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)

67

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.

68

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 as69

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)

70

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 ( 27kg/m2. Chronic obesity leads to increased insulin resistance that can develop

78

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 diabetes between normal risk glucose for homeostasis diabetes and and which increases future

cardiovascular disease. Studies have shown that people with

79

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

80

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. i. Hypertensive Cardiovascular Disease 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

81

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.

82

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)

83

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

84

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)

85

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)

86

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 and87

(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

88

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)

89

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.

90

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.

91