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b.

Synthesis of the Disease (Book – based)

1. Acute Coronary Syndrome Non ST- Elevation Myocardial


Infarction

i. Definition of the disease

Acute coronary syndrome Non ST Elevation Myocardial Infarction


defined as a series of a transient coronary occlusion and reperfusion
leading to myocardial cellular injuries and the appearance of markers of
myocardial cellular injury. These transient coronary occlusions is brought
about by either as a result of an atherosclerotic plaque formation or plaque
rupture leading to clot formation which are not big enough to totally
occlude the artery (see figure 1 and 2), other reasons include coronary
vasoconstriction, progressive mechanical obstruction and secondary
unstable angina. (Vidya Banka, 2008)

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As a normal response of the body, chemical mediators would be
released thus activating thrombosis promoting repair of the ruptured
plaque wherein endothelium would be replaced with fibrotic tissues which
contributes to narrowing of the artery and loss of its elasticity which may
eventually result in another episode of occlusion (figure 3). This
transformation of an atherosclerotic plaque to an unstable lesion follows
the different stages in platelet activation and aggregation. Rupture or
ulceration of an atherosclerotic plaque exposes the subendothelial matrix
(primarily composed of collagen and tissue factor) to circulating blood.
This particular event will result to platelet adhesion through the binding of
platelet glycoprotein (GP) Ib to von Willerbrand factor and GP VI binding
to collagen. Platelet activation ensues leading to a (1) change in shape of
the platelet (from smooth discoid to spiculated form) which increases the
surface area on which thrombin generation can occur, (2) degranulation of
the platelet alpha and dense granules, releasing thromboxane A2,
serotonin and other platelet aggregatory and chemoattractant agents; and
(3) increased expression of GP IIb/IIIa which enhances affinity to
fibrinogen. Lastly platelet aggregation takes place wherein fibrinogen
binds to activated platelet GP IIb/IIIa, creating a growing platelet
aggregate. This process continuously happening which decreases the
arterial lumen in the long run. In line with this, secondary hemostasis
happens wherein plasma coagulation system is activated. Tissue factor
will cause the activation of Factor X changing it to Factor Xa which leads
to formation of thrombin (factor IIa) which play a central role in arterial
thrombosis: (1) thrombin converts fibrinogen to fibrin (2) thrombin
powerfully stimulates platelet aggregation; and (3) it activates factor XIII
leading to cross – linking and stabilization of fibrin clot. Thrombin
molecules will eventually incorporated to coronary thrombi forming the
nidus of rethrombosis.

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Figure
3

According to Cannon and Braunwald coronary vasoconstriction


contributes to the mechanism of the development of NSTEMI. They have
identified three settings in which the process of dynamic coronary
obstruction is identified: (1) prinzmetal variant angina (2) coronary
vasoconstriction causing “microcirculatory angina” and (3) local
vasoconstrictors released from platelet, serotonin and thromboxane A2 as
well as those present within the thrombus such as thrombin. Dysfunctional
coronary endothelium with reduced production of nitric oxide with increase
production of endothelin will cause vasoconstriction. Adrenergic stimuli,
cold immersion and mental stress can cause vasoconstriction.

Progressive Mechanical Obstruction is the progressive luminal


narrowing by the process of restenosis following a percutaneous coronary
intervention (PCI) secondary to rapid cellular proliferation. Lastly,
secondary unstable angina which results from an imbalance in myocardial
oxygen supply and demand caused by conditions extrinsic to the coronary
arteries in patient with prior coronary stenosis increases the chances of
the patient to experience NSTEMI. These conditions include tachycardia
(e.g. atrial fibrillation with rapid ventricular response) fever, thyrotoxicosis,
hyperadrenergic states and elevation of left ventricular afterload such as

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hypertension or aortic stenosis. All of these conditions increase the
myocardial oxygen demand. On the other hand, anemia, hypoxemia,
hyperviscosity states and hypotension bring impaired oxygen delivery.

