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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
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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.
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Modifiable risk factors:
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reveal that CO may also be a chemical irritant causing endothelial
injury. (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)
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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.
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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.
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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)
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leading to strokes, coronary heart disease, and other large
blood vessel diseases or what is commonly known as
macrovascular complications.
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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)
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into diabetes because fat interferes with the body's ability to use
insulin. (Fauci et.al 2008)
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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)
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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
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arrhythmias, and CHF that are caused by direct or indirect
effects of elevated BP. (Monahan et.al 2006)
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Certain factors can increase the risk of developing diabetes.
These risk factors include:
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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)
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► Sweating
► Dizziness
► Nausea
► Shortness of breath
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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)
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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)
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Malnutrition – malnutrition weakens the immune system
predisposing an individual to infections. (Joyce Black, 2008)
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Signs of consolidation such as
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