1. Three consequences of pathologic change in blood vessels?
    • Narrowing and obstructing the lumen, slowly by athrosclerosis or quickly by thrombotic embolus
    • weakening the vessel wall; can lead to dissection dilation , and rupture
    • causing thrombosis deposits, have the ability to embolize
  2. Reduplicated vessels
    • anomalous vessels
    • interest to surgeons
  3. What is a berry aneurysm
    • vascular outpouching resulting from congenital vascular wall weakness
    • Mostly found in cerebral vessels
  4. Abnormal communication between artery and vein?
    • arteriovenous fistula
    • can be secondary to trauma, inflammation, or a healed ruptured aneurysm
    • causes a left to right shunt, leads to increased venous return predisposing to high output heart failure
  5. Arteriosclerosis?
    arterial wall thickening and loss of elasticity
  6. Three patterns of arteriosclerosis?
    • atherosclerosis
    • arteriolosclerosis, associated with HTN
    • Monckeberg medial calcific sclerosis; medial calcification to small and medium sized muscular arteries. after age 50. non obstructive and clinically insignificant
  7. What vessels is atherosclerosis usually found?
    • elastic and large to medium sized vessels
    • abdominal aorta, coronary arteries, popliteal, descending thoracic aorta, internal carotid, circle of willis
  8. Characteristics of atherosclerosis
    • elevated intimal based fibrofatty plaques composed of lipids
    • proliferating smooth muscle
    • increased extra cellular matrix
  9. Morphology of an atheroma
    • white yellow intimal based lesion protruding into the vessel
    • composed of a superficial fibrous cap containing SMC. leukocytes, and dense connective tissue ECM overlying a necrotic zone
    • necrotic core contains dead cells, lipid, cholesterol, foam cells, proteins
  10. What is a fatty streak?
    • early lesion composed of intimal lipid laden macrophages and SMCs
    • no real relationship between fatty streaks and plaques
  11. complicated plaque?
    • calcified, hemorrhagic, fissured, or ulcerated atheroma
    • predisposed to local thrombus, cholesterol microemboli, and aneurysmal dilation
  12. Risk factors for developing atherosclerosis, major
    • age
    • smoking
    • hypercholestrol
    • diabetes
  13. Minor risk factors for atherosclerosis
    • obesity
    • sedentary life style
    • high stress life
    • type A personality
  14. CRP?
    • an indicator of systemic inflammation and is correlated with atherosclerosis risk
    • acute phase reactant synthesized in the liver
    • downstream of many inflammatory triggers
    • opsonizes bacteria and activates compliment
    • withing intimal cells it can activate local endothelial cells and induce a prothrombotic state, increasing leukocyte adhesion
  15. causes of endothelial cell injury that promotes atherosclerosis
    • hyperlipidemia
    • hemodynamic disturbances
    • smoking,
    • HTN
    • toxins and infections
  16. EC injury causes?
    • increased permeability
    • white blood cell and platelet adhesion
    • coagulation activation
  17. response to injury hypothesis of athersclerosis
    considered to be a chronic inflammatory response to arterial wall injury
  18. Stages of atherosclerosis pathogenesis
    • EC injury, endothelial dysfunction causes increased permeability, and increased expression of adhesion molecules
    • blood monocytes and leukocytes adhere
    • monocytes migrate into intima and become macrophages that ingest lipids to form foam cells
    • LDL and VLDL enter the vessel wall at site of injury
    • macrophages oxidize lipoproteins
    • platelets adhere
    • PDGF is released which causes SMCs to migrate to the intima
    • SMCs proliferate in the intima and secretes ECM leading to collagen and proteoglycan accumulation
    • Lipids accumulate in the SMC and macrophages
    • inflammation mediates lesion progression, initially foam cell formation is protective by removing lipids but then activated macrophages secrete cytokines that recruit more monocytes and T cells, and produce oxygen radicals that oxidize LDLs. The t cell macrophage cross talk initiates chronic inflammation
  19. Stenosis in the popliteal artery causes?
    gangrene in the lower leg
  20. What can cause sudden lumina occlusion
    • plaque rupture
    • superficial erosion followed by superimposed thrombus formation
    • embolism
  21. What is the single most important risk factor in coronary heart disease and cerebral event
    • hypertension
    • can also be a leading cause of congestive heart failure, renal failure, and aortic dissection
  22. hypertension is defined as?
