GENERAL NURSING SCIENCE I

(GN-EN 104)
2020

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Course Description:
This course aims to equip students with the practical knowledge of the scientific nursing
process in the clinical care of patients with conditions of the genito-urinary system,
cardiovascular system, respiratory system and gastro-intestinal system including
communicable diseases in a general hospital.

Outcomes of Learning:
At the end of this course students will be able to:
 Apply the legal and ethical implications of disease management.
 Initiate and maintain a successful medical rehabilitation program for patients with
different health conditions.
 Demonstrate competence in the assessment and management of gastro-intestinal,
respiratory, cardiovascular and genito-urinary diseases/ disorders and their
comorbidities.
 Demonstrate competence in using palliative care approach in the care for patients with
advanced gastro-intestinal, respiratory, cardiovascular and genito-urinary disease/
disorders.

Course Outline:
 Medico-legal hazards in disease management
 Medical rehabilitation
 Assessment, and management of gastro-intestinal, respiratory, cardiovascular and
genito-urinary diseases/ disorders and their comorbidities.

Recommended Textbook
 Peate I., Wild K., 2018, Nursing Practice: Knowledge and Care, Wiley Blackwell,
ISBN-13: 978-1119237471
 CLINICAL COMPANION TO MEDICAL-SURGICAL NURSING: Assessment and
Management of Clinical Problems. 10th Edition, Sharon L. Lewis, et.al, ISBN
9780323371179, 2016
 Wilson, B. et al (2012). Nurse’s drug guide 2012 New Jersey: Prentice Hall. ISBN-
10: 0-13-259867-X or ISBN-13: 978-0-13-255867-9
Assessment
Objective Structured Clinical Examination (OSCE) pre-clinical placement, Log-book
practical procedures competency evaluations by clinical supervisors during clinical
placement, 3 procedures competency evaluations by clinical facilitator/lecturer during clinical
placement and Final OSCE post-clinical placement. Minimum pass rate for each competency
evaluation and OSCE is 70%.

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UNIT 1: ASSESSMENT AND MANAGEMENT OF CARDIOVASCULAR
DISORDER/DISEASES (CVDs)
Learning objectives
By the end of this session, students should be able to
 Define cardiovascular diseases/disorder
 List the risk factors for CVDs
 Outline the types of Cardiovascular diseases/disorder (CVDs)

INTRODUCTION
According to World Health Organization (2017), “Cardiovascular diseases/disorders (CVDs)
are the number 1 cause of death globally, more people die annually from CVDs than from
any other cause. An estimated 17.9 million people died from CVDs in 2016, representing
31% of all global deaths. Of these deaths, 85% are due to heart attack and stroke. Over three
quarters of CVD deaths take place in low- and middle-income countries. Out of the 17
million premature deaths (under the age of 70) due to noncommunicable diseases in 2015,
82% are in low- and middle-income countries, and 37% are caused by CVDs”.

DEFINITION
The cardiovascular/circulatory system supplies the body with blood and it consists of the
heart, arteries, veins, and capillaries.
Cardiovascular diseases/disorder (CVDs) is a general term which is used for conditions
affecting the heart or blood vessels. It's usually associated with a build-up of fatty deposits
inside the arteries (atherosclerosis) and an increased risk of blood clots.

CVDs can also be associated with damage to arteries in organs such as the brain, heart,
kidneys and eyes.

Most cardiovascular diseases can be prevented by addressing behavioural risk factors such as
tobacco use, unhealthy diet and obesity, physical inactivity and harmful use of alcohol using
population-wide strategies.

People with cardiovascular disease or who are at high risk of cardiovascular diseases (due to
the presence of one or more risk factors such as hypertension, diabetes, hyperlipidemia (any

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several acquired or genetic disorder or already established disease) need early detection and
management using counselling and medicines, as appropriate.

RISK FACTORS FOR CARDIOVASCULAR DISEASES/DISORDER

 Family history
 Unhealthy diet
 Physical activity
 Tobacco use
 Harmful use of alcohol
 Raised blood pressure (Hypertension)
 Raised blood glucose (diabetes)
 Raised blood lipids
 Overweight and obesity
 Age

TYPES OF CARDIOVASCULAR DISEASES/DISORDER

CVDs comprises many different types of condition. Some of these might develop at the same
time or lead to other conditions or diseases within the group.

Coronary heart disease – disease of the blood vessels supplying the heart muscle;

Cerebrovascular disease – disease of the blood vessels supplying the brain;

Peripheral arterial disease – disease of blood vessels supplying the arms and legs;

Rheumatic heart disease – damage to the heart muscle and heart valves from rheumatic
fever, caused by streptococcal bacteria (throat infection) that causes inflammation in the heart
and which can affect the function of heart valves.

Congenital heart disease – malformations of heart structure existing at birth;

deep vein thrombosis and pulmonary embolism – blood clots in the leg veins, which can
dislodge and move to the heart and lungs.

Heart attack- a sudden blockage to the heart’s blood flow and oxygen supply. It is also
known as myocardial infarction.

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Heart failure - wherein the heart cannot contract or relax normally.

Dilated cardiomyopathy - when the heart gets larger and cannot pump blood efficiently

Hypertrophic cardiomyopathy - when the heart muscle walls thicken and problems with
relaxation of the muscle, blood flow, and electrical instability develop.

Mitral regurgitation - when blood leaks back through the mitral valve of the heart during
contractions.

Mitral valve prolapse - part of the mitral valve bulges into the left atrium of the heart while
it contracts, causing mitral regurgitation.

Pulmonary stenosis - narrowing of the pulmonary artery reduces blood flow from the right
ventricle (pumping chamber to the lungs) to the pulmonary artery (blood vessel that carries
deoxygenated blood to the lungs).

Aortic stenosis - a narrowing of the heart valve that can cause blockage to blood flow
leaving the heart.

Atrial fibrillation - an irregular rhythm that can increase the risk of stroke

Aneurysm - a bulge or enlargement in an artery that can rupture and bleed

Atherosclerosis - in which plaque forms along the walls of blood vessels, narrowing them
and restricting the flow of oxygen rich blood.

Strokes are caused by disruption of the blood supply to the brain. This may result from either
blockage (ischaemic stroke) or rupture of a blood vessel (haemorrhagic stroke).

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MYOCARDIAL INFACTION (HEART ATTACK)

Learning objectives

At the end of this session, students should be able to

 Define myocardial infarction

 Describe the pathophysiology of myocardial infarction
 List the signs and symptoms of myocardial infarction
 Briefly describe how to diagnose heart attack
 Describe complication of myocardial infarction
 Enumerate the prevention of myocardial infarction
 Outline nursing intervention of myocardial infarction
 Outline the health education that should be given to patients

DEFINITION

Myocardial infarction (Heart attack) is a sudden blockage to the heart’s blood flow and
oxygen supply. It is the death of a segment of heart muscle caused by a loss of blood supply.
The blood is usually cut off when an artery supplying the heart muscle is blocked by a blood
clot.

A dynamic process by which one or more regions of the heart experience a prolonged
decrease or cessation in oxygen supply due to insufficient coronary blood flow, necrosis and
death of the myocardiac tissues (Lippincott, 2010)

Pathophysiology & Etiology

 Severe atherosclerosis precipitate thrombus

 Thrombus formation begins with plaque rupture and platelets' adhesion to the
damaged area with fibrinogen binding to them
 As the adhesion of platelets continues, thrombus grow bigger and occlude the artery
 Other etiologic factors include coronary artery spasm, embolism, inflammation of
arteries, severe exertion & surgical procedures
 Different degree of damage occurs to the heart muscle:
- Zone necrosis: death of heart muscle due to extensive & complete oxygen
deprivation-irreversible damage

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 - Zone of injury: heart muscle surrounding the area of necrosis inflamed,
&injured but still viable provided they receive oxygen
- Zone of ischemia: heart muscle surrounding the area of injury is ischemic&
viable not endangered unless infarction continues.
 Left Ventricle is a common & dangerous location because it is the pumping chamber
 The prognosis myocardial infarction is determined by the severity of the attack.

CLINICAL MANIFESTATION (signs and symptoms)

 Pain, fullness, and/or squeezing and crushing sensation of the chest. Pain may last for
more than 15minutes
 Jaw pain, toothache, headache
 Shortness of breath
 Nausea, vomiting, and/or general epigastric (upper middle abdomen) discomfort
 Diaphoresis- sweating, cold clammy skin, facial pallor, fainting, tachycardia &
bradycardia
 Heartburn and/or indigestion
 Arm pain (more commonly the left arm, but may be either arm); Upper back pain
 General malaise (vague feeling of illness)
 Heart palpitation

NB: Kindly take note that some patients does not have symptoms (Approximately one
quarter of all heart attacks are silent, without chest pain or new symptoms). Silent heart
attacks are especially common among patients with diabetes mellitus.

WARNING SIGNS

 discomfort, pressure, squeezing, or fullness in the chest that lasts several minutes or
resolves then returns
 pain or discomfort in the arms, neck, back, stomach, or jaw
 sudden shortness of breath
 Other signs can include a cold sweat, lightheadedness or sudden dizziness.

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CLINICAL DIAGNOSIS

 Electrocardiogram (ECG): This first test done to diagnose a heart attack records
electrical signals as they travel through your heart. the ECG may show that a heart
attack has occurred or is in progress.
 Blood tests: Certain heart proteins slowly leak into your blood after heart damage
from a heart attack.
 Chest X-ray: chest X-ray allows the doctor to check the size of the heart and its
blood vessels and to look for fluid in the lungs.
 Echocardiogram: Sound waves (ultrasound) create images of the moving heart.
Doctors can use this test to see how the heart's chambers and valves are pumping
blood through your heart. An echocardiogram can help identify whether an area of the
heart has been damaged.
 Coronary catheterization (angiogram): A liquid dye is injected into the arteries of
the heart through a long, thin tube (catheter) that's fed through an artery, usually in the
leg or groin and the dye goes to the arteries in the heart. The dye makes the arteries
visible on X-ray, revealing areas of blockage.
 Cardiac CT or MRI: These tests create images of the heart and chest. Cardiac CT
scans use X-rays. Cardiac MRI uses a magnetic field and radio waves to create
images of the heart. For both tests, the patient must lie on a table that slides inside a
long tube-like machine. Cardiac CT and MRI can be used to diagnose heart problems,
including the extent of damage from heart attacks.
Treatment of myocardial infarction
 Aspirin: Aspirin reduces blood clotting, thus helping maintain blood flow through a
narrowed artery.
 Thrombolytics: These drugs, also called clot-busters, helps in dissolving blood clot
that's blocking blood flow to the heart. The earlier the patient receive a thrombolytic
drug after a heart attack, the greater the chance survival and less damage to the heart.
 Antiplatelet agents: help to prevent new blood clots and keep existing clots from
getting larger.
 Other blood-thinning medications: patients can also be given other medications,
such as heparin, to make blood less "sticky" and less likely to form clots. Heparin is
given by IV or by an injection under the skin.
 Pain relievers: pain relieve medication can be given to patient, such as morphine.

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  Beta blockers. These medications help relax the heart muscle, slows the heartbeat
and decrease blood pressure. Beta blockers can limit the amount of heart muscle
damage and prevent future heart attacks.
 Statins: drugs that helps in controlling blood cholesterol.
 Nitroglycerin: This medication is used to treat chest pain (angina), can help improve
blood flow to the heart by widening (dilating) the blood vessels.
 ACE inhibitors: These drugs lower blood pressure and reduce stress on the heart.
 Surgery: Coronary angioplasty and stenting or Coronary artery bypass surgery.

COMPLICATIONS OF HEART ATTACK

Complications are often related to the damage done to the heart during a heart attack, which
can lead to:

 Abnormal heart rhythms (arrhythmia): Electrical "short circuits" can develop,

resulting in abnormal heart rhythms, some of which can be serious, and may lead to
death.
 Heart failure: A heart attack might damage so much heart tissue that the remaining
heart muscle can't pump enough blood out of your heart. Heart failure can be
temporary, or it can be a chronic condition resulting from extensive and permanent
damage to your heart.
 Sudden cardiac arrest: Without warning, your heart stops due to an electrical
disturbance that causes an abnormal heart rhythm (arrhythmia). Heart attacks increase
the risk of sudden cardiac arrest, which can cause death without immediate treatment.
 Cardiogenic shock: this is similar to heart failure, but it is even more serious. It
occurs when the heart muscle is so damaged to the extent that it can no longer pump
enough blood to maintain the body’s functions.
 Pulmonary edema: condition where fluid accumulates in and around the lungs
making it difficult to breathe.
 Deep vein thrombosis: formation of blood clots in the deep veins, generally in the
leg and pelvic areas.
 Ventricular fibrillation: abnormal heart rhythm that occurs when the heart beats
with rapid and erratic electrical impulses. This causes pumping chambers in the heart
(the ventricles) to quiver (shaking) instead of pumping blood.

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PREVENTION OF HEART ATTACK

It's never too late to take steps to prevent a heart attack — even if you've already had one.
Here are ways to prevent a heart attack.

 Lifestyle factors: Maintain a healthy weight with a heart-healthy diet, avoid smoking,
exercise regularly, manage stress and control conditions that can lead to a heart attack,
such as high blood pressure, high cholesterol and diabetes.
 Medications: Taking medications can reduce your risk of a subsequent heart attack
and help your damaged heart function better. Continue to take what your doctor
prescribes, and ask your doctor how often you need to be monitored.
 Going for general check up is highly important for early detection.

NURSING ASSESSMENT

 Gather information regarding the patient’s pain: nature, onset, duration, location,
precipitating factors
 Ask patient about other symptoms experienced
 Evaluate cognitive, behavior & emotional status
 Ask the patient about previous health status and also check the health passport for
previous health history
 Identify patient’s social support system & potential care givers

NURSING DIAGNOSIS

 Anxiety related to chest pain, fear of death, threatening environment

 Activity intolerance related to insufficient oxygenation to perform activities of daily
living
 Risk of injury related to dissolution of protective clots
 Risk of lower cardiac tissue perfusion related to coronary restenosis
 Lack of self esteem related loss of control, change in life style

NURSING INTERVENTION

 Alleviate anxiety by calming the patient

 Take vital signs (Bp, pulse, respiration, saturation, temperature, Hgt, ECG), notify the
doctor about any abnormality detected and record your findings
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  Assess the level of consciousness of the patient frequently
 Reassure patient & family members
 Teach the progressive muscle relaxation massage to allow patient to relax .

PATIENT HEALTH EDUCATION

After patient has recovered from heart attack, the following health education should be given
to the patient and family members:

- Design individualized activity progression program that will assist patient to cope
with his/her condition at home
- Educate patients about complication that can arise after heart attack episode
- Educate on how to take the medications as prescribed by the doctor
- Advise patient on change in lifestyle. This include quitting smoking and alcohol,
regular exercise.
- Advise patient on healthy balanced diet. Patient can be referred to a dietician
- Patient can resume sexual activity on doctor’s advice, or when patient have achieved
activity tolerance.

Case scenario

Mr. X is 60 year old man admitted in your unit with a diagnosis of an acute Myocardial
Infarction (MI).

Subjective data: Mr. X is complaining of severe, crushing chest pain unrelieved by rest,
which has lasted for 2hrs. The pain is substernal & does not radiate. He tells you that he
smoke two packs of cigarettes a day, is a manager of tobacco irrigation project in Zambezi,
and his father died at the age of 58 of heart attack.