ii. Risk Factors

Risk factors are characteristics or conditions that are statistically


associated with a high incidence of a disease. Incidences of Acute
Coronary Syndrome Non ST Elevation Myocardial Infarction are
influenced by the following:

Non - modifiable risk factors:

Age, Gender, Ethnicity – Incidence of MI is highest among white


though cases of cardiovascular disorder among blacks are severe
compared with whites. Literatures have also revealed that during
the middle age years, MI is more prevalent among men and
becomes equal when women reach the age of 60 and above.
(Eugene Braunwald, 2007)

Familial history and Genetics – genetic predisposition plays an


important factor in the occurrence of CAD and other cardiovascular
disease though the exact mechanism of inheritance is still
unknown. Familial Hypercholesterolemia is the leading autosomal
genetic disorder that is associated with the development of CAD
and myocardial infarction. (Eugene Braunwald, 2007)

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Modifiable risk factors:

Elevated serum lipids – The risk of having CAD or for an individual


to experience a heart attack is associated to a serum cholesterol
level of more than 200 mg/dl or a serum triglyceride of more than
150 mg/dl. (Eugene Braunwald, 2007)

Hypertension – Hypertension increases the risk of CAD or MI


deaths by 10 folds in all persons. It is believed that due to the
increased pressure exerted against the arteries, rupture of
atherosclerotic plaque is more likely to develop due to the shearing
stress brought about by increased tension on the arterial wall
causing endothelial injury. Increased in the workload of the heart is
also associated with the development of left ventricular hypertrophy
and decreased stroke volume with each contraction (<70 ml).
(Eugene Braunwald, 2007)

Tobacco use – myriad of literatures explain how tobacco increases


the risk of experiencing CAD and other cardiovascular disorder. It is
believed that nicotine found in tobacco causes the release of
catecholamine producing sympathetic response increasing
myocardial oxygen demand. Nicotine also increases platelet
adhesion, which increases the risk of emboli formation. Carbon
monoxide (CO) which is a by – product of combustion found in
tobacco smoke affects the oxygen carrying capacity of hemoglobin
by reducing the site available for oxygen transport. Literatures also

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reveal that CO may also be a chemical irritant causing endothelial
injury. (Eugene Braunwald, 2007)

Physical inactivity – physical inactivity implies a lack of adequate


physical exercise on a regular basis. According to National Heart,
Lung and Blood Institute (NHLBI) a person must have at least 150
hours of exercise/ week. The mechanism why physical inactivity
contribute to development of CAD and other cardiovascular disease
is unknown though literatures suggest that exercise increases HDL
levels, enhances fibrinolytic activity thus reducing clot formation.
(Eugene Braunwald, 2007)

Obesity – obesity contributes to the development of hypertension. It


is also believed that with obesity, the heart size grows thus
increasing myocardial oxygen consumption. Obesity is also
associated with the development of atherosclerotic plaque due to
increased serum lipid. It is also believed that obesity increases
insulin resistance thus increasing blood glucose level. (Eugene
Braunwald, 2007)

Diabetes mellitus – Undiagnosed DM is frequently discovered at


the time of MI. It is believed that patients with DM have an
increased tendency toward connective tissue degeneration and
endothelial dysfunction which is believed that this contributes to
atheroma development. Clients with DM tend to have alteration in
lipid metabolism thus increasing cholesterol and triglyceride levels.
(Eugene Braunwald, 2007)

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Psychologic states – according to Framingham study there are
certain lifestyle and behaviors that are conducive to the
development of CAD. Persons with type A personality often
suppresses anger and hostility, sense of time urgency, impatient
and often creates stress and tension which are actually activities
that stimulates sympathetic response making them prone to MI.
Stress – induced mechanism can cause elevated lipid and glucose
levels and alterations in blood coagulation which can lead to
atherogenesis. Furthermore negative psychologic or behavioral
states such as depression, hopelessness, anxiety, hostility and
anger increases the circulating catecholamine that contributes to
endothelial injury and inflammation and platelet activation. (Eugene
Braunwald, 2007)

