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Causes of increased interstitial fluid - EDEMA
- Increased hydrostatic pressure
- reduced oncotic pressure - hypoproteinemia
- Sodium-water retention
- Impaired lymphatic drainage - localized edema due to infection, tumor or surgery
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Hyperemia and congestion
- Hyperemia: - when arteries and arterioles dilate, increaseing the blood flow into cappilary beds - Active inflammation and neurogenic bluching
- Congestion: Also called Passive hyperemia - due to impaired venous return - blocks distal to blockage
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Hemorrhage
when blood escapes a vessel and a hemorrhage forms inside an organ or in a potential space - hematoma
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Hemostatis and thrombosis
- Hemostasis: Normal protective mechanism - with injury to endothelial cells, normal process
- 1st: Hemostatic plug -primary hemostasis ( at damaged site release of ADP, Thromboxane A1 and further platelet aggregation and activation)
- 2nd: tissue factor, activates the coagulation cascade, meshwork of Fibrin formed - permanent hemostatic plug
Thrombosis - pathological extension of normal hemostasis
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Factors required for thrombogenesis: Virchow's triad
- Damage to the vascular lining
- Stasis or turbulence of blood flow
- Increased coagulability of blood
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Morphological features of thrombi
- Lines of Zahn: mostly in arterial thrombi
- Arterial thrombi almost always attached to an atherosclerotic plaque
Venous thrombi: less-defined lines of Zahn; most often form in popliteal, femoral and iliac veins
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What can happen to a thrombus?
- Propagate, enlarge, etc.
- Embolize
- Be removed by fibrinolytic action - most likely in early stages
- Organize and recanalize - initially - a thrombus becoming attache to the vessel wall
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Blood clots
Form only post-mortem
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Hypoxia
Ischemia
- Hypoxia - low oxygen supply; - glycolitic energy production by cells can continue
- Ischemia - specifically reduced blood flow; lack of flow reduces the delivery of substrates and removal of metabolites, so isolated ischemia tends to injure tissues more quickly than isolated hypoxia.
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Infarct
- localized area of ischemic necrosis
- Size and shape may be affected by the presence of collateral circulation
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Infarcts can be: anemic or hemorrhagic
- an anemic infarct can become hemorrhagic if blood flow is re-established in the occluded vessel after the tissue becomes necrotic
- In such cases blood leaks out through the damaged vessels in the infarcted area
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Atrial Fibrillation and Stroke
- During atrial fibrillation, the atrium does not contrace in a coherent way -> Stasis
- Favors development of mural thrombi
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Righ-sided CHF:
clinical findings:
pathogenesis:
etiology:
- clinical findings: dependent edema; chronic passive congestion (liver, spleen, GI)
- pathogenesis: increased pressure in systemic capillaries
- etiology: anything that interferes with passage of blood through the heart
- vena cava
- right atrium
- tricuspid valve
- right ventricle
- pulmonary valve
- pulmonary artery
- intrinsic lung disease
- left-sided CHF
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Hypoxemia:
clinical findings:
pathogenesis:
etiology:
- clinical findings: weakness, drowsiness, cyanosis, clubbing, polycythemia
- pathogenesis: decreased FLOW in pulmonary arteries
- etiology: heart malformations with right to left shunt, pulmonary hypertension, lung disease which produced increased resistance to blood flow
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Left-sided CHF
clinical findings:
pathogenesis:
etiology:
clinical findings: dyspnea, orthopnea, hemoptysis
pathogenesis: increased pressure in pulmonary capillaries
- etiology: anything that interferes with passage of blood through the left heart
- pulmonary veings
- left atrium
- mitral valve
- left ventricle
- aortic valve
- systemic hypertension
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Hypoperfusion:
clinical findings:
pathogenesis:
etiology:
- clinical findings: syncope/coma, renal failure, tissue necrosis: heart, liver, GI, etc.