Objective data: vital signs: P 110, irregular; Bp 90/68mmHg, R 28 b/m, SP02 90%. His
cardiac monitor shows sinus tachycardia, with frequent premature ventricular contraction and
his 12 lead ECG shows ST elevation in lead II, III, & Anterior Ventricle Fibrillation. He is
pale, diaphoretic & clutching his chest.

Questions

What’s your nursing Dx?

Draw up a nursing care plan for Mr. X.

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 ANGINA PECTORIS

Learning objectives

At the end of this session, students should be able to

 Define angina pectoris

 Describe the types of angina pectoris
 List the risk factors of angina pectoris
 Outline nursing assessment, nursing diagnosis & nursing intervention of angina

DEFINITION

Angina pectoris is defined as the chest pain that happens due to insufficient blood that is
going to part of the heart. It can feel like a heart attack, with pressure or squeezing a person’s
chest. It’s sometimes called ANGINA OR ISCHEMIC CHEST PAIN.

It is very important to understand that angina usually goes away quickly BUT it can be a sign
of a life-threatening heart problem, therefore, it is very important to find out what is going on
and what can be done to prevent a heart attack.

TYPES OF ANGINA PECTORIS

• Stable -attacks are related to known triggering factors such as stress and physical activities,
such attacks usually go within few minutes. May be alleviated by resting or a known dose of
nitrate. This is not a heart attack, but it can be a sign that a person is more likely to have one.

• Unstable –the pattern of attack and triggering factors are unpredictable but are usually
triggered when a person is at rest or not very active. The number of attacks and the intensity
and duration of the attack have a tendency to increase due to the fact that it can be a signal a
person is about to have heart attack.

• Nocturnal -attacks only occur in the night and only during sleep

• Decubitus -the attacks occur when lying down and is relieved by standing up

• Intractable -a potentially serious form of angina characterized by severe and incapacitating

attacks that do not respond to treatment

• Variant -occurs as result of coronary artery spasm. Attacks may occur unpredictably or
during sleep. Attacks can be relieved by calcium channel blockers or when you stand up.

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 CAUSES OF ANGINA PECTORIS

 A fatty substance called plaque builds up in the arteries causes blockage of blood flow
to the heart muscle which in turn lead to inadequate supply oxygen to the heart.
 Blood clot in the arteries
 A blockage in a major artery of the lungs (pulmonary embolism)
 An enlarged or thickened heart (hypertrophic cardiomyopathy)
 Narrowing of a valve in the main part of the heart (aortic stenosis)
 Swelling of the sac around the heart (pericarditis)
 Tearing in the wall of the aorta, the largest artery in the body (aortic dissection)

RISK FACTORS OF ANGINA PECTORIS

- Older age
- Family history of heart disease
- High blood pressure, high cholesterol, and diabetes
- Obesity
- Stress
- Using tobacco
- Not getting enough exercise

CLINICAL MANAGEMENT

 Surgical treatment
- Coronary Artery Bypass Grafting (CABG) to increase myocardial coronary
blood flow and to provide symptomatic relief in many cases up to 80%. To
disable angina that is refractory to medical therapy, significant abnormal ECG
response to exercise. It is used when there is 50% or greater obstruction of left
main coronary artery and significant obstructive lesions in all three coronary
arteries.
- Percutaneous Transluminal Coronary Angioplasty (PTCA) is a laternative
approach to CABG with the attempt to restore luminal patency by
compressing atheromatous plaques. This is used for a single-vessel disease in
which there are high degree of stenosis, good ventricular function and recent
angina refractory to medical therapy.

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  Chemotherapeutic management: Vasodilators short acting nitrates sublingual
nitroglycerin 0.4-0.6 mg, isosorbine dinitrate 5 mg.

NURSING ASSESSMENT OF ANGINA PECTORIS

In assessing the patient with angina, the nurses to

 Ask the patient the location, onset and characteristics of pain

 Ask the patient for any other symptoms that occur with pain
 Ask the patient about previous health status and also check the health passport for
previous health history
 Evaluate cognitive, behavior & emotional status
 Identify patient’s social support system & potential care givers
 Assess the level of pain (Pain scale: 1-5 moderate, 6-10 severe)
 Assess for the cause of pain.

NURSING DIAGNOSIS

Based on the assessment data, major nursing diagnosis may include:

 Ineffective cardiac tissue perfusion secondary to CAD as evidenced by chest pain or

other prodromal symptoms.
 Death, anxiety related to cardiac symptoms.
 Deficient knowledge about the underlying disease and methods for avoiding
complication
 Noncompliance, ineffective management of therapeutic regimen related to failure to
accept necessary lifestyle changes.

NURSING INTERVENTIONS

 The nurse should put the patient in a semi-fowler’s position when they experience
angina, and administer nitroglycerin sublingually as prescribed.
 Reduce anxiety by informing the patient about the implications and its treatment, and
methods of preventing its progression.
 Balancing activity and rest are an important aspect of the educational plan for the
patient and family. Encourage bed rest.

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CONGESTIVE CARDIAC FAILURE(CCF)

Learning objectives

At the end of this session, students should be able to

 Define congestive cardiac failure
 Describe the types of congestive cardiac failure
 Describe the pathophysiology of congestive cardiac failure
 Briefly describe the causes of congestive cardiac failure
 List the clinical manifestation of congestive cardiac failure
 Briefly describe the prevention of congestive cardiac failure
 Describe the clinical management of CCF
 Outline the nursing diagnosis and nursing management of CCF
 Describe the nursing intervention of CCF

DEFINITION

Congestive cardiac failure is also known as Heart failure. It is the inability of the heart to
pump sufficient blood to meet the needs of the tissues for oxygen and nutrients.

CCF is often a progressive, life-long condition that is managed with lifestyle changes and
medications to prevent episodes of acute decompensated heart failure.

It is very essential to take note that heart failure can affect both women and men, although
the mortality is higher among women. There are also racial differences; at all ages death rates
are higher in African American than in non-Hispanic whites. Heart failure is usually a disease
of older adults, affecting 6% to 10% of those older than 65. It is also the leading cause of
hospitalization in older people.

TYPES CCF

There are two types of CCF and they are as follows:

 Left-Sided Heart Failure

Left-sided heart failure or left ventricular failure have different manifestations with right-
sided heart failure.

Pulmonary congestion occurs when the left ventricle cannot effectively pump blood out of
the ventricle into the aorta and the systemic circulation.

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Pulmonary venous blood volume and pressure increase, forcing fluid from the pulmonary
capillaries into the pulmonary tissues and alveoli, causing pulmonary interstitial edema and
impaired gas exchange.

 Right-Sided Heart Failure

When the right ventricle fails, congestion in the peripheral tissues and the viscera
predominates.

The right side of the heart cannot eject blood and cannot accommodate all the blood that
normally returns to it from the venous circulation.

Increased venous pressure leads to JVD (jugular vein distension) and increased capillary
hydrostatic pressure throughout the venous system.

PATHOPHYSIOLOGY OF CCF

 When heart failure occurs, the body activates neurohormonal compensatory

mechanisms.
 Systolic heart failure results in decreased blood volume being ejected from the
ventricle.
 The sympathetic nervous system is then stimulated to release epinephrine and
norepinephrine which leads to the decrease in renal perfusion causes renin release,
and then promotes the formation of angiotensin I.
 Angiotensin I is then converted to angiotensin II by ACE which constricts the blood
vessels and stimulates aldosterone release that causes sodium and fluid retention.
 During this process, there is a reduction in the contractility of the muscle fibers of the
heart as the workload increases which make the heart compensates for the increased
workload by increasing the thickness of the heart muscle.

CAUSES OF CCF

Coronary artery disease: Atherosclerosis of the coronary arteries is the primary cause of
heart failure, and coronary artery disease is found in more than 60% of the patients with heart
failure.

Ischemia: it deprives heart cells of oxygen and leads to acidosis from the accumulation of
lactic acid.

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Cardiomyopathy: heart failure that occur due to cardiomyopathy is usually chronic and
progressive.

Systemic or pulmonary hypertension: it increases the workload of the heart and leads to
hypertrophy of myocardial muscle fibers.

Valvular heart disease: Blood has difficulty moving forward which in turn increase pressure
within the heart and increasing cardiac workload.

CLINICAL MANIFESTATIONS OF CCF

Impaired myocardial function

 Tachycardia
 Pallor
 Exercise or activity intolerance which leads to shortness of breath

Pulmonary Congestion

 Tachypnea
 Cyanosis
 Retractions and nasal flaring, grunting
 Cough

Systemic Venous Congestion

 Hepatomegaly
 Peripheral edema, scrotal and orbital
 Water weight gain
 Decreased urine output

COMPLICATIONS OF CCF

 Pulmonary edema
 Metabolic acidosis
 Failure to thrive
 URI (upper respiratory infection)
 Arrhythmias
 Death

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 PREVENTION OF CCF

Prevention of heart failure mainly lies in lifestyle management.

 Healthy diet: Avoiding intake of fatty and salty foods greatly improves the
cardiovascular health of an individual.
 Quitting smoking: Nicotine causes vasoconstriction that increases the pressure along
the vessels.

 Engaging in cardiovascular exercises thrice a week could keep the cardiovascular

system up and running smoothly.

CLINICAL MANAGEMENT OF CCF

The main goals of management of CCF are to relieve patient symptoms, to improve
functional status and quality of life as well as extending patient’s survival. The clinical
management are as follows:

 Pharmacologic Therapy
 ACE Inhibitors are used to slow the progression of heart failure, improve exercise
tolerance and to decrease the number of hospitalizations for heart failure. It also
promotes vasodilation and diuresis by decreasing afterload and preload.
 Angiotensin II Receptor Blockers are used to block the conversion of angiotensin I
at the angiotensin II receptor and cause decreased blood pressure, decreased systemic
vascular resistance, and improved cardiac output.
 Beta Blockers are used to reduce the adverse effects from the constant stimulation of
the sympathetic nervous system.
 Diuretics are used to remove excess extracellular fluid by increasing the rate of urine
produced in patients with signs and symptoms of fluid overload.
 Calcium Channel Blockers causes vasodilation which reduce systemic vascular
resistance. It is contraindicated in patients with systolic heart failure.
 Nutritional Therapy

A low sodium diet of 2 to 3g/day reduces fluid retention and the symptoms of peripheral and
pulmonary congestion. It also decrease the amount of circulating blood volume which
decreases myocardial work.

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Patient compliance to strict diet highly is important because dietary indiscretions may result
in severe exacerbations of heart failure requiring hospitalizations.

 Surgical therapy
Cardiac Transplant is recommended for some patients with end-stage heart failure,
cardiac transplant is the only option for long term survival.
 Additional Therapy
 Supplemental Oxygen: The need for supplemental oxygen is based on the degree of
pulmonary congestion and resulting hypoxia.
 Cardiac resynchronization therapy: this involves the use of a biventricular
pacemaker to treat electrical conduction defects.
 Ultrafiltration: this is an alternative intervention for patients with severe fluid
overload.

NURSING ASSESSMENT OF CCF

 Observe the effectiveness of therapy on the patient

 Carry all the required vital signs
 Assess the signs and symptoms such as dyspnea, shortness of breath, fatigue, and
edema.
 Assess for sleep disturbances, especially sleep suddenly interrupted by shortness of
breath.
 Assess the patient’s understanding of HF, self-management strategies, as well as the
willingness to adhere to those strategies. This include change in lifestyle.

NURSING DIAGNOSIS FOR CCF

Based on the nursing assessment, major nursing diagnoses for the patient with HF include the
following:

 Activity intolerance related to decrease CO.

 Excess fluid volume related to the HF syndrome.
 Anxiety related to breathlessness from inadequate oxygenation.
 Powerlessness related to chronic illness and hospitalizations.
 Ineffective therapeutic regimen management related to lack of knowledge.

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NURSING INTERVENTIONS

 Promoting activity tolerance: daily exercise should be encouraged; the nurse and
the physiotherapist should collaborate to develop a schedule that promotes pacing and
prioritization of activities.
 Managing fluid volume: The patient’s fluid status should be monitored closely,
auscultating the lungs, monitoring daily body weight, and assisting the patient to
adhere to a low sodium diet.
 Controlling anxiety: the nurse should promote physical comfort and provide
psychological support. Patient must be educated on ways to control anxiety and avoid
anxiety-provoking situations.
 Encourage the patient to verbalize their concerns and provide the patient with
decision-making opportunities.
 Teach the patient and their families about medication management, low-sodium diets,
activity and exercise recommendations, smoking cessation, and learning to recognize
the signs and symptoms of worsening heart failure. (nurseslab, 2020)

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 RHEUMATIC HEART DISEASE

Learning objectives

At the end of this session, students should be able to

 Define rheumatic heart disease

 Briefly describe the pathophysiology of rheumatic heart diseases
 List the clinical of rheumatic heart diseases
 Outline clinical diagnosis of rheumatic heart diseases
 Outline nursing management of rheumatic heart diseases
 Outline the nursing Interventions of rheumatic heart diseases

DEFINITION

Rheumatic heart disease is defined as a chronic condition resulting from rheumatic fever
which involves all the layers of the heart.

Refers to heart disease that occurs as a result of rheumatic fever.

Rheumatic fever is defined as a diffuse inflammatory disease which is characterized by a

delayed response to an infection by group A beta- hemolytic streptococci in the
tonsilopharyngeal area, affecting, joints, central nervous system, skin and subcutaneous
tissues.

PATHOPHYSIOLOGY

 During the initial throat infection, the immune system produces antibodies for the
organism which reacts with the tissues of the body forming wide spread inflammatory
lesions especially around small blood vessels.
 The heart valves and the joints are the sites where the inflammatory process is most
symptomatic
 Rheumatic fever occurs due to delayed reaction to throat infection (Group A
Streptococcus (beta-haemolytic streptococci), it can be contracted in conditions of
poverty, overcrowding, and poor socioeconomic conditions as they encourage the
spread of strains of Group A Streptococci that causes rheumatic fever.

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CLINICAL MANIFESTATIONS (Signs and Symptoms)

 Pyrexia
 General malaise
 Wandering joint pains
 Cardiac involvement resulting in tachycardia
 Arthritis with acute migratory joint pains
 Acute rheumatic carditis with presence of heart murmurs, tachycardia, heart
enlargement, and congestive cardiac failure
 Subcutaneous nodules: these are painless swellings found under the skin in the area of
the major joints and under the skin in the area of the major joints and near bony
prominences.
 Erythema marginatum: a pinkish skin rash which occurs in patches found mainly on
the trunk.
 Gastrointestinal upset
 Abdominal pain
 Epistaxis

CLINICAL DIAGNOSIS OF RHEUMATIC HEART DISEASES

 Include a raised erythrocyte sedimentation rate (ESR) and white cell count
 Positive throat swab for Group A Streptococci. A high titre of anti-streptococcal
antibodies is suggestive of rheumatic fever

NURSING MANAGEMENT OF RHEUMATIC HEART DISEASES

 Give supportive measures to reduce mortality

 Provide bed rest for the patient
 Administer prescribed antibiotics and anti-inflammatory agents as prescribed by the
doctor
 Monitor for signs of progression of the disease and signs of worsening cardiac
involvement
 Give treatment for congestive cardiac failure as prescribed if signs of cardiac failure
develop.

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NURSING INTERVENTIONS OF RHEUMATIC HEART DISEASES

 Observe patient for signs of pain

 Ensure mobility of the patient with care to avoid over-activity
 Observe also for possible complications
 Monitor the patient’s vital signs especially pulse when patient is sleeping
 Monitor and record ECG daily

COMPLICATIONS OF RHEUMATIC HEART DISEASES

The following conditions are the complication that can arise after the episode of rheumatic
heart disease:

 Valvular heart disease which disrupts the function of heart due to structural damage of
the heart valves following rheumatic fever.
 Bacterial endocarditis inflammation of the endocardium including interior cardiac
structures as the heart valves, and the chordae tendinea.