Increased Homocysteine level – Homocysteine is sulfur –


containing amino acid, this is produced by the breakdown of the
essential amino acid methionine which is found in dietary protein.
Deficiencies in vitamin B6, B9, and B12 can increase homocysteine
level. Increase in homocysteine level contributes to atherosclerosis
by (1) damaging the inner lining of blood vessels by degrading and
inhibiting the formation of the three main structural components of
artery which are collagen, elastin and proteoglycans (2) promoting
plaque buildup, and (3) altering the clotting mechanism to make
clots more likely to occur. (Eugene Braunwald, 2007)

iii. Signs and symptoms

ACS NSTEMI presents the following signs and symptoms:

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 Pain in the chest which may radiate down the left arm or both arms
and/ or in the jaw is due to lactic acid accumulation in the
myocardium as a by- product of anaerobic respiration as a
compensatory mechanism of the body to the decreased perfusion
of the myocardium. This is often described as:
► a tightness
► indigestion like pain
► rushing
► a band around the chest
► ‘like someone sitting on my chest’.
 Pain may be accompanied by:
► Sweating – pain is considered as a stressor and sweating is
induced by stress.
 Elevated Troponin T and CK – MB – Troponin T and CK – MB are
enzymes found inside the cells of the myocardium, when the
myocardium is damaged or injured, these enzymes are released in
the blood stream.

 Elevation of C-reactive protein** – C-reactive protein is an acute


reactant during tissue damage to activate complement system.

 Elevation of Myeloperoxidase** – a heme protein expressed by


Neutrophils. Myeloperoxidase serves as inflammatory marker.

 Elevation of WBC** – WBC serves as marker of inflammation.

 S3, S4 sounds – this abnormal heart sounds may be heard on


patient who had ACS NSTEMI due to the weakening of the heart
muscle due to necrosis.

 Rales on lung examination – this is brought about by pulmonary


congestion secondary to ineffective circulation of the blood going to
the aorta thus the blood goes back to the lungs causing congestion.

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 Hypertension initially followed by hypotension – hypertension is
manifested as a compensatory mechanism of the body in attempt
to deliver blood among the major organs of the body to improve
perfusion. Eventually due to the increasing oxygen demand of the
heart muscles due to its increased workload, it will eventually slow
down causing hypotension.

 ST segment deviation/depression – ST segment deviation or


depression is associated with ischemia.

 Tachycardia or ventricular dysrrhytmias – tachycardia or ventricular


dysrrhythmias are compensatory mechanism of the body in attempt
to pump the blood to the systemic circulation.

 Decrease in serum lipids - serum lipids decreases up to 30 to 40 %


beginning 24 hours following a STEMI or NSTEMI attack. This due
to the activation of the platelet trapping the lipids in the blood.

 diminished left ventricular function – the most affected part during


ischemic attack on the myocardium is the muscles on the left
ventricles as the left ventricles has the greater workload as to
compare with the right ventricle thus needing more oxygen. Due to
damage of the left ventricle, the function of the left ventricle is also
diminished.

** Inflammation on ACS cases increases the risk of death.

2. Diabetes Mellitus Type 2

i. Definition of the disease

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Diabetes mellitus type 2 is a metabolic disorder that is
primarily characterized by insulin resistance, relative insulin
deficiency, and hyperglycemia. In type 2 diabetes, patients can
still produce insulin, but do so relatively inadequately for their
body's needs, particularly in the face of insulin resistance. This
actually means the pancreas produces larger than normal
quantities of insulin. A major feature of type 2 diabetes is a lack
of sensitivity to insulin by the cells of the body. (Joyce Black
2008)