    • systolic above 140
    • diastolic above 90
  23. Essential hypertension?
    no known cause
  24. Secondary causes of hypertension?
    • renal disease
    • renal artery stenosis
    • endocrine abnormality
    • vascular malformation
    • neurologic disorders
  25. Renal causes of hypertension
    • acute glomerulonephritis
    • chronic renal disease
    • polycystic disease
    • renal artery stenosis
    • renal artery fibromuscular dysplasia
    • renal vasculitis
    • renin producing tumor
  26. Endocrine causes of HTN
    • adrenocortical hyperfunction; cushings, primary aldosteronism, adrenal hyperplasia, licorice ingestion
    • exogenous hormones; pregnancy and oral contracetives,
    • pheochromatomas
    • acromegly
    • hypothyroidism
    • hyperthyroidism
    • pregnancy induced
  27. Cardiovascular causes of HTN
    • coarctation of the aorta
    • vasculitis
    • increased volume
    • increased cardiac output
    • rigid aorta
  28. Neurologic causes of HTN
    • psychogenic
    • increased intercranial pressure
    • sleep apnea
    • acute stress; surgery
  29. What three things affect blood volume
    • sodium load
    • mineralocroticoids
    • naturetic factor
  30. five main vasoconstrictors
    • angiotensin II
    • catecholomines
    • thromboxane
    • leukotrienes
    • endothelin
  31. 4 main vasodilators
    • kinins
    • NO
    • prostaglandins
    • adenosine
  32. Regional auto regulation of blood flow?
    increased blood flow leads to vasoconstriction
  33. Two fundamental causes of essential hypertension
    • increased blood volume; reduced renal sodium secretion
    • increased peripheral resistance; increased vasoconstrictor agents, increased sensitivity of smooth muscle, neurologic factors
  34. Two renal systems that play a part in HTN
    • renin angiotensin system
    • sodium homeostasis
  35. What vasculature doe HTN mainly effect
    • arterioles
    • small arteries, mainly in the kidney
  36. Hyaline arteriosclerosis
    • occurs in the elderly with mild hypertension and mild diabetes
    • lesion reflects EC injury with plasma leakage into vessel wall and ECM synthesis by SMC
    • diffuse pink, hyaline arteriolar thickening
  37. Hyperplastic arteriolosclerosis
    • characteristic of malignant HTN; acute severe elevation in BP
    • concentric lamina ( onion skin) arteriolar thickening
    • associated with fibrin deposits and wall necrosis, necrotizing arteriolitis
  38. What is an aneurysm?
    focal abnormal vascular dilation
  39. Difference between a true aneurysm and a pseudoaneurysm
    • true; bounded by all three layers
    • false; extravascular hematoma that communicates with the intravascular space. part of the vessel wall is missing
  40. Morbidity and death due to aneurism is due to?
    • rupture
    • impingement of adjacent structures
    • occlusion of proximal vessel by extrinsic pressure or superimposed thrombus
    • embolus from a mural thrombus
  41. Causes of aneurysms, 7
    • cystic medial degeneration
    • atherosclerosis
    • syphilis
    • trauma
    • polyarteritis nodosa
    • congenital defects
    • infection
  42. Most common location of an aneurysm caused by atherosclerosis
    abdominal aorta, between the renal arteries and iliac bifurcation
  43. AAA are what type of aneurysm
  44. Why do patients with a AAA have a high rate of ischemic heart disease
    aortic atherosclerosis is usually accompanied by coronary atherosclerosis
  45. Syphilitic aneurysm
    • syphilitic aortitis
    • arises in the tertiary stage of syphilis
    • confined to sac aorta and arch, may extend retrograde into the aortic valve
    • starts in the adventicia as inflammation, results in aortic medial ischemia and patchy elastic fiber loss with wall thickening and scarring
    • symptoms usually occur due to valvular insufficiency or impingement of surrounding organs
  46. Cor bovinum?
    LV hypertrophy due to aortic insufficiency from tertiary syphilis
  47. obliterative endarteritis
    affected vaso vasorum with syphilis have a perivascular infiltrate of lymphocytes and plasma cells, with hyperplastic thickening of the walls
  48. Aortic dissection
    • a blood filled channel along the laminar plane of the aortic media
    • it ofter ruptures
    • not associated with previous dilation
  49. Dissection in men 40-60
    • HTN
    • nonspecific degenerative histologic changes including elastic fragmentation and excess ECM
  50. Dissection in younger individuals
    connective tissue defects, marfan syndrome
  51. risk complications of aortic dissection
    • rupture
    • extension into the great vessels and other aortic branches
    • retrograde dissection of the aortic valve
  52. Two types of aortic dissection
    • type A; ascending aorta. Usually an intimal tear within 10cm of aortic valve.
    • Type B; distal to the subclavian artery
  53. clinical presentation of aortic dissection
    sudden onset of excruciating pain, beginning in the anterior chest and radiating to the back and moving downward as the dissection progresses
  54. Without intimal tear what is the likely cause of a type A dissection?
    rupture of an intramural portion of the vasa vasorum is the likely cause of hemorrhage
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