PATIENT EDUCATION

 Advise the patient about the continuity of the prophylactic antibiotic therapy
 Teach the patient how to take the medication and side effects
 Advise the patient to take antibiotic prophylaxis before undergoing dental or
urological procedures
 Teach the patient that infections must be treated promptly
 Advise patient to seek medical assistance immediately if the patient experiences
fatigue, dizziness palpitations and/or dyspnoea
 Encourage the patient to live a healthy lifestyle and ensure good health practices

PREVENTION OF RHEUMATIC FEVER

 Treating Streptococcal throat infections promptly is the main key to prevention of

rheumatic fever
 Throat swabs should be taken from children who present with fever and sore throat
and treat those with Group A Streptococcal throat infection with appropriate
antibiotics.

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 HYPERTENSION

Learning objectives

 Define the related concepts

 Describe the causes/predisposing factors of hypertension
 Describe the patho-physiological changes that occur as a result of hypertension
 Describe the signs and symptoms/clinical manifestations of hypertension
 List the complications of hypertension
 Enumerate the clinical diagnosis of hypertension
 Outline the nursing diagnosis of hypertension
 Outline the nursing management of hypertension

DEFINITIONS

Hypertension is a disease of vascular regulation in which the mechanisms that control

arterial pressure within the normal range are altered.

Hypertension is also defined as persistent levels of blood pressure in which the systolic
pressure is above 140 mmHg and the diastolic pressure is above 90 mmHg.

Therefore, hypertension is when the blood pressure is higher/ above normal range.

Hypertensive crisis is a term used to indicate either a hypertensive urgency or emergency.

Hypertensive crisis occurs at systolic BP greater than 180 mm Hg and/or diastolic BP greater
than 120 mm Hg. BPs often can be greater than 220/140 mm Hg.

ETIOLOGY OF HYPERTENSION

Hypertension can result from either primary or secondary causes.

Primary Hypertension

 Primary hypertension (essential or idiopathic) is the elevated BP without an identified

cause. It accounts for 90% to 95% of all cases of hypertension.
 The exact cause for primary hypertension is unknown, however, there are multiple
contributing factors.

Common causes of primary hypertension

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  Changes in endothelial function related to either vasoconstricting or vasodilating
agents.
 Overproduction of sodium-retaining hormones
 Increased sodium intake
 Overweight
 Age and family history
 Ethnicity
 Diabetes
 Tobacco use and excess alcohol intake.

Secondary Hypertension

 Secondary hypertension is the elevated BP with a specific cause that often can be
identified and corrected.
 Secondary hypertension can become resistant, causing cardiovascular complications if
left untreated. This type of hypertension accounts for 5% to 10% of hypertension in
adults. Secondary hypertension should be suspected in people who suddenly develop
high BP, especially if it is severe.
 According to findings, secondary hypertension relates to the underlying cause, For
example, an abdominal bruit heard over the renal arteries may indicate renal disease.
 It is often present in patients with obstructive sleep apnea. Treatment is aimed at
removing or treating the underlying cause.

Common Causes of secondary hypertension

 Cirrhosis
 Coarctation or congenital narrowing of the aorta
 Drug-related: estrogen replacement therapy, oral contraceptives, corticosteroids,
nonsteroidal anti-inflammatory drugs (e.g. cyclooxygenase-2 inhibitors), SNS
stimulants (e.g., cocaine, monoamine oxidase)
 Endocrine disorders (e.g., pheochromocytoma, Cushing syndrome, thyroid disease)
 Neurologic disorders (e.g., brain tumors, quadriplegia, traumatic brain injury)
 Pregnancy-induced hypertension
 Renal disease (e.g., renal artery stenosis, glomerulonephritis)
 Sleep apnea

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  Stress

PATHOPHYSIOLOGY OF HYPERTENSION
 Elevated diastolic pressure leads to strain on the arterial wall which over time causes
thickening and calcification of the arterial media (called sclerosis) and eventually
narrowing of the blood vessel lumen.
 Elevated blood pressure occurs when there is increased output and peripheral
resistance.

CLASSIFICATION OF HIGH BLOOD PRESSURE

CLINICAL MANIFESTATIONS

In most cases, hypertension is asymptomatic which is why its referred to as Silent Killer.
However, it is essential to look out for the following signs and symptoms:

 Headaches
 Dizziness
 Blurred vision
 Epistaxis
 Fainting attacks
 heart failure

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  Dyspnoea
 Oedema
 Ischaemic heart disease
 Angina and renal impairment
 Albuminuria
 Polyuria
 decreased specific gravity
 Nausea & vomiting
 Mental confusion
 Convulsions
 Pulmonary oedema

COMPLICATIONS OF HYPERTENSION

 Renal failure
 Angina/Myocardial infarction
 Stroke/Cerebral Vascular Accident (CVA)
 Retinopathy (eye problems)
 Accelerated hypertension
 CCF
 Impotence

CLINICAL DIAGNOSIS

 Outpatient ambulatory BP measurements (vital signs)

 ECG: To determine effects of hypertension on heart, e.g. left ventricular hypertrophy
 Chest X-Rays: to show cardiomegaly and any other abnormality
 Urine Test: Proteinuria shows elevated serum blood urea
 Indication of kidney disease as a cause or effect of hypertension
 Renal scan: To detect renal vascular diseases

NURSING DIAGNOSES

Nursing diagnoses and collaborative problems for the patient with

hypertension include:

27
  Altered blood pressure
 Ineffective tissue perfusion
 Impaired sexual function
 Potential complication: stroke, MI

NURSING MANAGEMENT

Health education should be given to patient with regards to:

 Periodic BP monitoring
 Home BP monitoring
 Ambulatory BP monitoring (It is a non-invasive, fully automated
system that measures BP at preset intervals over a 12- to 24-hour
period. The equipment is worn continuously for 24 hours and must be
reviewed by the nurse)
 After BP has been stabilized, patient should go for regular check up
 Nutritional therapy: patient must be put on
 Restrict salt and sodium
 Restrict cholesterol and saturated fats
 Maintain adequate intake of potassium and calcium (patient can be
referred to a dietitian)
 Weight management and regular, moderate physical activity
 Tobacco cessation and Moderation of alcohol intake
 Stress management techniques
 Educate patient on the dose of medication and advice patient not to miss his/her
medication and must not double dose in case he/she missed a dose.
 Educate not to stop his/her medication without consulting a healthcare provider
 Educate patient on the side effect of antihypertensive drugs such as erectile
dysfunction, decreased libido, fatigue, diarrhea etc.
 Assess patients for hypertension risk factors and develop risk modification plans.
 Monitor for adverse effects of antihypertensive drugs.
 Teach about home BP monitoring, including the correct use of automatic BP
monitors.

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UNIT 2: RESPIRATORY DISEASES/DISORDERS

Learning objectives

By the end of this session, students should be able to

 Define related concepts

 List respiratory tract infections
 Differentiate between LRTIs and URTIs

Definition

Respiratory system is a series of organs responsible for taking in oxygen and expelling
carbon dioxide. The primary organs of the respiratory system are the lungs, which carry out
this exchange of gases as we breathe. Respiratory organs include the nose, mouth, bronchial
tubes, alveoli, lungs, larynx, epiglottis, trachea etc.

Respiratory system diseases/ disorders are the conditions that affect the respiratory organs.

Respiratory system is divided into 2 parts: upper respiratory tract and lower respiratory tract
and they are affected by different conditions.

Upper respiratory tract is responsible for warming up and filtering the inhaled air to allow the
lower respiratory tract to accomplish gas exchange.

Respiratory tract infection

 Bronchitis
 Asthma
 Empyema
 Atelectasis
 Chronic obstructive pulmonary diseases (COPD)
 Lung abscess
 Pneumonia
 Pulmonary tuberculosis
 Pleural effusion
 Chest injuries
 Cyst and tumors
 Pulmonary embolism

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  Rhinitis

UPPER RESPIRATORY TRACT DISEASES

There are lots of upper respiratory tract infections. Upper respiratory infections affect the
nasal cavity, ethmoidal air cells, and frontal, maxillary & sphenoid sinuses, pharynx, larynx,
and trachea. Some of these disorders will be discussed in this unit.

RHINITIS

Learning objectives

At the end of this session, students should be able to

 Define rhinitis, viral rhinitis and allergic rhinitis

 List the causes rhinitis
 Enumerate the clinical manifestation of rhinitis
 Outline the clinical management of rhinitis
 Outline the nursing management of rhinitis

DEFINITIONS

Rhinitis is a group of disorders characterized by inflammation and irritation of mucous

membranes of the nose. There are two types of rhinitis: viral rhinitis and allergic rhinitis.

Viral rhinitis is a general term used to refer to symptoms of upper respiratory tract infection
such as cough, sore throat as well as nasal congestion. Cold is an inflammation of the nasal
cavity including the mucus membrane which can be acute or chronic. Viral rhinitis is non-
allergic. This is also known as common cold.

Allergic rhinitis is caused by the reaction of the body’s immune system to environmental
trigger such as mold.

CAUSES OF RHINITIS

 Changes in temperature or humidity

 Use of over-the-counter medication and over use of prescribed nasal decongestants
 Presence of a foreign body in the nose
 Infection
 Age
 Systemic disease such as asthma

30
  Allergic reaction to certain food such as egg, fish, milk, peanut etc.
 Allergic reaction to pollen, grass, mold, dust, trees and animals (cat)
 Allergic reaction to certain medications such as penicillin, amoxicillin, cotrimoxazole

CLINICAL MANIFESTATION

 Rhinorrhea: excessive nasal drainage, runny nose

 Nasal congestion
 Nasal discharge: purulent with bacterial rhinitis
 Sneezing
 Pruritus of the nose, roof of the mouth, throat, eyes, and ears.
 Headache
 Red, swollen, and itching eyes
 Fatigue and malaise

CLINICAL MANAGEMENT

 Do vital signs and carry out physical examination

 The nurse asks the patient about recent symptoms as well as possible exposure to
allergens in the home, environment, or workplace.
 If viral rhinitis is the cause, medications may be prescribed to relieve the symptoms.
 In allergic rhinitis, allergy tests may be performed to identify possible allergens.
 Depending on the severity of the allergy, desensitizing immunizations and
corticosteroids may be required.
 Oral decongestant agents may be used for nasal obstruction.
 Saline nasal spray can act as a mild decongestant and can liquify mucus to prevent
crusting. Two inhalations of intranasal ipratropium (Atrovent) can be administered in
each nostril two to three times per day for symptomatic relief of rhinorrhea
 Intranasal corticosteroids may be used for severe congestion, and ophthalmic agents
(cromolyn ophthalmic solution 4%) may be used to relieve irritation, itching, and
redness of the eyes.
 The choice of medications depends on the symptoms, adverse reactions, adherence
factors, risk of drug interactions, and cost to the patient.

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NURSING MANAGEMENT OF RHINITIS

 Advise patient with allergic rhinitis to avoid or reduce exposure to allergens and
irritants, such as dusts, molds, animals, fumes, odors, powders, sprays, and tobacco
smoke.
 Patient education is essential when assisting the patient in the use of all medications.
To prevent possible drug interactions, the patient is cautioned to read drug labels
before taking any OTC medication
 Educate patient on hand hygiene
 Advise patient to use nasal decongestant with caution

PHARYNGITIS AND TONSILITIS

Learning objectives

By the end of this unit, students should be able to

 Define pharyngitis and tonsilitis

 List the clinical manifestation of acute and chronic pharyngitis
 List the clinical diagnosis of pharyngitis
 Outline the clinical management and nursing management of pharyngitis

DEFINITIONS

Pharyngitis is the inflammation of the pharynx which is basically known as sore throat. It is
mostly caused by a virus and/or bacteria. Pharyngitis is simply the inflammation of the throat.
Pharyngitis can either be an acute or a chronic condition.

Tonsiolpharyngitis is the inflammation of the throat and tonsils

Acute pharyngitis is a sudden painful inflammation of the pharynx, the back portion of the
throat that includes the posterior third of the tongue, soft palate, and tonsils. It is caused by
virus and bacteria and it is common during winter and when the weather is changing.

Chronic pharyngitis is a persistent inflammation of the pharynx. It is common in adults who

work in dusty surroundings, use their voice to excess, suffer from chronic cough, or
habitually use alcohol and tobacco.

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PATHOPHYSIOLOGY

 Ten percent of adults with pharyngitis have group A beta-hemolytic streptococcus

(GABHS), which is commonly referred to as group A streptopccocus(GAS)
 The body responds by triggering an inflammatory response in the pharynx.
 Results in pain, fever, vasodilation, oedema, and tissue damage, manifested by
redness and swelling in the tonsillar pillars, uvula, and soft palate.
 Bacterial organisms which causes acute pharyngitis include Mycoplasma
pneumoniae, Neisseria gonorrhoeae, and H. influenzae type B, and M. pneumoniae
which is one of the most common known bacterial pathogens of the respiratory tract.
 Uncomplicated viral infections usually subside promptly, within 3 to 10 days after the
onset.
 Pharyngitis can become complicated and life threatening if not treated on time.
 Complication condition include peritonsillar abscess, otitis media, mastoiditis,
sinusitis, bacteremia, fever, nephritis & cervical adenitis.
 A creamy (yellowish) exudate may be present in the tonsillar pillars which indicate
sepsis and will require antibiotics.

CLINICAL MANIFESTATION

Acute pharyngitis

 Fiery-red pharyngeal membrane and tonsils

 Swollen lymphoid follicles flecked with white-purple exudate
 Enlarged and tender cervical lymph nodes
 Fever higher than 38.3C
 Malaise
 Sore throat may be present.
 Patients with group A streptopccocus(GAS) may develop anorexia, vomiting &
scarlet.
 No cough

Chronic pharyngitis

 Constant sense of irritation or fullness in the throat

 Collection of mucus in the throat and can be expelled by coughing

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  Dysphalgia: difficulty in swallowing.
 Inflammation of the pharynx.
 A sore throat that is worse with swallowing in the absence of pharyngitis suggests the
possibility of thyroiditis, and patients with this symptom are referred for evaluation
for possible thyroiditis.

CLINICAL DIAGNOSIS

 Treatment should be initiated early

 Throat swab can be taken to check the type of pharyngitis (virus/bacteria)
 Thorough physical examination should be done
 In case of chronic pharyngitis, ask patient about previous health history

CLINICAL MANAGEMENT

 Viral pharyngitis is treated with supportive measures due to the fact that antibiotics
have no effect on the causal organism.
 Bacterial pharyngitis is treated with a variety of antimicrobial agents.
 Penicillin V potassium is the treatment of choice for bacterial pharyngitis but
erythromycin, azithromycin, cephalosporins can be used in patients allergic to
penicillin.
 Analgesic is given to relieve pain
 Benzocaine can be used to gargle to relieve symptoms
 Antihistamine to alleviate itchy throat
 In severe cases, tonsillectomy can be an option
 Nutritional therapy:
- Soft or liquid diet is provided depending on the level of throat pain
- Warm liquids and cold desert can be soothing to the throat

NURSING MANAGEMENT

 Monitor the vital signs of the patient

 Do thorough physical examination
 Encourage bed rest
 Educate patient on how to the prescribed medication

34
  Teach patient on the home remedies that can alleviate symptoms such as gargling of
salty water etc.
 Advise patient to dispose toilet tissues used correctly to prevent spread of the
infection in the house.
 Encourage patient on adequate intake of fluid
 Advise patient to avoid smoking, drinking of alcohol, exposure to cold environment
etc.