In addition to the problems with an increase in insulin


resistance, the release of insulin by the pancreas may also be
defective and suboptimal. In fact, there is a known steady
decline in beta cell production of insulin in type 2 diabetes that
contributes to worsening glucose control. (This is a major factor
for many patients with type 2 diabetes who ultimately require
insulin therapy.) Finally, the liver in these patients continues to
produce glucose through a process called gluconeogenesis
despite elevated glucose levels. The control of gluconeogenesis
becomes compromised. (Fauci et.al 2008)

People who are overweight are more likely to have


insulin resistance, because fat interferes with the body's ability
to use insulin. Type 2 diabetes usually occurs gradually. Most
people with the disease are overweight at the time of diagnosis.

Over time, diabetes can lead to blindness, kidney failure,


and nerve damage. These types of damage are the result of
damage to small vessels, referred to as microvascular disease.
Diabetes is also an important factor in accelerating the
hardening and narrowing of the arteries (atherosclerosis),

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leading to strokes, coronary heart disease, and other large
blood vessel diseases or what is commonly known as
macrovascular complications.

ii. Risk Factors

Risk factors are characteristics or conditions that are


statistically associated with a high incidence of a disease.
Certain factors can increase the risk of developing diabetes.
These risk factors include:

Non - modifiable risk factors:

Age and Ethnicity – Incidence of DM is highest among


African Americans, Hispanic Americans, Native Americans,
Asian Americans, Pacific Islanders. Age of 45 years and above
contributes to an increased risk. Incidence is equal in men and
women and rises with age. (Fauci et.al 2008)

Genetics and Familial History – Genetic factors, usually


polygenic, are present in most patients, having relatives
(especially first degree) with type 2 is a considerable risk factor

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for developing type 2 diabetes. Mutation of glucokinase or the
islet transcription factor which catalyzes the formation of
glucose-6-phosphatase from glucose is another autosomal
genetic disorder that can be transmitted through generation.
The action of glucokinase is also essential for glucose sensing
of the beta cells and by the liver for storing excess glucose in
the blood. Therefore alteration to function of the glucokinase will
warrant a higher glucose concentration before eliciting stimuli to
release insulin which may in time result to glucose
desensitization. (Fauci et.al 2008)

Mutation or abnormal levels of adipokines - Several


adipokines, secreted by fat cells, can affect insulin action in
obesity. Two of these, leptin and adiponectin, seem to increase
sensitivity to insulin, presumably by increasing hepatic
responsiveness. Two others - tumor necrosis factor-α, which
inactivates insulin receptors, and the newly discovered peptide
resistin - interfere with insulin action on glucose metabolism.

Modifiable risk factors:

Obesity – There is a direct relationship between the


degree of obesity and the risk of developing type 2 diabetes,
and this holds true in children as well as adults. It is estimated
that the chance to develop diabetes doubles for every 20%
increase over desirable body weight or BMI > 27kg/m2. Chronic
obesity leads to increased insulin resistance that can develop

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into diabetes because fat interferes with the body's ability to use
insulin. (Fauci et.al 2008)

Sedentary lifestyle and lack of exercise – Exercise may


affect the deposition of visceral fat as suggested by CT scans of
Japanese wrestlers, whose extreme obesity is predominantly
subcutaneous. Their daily vigorous exercise program prevents
accumulation of visceral fat, and they have normal serum lipids
and euglycemia despite daily intakes of 5000-7000 kcal and
development of massive subcutaneous obesity. (Fauci et.al
2008)

Physiologic or emotional stress – Stress can cause


prolonged elevation of stress hormone levels (cortisol,
epinephrine, glucagon and growth hormone). This raises blood
glucose levels which in turn places increased demands on the
pancreas. (Fauci et.al 2008)

Certain medications – Some medications can antagonize the


effect of insulin, including thiazide diuretics, adrenal
corticosteroids, and hormonal contraceptives. (Fauci et.al 2008)

