Ostrow's Lectures

• Increased hydrostatic pressure
• reduced oncotic pressure - hypoproteinemia
• Sodium-water retention
• Impaired lymphatic drainage - localized edema due to infection, tumor or surgery

• 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

when blood escapes a vessel and a hemorrhage forms inside an organ or in a potential space - hematoma

• 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

• Damage to the vascular lining
• Stasis or turbulence of blood flow
• Increased coagulability of blood

• 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

• 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

Form only post-mortem

• 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.

• localized area of ischemic necrosis
• Size and shape may be affected by the presence of collateral circulation

• 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

• During atrial fibrillation, the atrium does not contrace in a coherent way -> Stasis
• Favors development of mural thrombi

• 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

• 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

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

• 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

• Capacitance arteries
• Regulatory arteries and arterioles
• Exchange: Capillaries

• 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

affects predominantly elastic arteries (aorta and major branches) and large and medium size muscular arteries(coronary, renal, cerebral, popliteal)

• 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

• 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

• 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

• 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

• Plaques: usually much more extensive and advance in abdominal aorta than thoracic
• Turbulence or shear stress

• Fusiform: gradual, progressive dilatation of the entire circumference of the vessel
• Saccular: nearly spherical, involving only a portion of the wall

• 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.

• 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.