TONSILLITIS AND ADENOIDITIS

Learning objectives

At the end of this unit, student should be able to

 Define tonsillitis and adenoiditis

 Outline the pathophysiology of tonsillitis and adenoiditis
 Outline the clinical manifestation
 Mention the nursing management

DEFINITIONS

Tonsillitis in an inflammation (infection) of the tonsils. It is composed of lymphatic tissue

and are situated on each side of the oropharynx. Acute tonsillitis can be confused with acute
pharyngitis. Tonsillitis is a common illness in children but it can also affect adult.

Adenoiditis is an inflammation of the adenoids. Adenoids are lymphatic tissues near the
center of the posterior wall of the nasopharynx which helps to filter out germs from the body.

Infection of the adenoids usually accompany tonsillitis.

PATHOPHYSIOLOGY

 A ring of lymphoid tissue encircles the pharynx, forming a protective barrier

against upper respiratory infection.
 This ring consists of groups of lymphoid tonsils, including the faucial or palatine
tonsils, the commonly known tonsils; pharyngeal, known as adenoids; and lingual
tonsils.

35
  Lymphoid tissue normally enlarges progressively in childhood between the ages
of 2 and 10 years and shrinks during preadolescence.
 When the tissue itself becomes a site of acute or chronic infection, it may become
hypertrophied and can interfere with breathing, may cause partial deafness, or
may become a source of infection in itself.
 Epstein-Barr virus (EBV) may cause tonsillitis in the absence of systemic
mononucleosis. In one study, EBV was found to be responsible for 19% of
exudative tonsillitis in children.
 Anaerobic bacteria play an important role in tonsillar disease, most cases of
bacterial tonsillitis are caused by group A beta-hemolytic Streptococcus pyogenes
(GABHS). S. pyogenes adheres to adhesin receptors that are located on the
tonsillar epithelium; immunoglobulin coating of pathogens may be important in
the initial induction of bacterial tonsillitis.
 . Local immunologic mechanisms also play a role in chronic tonsillitis; the
distribution of dendritic cells and antigen-presenting cells is altered during
disease, with fewer dendritic cells on the surface epithelium and more in the
crypts and extrafollicular areas.

CLINICAL MANIFESTATION

 Sore throat
 Fever (38OC and above)
 Snoring
 Difficulty swallowing
 Enlarged adenoids may cause mouth-breathing, earache, draining ears, frequent head
colds, bronchitis, foul-smelling breath, voice impairment, and noisy respiration

36
CLINICAL DIAGNOSIS

 Throat swab cultures are performed to diagnose tonsillitis and the causative organism.
 For patients in whom acute tonsillitis is suspected to have spread to deep neck
structures, radiologic imaging using plain films of the lateral neck or CT scan and
Xray can be done.

CLINICAL MANAGEMENT

 Antibiotic therapy must be comprehensive and cover all likely pathogens according to
the severity of the infection. E.g pen V.K, amoxicillin, azithromycin, cefurozime etc.
 Corticosteroids can be given because it has an anti-inflammatory properties and cause
profound and varied metabolic effects; these agents modify the body’s immune
response to diverse stimuli. Corticosteroids reduce inflammation, which may impair
swallowing and breathing.
 Immunoglobulins can be used to improve clinical aspects of the diseases because it
stimulates immune cells which reduces the severity of infection.
 Analgesics must be given to control pain and fever. Analgesics with antipyretic
properties ensure patient comfort, promote pulmonary function, and have sedating
properties, which are beneficial for patients who experience pain.
 Tonsillectomy is indicated for individuals who have experienced more than six (6)
episodes of streptococcal pharyngitis (confirmed by positive culture) in 1 year, 5

37
 episodes in 2 consecutive years, or 3 or more infections of tonsils and/or adenoids per
year for 3 years in a row despite adequate medical therapy, or chronic or recurrent
tonsillitis associated with the streptococcal carrier state that has not responded to beta-
lactamase–resistant antibiotics.
 Adenoidectomy:due to the fact that adenoid tissue has similar bacteriology to the
pharyngeal tonsils and because minimal additional morbidity occurs with
adenoidectomy if tonsillectomy is already being performed, most surgeons perform an
adenoidectomy if adenoids are present and inflamed at the time of tonsillectomy.

NURSING MANAGEMENT
 Monitor the vital signs of the patient
 Do thorough physical examination and ask patient about previous health history
 Encourage bed rest
 Educate patient on how to the prescribed medication
 Teach patient on the home remedies that can alleviate symptoms such as gargling of
salty water etc.
 Encourage patient on plenty intake of fluid
 In case surgery was done (tonsillectomy/adenoidectomy) nurses should do the
following:
 monitor vital signs of the patient
 place the patient in a comfortable position with the head turned
the side to drainage from the mouth and pharynx.
 Provide liquid/soft for the patient
 Administer medication as prescribed by the doctor

NURSING ASSESSMENT OF UPPER RESPIRATORY TRACT INFECTION

 Proper history taken to identify signs and symptoms such as headache, sore throat,
pain around the eyes and on either side of the nose, difficulty in swallowing, cough,
hoarseness, fever, stuffiness, and generalized discomfort and fatigue.

38
 Determine when the symptoms began, what precipitated them, what the the patient
has done to relieve them as well as what aggravates the symptoms.
 The nurse should also determine any history of allergy or the existence of a
concomitant illness.
 Inspection may reveal swelling, lesions, or asymmetry of the nose as well as bleeding
or discharge. The nurse should inspect the nasal mucosa for abnormal findings such as
increased redness, swelling, exudate, and nasal polyps, which may develop in chronic
rhinitis.
 The nurse palpates the frontal and maxillary sinuses for tenderness, which indicate
inflammation, and then inspects the throat by having the patient open the mouth wide
and take a deep breath.
 Inspect the throat for redness, asymmetry, or evidence of drainage, ulceration, or
enlargement of the tonsils and pharynx.
 Palpate the lymph nodes in the neck for enlargement and tenderness.

NURSING DIAGNOSES

 Ineffective airway clearance related to excessive mucus production secondary to

retained secretions and inflammation
 Acute pain related to upper airway irritation secondary to an infection
 Impaired verbal communication related to physiologic changes and upper airway
irritation secondary to infection or swelling
 Deficient fluid volume related to decreased fluid intake and increased fluid loss
secondary to diaphoresis associated with a fever
 Deficient knowledge regarding prevention of URIs, treatment regimen, surgical
procedure, or postoperative care.

COMPLICATIONS

Based on assessment data, potential complications include:

 Sepsis
 Meningitis or brain abscess
 Peritonsillar abscess, otitis media, or sinusitis

39
 LOWER RESPIRATORY TRACT DISEASES/DISORDER

 Lower respiratory tract infections are the infection that affects the lungs and/ or
occur below the voice box. Conditions that affect the lower respiratory tract range
from acute problems to chronic disorders and they can be life threatening. These
include atelectasis, pneumonia, pneumothorax, hemothorax, pleural effusion, acute
respiratory distress, bronchitis, tuberculosis, asthma, Chronic obstructive pulmonary
diseases (COPD) etc. Common LRTIs will be discussed in this unit

ASTHMA

Learning objectives

At the end of this unit, student should be able to

 Define asthma
 Describe the classification of asthma
 Describe the pathophysiology of asthma
 Outline the clinical manifestation of asthma
 Outline the nursing intervention and patient education for asthma

DEFINITION

Asthma is a respiratory condition in which the responsiveness of the airways to a variety of

stimuli is increased.

CLASSIFICATION OF ASTHMA

Extrinsic Asthma associated with Type 1 hypersensitivity. The individual is genetically

predisposed to form antibodies against a variety of substances which include pollens, animal
fur, house dust and fungi.

INTRINSIC ASTHMA develops later in life in individuals with no previous history of

allergy. Attacks are triggered by infection and exposure to irritants.

PATHOPHYSIOLOGY

 After exposure to the stimulus, immune cells in the bronchial tree like the mast cells,
basophils and macrophages get activated.

40
  When these cells are activated, they release chemical mediators that cause constriction
of the bronchial smooth muscles leading to increased capillary permeability in the
airways resulting in a bronchospasm.
 Asthma can be triggered by exposure to a stimulus which include allergen, infectious
agent, drug, dust or pollutants in the environment, substances in the workplace, etc.

CLINICAL MANIFESTATIONS

 Dyspnoea
 Coughing and wheezing
 Tachypnoea
 Tachycardia
 Raised systolic pressure
 Development of pulsus paradoxus
 Hypoxia
 Metabolic acidosis in severe obstruction
 Cyanosis
 Absence of breath sounds indicating complete closure of the airways
 Extensive mucous plugging (atelectasis)occur due to the thickness of the secretions
 Spontaneous pneumothorax occurs due to over inflation of lungs (rare)

CLINICAL MANAGEMENT

 Drug therapy is the main choice in controlling and managing asthma and acute
attacks of asthma
- Sympathomimetic agents e.g hexoprenaline or salbutamol relax bronchial smooth
muscle and decrease the release of bronchoconstrictor substances.
- Anticholinergics e.g ipatropium bromate inhibit the effects on the airways of the
sympathetic nervous stimulation.
- Mast cell inhibitors e.g cromolyn sodium prevent the release of bronchoconstrictor
chemicals like histamine and serotonin from the mast cells.
- Steroids e.g methylprednisolone, beclamathazone is used to reduce inflammatory and
allergic reactions in the lungs that cause asthmatic attacks
 Status Asthmaticus

41
 - Inhaled beta-adrenergic agents e.g hexoprenaline or salbutamol
- Intravenous aminophylline to relieve acute bronchospasms
- Large doses of steroids can be given to alleviate inflammatory and allergic reaction in
the lungs and aid the effectiveness of other agents
- Antibiotic to prevent infection during the acute episodes
- Bronchodilators e.g epinephrine 1:1000 0.2-0.5 ml subcutaneously q15-30 min for 3
doses
- Aerosols 1 or 2 inhalations from hand nebulizer in 2.5ml or 3 ml normal saline by
nebulization.
 Corticosteroids: Hydrocortisone sodium succinate 100-250 mg to be given with the
first oral dose: Prednisolone 40-60 mg/d in divided doses.

NURSING INTERVENTIONS

 Assess ventilation including breathing rate, rhythm, and depth, chest expansion,
dyspnoea, shortness of breath and nasal flaring
 Assess peak expiratory flow rate or forced expiratory volume as prescribed
 Identify contributing factors such as allergens
 Maintain patient position to facilitate ventilation such as semi fowler’s position
 Instruct patient in pulmonary hygiene routines to facilitate effective breathing
 Assess the patient for tiring in relation to attempts to breathe
 Reassure and calm patient down and provide a restful environment
 Encourage the patient to use adaptive breathing techniques
 Cover pillows with allergen-proof covers to eliminate dust and other irritants

PATIENT EDUCATION

 Ensure the patient understands the medication regime and make sure that inhaler is
within reach at all time
 Advise the patient and family members to avoid allergens and irritants
 Advise the patient to seek medical care for upper respiratory tract infections
 Explore stress management techniques with the patient
 Advise the patient to avoid extremes of weather.

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ACUTE RESPIRATORY DISTRESS SYNDROME (ARDs)

Learning objectives

 Define Acute respiratory distress syndrome

 Identify the predisposing factors of ARDS
 Describe the Pathophysiology of ARDS
 Outline the clinical manifestation of ARDS
 Mention the clinical diagnosis of ARDS
 Outline the clinical management of ARDS
 Describe the nursing management of ARDS

Definition

Acute respiratory distress syndrome (ARDS) is a life-threatening condition which is

characterized by severe inflammatory process or acute lung injury characterized by
pulmonary oedema at the level of the alveoli, it causes severe hypoxemia and decreasing
compliance of the lungs which is unresponsive to oxygen supplement.

PREDISPOSING FACTORS

 Localized infection such as pneumonia

 Respiratory complications such as pulmonary emboli
 GI complication such as stress ulcer
 Cardiac complication
 Indirect lung injury e.g. shock and trauma (e.g head injury)
 Renal failure
 Direct lung injury such prolonged inhalation of concentration of oxygen and smoke
 Aspiration (e.g. gastric secretions and drowning)
 Fat or air embolism
 Systemic sepsis
 Metabolic disorders (pancreatitis, uremia)
 Drug ingestion and overdose

PATHOPHYSIOLOGY

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  ARDS developed as a result of diffuse alveolar damage which is triggered by
combinations of ischemic tissue injury, release of toxic cellular substance and
sustained inflammatory response.
 Severe ventilation –perfusion mismatching occurs.
 Alveoli collapse due to inflammation infiltrate, blood function and surfactant
dysfunction
 Due to interstitial fluid and bronchial obstruction, the air way become narrowed,
gaseous exchange becomes impaired resulting in severe hypoxemia.
 There is significant amount of secretion in the airway.

CLINICAL MANIFESTATION

 Acute onset of severe dyspnea, tachypnea, tachycardia, cyanosis and use of accessory
muscles.
 Arterial hypoxemia and increase requirement of oxygen therapy
 Scattered crackles and rhonchi heard on auscultation
 Decrease pulmonary compliance characterized pressure required to ventilate patient
on mechanical ventilators (stiff lungs)

CLINICAL DIAGNOSIS

 Pulmonary function: Alveolar-arterial oxygen P (A-a ) O2

 Arterial blood gases: Indicate hypoxia
 Lactic acid level: to check for increase in tissue hypoxia normal value : 0.5-
2.2meq/L (venous blood)
 Chest roentgenograms: to check for fluid in the lungs
 Chest X-ray: Thickened or unclear margins of the bronchi or vessel and bilateral
infiltrates

CLINICAL MANAGEMENT

 The main focus in the management of ARDS includes identification and treatment
of the underlying condition.
 Aggressive, supportive care must be provided to compensate for the severe
respiratory dysfunction. This includes intubation and mechanical ventilation.

44
  Circulatory support, adequate fluid volume, and nutritional support are important.
Supplemental oxygen is used as the patient begins the initial spiral of hypoxemia
and as the hypoxemia progresses, intubation and mechanical ventilation are
instituted.
 The concentration of oxygen, ventilator settings, and modes are determined by the
patient’s status which is monitored by arterial blood gas analysis, pulse oximetry,
and bedside pulmonary function testing.
 Oxygen support via face mask may be used at very early stage but will not be
adequate as symptom get worse.
 There is no specific pharmacological treatment for ARDS, however, patient can
be treated symptomatically. The medication that can be given to the patient
include the following:
 Morphine 3 to 5 mg/hr IV is given as a sedation for restlessness in
patient on ventilator and experience tachypnea.
 Vecuronium bromide is used as neuromuscular blocking agent and
compel paralyze voluntary respiration
 Give antibiotic and Bronchodilators as prescribed
 Intubation Mechanical ventilation can also be used to increase the inspiratory
flow rate and exert Positive End-expiratory Pressure (PEEP).

NURSING MANAGEMENT

 Patient should be monitored closely because ARDS is a life-threatening condition

 Assess patient frequently to check the effectiveness of treatment
 Administer medication as prescribed by the doctor
 Place patient in a comfortable condition and change position frequently to improve
ventilation, perfusion in the lungs as well as enhancing secretion drainage.
 Keep patient calm to prevent anxiousness
 Encourage resting and ensure that the environment is quiet

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 PNEUMONIA

Learning objectives

 Define pneumonia
 Describe the classification of pneumonia
 Describe the pathophysiology of pneumonia
 Outline the clinical manifestation and complication of pneumonia

Definition

Pneumonia is defined as an inflammation of the lung parenchyma which is caused by

various microorganisms such as bacteria, mycobacteria, fungi, and viruses.