Previously identified impaired fasting glucose or impaired


glucose tolerance – This refers to a metabolic stage
intermediate between normal glucose homeostasis and
diabetes which increases risk for future diabetes and
cardiovascular disease. Studies have shown that people with

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pre-diabetes can prevent or delay the development of type 2
diabetes by up to 58 percent through changes to their lifestyle
that include modest weight loss and regular exercise. (Fauci
et.al 2008)

Low HDL, High triglyceride, High blood pressure -


Triglyceride is the most common type of fat in the body. Many
people who have heart disease or diabetes have high
triglyceride levels. Normal triglyceride levels vary by age and
sex. A high triglyceride level combined with low HDL cholesterol
or high LDL cholesterol seems to speed up atherosclerosis. Up
to 65% of people with diabetes also suffer from hypertension, or
high blood pressure. Blood pressure increases when arteries
are narrowed, due to atherosclerosis or to chronically high blood
glucose levels, and blood flow is restricted. The long-term stress
of high blood pressure levels increases the risk of other diabetic
complications such as stroke, coronary artery disease (CAD),
diabetic retinopathy, and nephropathy (kidney disease). (Fauci
et.al 2008)

Women who had gestational diabetes, or who have had a


baby weighing 9 pounds or more at birth - Women who get
diabetes while they are pregnant are more likely to have a
family history of diabetes, especially on their mothers' side.
Older mothers and overweight women are more likely to get
gestational diabetes. (Fauci et.al 2008)

iii. Signs and symptoms

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DM Type II does have the following signs and symptoms:

 Polyuria
 Polydipsia
 Polyphagia
 Fatigue
 Weakness
 Sudden vision changes
 Tingling or numbness in hands or feet
 Dry skin
 Skin lesions or wounds that are slow to heal
 Recurrent infections

3. Hypertensive Cardiovascular Disease

i. Definition of the disease

Uncontrolled and prolonged elevation of blood pressure


(BP) can lead to a variety of changes in the myocardial
structure, coronary vasculature, and conduction system of the
heart. These changes in turn can lead to the development of left
ventricular hypertrophy (LVH), coronary artery disease, various
conduction system diseases, and systolic and diastolic
dysfunction of the myocardium, which manifest clinically as
angina or myocardial infarction, cardiac arrhythmias (especially
atrial fibrillation), and congestive heart failure (CHF). Thus,
hypertensive heart disease is a term applied generally to heart
diseases, such as LVH, coronary artery disease, cardiac

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arrhythmias, and CHF that are caused by direct or indirect
effects of elevated BP. (Monahan et.al 2006)

Hypertensive cardiovascular disease also known as


hypertensive heart disease occurs due to the complication of
hypertension or high blood pressure. In this condition the
workload of the heart is increased manifold and with time this
causes the heart muscles to thicken. The heart continues
pumping blood against this increased pressure and over a
period of time the left ventricle of the heart enlarges and this in
turn causes the blood pumped by heart to reduce. If proper
treatment is not taken at this stage then symptoms of
congestive heart failure may be observed. (Monahan et.al 2006)

High blood pressure or hypertension is among the top


most factors associated with cardiovascular diseases. This can
result in ischemic heart disease. High blood pressure is also a
contributing factor to the eventual thickening of walls of blood
vessels. This increases the possibility of heart attacks and
strokes. Hypertensive cardiovascular disease is among the
leading killers in present times. Around 7 people out of every
1000 suffer from this disease. (Monahan et.al 2006)

ii. Risk Factors

Risk factors are characteristics or conditions that are


statistically associated with a high incidence of a disease.

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Certain factors can increase the risk of developing diabetes.
These risk factors include:

Non - modifiable risk factors:

Age, Gender, Ethnicity – Systolic BP increases with age.


