Ostrow's Lectures

  1. 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
  2. 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
  3. Hemorrhage
    when blood escapes a vessel and a hemorrhage forms inside an organ or in a potential space - hematoma
  4. 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
  5. Factors required for thrombogenesis: Virchow's triad
    • Damage to the vascular lining
    • Stasis or turbulence of blood flow
    • Increased coagulability of blood
  6. 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
  7. 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
  8. Blood clots
    Form only post-mortem
  9. Hypoxia
    • 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.
  10. Infarct
    • localized area of ischemic necrosis
    • Size and shape may be affected by the presence of collateral circulation
  11. 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
  12. Atrial Fibrillation and Stroke
    • During atrial fibrillation, the atrium does not contrace in a coherent way -> Stasis
    • Favors development of mural thrombi
  13. Righ-sided CHF:
    clinical findings:
    • 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
  14. Hypoxemia:
    clinical findings:
    • 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
  15. Left-sided CHF
    clinical findings:
    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
  16. Hypoperfusion:
    clinical findings:
    • 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
  17. Vascular system can be divided into:
    • Capacitance arteries
    • Regulatory arteries and arterioles
    • Exchange: Capillaries
  18. 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
  19. Atherosclerosis
    affects predominantly elastic arteries (aorta and major branches) and large and medium size muscular arteries(coronary, renal, cerebral, popliteal)
  20. 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
  21. 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
  22. 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
  23. 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
  24. Distribution of Atherosclerosis
    • Plaques: usually much more extensive and advance in abdominal aorta than thoracic
    • Turbulence or shear stress
  25. Aneurysms: 2 types
    • Fusiform: gradual, progressive dilatation of the entire circumference of the vessel
    • Saccular: nearly spherical, involving only a portion of the wall
  26. 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.
  27. 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.
Card Set
Ostrow's Lectures
Cardio review