Pneumonitis is a general term that is used to describe an inflammatory process in the lung

tissue that may predispose or place the patient at risk for microbial invasion.

Classification of pneumonia

Pneumonia can be classified into 4 categories and they are as follows:

1. Community-acquired pneumonia (CAP): an acute infection of the lung occurring in

patients who have not been hospitalized or lived in a long-term care facility within 14
days of the onset of symptoms. It is more prevalent in winter period.
2. Hospital-acquired pneumonia (HAP): This is also known as nosocomial pneumonia
(infection). This is defined as the onset of pneumonia symptoms more than 48 hours
after admission in patients with no evidence of infection at the time of admission.
Mostly occur in patient with pre-existing lung diseases, cancer, etc.
3. Pneumonia in the immunocompromised host: this is also known as opportunistic
pneumonia. It is an inflammation and infection of the lower respiratory tract in
immunocompromised patients. It occurs with use of corticosteroids or other
immunosuppressive agents, chemotherapy, nutritional depletion, use of broad-
spectrum antimicrobial agents, acquired immunodeficiency syndrome (AIDS), genetic
immune disorders, and long-term advanced life-support technology (mechanical
ventilation).
4. Aspiration pneumonia: occurs due to the abnormal entry of material from the mouth
or stomach into the trachea and lungs. Conditions that increase the risk for aspiration
include decreased level of consciousness, difficulty swallowing, and insertion of

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 nasogastric (NG) tubes with or without enteral feeding. With loss of consciousness,
the gag and cough reflexes are depressed and aspiration is more likely to occur. The
aspirated material includes food, water, vomitus as well as oropharyngeal secretions
which eventually triggers an inflammatory response. The most common form of
aspiration pneumonia is bacterial infection which occur due to aspiration of bacteria
that normally reside in the upper airways. Aspiration pneumonia may occur in the
community or hospital setting.
5. Necrotizing Pneumonia: it is a rare complication of bacterial lung infection. It
causes the lung tissue to turn into a thick, liquid mass. In some situations, cavitation
occurs as well as lung abscess.

PATHOPHYSIOLOGY OF PNEUMONIA

 Almost all pathogens can trigger an inflammatory response in the lungs

 Inflammation which occur in the lungs is characterized by an increase in blood
flow and vascular permeability which activates neutrophils to engulf and kill the
offending pathogens.
 As a result, the inflammatory process attracts more neutrophils, edema of the
airways occurs, and fluid leaks from the capillaries and tissues into alveoli.
 Normal oxygen transport is affected, leading to manifestations of hypoxia (e.g.,
tachypnea, dyspnea, tachycardia).

 Due to hypoventilation, a ventilation–perfusion mismatch occurs in the affected

area of the lung.
 Venous blood entering the pulmonary circulation passes through the under-
ventilated area and travels to the left side of the heart which is poorly oxygenated
 This can potentially obstruct airflow, impair gas exchange, and cause the signs
and symptoms associated with bacterial infection.

CLINICAL MANIFESTATION OF PNEUMONIA

 Cough (may be productive or non-productive. Sputum may be green, yellow, or

even rust colored)
 Fever
 Chills
 Dyspnea

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  Tachypnea
 Pleuritic chest pain that is aggravated by deep breathing and coughing.
 Some patients may have sore throat and nasal congestion

COMPLICATIONS

 Atelectasis
 Pleurisy, an inflammation of the pleura.
 Pleural effusion: fluid in the pleural space.
 Bacteremia: bacterial infection in the blood, is more likely to occur in infections with
Streptococcus pneumoniae and Haemophilus influenzae.
 Pneumothorax: occur when air collects in the pleural space, causing the lungs to
collapse.
 Acute respiratory failure is one of the leading causes of death in patients with severe
pneumonia. Failure occurs when pneumonia damages the lungs’ ability to exchange
O2 and
 CO2 across the alveolar-capillary membrane.
 Sepsis/septic shock can occur when bacteria within alveoli enter the bloodstream.
Severe sepsis can lead to shock and multisystem organ dysfunction syndrome
(MODS)

CLINICAL DIAGNOSIS

 Proper history should be taken and physical examination must be done

 Chest X-ray to show the patterns and characteristics of the infecting pathogen and
also to check for pleural effusion
 Arterial blood gases (ABGs) may be obtained to assess for hypoxemia
 Sputum: Gram stain, culture and sensitivity test.

CLINICAL MANAGEMENT

 Appropriate antibiotics should be administered and should be early to prevent

complications
 Administer pain medications as appropriate
 Ensure that patient is well ventilated

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NURSING MANAGEMENT

 Increase fluid intake to at least 3litre per day

 Administer medication as prescribed by the doctor
 Administer oxygen if needed
 Chest physiotherapy (percussion and postural drainage) is important in loosening and
mobilizing secretion
 Encourage bed rest
 Educate patient and family members on nutrition

PNEUMOTHORAX AND HAEMOTHORAX

Learning objectives

At the end of this session, students should be able to

 Define pneumothorax and haemothorax

 Describe the classification of pneumothorax
 Describe the pathophysiology of pneumothorax
 Outline the clinical manifestation of pneumothorax

DEFINITION

Pneumothorax is air in the pleural space occurring spontaneously or from trauma.

In patients with chest trauma, it is usually the result of a laceration to the lung parenchyma,
tracheobronchial tree or oesophagus. The clinical status of the patient depends on the rate of
air leakage and size of the wound.

Haemothorax is an accumulation of blood in the pleural space. It is caused by intercostal and

intracostal vessel injury, non-penetrating (blunt) chest injuries to the heart or aorta from
motor vehicle accidents, injuries, fails and blows. It may also resulted from internal bleeding
from punctured organs. A haemothorax is not obvious and difficult to diagnose.The
accumulation of blood in the thoracic cavity restricts the heart to pump blood or the lungs to
expand and effect meaningful respiration.

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 CLASSIFICATION

Spontaneous Pneumothorax: Sudden onset of air in the pleural space with deflation of the
affected lung in the absence of trauma.

Tension Pneumothorax: Build up air under pressure in the pleural space resulting in
interference with filling of both the heart and the lungs

Open Pneumothorax: Open pneumothorax implies an opening in the chest wall large
enough to allow air to pass freely in and out of the thoracic cavity with attempted respiration.

PATHOPHYSIOLOGY

 Increased pressure forces the mediastinum heart, trachea, oesophagus and great
vessels to shift laterally from the middle
 With the shift the heart and other vital structures are compressed
 Venous return to the heart is compromised
 Air continues to enter with each inspiration and becomes trapped and not expelled
during expiration
 Pressure builds up in the chest resulting lung-expansion and impaired gas exchange

CLINICAL MANIFESTATIONS

 Moderate to very severe dyspnoea, severe chest discomfort radiating to the back
 Hyper resonance and diminished breath sounds on affected side
 Reduced mobility of affected half of the thorax
 Tracheal deviation away from affected side in tension pneumothorax
 Clinical picture of an open or tension pneumothorax is air hunger, agitation,
hypotension and cyanosis.

CLINICAL MANAGEMENT

Diagnostic evaluation = Chest X-Ray

Spontaneous Pneumothorax:

o Observe and allow spontaneous recovery for less than 50% pneumothorax in a
healthy person
o Needle aspiration or chest tube if less than 50% pneumothorax

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 o Pleurodesis may be done to prevent recurrence. Chemical pleurodosis uses
various solutions
o Thoracotomy to remove apical blebs (air bubble)

Tension Pneumothorax:

o Immediate decompression to prevent cardio- vascular collapse

o Insertion of chest drain with underwater-sealed suction

Open Pneumothorax:

o Close chest wound immediately

o Pressure dressing
o Chest tube and water sealed drainage
o Surgical intervention to repair trauma

COMPLICATIONS

 Acute respiratory failure

 Cardiovascular collapse with tension pneumothorax

NURSING ASSESSMENT

 Obtain history for chronic respiratory diseases, trauma and onset of symptoms
 Inspect chest for reduced mobility and tracheal deviation
 Auscultate chest for diminished breath sounds and percuss for hyperresonance
 Assess chest expansion: Chest expansion may be asymmetrical due to collapsed lung
 Assess oxygenation and provide supplemental O2 as appropriate
 Assess the level of pain and administer pain medication as appropriate.

Assessment of haemothorax

 On percussion there will be a dullness on the affected side

 On auscultation there will be decreased breath sounds
 Assess for dyspnoea and shortness of breath
 Assess for Tachycardia and hypotension
 Assess for shock and increase jugular vein pressure resulting in distended neck
veins

NURSING DIAGNOSES

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  Ineffective breathing pattern related to air in the pleural space
 Impaired gas exchange related to atelectasis and collapse of the lung

NURSING INTERVENTIONS

 Achieving effective breathing pattern:

o Provide emergency care as indicated: petroleum gauze to sucking wound and
assist with thoracentesis or thoracostomy
o Maintain open airway and suction as needed
o Position patient upright
o Maintain patency of chest tubes
o Assis patient to splint chest when turning or coughing
o Administer analgesics as needed
 Resolving impaired gas exchange
o Educate patient on chest expansion exercises such as deep breathing, cough,
and use of incentive spirometer.
o Monitor oximetry and levels of oxygenation and oxygen as needed
o Place patient in high fowler’s position or position of comfort. Good-lung down
positioning.

Emergency care of haemothorax

 Thoracocentesis
 Monitor intercostal drainage
 Monitor haemoglobin
 Blood transfusion if needed
 Strict fluid balance
 Strict monitoring of vital signs
 Administer oxygen via face mask/nasal catheter

PLEURAL EFFUSION

Learning objectives

At the end of this session, student should be able to

 Define pleural effusion

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Pleural effusion, also called hydrothorax, is the accumulation of watery fluid in the pleural
cavity, between the membrane lining the thoracic cage and the membrane covering the lung.

There are many causes of pleural effusion, including pneumonia, tuberculosis, and the spread
of a malignant tumors from a distant site to the pleural surface.

Pleural effusion often develops as a result of chronic heart failure because the heart cannot
pump fluid away from the lungs, and fluid that seeps from the lungs places additional stress
on the dysfunction heart. Large pleural effusions can cause disabling shortness of breath.

CLINICAL MANIFESTATIONS

 Fever
 Chills
 Pleuritic chest pain
 Coughing
 Underlying causes such as pneumonia
 Shortness of breath in severe cases

CLINICAL ASSESSMENT

 Physical examination: percussion

 Chest x-ray, chest CT and thoracentesis to confirm presence of fluid
 Pleural fluid is analyzed by bacterial culture
 Pleural biopsy may also be performed

CLINICAL MANAGEMENT

 Thoracocentesis is performed to remove fluid and obtain specimen analysis.

Thoracocentesis is the insertion of the needle over the 2nd intercostal space.
 Under certain conditions, such as malignant disease of the pleura (i.e., mesothelioma),
pleural effusion can be treated by introducing an irritating substance called a
sclerosing agent into the pleural space in order to stimulate an inflammatory reaction
of the pleural surfaces.
 As the inflammation heals, tissue adhesions obliterate the pleural space, thereby
preventing the accumulation of more fluid.
 Examples of sclerosing agents that cause an inflammatory reaction of the pleural
surfaces include talc, doxycycline, and bleomycin.

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  Intercostal Drain - Costal drain is inserted on the 5th intercostal space, midaxillary
line
 Thoracotomy- Surgical opening of the thorax.

Nursing management

 Administer treatment as prescribed.

 Monitor vital signs
 Prepare patient for procedures to be performed
 Place patient in position that is less painful and turn patient frequently to facilitate
adequate spreading of talc over the pleural space

UNDERWATER DRAINAGE SYSTEM

A chest tube (chest drain or tube) is a flexible plastic tube that is inserted through the
Lateral/ or Mediastinal of the chest into the pleural space. It is used to remove excess air
or fluid, or pus from the intrathoracic space and to help regain –ve pressure.

INDICATIONS FOR UNDERWATER DRAINAGE

 To remove the residual air and drainage fluid from the pleural space. This assists
in the re expansion of remaining lung tissue.

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  To restore negative pressure.
 Chest tube used during and immediately after thoracic surgery (e.g. open-heart
surgery). Mediastinal.

CARE OF UNDERWATER DRAINAGE SYSTEM

 Keep the system closed and below chest level. Make sure all connections are taped
and the chest tube is secured to the chest wall.
 Make sure the water-seal chamber is filled with sterile water to the level specified by
the manufacturer.
 You should see fluctuation (tidaling) of the fluid level in the water-seal chamber; if
you don’t, the system may not be patent or working properly, or the patient’s lung
may have re-expanded.
 Look for constant or intermittent bubbling in the water-seal chamber, which indicates
leaks in the drainage system.
 Identify external leaks and notify the R/N immediately if you can’t identify an
external leak or correct it.
 Assess the amount, color, and consistency of drainage in the drainage tubing chamber.
 Mark the drainage level on the outside of the collection chamber (with date, time, and
initials).
 Report drainage that’s excessive, cloudy, or unexpectedly bloody.
 Encourage the patient to perform deep breathing, coughing, and incentive spirometry.
 Assist with repositioning or ambulation as ordered.
 Provide adequate analgesia
 Assess vital signs, breath sounds, SpO2, and insertion site for subcutaneous
emphysema as ordered
 When the chest tube is removed, immediately apply sterile occlusive petroleum gauze
dressing over the site to prevent air from entering the pleural space
 Don’t let the drainage tubing kink, loop, or interfere with the patient’s movement.
 Don’t aggressively manipulate the chest tube; don’t strip or milk it
 A patient who is free from pain, to the degree that an effective cough can be
produced, will generate a much higher pressure than can safely be produced with
suction;

55
  If a patient cannot re-inflate his own lung, high volume, low pressure "thoracic"
suction in the range of 15-25 cm of water can help.
 Patients on mechanical ventilators cannot produce an effective cough and therefore
suction is advised.
 The water seal chamber and suction control chamber provide intrathoracic pressure
monitoring.
 Slow, gradual rise in water level over time means more negative pressure in pleural
space and signals healing.
 When applying suction: Level of water in suction control + level of water in water
seal chamber = intrathoracic pressure.

CLAMPING OF THE TUBE

 The decision whether to clamp a chest tube is taken when the drainage system has
been knocked over and disconnected or otherwise disrupted which is based on initial
assessment of the water seal chamber and air leak meter.
 If there has been no bubbling in the water seal, you can deduce there is no air leak
from the lung.
 Therefore, the tube may be clamped for the short time it takes to reestablish drainage.
 If there has been bubbling and assessment has determined there is an air leak from the
lung, you must not clamp the chest tube because it can cause air to accumulate in the
pleural cavity since the air has no means of escape and it can rapidly lead to tension
pneumothorax.
 The few times you should clamp a chest tube are when:
o you are performing a physician-ordered procedure such as sclerosing;
o you are assessing for a leak.
o prior to removing the chest tube to determine if the patient can do without the
chest tube (with a physician order).
o You should never clamp a chest tube during patient transport unless the chest
drainage system becomes disrupted during patient movement, and then only if
there is no air leak.

COMPLICATIONS

o Hemothorax, usually from laceration of intercostals vessel (may require thoracotomy)

o Lung laceration (placed too deep).