- pathogenesis: decreased flow in systemic capillaries
- etiology: low pressure of volume: MI, Fibrillation, Blood loss, Sepsis, Vasodilation
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Vascular system can be divided into:
- Capacitance arteries
- Regulatory arteries and arterioles
- Exchange: Capillaries
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Mechanisms by which they are changed
- narrowing or obstruction of the lumen
- increased resistance to flow
- production of turbulence
- providing a nidus for thrombosis
- weakening of the wall, leadin to aneurysm formation
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Atherosclerosis
affects predominantly elastic arteries (aorta and major branches) and large and medium size muscular arteries(coronary, renal, cerebral, popliteal)
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Monckeberg's medial calcific sclerosis
- calcium deposition in the media of muscular arteries
- usually in older peiople
- arteries become rigid and visible on x-rays, but seldom encroach on the lumen and usually are not clinically significant
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Arteriosclerosis
- affects small arteries and arterioles and often produced enough narrowing of the lumen to cause ischemia
- often a hallmark of hypertension
- Hyaline arteriolosclerosis: frequently encountered in older patients, but more generalized an more severe in patients with HTN
- Hyperplastic arteriolosclerosis: and
- Necrotizing arteriolosclerosis (arteriolitis) typically seen in more sever or acute ("malignant") hypertension
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Pathology of atherosclerosis
- Fatty streaks: form first - the earliest lesions; made of lipid-containing smooth muscle cells ( foam cells) that have migrated into the intima
- Atheroma: (fibrous of fibrofatty plaque) raised lesions that impinge on the lumen of the arteries in which they occur; contain smooth muschel cells, connective tissue fibers and lipid in varying proportions, along with occasional inflammatory cells.
- Complicated plaques: continue to enlarge and evolve
- Hemorrhage - into the plaque, often leading to a sudden increase in plaque size with abrupt narrowing of the lumen and distal ischemia
- Ulceration or rupture - which may begin as a cracking of fissure in the surface, releasing the underlying lipid-rich material into the circulation as an atheromatous embolus or providing a nidus for thrombosis on the damaged intimal surface
- Thrombus formation - on the surface of the plaque, usually if there is already a fissure
- Calcification - may render the plaque brittle and more prone to the other complications; often visible on x-rays or CT-scans
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Risk factors for atherosclerosis
- Age
- Sex
- HTN
- Cigarette smoking
- Diabetes
- Hyperlipidemia and diet
- Obesity
- Lifestyle (stress, exercise)
- Family history/genetic influences
- Elevated homocysteine levels
- Inflammation (C-reactive protein)
- Others
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Distribution of Atherosclerosis
- Plaques: usually much more extensive and advance in abdominal aorta than thoracic
- Turbulence or shear stress
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Aneurysms: 2 types
- Fusiform: gradual, progressive dilatation of the entire circumference of the vessel
- Saccular: nearly spherical, involving only a portion of the wall
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Causes of aneurysms
- Atherosclerosis: the most common etiology for abdominal aortic aneurysms, often filled with organizing laminated thrombus material
- Increasing diameter leads to increased wall tension and greater likelihood of rupture
- Vasculitis: several inflammatory and autoimmune disorders involve damage to vessels
- The inflammatory response to these may produce vessel occlusion, hemorrhage, or aneurismal distension of the vessel due to scarring and loss of tensile strength
- Syphilis: the vasa vasorum of the aorta are the major site of attach, and undergo obliterative endarteritis; this leads to ischemia in the media, and the elastic and muscle layers are replaced by scar tissue
- Syphilitic aneurysms are usually saccular and are almost always located in the thoracic aorta, especially the ascending portion and the arch.
- Mycotic: when referring to an aneurysm, this term means infectious in the broadest sense, not necessarily fungal, as is the usual implication of 'mycotic'.
- Congenital: these are sometimes called "berry" aneurysms, are seen at branch points of the cerebral arteries. These are not really present at birth but form later at places where a congenital defect in the media
- With the passage of time, and abetted by HTN, these enlarge and can undergo catastrophic rupture.
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Abdominal aneurysms can:
- Compress the true lumen or some of the branch points: distal ischemia and possibly infarction of organs
- Rupture outward into a body cavity: the most common cause of death; rupture into the plaural or peritoneal cavity can cause massive hemorrhage; in the pericardial cavity, it will produce pericardial tamponade
- Rupture through the intima back into the lumen, producing a "double-barreled" aorta.
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