The prevalence of hypertension is higher in men than in women
younger than 55 years but is higher in women older than 55
years. In the United States, hypertension is more prevalent in
African Americans than in Hispanic and non-Hispanic whites. In
addition, hypertension is the most common etiology of heart
failure in African Americans in the United States. (Monahan et.al
2006)

Genetics and Familial History – Genetic factors, usually


polygenic, are present in most patients, having relatives
(especially first degree) with type 2 is a considerable risk factor
for developing type 2 diabetes. (Monahan et.al 2006)

Modifiable risk factors:

Obesity – The risk of LVH is increased 2-fold by


associated obesity.(Monahan et.al 2006)

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High blood pressure - Elevated BP leads to adverse
changes in cardiac structure and function in 2 ways: directly by
increased afterload and indirectly by associated neurohormonal
and vascular changes. Elevated 24-hour ambulatory BP and
nocturnal BP have been demonstrated to be more closely
related to various cardiac pathologies, especially in African
Americans. High blood pressure is also a contributing factor to
the eventual thickening of walls of blood vessels. This increases
the possibility of heart attacks and strokes. (Monahan et.al
2006)

iii. Signs and symptoms

It usually takes some time for the problem of high blood


pressure to eventually lead to hypertensive cardiovascular
disease and therefore high blood pressure is often called the
silent killer. Eventually hypertensive heart disease can also lead
to congestive heart failure.

 Some symptoms of hypertension and the eventual


congestive heart failure include:
► Arrhythmias
► Shortness of breath
► weakness and fatigue
► Swelling in lower extremities
► Nocturia

 Hypertensive cardiovascular disease may also result in


ischemic heart condition and in this case there might be:
► Chest pain

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► Sweating
► Dizziness
► Nausea
► Shortness of breath

4. Community Acquired Pneumonia

i. Definition of the disease

Pneumonia is an inflammatory process in the lung


parenchyma usually associated with a marked increase in
interstitial or alveolar fluid. Pneumonia is commonly caused by
bacteria, viruses, mycoplasma, fungal agents, and protozoa. On
the other hand this may also result from aspiration of food, fluids
or vomitus or from inhalation of toxic materials or it may also
result from pulmonary congestion secondary to the ineffective
circulation of the blood causing the back flow of the blood to the
lungs. (http://www.doh.gov.ph/faqs/pneumonia)

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Furthermore, pneumonia is classified as to (1) community –
acquired (2) hospital acquired, and (3) idiopathic pneumonia. According to
Porth, community acquired pneumonia is defined as the infection that
begins outside the hospital or is diagnosed within 48 hours after admission
to the hospital in a person who has not resided in a long - term care facility
for 14 days or more before admission. On the other hand, hospital –
acquired pneumonia or also termed as nosocomial pneumonia is defined
as a lower respiratory tract infection that was not present or incubating on
admission to the hospital. Usually infections occurring 48 hours or more
after admission are considered hospital acquired. More so, idiopathic
pneumonia per se is a diffuse lung disease wherein the reason is actually
unknown though certain literatures suggest that this is probably caused by
tobacco use. (http://www.doh.gov.ph/faqs/pneumonia)

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Pneumonia has four characteristic stages which are the following:
(1) Congestion – after the organisms or the foreign bodies reach the
alveoli, there would be an outpouring of fluid in the alveoli causing
pulmonary congestion. (2) Red hepatization – due to congestion, there
would be a massive dilation of the capillaries to compensate and resume
the normal function of the respiratory system. Alveoli will be filled with
organisms, fluids, Neutrophils, and RBCs. (3) Gray Hepatization and
deposition of fibrin- the deposition fibrin promotes formation of blood clots
decreasing the blood flow in the lungs, neutrophils becomes exudates and

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(4) Resolution or healing takes place.
(http://www.doh.gov.ph/faqs/pneumonia)

ii. Risk Factors

Pneumonia is more likely to result when defense mechanisms


become incompetent or overwhelmed by the virulence or quantity of
infectious agents. Risk factors or predisposing factors involve regarding
pneumonia are determined as follows:

Non - modifiable risk factors:

Age – Patients of the extreme ages are most at risk in acquiring


pneumonia. Children below 5 years old are believed to have a
weaker immune system compared to school aged children
predisposing them to respiratory tract infections and alterations. On
the other hand geriatrics or those who belong to 60 years old and
above are at risk of acquiring pneumonia due to the mucociliary
impairment as a normal change in aging thus losing the ability to
trap foreign bodies at the trachea. (Joyce Black, 2008)

Modifiable risk factors:

Air Pollution, Cigarette Smoking – polluted air acutely stimulate the


secretory function of the mucociliary blanket of the tracheobronchial

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tree and thus may result to fluid additions to the mucus layer from
mucosal to submucosal secretory cells or alterations of epithelial
permeability. According to a study conducted by Nalan et. al.
smoking decreases the mucociliary clearance mechanism by
paralyzing the cilia of an individual retaining more fluids in the
lungs. (Joyce Black, 2008)

Altered oropharyngeal flora secondary to antibiotic – normal flora


present on the oropharyngeal area helps in preventing the entry of
other foreign bodies. Decreased amounts of oropharyngeal flora
brought about by antibiotic therapy allows the entrance of foreign
bodies in the tracheobronchial tree thus stimulating the mucociliary
blanket increasing its secretory function. (Joyce Black, 2008)

Bed rest and prolonged immobility - bed rest and prolonged


immobility pools the secretion in the lungs promoting congestion.
(Joyce Black, 2008)

Chronic Diseases such as lung diseases, DM, heart and renal


diseases and cancer – chronic diseases weakens the immune
system predisposing an individual to infections. (Joyce Black, 2008)

Immunosuppressive drugs – immunosuppressive drugs such as


corticosteroids suppresses the immune system predisposing an
individual to infection. (Joyce Black, 2008)

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Malnutrition – malnutrition weakens the immune system
predisposing an individual to infections. (Joyce Black, 2008)

State of Altered Consciousness such as alcoholism, head injury,


seizures, anesthesia and stroke – decrease consciousness
depresses the cough and epiglottal or gag reflex allowing aspiration
or oropharyngeal secretions thus predisposing an individual to
acquire pneumonia brought about by aspiration. (Joyce Black,
2008)

Tracheal and nasogastric intubation - tracheal intubation interferes


with the mucociliary function and normal cough reflex predisposing
individual to aspiration type of pneumonia. (Joyce Black, 2008)

iii. Signs and symptoms

Pneumonia presents the following sign and symptoms:

 Fever – fever occurs as a part of the normal inflammatory response


of the body against infection or injury.

 Chills – this usually occur at the start of infection and as a response


to fever.

 Shortness of Breath – this is due to decrease respiratory function


related to pulmonary congestion.

 Productive cough – this is the normal response of the body t expel


the excess fluid in the lungs.

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 Signs of consolidation such as

o Dullness upon percussion – this denotes that fluid instead of


air is in the air containing tissues of the lungs.

o Increased tactile fremitus – this is explained by the fact that


sounds travel much faster on solid or liquid state rather than
on gaseous state.

o Crackles or rales – this are present due to the passage of air


onto a fluid filled alveoli.

 Unequal chest expansion –this is present if large area of the lungs


is involved wherein there would be a decrease in distensibility of
the lung.

 Weakness – this is due to decrease perfusion of the muscles of the


body related to decreased oxygenation capability of the lungs.

 Tachypnea – this is present as a response of the body to decrease


oxygen saturation in the body thus increasing the respiratory rate.

 Elevated WBC count – elevation of the WBC count is a normal


response of the body against infection.

 Single or multiple lobar consolidations on Chest X – ray –


consolidation appears as white areas on the x – ray film.

 Respiratory Acidosis on ABG analysis – this due to increased


concentration of carbon dioxide in comparison to oxygen level.

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