56
o Diaphragm / Abdominal cavity penetration (placed too low)
o Tube placed subcutaneously (not in thoracic cavity)
o Tube placed too far (pain)
o Tube falls out (not secured)

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 UNIT 3: GASTRO-INTESTINAL DISEASES/ DISORDERS

Learning objectives

At the end of this unit, student should be able to

 Define gastro-intestinal diseases/ disorders

 Factors may upset the GI tract

Definition

Gastrointestinal disorder is the term used to refer to any condition or disease that occurs
within the gastrointestinal tract. The organs that make up GI tract are mouth, esophagus,
stomach, small intestine, large intestine, and anus.

Gastrointestinal disorders include conditions such as constipation, irritable bowel

syndrome, hemorrhoids, anal fissures, perianal abscesses, anal fistulas, perianal
infections, diverticular diseases, colitis, colon polyps and cancer.

Functional disorders are the conditions in which the gastrointestinal (GI) tract looks
normal but doesn't work properly. They are the most common problems affecting the GI
tract (including the colon and rectum), examples of functional disorders are Constipation
and irritable bowel syndrome (IBS).

Factors may upset the GI tract

 Eating a diet low in fiber.

 Not enough exercise.
 Traveling or other changes in routine.
 Eating large amounts of dairy products.
 Stress.
 Resisting the urge to have a bowel movement.
 Resisting the urge to have bowel movements due to pain from hemorrhoids.
 Overusing laxatives (stool softeners) that, over time, weaken the bowel muscles.
 Taking antacid medicines containing calcium or aluminum.
 Taking certain medicines (especially antidepressants, iron pills, and strong pain
medicines such as narcotics).
 Pregnancy.

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 SOME GASTROINTESTINAL DISEASES/DISORDER

Anal disorders

At the end of this session, students should be able to

 Define hemorrhoid, anal fissures, internal and external hemorrhoid

 Outline treatment of hemorrhoid

Hemorrhoids

Hemorrhoids are swollen blood vessels that line the anal opening. They are caused by chronic
excess pressure from straining during a bowel movement, persistent diarrhea or pregnancy.
There are two types of hemorrhoids: internal and external.

Internal hemorrhoids

Internal hemorrhoids are blood vessels on the inside of the anal opening. When they fall
down into the anus as a result of straining, they become irritated and start to bleed.
Ultimately, internal hemorrhoids can fall down enough to prolapse (sink or stick) out of the
anus.

Treatment includes:

 Improving bowel habits (such as avoiding constipation, not straining during bowel
movements and moving your bowels when you have the urge).
 Your doctor using elastic bands to eliminate the vessels.
 Your doctor removing them surgically. Surgery is needed only for a small number of
patients with very large, painful and persistent hemorrhoids.

External hemorrhoids

External hemorrhoids are veins that lie just under the skin on the outside of the anus.
Sometimes, after straining, the external hemorrhoidal veins burst and a blood clot forms
under the skin. This very painful condition is called a pile.

Treatment includes removing the clot and vein under local anesthesia and /or removing the
hemorrhoid itself.

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Anal fissures

Anal fissures are splits or cracks in the lining of the anal opening. The most common cause of
an anal fissure is the passage of very hard or watery stools. The crack in the anal lining
exposes the underlying muscles that control the passage of stool through the anus and out of
the body. An anal fissure is one of the most painful problems because the exposed muscles
become irritated from exposure to stool or air, and leads to intense burning pain, bleeding or
spasm after bowel movements.

Treatment of anal fissures

 Initial treatment for anal fissures includes pain medicine, dietary fiber to reduce
the occurrence of large, bulky stools and sitz baths (sitting in a few inches of
warm water).
 If these treatments don't relieve pain, surgery might be needed to repair the
sphincter muscle.

DYSPEPSIA

Learning objectives

At the end of this session, student should be able to

 Define dyspepsia
 Outline the causes of dyspepsia
 List the clinical manifestation, and contributing factors of dyspepsia
 Mention the treatments of dyspepsia
 What are the health education that you will give your patient?

DEFINITION

Dyspepsia is an impaired gastric function or stomach upset which is due to some disorders of
the gastrointestinal system characterized by belly pain or discomfort, bloating as well as
feeling uncomfortably full after eating.

CAUSES OF DYSPEPSIA
 Ulcers
 GERD

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  Gastro paresis
 Stomach infections
 Irritable bowel syndrome
 Chronic pancreatitis
 Thyroid diseases
 Hiatal hernia

CONTRIBUTING FACTORS

 Medications such as NSAIDs such as aspirin, ibuprofen, estrogen and oral

contraceptives
 steroid medications
 Drinking too much alcohol
 Cigarette smoking
 Stress and fatigue
 Lactose intolerance

CLINICAL MANIFESTATION

 Loss of appetite
 Heartburn
 Regurgitation
 Acidic taste
 Bloating
 Nausea and vomiting.

CLINICAL DIAGNOSIS

 Abdominal x-ray
 Endoscopy
 Abdominal ultrasound
 Barium swallow
 Blood tests such as FBC, ESR, LFT, H pylori

TREATMENT

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  Proton Pump Inhibitor (PPIs) such as omeprazole, may be recommended if there is a
heartburn along with indigestion.
 H-2-receptor antagonists (H2RAs), which can also reduce stomach acid.
 Prokinetics, which may be helpful if stomach empties slowly.
 Antibiotics, if H. pylori bacteria are causing indigestion.
 Antidepressants or anti-anxiety medications, which may ease the discomfort from
indigestion by decreasing sensation of pain.

HEALTH EDUCATION

Lifestyle changes may help ease indigestion these includes;

 Avoiding foods that trigger indigestion such as fatty, spicy food.

 Do not exercise with full stomach and do not lie down right after eating.
 Eating five or six small meals a day instead of three large meals
 Reducing or eliminating the use of alcohol and caffeine
 Avoiding certain pain relievers, such as aspirin, ibuprofen (Advil, Motrin IB, others)
 Controlling stress and anxiety.

GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)

Learning objectives

By the end of this session, student should be able to

 Define GERD
 Outline the causes of GERD
 Describe the pathophysiology of GERD
 List the clinical manifestation
 Outline the clinical management and patient education of GERD

DEFINITION

Gastro-esophageal reflux disease (GERD) is a digestive disorder that affects the ring of
muscle between your esophagus and your stomach. It is a disease of upper abdominal and
epigastric area caused by the reflux of acids, fluids or food into the oesophagus which can

62
lead to the inflammation of the oesophagus called oesphagitis. GERD occur due to poor
functioning of the musculature of the lower oesophageal segment including the cardiac
sphincter, which permits a reflux of the stomach contents.

CAUSES OF GERD

 Poor function of lower oesophageal sphincter

 Medications such as nitrates, contraceptives, calcium channel blockers and
benzodiazepines.
 Mechanical injury or trauma to the esophageal mucosa caused by rough or sharp
instruments e.g scopes
 Smoking, alcohol
 Caffeinated beverages, oily food, chocolates, citrus fruits and juices
 Slow stomach emptying as in pyloric stenosis
 Hiatus hernia
 Abdominal distension or raised abdominal pressure from pregnancy, obesity or
gastric obstruction such tumours, pyloric stenosis.

PATHOPHYSIOLOGY

 In gastro oesophageal reflux associated with an incompetent lower oesophageal

sphincter, the acidic gastric contents flow backwards through the weak cardiac
sphincter into the oesophagus.
 Contributory factors include impaired gastric emptying from gastro paresis or partial
gastric outlet obstruction and mucosal damage of the oesophagus.

CLINICAL MANIFESTATION

 Regurgitation with heart burn

 Retrosternal chest pain
 Vomiting
 Anorexia and loss of appetite
 Dysphagia
 Belching
 Bloating
 Shortness of breath on lying down especially at night

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  Hoarseness and pharyngitis

CLINICAL DIANOSIS

 Blood tests- FBC, ESR

 Barium swallow
 H pylori test
 Oesophagoscopy and gastroscopy

CLINICAL MANAGEMENT

 Medical management includes: antacids, histamine receptor blockers, proton pump

inhibitors to block gastric secretion.
 Surgical management – vagotomy to reduce the acidity of the stomach contents and
tightens sphincter muscles to reduce reflux.
 Gastrostomy may be performed to assist with nutrition where swallowing is not
possible.

PATIENT EDUCATION

 Avoid any situation that decreases pressure at lower oesophageal sphincter or causes
oesophageal mucosa irritation such as smoking and alcohol.
 stress management - stress increases the amount of stomach acid reflux.
 Diet rich in high protein, low in fat.
 Avoid spicy foods, carbonated drinks and beverages containing caffeine as well as
chocolate.
 Advice patient not to prop his/ her head with more than one pillow, as the abdomen
folds increase the reflux.
 Advice on weight reduction if patient is obese
 Over eating should be avoided because it lowers oesophageal sphincter relaxation.

GASTRO ENTERITIS (GE)

Learning objectives

At the end of this session, student should be able to

 Define gastro enteritis (GE)

 Outline the causes of GE

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  Briefly describe the pathophysiology of GE
 List the clinical manifestation and complication of GE
 Discuss the nursing management and patient education of GE

DEFINITION

Gastroenteritis is a medical condition characterized by inflammation of the gastrointestinal

tract that involves both the stomach and the small intestine resulting in combination of
diarrhea, vomiting, and abdominal pain and cramping. Gastroenteritis is known to as gastro,
stomach bug, stomach virus, stomach flu and gastric flu.

CAUSES OF GASTROENTERITIS

 Virus Rotavirus, norovirus, adenovirus, and astrovirus are known to cause viral
gastroenteritis. Rotavirus is the most common cause of gastroenteritis in children.
 Parasites such as histolytica is pathogenic; infection can lead to amoebic dysentery or
amoebic liver abscess.
 Cryptosporidium is the organism most commonly isolated in HIV positive patients
presenting with diarrhea.
 Bacteria are the cause in about 15%the most of cases, with the most common types
being Escherichia coli, Salmonella, Shigella and Campylobacter.
 Transmission may occur via consumption of contaminated water or/and food
 Bottle-feeding of babies with improperly sanitized.
 Poor hygiene as well as poor nutritional status.

PATHOPHYSIOLOGY

 The intestinal mucosa secretes large amount of water and electrolytes into the
intestinal lumen as a response to irritation by ineffective organisms or the osmotic
pressure exerted by the particles that are not absorbed in the chyme.
 Peristalsis is increased leading to the frequency in bowel emptying.
 Depending on the severity of the diarrhea, electrolyte imbalance occurs.

CLINICAL MANIFESTATION

 Frequent explosive watery stools (diarrhea)

 Abdominal pain and cramps
 Abdominal distension, tenesmus and anorexia

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  Nausea and vomiting
 Fever
 Dehydration- increased thirst, loss of skin turgor, decreases urinary output.
 Dry and inelastic skin and mucus membrane

COMPLICATIONS

 Dehydration
 Shock
 Delirium
 Electrolyte imbalance

CLINICAL DIAGNOSIS

 Stools MCS to identify the causative organism

 Endoscopy
 Upper and lower gastrointestinal radiological studies such as barium contrast to detect
any mucosal lining diseases as well as any structural abnormality.

CLININCAL MANAGEMENT OF GE

 Oral rehydration solution: World Health Organization (WHO) recommend oral

rehydration solution (ORS) as the treatment of choice for children with mild-to-
moderate gastroenteritis in both developed and developing countries.
 NG feeding: For patients who do not tolerate ORS by mouth, nasogastric (NG)
feeding is a safe and effective alternative.
 IV rehydration: IV access should be obtained in severe dehydration and patients
should be administered a bolus of 20-30 mL/kg lactated Ringer (LR) or normal saline
(NS) solution over 60 minutes.
 Diet: children with gastroenteritis should be returned to a normal diet as rapidly as
possible; early feeding reduces illness duration and improves nutritional outcome.
 Administer treatment as prescribed to reduce morbidity, prevent complications, and
provide prophylaxis. Drugs such as metronidazole is recommended as the treatment of
choice for mild-to-moderate cases of C difficile colitis.
 Vaccines: vaccinating children against Rotavirus very important, it prevent children
from rotavirus gastroenteritis.

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  Antiemetics: drugs such as ondansetron reduce vomiting and the need for intravenous
(IV) rehydration and hospital admission, IV ondansetron and metoclopramide reduce
the number of episodes of vomiting and hospital admission, and dimenhydrinate
suppository reduce the duration of vomiting.

NURSING MANAGEMENT

 Prevent dehydration by replacing fluid and electrolyte to achieve acid base balance.
 Strictly monitoring intake and output
 Monitor vital signs closely
 Provide the patient with bed pan at all times and clean it after every use
 Ensure that patient wash hands after each stool
 Prevent peri anal skin breakdown by ensuring good personal hygiene. Make sure that
the patients perineum is washed and dried after each bowel motion to prevent
excoriation and promote comfort.
 Maintain normal nutritional intake- encourage balanced diet to maintain nutritional
status which may also assist in getting the stool formed.
 Administer antidiarrheal medication as prescribed

PATIENT EDUCATION

 Encourage patient to increase clean and clear fluid intake such as water, apple, juice
 Encourage bed rest
 Avoid smoking, alcohol and irritating foods such as coffee, chocolate, fried foods or
highly spiced foods.
 Encourage patient to eat foods that are less irritating to the stomach. Add foods such
as white bread, crackers, oatmeal, rice cereals, fish or chicken, potatoes, rice and most
vegetables.
 Educate patient on the importance of hand washing after using the toilet and also
before handling food
 Do not participate in food handling or preparation until the illness has gone away.
 Educate patient on dosage of medication and advise patient to complete antibiotic
treatment course.
 Take antidiarrheal medicines only if doctor has prescribed them.

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 DEHYDRATION

Learning objectives

At the end of this session, student should be able to

 Define dehydration

DEFINITION

Dehydration can be defined as an excessive loss of fluid from the body as a result of
persistent vomiting, diarrhea, sweating or from lack of fluid intake. Dehydration can be
classified as some, mild or severe dehydration.

Severe dehydration is a serious condition that may lead to fatal shock and the accumulation
of waste products in the body.

CAUSES

 Vomiting and diarrhea

 Heat exposure
 Fever
 Increased urination due to infection
 Impaired ability to drink for instance someone in coma or on a respirator
 Injuries to skin such as burns or mouth sores or severe skin diseases or infections.

CLINICAL MANIFESTATION

 Increased thirst
 Dry mouth and tongue
 Palpitations
 Confusion
 Sluggish with fainting
 Decreased urine output
 Poor skin turgor
 Sunken eyes

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Dehydrated patient

NURSING MANAGEMENT OF PATIENT WITH DEHYDRATION

 Administer IV therapy to replace fluid and electrolyte loss

 Monitor intake and output
 Encourage intake of extra fluids
 Provide nasogastric tube feeding as prescribed
 Monitor the vital signs closely
 Provide hygiene care
 Observe for signs of shock
 Patient education

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UNIT 4: GENITO-URINARY DISEASES/ DISORDERS

Learning objectives

At the end of this session, student should be able to

 Define
 Outline the risk factors of Genito-urinary diseases/ disorders
 Classify renal system disorder
 Define the concepts related to Genito-urinary diseases/ disorders

DEFINITION

Genito-urinary diseases/ disorders are the conditions that affect the urinary and genital
organs. Renal system is also known as urinary system and it maintains homeostasis in the
body. Urinary tract is divided into upper urinary tract (kidneys and ureter) and lower urinary
tract t (bladder and urethra).

