICANCE/INTERPRETATION

DATE TYPE OF EXAMINATION INTERPRETATION REMARKS: SIGNIFICANCE/INTERPRETATION

DATE TYPE OF EXAMINATION PATIENT’S RESULT REFERENCE RANGE SIGNIFICANCE/INTERPRETATION

DATE TYPE OF EXAMINATION PATIENT’S RESULT REMARKS SIGNIFICANCE/INTERPRETATION

WHOLE ABDOMEN Axial slices of the whole No remarks seen on the

DATE TYPE OF EXAMINATION PATIENT’S RESULT REMARKS SIGNIFICANCE/INTERPRETATION

MACROSCOPIC 09-24-22 09-25-22 09-25-22 10-01-22

TEST UNIT NORMAL 09-16-

Name of the Mechanism Indication/s Side Effects Nursing

Name of the Mechanism Of Indication/s Side Effects Nursing

Name of the Mechanism Of Indication/s Side Effects Nursing

Reference: J.Rebamipide Drug study, retrieved April 21,2021 from

Generic Citicoline Supportive

Reference/Source: Availability. CHOLINE SALICYLATE. (n.d.). Retrieved November

Reference/Source: Atorvastatin. Uses, Interactions, Mechanism of Action |

Name of the Mechanism Indication/s Side Effects Nursing