Kidneys secrete hormones such as renin, erythropoietin, renal prostaglandins which play a
role in normal functioning of the system. In females, kidney is close proximity to the
reproductive system while in males, it is shared with reproductive system.

RISK FACTORS

 Dehydration and inadequate intake of water

 Hypertension, diabetes mellitus
 Nephrotoxic medications such as antibiotics such as aminoglycosides
 Infections: pyelonephritis, glomerulonephritis, cystitis, urethritis
 Instrumentation to the urinary tract.
 Diet rich in calcium

CLASSIFICATION OF RENAL SYSTEM DISORDERS

Classification was done according to the causative factor and they are as follows:

 Infections- pyelonephritis, glomerulonephritis, cystitis, urethritis, UTI

 Obstructive disorder- tumors, cancer of the bladder, renal calculi, Structural defects,
renal failure, Congenital defects, solitary kidney, ectopic/ duplicate ureter
 Trauma: accident

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KEY CONCEPTS

 Anuria- absence of urine, volume less than 100ml/24 hrs

 Enuresis- involuntary voiding during the night
 Haematuria- presence of blood in urine
 Polyuria- passing large volumes of urine more than 1500mls in 24 hours.
 Proteinuria- presence of protein in urine
 Uraemia- accumulation of urea in circulating blood.
 Oliguria- decreased volume of less than 500 mls of urine pass over 24hour period
 Retention- inability to pass urine even though the bladder is full.
 Stress incontinence- involuntary voiding due to sudden increase in abdominal
pressure causing urine to leak, such as running, lifting of heavy object, sneezing,
coughing. Stress incontinence has nothing to do with psychological stress.

COMMON CLINICAL MANIFESTATION

 Pain- back pain radiating to the abdomen flank pain (between ribs and ileum),
suprapubic pain
 Dysuria
 Change in patterns of urinary elimination such as incontinence, retention, oliguria,
discharge etc.
 Systemic manifestation such as oedema, signs and symptoms of shock, loss of weight.

CLINICAL DIAGNOSIS

 Urine test
 Urine MCS
 Blood tests- FBC, U+E, BUN
 Pyelography
 Cystography
 CT scan
 Ultrasound
 MRI

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 ACUTE RENAL FAILURE

Learning objectives

At the end of this session, student should be able to

 Define Acute renal failure

 Describe the causes of renal failure
 Describe the pathophysiology of renal physiology
 List the clinical manifestation of renal failure
 Outline the clinical management and nursing management of renal failure

DEFINITION

Acute renal failure is defined as rapid decline or loss of kidney function due to sudden
decrease in the glomerular filtration rate, resulting in acute tubular necrosis. It occurs when
the kidney lost its filtering ability, then cause dangerous levels of wastes to accumulate which
in turn, can lead to imbalance in blood's chemical makeup.

CAUSES OF ACUTE RENAL FAILURE

 Pre-renal causes: conditions that cause a drop in the blood supply to the kidneys,
resulting in hypo perfusion of the kidneys and thus a drop in the glomerular filtration
rate. Major causes of pre-renal causes include Fluid volume depletion, vasodilation&
impaired cardiac function.
 Intra-renal causes: conditions that cause structural damage to parenchyma or tubules
of the kidneys. These include infections, crush injuries, nephrotic agents such as non-
steroidal anti-inflammatory drugs.
 Post-renal causes: Obstruction in the collecting system above the urinary bladder or
anywhere in the bladder. Obstruction causes reflux of urine and an increase in the
pressure inside the kidneys. Obstruction can be caused by renal stones, blood clots
from trauma, strictures, enlarged prostate gland, cancer of the cervix, bladder tumors.
 PATHOPHYSIOLOGY
Occurs as a result of a direct decrease in renal blood supply, causing ischaemic
damage to the kidneys.
 Tubular damage that occurs includes the sequestration of the glomerular filtrate in
tubules whereby the lumen will be blocked by sloughed necrotic tubular cells.

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  The filtrate then leaks back into the interstitial through damage tubular cells and
stimulates the renin-angiotensin mechanism, resulting in a raised blood pressure.
 Afferent arterioles constrict and glomerular filtration pressure drops, resulting in
hypovolemia and increased blood pressure

PHASES OF ACUTE RENAL FAILURE

 Initiation phase- starts with initial cause and end with the occurrence of oliguria
or anuria
 Oliguric phase: occurs within 48 hours of the initial cause and may last up to 4- 6
weeks. Metabolites are not adequately excreted by kidney, resulting in their
retention.
 Diuretic phase: characterized by excretion of excess fluid retained during oliguric
phase. It takes up to 7 or more days.
 Recovery phase: starts when the kidney shows signs of improved renal function.
It takes from 3 to 12 months to recover.

CLINICAL MANIFESTATION

 Edema
 Distended neck veins
 Decreased urine output
 Headache
 Signs of dehydration
 Dyspnea
 Patient may appear very ill, lethargic and has an impaired memory

CLINICAL MANAGEMENT

 Dialysis is indicated when there is fluid overload and uncontrolled hyperkalemia.

 Diuretics such as furosemide are prescribed if oliguria and fluid retention persist
 Anti-hypotensive drugs to regulate adequate renal perfusion and urine production.
 High caloric diet should be given to meet energy requirements.

NURSING MANAGEMENT

 Monitoring intake and output of the patient

 Assess and care for edematous skin

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  Assist the patient with frequent position changes and take care of the pressure areas in
the body
 Patient should be kept on bed rest to reduce oxygen and metabolic demand
 Monitor vital signs closely and fever should be treated promptly
 Prevention of infection by practicing aseptic procedures.

CHRONIC RENAL FAILURE

Learning objectives

At the end of this session, students should be able to

 Define chronic renal failure

DEFINITION

Chronic renal failure is a progressive, irreversible loss of function of nephrons that results
in the retention of metabolic waste products in the body as well as electrolyte imbalances.

CAUSES OF CHRONIC RENAL FAILURE

 Diabetes
 High blood pressure (hypertension)
 Heart disease
 Infection
 Trauma
 Cancer

PATHOPYSIOLOGY

 Renal function declines and waste products accumulate in the body.

 Stage 1- the nephrons loose function
 Stage 2 – renal insufficiency, 75%-90% nephron functioning is lost, anemia develops
and polyuria.
 Stage 3- less than 10% functioning ability of the kidney. Compromised regulatory
functioning.
 Characterized by uremia, proteinuria, hypertension. dialysis is usually indicated at this
stage.

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CLINICAL MANIFESTATION

 Metallic taste in the mouth

 Increased respiratory rate
 Edema of the hands and feet
 Distended neck veins
 Hypertension
 Decreased libido
 Hyperglycemia
 Loss of muscle strength

CLINICAL MANAGEMENT

 Drug therapy- anti-hypertensive, diuretics, vitamins

 Diet - avoid food rich in protein, potassium and sodium intake
 Fluid restriction
 Encourage rest because of the effects of waste in the body and treatment.
 Dialysis

NURSING MANAGEMENT

 Monitor intake and output on daily basis

 Weigh patient daily and restrict fluid intake. Advice patient to avoid alcohol
 Administer medication as prescribed
 Take all the infection prevention control measures such as aseptic technique
 Assist the patient with frequent position changes and take care of the pressure areas in
the body
PATIENT EDUCATION

 Give health education on medication regimen and rationale

 Educate patient on diet- restriction protein, sodium and potassium intake
 Educate patient on infection prevention; Personal hygiene, rest and exercises
 Advice patient to adhere to follow up dates.

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 DIALYSIS

Learning objectives

At the end of this unit, students should be able to

 Define dialysis

DEFINITION

Dialysis is the process that involves selective movement of solutes and water from one
compartment to another through the semi permeable membrane. Dialysis is used to filter the
waste product that the kidneys are not able to filter from the blood.

It is used as life saving measure in renal failure to remove excess body fluid, urea, to correct
electrolytes and acid base imbalances. So basically, dialysis performs the duty of the kidneys.
It can be temporary until kidneys function is restored and it can be permanent in a situation
where there is extensive damage to the nephrons.

METHODS OF DIALYSIS

1.Peritoneal dialysis

 Peritoneum of the patient with renal failure is used as a semi permeable membrane.
 Sterile catheter is inserted through a small incision in the abdominal wall.
 Catheter is sutured in position and covered with sterile dressing.
 Solution (electrolyte and glucose) is instilled in the peritoneal cavity and remain there
for a prescribed period of time.
 During this process, osmosis and diffusion takes place

COMPLICATIONS PERITONEAL DIALYSIS

 Infections: An infection of the abdominal lining (peritonitis) is a common

complication of peritoneal dialysis. An infection can also develop at the site where the
catheter is inserted to carry the cleansing fluid (dialysate) into and out of the
abdomen. The risk of infection is greater if the person doing the dialysis isn't
adequately trained.
 Weight gain: The dialysate contains sugar (dextrose). Absorbing some of the
dialysate might cause extra calories daily, leading to weight gain.

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  Hernia: Holding fluid in your abdomen for long periods may strain your muscles.
 Inadequate dialysis: Peritoneal dialysis can become ineffective after several years.
Patient might need to switch to hemodialysis.

2. Hemodialysis

 Aim is to remove toxic nitrogenous substances and excess water from the blood.
 Blood is removed from the patient, pumped through an artificial kidney (dialyzer) and
returned to the patient.
 As patients’ blood circulates through the dialyzer, it is exposed to the semi permeable
and dialysate where the toxins are removed from the blood by diffusion and water by
osmosis.

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COMPLICATIONS OF HEMODIALYSIS

 Hypotension
 Hemolysis
 Embolism
 Headache
 Psychological problems such as depression and anxiety.

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UNIT 5: ENDOCRINE DISORDERS

Learning objectives

At the end of this unit, student should be able to

 Define endocrine disorder

 Describe various types of endocrine disorders

DEFINITION

Endocrine diseases/ disorders are the conditions that affects the endocrine system. The
endocrine system involves the release of chemical substances known as hormones to regulate
and integrate body functions.

The endocrine system is composed of several glands: the pituitary, the thyroid gland,
parathyroid glands, adrenal glands, pancreatic islets, ovaries, and testes. Most hormones
secreted from endocrine glands are released directly into the bloodstream. These hormones
help to regulate organ function in concert with the nervous system.

Endocrine diseases occur when a gland produces too much or too little of an endocrine
hormone, called a hormone imbalance.

TYPES OF ENDOCRINE SYSTEM DISORDER

There are various types of endocrine disorders of which some are listed below:

 Diabetes
 Hyperthyroidism (thyroid gland condition)
 Hypothyroidism (thyroid gland condition)
 Cushing syndrome
 Hypopituitarism
 Polycystic ovary syndrome (PCOS)

Management of endocrine disorders depend on the type of disorders. Some of these

conditions are discussed below.

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 DIABETES MELLITUS

Learning objectives

At the end of this session, student should be able to

 Define diabetes mellitus

 Describe the pathophysiology of diabetes mellitus
 Describe the classification of diabetes mellitus
 Outline the clinical manifestation, clinical diagnosis and clinical management of
diabetes mellitus
 Outline the nursing intervention of diabetes mellitus

DEFINITION

Diabetes mellitus is a group of metabolic diseases characterized by increased levels of

glucose in the blood (hyperglycemia) resulting from defects in either insulin secretion, insulin

action, or both.

Diabetes is the third leading cause of death from disease, primarily because of the high rate of
cardiovascular disease (myocardial infarction, stroke, and peripheral vascular disease) among
people with diabetes. The economic cost of diabetes continues to increase because of
increasing health care costs and an aging population.

PATHOPHYSIOLOGY

 Insulin is secreted by beta cells in the pancreas and it is an anabolic hormone.

 When food is consumed, insulin moves glucose from blood to muscle, liver, and fat
cells as insulin level increases.
 The functions of insulin include the transport and metabolism of glucose for energy,
stimulation of storage of glucose in the liver and muscle, serves as the signal of the
liver to stop releasing glucose, enhancement of the storage of dietary fat in adipose
tissue, and acceleration of the transport of amino acid into cells.
 Insulin and glucagon maintain a constant level of glucose in the blood by stimulating
the release of glucose from the liver.

CLASSIFICATION OF DIABETES

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The major types of diabetes are type 1 diabetes mellitus, type 2 diabetes mellitus, and
gestational diabetes.

The different types of diabetes mellitus vary in cause, clinical course, and treatment

Type 1 Diabetes Mellitus

 Type 1 diabetes mellitus is characterized by destruction of the pancreatic beta cells.

 A common underlying factor in the development of type 1 diabetes is a genetic
susceptibility.
 Destruction of beta cells leads to a decrease in insulin production, unchecked glucose
production by the liver and fasting hyperglycemia.
 Glucose taken from food cannot be stored in the liver anymore but remains in the
blood stream.
 The kidneys will not reabsorb the glucose once it has exceeded the renal threshold, so
it will appear in the urine and be called glycosuria.
 Excessive loss of fluids is accompanied by excessive excretion of glucose in the urine
leading to osmotic diuresis.
 There is fat breakdown which results in ketone production, the by-product of fat
breakdown.
 There is also evidence of an autoimmune response in type 1 diabetes. The abnormal
response in which antibodies are directed against normal tissues of the body,
responding to these tissues as if they were foreign.
 Environmental factors such as viruses or toxins, that may initiate destruction of the
beta cell can also cause type 1 diabetes but are being investigated.

Type 2 diabetes mellitus

 Type 2 diabetes mellitus has major problems of insulin resistance and impaired
insulin secretion.
 It occurs more commonly among people who are older than 30 years of age
 and obese
 Insulin could not bind with the special receptors so insulin becomes less effective at
stimulating glucose uptake and at regulating the glucose release.

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  There must be increased amounts of insulin to maintain glucose level at a normal or
slightly elevated level.
 However, there is enough insulin to prevent the breakdown of fats and production of
ketones.
 Uncontrolled type 2 diabetes could lead to hyperglycemic, hyperosmolar nonketotic
syndrome.
 The usual symptoms that the patient may feel are polyuria, polydipsia, polyphagia,
fatigue, irritability, poorly healing skin wounds, vaginal infections, or blurred vision.

Gestational Diabetes Mellitus

 Gestational diabetes mellitus (GDM) is any degree of glucose intolerance with its
onset during pregnancy.
 Hyperglycemia develops during pregnancy because of the secretion of placental
hormones, which causes insulin resistance.
 Gestational diabetes occurs in as many as 14% of pregnant women and increases their
risk for hypertensive disorders during pregnancy
 After delivery, blood glucose levels in women with GDM usually return to normal or
later on develop type 2 diabetes.

CLINICAL MANIFESTATION OF DIABETES MELLITUS

 Elevated blood glucose

 Polyuria (increased urination)
 Polydipsia (increased thirst)
 Polyphagia (increased appetite)
 Fatigue and weakness
 Sudden vision changes.
 Sudden weight loss
 Prolong wound healing
 Numbness or tingling of hand and feet
 Infection such as vaginal infection
 Sexual problem
 Dry skin

CLINICAL DIAGNOSIS

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  An abnormally high blood glucose level is the basic criterion for the diagnosis of
diabetes.
 Fasting plasma glucose (FPG), random plasma glucose can be used.
 Glucose level 2 hours after receiving glucose (2-hour post-load) may be used.
 Urine: Positive for glucose and ketones; specific gravity and osmolality may be
elevated.
 Cultures and sensitivities: to check for possible UTI, respiratory or wound infections.

CLINICAL MANAGEMENT

The main goal of diabetes treatment is to normalize the blood glucose levels to reduce the
development of vascular and neuropathic complications.

 Intensive therapy must be initiated with caution and must be accompanied by

thorough education of the patient and family and by responsible behavior of the
patient.
 Careful screening of patients is a key step in initiating intensive therapy.
 Nutrition, meal planning, and weight control are the foundation of diabetes
management
 It is recommended for patients that are obese to lose weight
 Nutritionist must draw up a meal plan for diabetic patient
 Patient must exercise regularly
 Monitor glucose level and ketone
 In type 1 diabetes, exogenous insulin must be administered for life because the body
loses the ability to produce insulin.
 In type 2 diabetes, insulin may be necessary on a long-term basis to control glucose
levels if meal planning and oral agents are ineffective.
 Oral antidiabetic agents may be effective for patients who have type 2 diabetes that
cannot be treated effectively with nutritional therapy and exercise alone

NURSING MANAGEMENT

 Assess the patient’s current knowledge and understanding about diabetes mellitus and
educate patient accordingly.
 Educate patient on healthy lifestyle, balanced diet. Involve a dietitian in this process
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  Assess for anxiety, tremors, and slurring of speech
 Monitor patient for signs of hypoglycemia
 Teach patient on how to administer insulin and any other anti-diabetic treatment at
home
 Advice patient on exercising daily and educate him/her on the importance of daily
exercise
 Advice patient to avoid getting injured because diabetic wound does not heal fast

THYROID DISORDERS

Learning objectives

At the of this session, student should be able to

 Define thyroid disorder

 Define hyperthyroidism, hypothyroidism and thyroidectomy
 Outline the clinical manifestation of each condition
 Outline the clinical management of each condition

DEFINITION

The thyroid gland is a small organ that’s located in the front of the neck, wrapped around
the windpipe (trachea). It’s shaped like a butterfly, smaller in the middle with two wide wings
that extend around the side of your throat. Thyroid gland secretes the hormones that control
the metabolism in the body. Thyroid hormone is secreted by anterior pituitary gland, which
stimulates the thyroid gland to secrete T3 (triiodothyronine) and T4 (thyroxine).

Thyroid disease/ disorder is a general term for a medical condition that prevent the thyroid
from making the right amount of hormones. Thyroid disorders can result in the disruption of
normal bodily functions.

The main abnormalities of the thyroid gland are: hyperthyroidism, hypothyroidism and
goitre.

HYPERTHYROIDISM

Hyperthyroidism is the hypersecretion of the thyroid hormone or the over activity of the
thyroid glands. It results from an excessive output of thyroid hormones caused by abnormal

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stimulation of the thyroid gland by circulating immunoglobulins It is 8 times more common
in females. Hyperthyroidism leads to goitre.

Hyperthyroidism disorder may appear after an emotional shock, stress, or an infection, but
the exact significance of these relationships is not understood. Other common causes of
hyperthyroidism include thyroiditis and excessive ingestion of thyroid hormone.

CAUSES

 Excess secretion of TSH

 Abnormal thyroid stimulator
 Acute thyroiditis
 Medicines e.g amiodarone
 Autonomous hyper function within the gland.

CLINICAL MANIFESTATION

 Anxiety, irritability and nervousness.

 Having trouble sleeping.
 Losing weight.
 Having an enlarged thyroid gland or a goiter.
 Having muscle weakness and tremors.
 Experiencing irregular menstrual periods or amenorrhea.
 Feeling sensitive to heat, pyrexia
 Having vision problems or eye irritation such as Exophthalmos and infrequent
blinking or inability to close the eyes
 Bulging eyes
 Rapid speech and body movements
 There may be a fine tremor of the hands.
 Tachycardia
 Polyuria
 Hair appear fine and silky

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 Goitre

CLINICAL DIAGNOSIS

Clinical diagnosis is made on the basis of the

 Symptoms
 Decrease in serum TSH
 Increased free T4
 An increase in radioactive iodine uptake.
 FBC, U+E
 ECG
 CXR

CLINICAL MANAGEMENT

 Hyperthyroidism treatment depends on the underlying cause and often consists of a

combination of therapies, including antithyroid agents, radioactive iodine,
 and surgery.
 Treatment of hyperthyroidism is directed toward reducing thyroid hyperactivity to
relieve symptoms and preventing complications
 Irradiation involving the administration of 131I or 123I for destructive effects on the
thyroid gland

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  Antithyroid medications that interfere with the synthesis of thyroid hormones I
administered to the patient to prevent manifestations of hyperthyroidism.
 Radioactive iodine is the most common form of treatment for Graves’ disease
 Beta-adrenergic blocking agents (eg, propranolol [Inderal]) are used as adjunctive
therapy for symptomatic relief, particularly in transient thyroiditis
 Surgical removal of most of the thyroid gland is a nonpharmacologic alternative.
 No treatment for thyrotoxicosis is without side effects, and all three treatments
(radioactive iodine therapy, antithyroid medications, and surgery) share the same
complications such as relapse or recurrent hyperthyroidism and permanent
hypothyroidism.

NURSING MANAGEMENT

 Provide adequate rest.

 Administer sedatives as prescribed.
 Provide a cool and quiet environment.
 Monitor patients’ weight on daily basis
 Provide a high-calorie diet.
 Avoid the administration of stimulants.
 Administer antithyroid medications (propylthiouracil [PTU]) that block thyroid
synthesis, as prescribed.
 Administer iodine preparations that inhibit the release of thyroid hormone as
prescribed.
 Administer propranolol (INderal) for tachycardia as prescribed.
 Prepare the client for radioactive iodine therapy, as prescribed, to destroy thyroid
cells.
 Prepare the client for thyroidectomy if prescribed by the doctor.

THYROIDECTOMY

Thyroidectomy is the surgical removal of all or part of your thyroid gland. A sub/total
thyroidectomy may be done for most patients suffering from a large and unsightly goiter is
causing pressure symptoms.When malignancy exists, then a total thyroidectomy will be done

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Postoperative care aims at early identification and prevention of complications, ie.
Hemorrhage, hypocalcaemia, hypothyroidism, and re-current laryngeal nerve palsy.

In the initial post-operative phase, bleeding leading to airway obstruction is the most
significant complication and the emergency trolley must be kept in readiness by the bedside.

Acute hypo-calcaemia indicated by laryngospasm and is a very significant complication.

A syringe of calcium chloride or calcium gluconate solution must be kept at the bedside to be
given in this instance

NURSING MANAGEMENT OF THYROIDECTOMY

Prevention of following complications:

1. Potential for airway obstruction

 Nurse patient in Fowler’s position to facilitate breathing and reduce neck swelling
 Support head between two sandbags to reduce strain or tension on the sutures
 Keep clip removal/suture removal set at bedside in case of an emergency to remove
suture/clips

2. Bleeding

 Monitor vital signs frequently – a low B/P and restlessness may indicate bleeding,
 Observe for obvious bleeding from the wound
 Be alert for signs of labored breathing and/or stridor, both of which may indicate
airway obstruction.
 If the patient’s breathing becomes labored the clips or sutures should be removed to
allow any blood or blood clot to escape and thereby releasing pressure on the trachea.
 The open wound should be covered with sterile/gauze that has been soaked in sterile
3. Loss of hoarseness of voice
 Observe the patient for any difficulty in breathing, dysphagia or hoarseness
 A tracheostomy set should be kept at the bedside in case it becomes necessary to carry
out an emergency tracheostomy – e.g when airway obstruction is due to edema or to
laryngo-spasm following severing of one or both recurrent laryngeal nerves during
surgery saline and the patient should be returned to theatre.

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 HYPOTHYROIDISM

Hypothyroidism results from suboptimal levels of thyroid hormone. It is the underactivity of

the thyroid gland i.e. low thyroid hormone levels. Thyroid deficiency can affect all body
functions and can range from mild, subclinical forms to myxedema, an advanced form. The
most common cause of hypothyroidism in adults is autoimmune thyroiditis (Hashimoto’s
disease), in which the immune system attacks the thyroid gland.

Hypothyroidism has gradual onset and it is often mistaken for ageing or depression. Its
diagnosis is easily missed and it primarily affects middle aged women.

Congenital hypothyroidism (cretinism)

Develops during intrauterine life or neonatal stage due to maternal deprivation of iodine,
genetic enzyme defects or absence of the thyroid gland.

Adult hypothyroidism (myxedema)

In this condition all the body process are slowed down, T3 and T4 levels are low.

CAUSES OF HYPOTHYROIDISM

 Congenital abnormality
 Iodine deficiency
 Post thyroidectomy
 Post thyroiditis
 Post radiotherapy for thyrotoxicosis
 Pituitary or hypothalamic malfunction
 Autoimmune disease (Hashimoto’s thyroiditis, post Graves’ disease)
 Atrophy of thyroid gland with aging
 Therapy for hyperthyroidism
 Radioactive iodine (131I)
 Medications
 Radiation to head and neck for treatment of head and neck cancers, lymphoma

CLINICAL MANIFESTATION

 Poor appetite with increased weigh gain

 Cold intolerance, Extreme fatigue

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  Impaired memory, sleeping for longer periods
 Constipation, abdominal distension
 Coarse skin and brittle hair and nails
 Swollen face and eyelids
 Large tongue
 Dry skin that flakes easily on rubbing

CLINICAL DIAGNOSIS

 Thyroid function test

 Thyroid stimulating hormone
 Fbc
 Cholesterol

CLINICAL MANAGEMENT

 Synthetic levothyroxine (Synthroid or Levothroid) is the preferred preparation for

treating hypothyroidism and suppressing nontoxic goiters. Dosage is based on the
patient’s serum TSH concentration.
 Prevent cardiac dysfunction because has had hypothyroidism for a long period is
almost certain to have elevated serum cholesterol, atherosclerosis, and coronary artery
disease.
 Prevent medication interactions by taking all the necessary precautions
 Arterial blood gases may be measured to determine carbon dioxide retention and to
guide the use of assisted ventilation to combat hypoventilation.
 Oxygen saturation levels should be monitored using pulse oximetry.
 Fluids are administered cautiously because of the danger of water intoxication.

NURSING MANAGEMENT

 Monitor vital signs such as temperature, respiratory rate, depth, pattern, pulse
oximetry, and arterial blood gases
 Monitor patient for increasing severity of signs and symptoms of hypothyroidism
 Observe for decreased level of consciousness as well as dementia
 Administer medication as prescribed by the doctor
 Provide stimulation through conversation and non-stressful activities

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  Encourage increased mobility within patient’s exercise tolerance
 Monitor patient’s response to increasing activities
 Encourage increased fluid intake within limits of fluid restriction
 Educate patient and family on how to manage hypothyroidism at home
 Educate patient on the importance of nutrition and diet to promote weight loss and
normal bowel patterns
 Provide foods high in fiber to prevent constipation
 Avoid and discourage use of external heat source (eg, heating pads, electric or
warming blankets) to reduce the effect of vasodilation and vascular collapse.
 Encourage deep breathing, coughing, and use of incentive spirometry.
 Maintain patent airway through suction and ventilatory support if indicated.

CUSHING’S SYNDROME

Learning objectives

At the end of this session, student should be able to

 Define Cushing’s syndrome

 List the causes of Cushing’s syndrome
 Outline the clinical manifestation of Cushing’s syndrome
 Outline the clinical diagnosis and clinical management of Cushing’s syndrome
 Describe the nursing intervention of Cushing’s syndrome

DEFINITION

Cushing’s syndrome is a disorder that occur due to excess cortisol or related corticosteroids.
Cushing’s syndrome is commonly caused by use of corticosteroid medications and is
infrequently the result of excessive corticosteroid production secondary to hyperplasia of the
adrenal cortex. It is related to adenoma of the pituitary or ACTH (adrenocorticotropic)
overproduction.

CAUSES

 Primarily Cushing’s syndrome a result of over-secretion of glucocorticoids and

androgens (sex hormones)

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  Excessive stress
 Carcinoma of the lungs
 Prolonged administration of high doses of corticosteroids.
 Ectopic production of ACTH by malignancies

CLINICAL MANIFESTATION

1.Manifestations caused by excess glucocorticoids

 Weight gain that leads to obesity

 Arrest of growth which leads to heavy trunk, thin extremities
 Buffalo hump” in the neck & supraclavicular area
 Rounded face (moon face),
 Fragile & thin skin; strae &acne, Muscle wasted-high catabolism
 Musculoskeletal changes: osteoporosis-kyphosis, backache,
 Mental disturbances: mood change, psychosis

2. Manifestations caused by access mineralocorticoids

 hypertension
 hypernatremia
 Weight gain.
 edema

3. Manifestations caused by excess androgens

 Hirsutism-excessive growth of hairs on the face & midline truck.

 Breast atrophy
 Clitoris enlargement
 Loss of libido (male &female)

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CLINICAL DIAGNOSIS

 An overnight dexamethasone suppression test is the most widely used and most
sensitive screening test for diagnosis of pituitary and adrenal causes of Cushing’s
syndrome.
 Blood samples are taken to check for excessive plasma levels, increase in blood
glucose level & glucose intolerance and decreased serum Potassium level
 Ct scan
 ACTH stimulation test

CLINICAL MANAGEMENT

 Adrenal enzyme inhibitors (eg, metyrapone [Metopirone], aminoglutethimide

[Cytadren], mitotane [Lysodren], and ketoconazole [Nizoral]) may be used to reduce
hyper-adrenalism if the syndrome is caused by ectopic ACTH secretion by a tumor
that cannot be eradicated.
 Surgery & Radiation can be performed
 Replacement therapy is done postoperatively
 Cortisone treatment-prenisolone/hydrocortisone can be administered

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NURSING INTERVENTIONS

 Maintain skin integrity: Assess skin frequently, avoid use of adhesive tape, monitor
intake & output
 Encourage active participation in self-care: assist in activities planning, encourage
rest,
 Reduce anxiety: answer questions about surgery, discuss nursing care with patient.
 Strengthen body image: encourage patient to verbalize concerns, refer for counseling,
identify disturbing situation
 Decrease risk of infection: The patient should avoid unnecessary exposure to others
 with infections. The nurse frequently assesses the patient for subtle signs of infection.

PATIENT EDUCATION

 Teach the patient on how to cope with lifelong treatment

 Teach patient about proper skin care
 Encourage diet rich in calcium, high protein, low in cholesterol and salt.
 Advice patient to avoid stressful situations
 Educate patient about the importance of taking medication as directed.
 Encourage patient on low calories diet to avoid obesity.

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20373112. Accessed on 07/09/2020

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https://nurseslabs.com/heart-failure/. Accessed on 10/09/2020

https://nurseslabs.com/tonsillitis-adenoiditis/. Accessed on 13/09/2020

Nittina, S.M. 2014. Lippincot Manual of Nursing Practise. 10 th Ed. Tokyo: Wolters
Kluwer/ Lippincott Williams & Wilkens.

Smeltzer, S.C., Bare, B.G., Hinkle, J.L.& Cheever, K. H. (2010) 12 th Ed. Brunner &
Suddarth’s Textbook of Medical-Surgical Nursing. Tokyo: Wolters Kluwer Health.

Vlok, M. E. 1998. Manual of Nursing, 9th Ed. Volume 1. Basic Nursing, Cape Town: Juta &
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Viljoen, M. J. 2000. Nursing Assessment: History Taking and physical Assessment. Cape
Town. Kasigo.

Mogotlane, S., Chauke, M, C., Matlaka, m., Mokoena, J., Young, A. Tuta’s Complete
Textbook of Medical and Surgical Nursing. (2013) Juta and Company LTD. Lansdowne.
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Assessed on 29/10/2020

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