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44 Cards in this Set
- Front
- Back
In what groups is there a higher level of hypertension?
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old people, family history, AA, exogenous factors like smoking
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What is essential hypertension?
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no cause is found
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What are some causes of hypertension?
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essential, excess aldosterone, excess NE or Epi, renin-producing tumors, hypercalcemia
neurogenic, iatrogenic, congenital structural lesions |
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What ist he leading cause of secondary hypertension?
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kidney disease
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How does kidney disease lead to hypertension?
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renal parenchymal scarring, obstruction, renovascular lesions
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How do kidneys influence blood pressure?
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modulate salt/water under aldosterone, renin --> angiotensin II which is a vasoconstrictor and stimulus for aldosterone secretion
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What increases blood pressure in renovascular idsease?
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renal ischemia increases renin-angiotensin system activity
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What causes higher blood pressure in renal parenchymal disease?
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decreased nephron mass leads to lower GFR, retention of sodium and fluid, increased ECV
decreased perfusion to parenchyma increases angiotensin, aldosterone, vasoactive substances |
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What are the most common complications of untreated hypertension?
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cardiac disease, stroke, renal and retinal disease
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Why does hypertension accelerate the decline in GFR?
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direct transmission of increased BP to injured glomerulus increases injury
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What is the gross lesion in "benign" nephrosclerosis?
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small kidneys with finely granular surface and thinned cortex
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What is the microscopic lesion in "benign" nephrosclerosis?
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interlobular arteries and afferent arterioles show hyalinization, medial hypertrophy
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How are the glomeruli in "benign" nephrosclerosis?
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ischemic collapse/sclerosis, tubular atrophy with proportional interstitial fibrosis
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What are the gross lesions in malignant nephrosclerosis?
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petechial subscapsular hemorrhage, mottling, occasional infarcts
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What are the microscopic lesions in malignant nephrosclerosis?
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fibrinoid necrosis of the arterioles, concentric onion-skin pattern of intimal fibrosis of interlobular arteries
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Which type of diabetes causes more renal disease?
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equal proportions of each
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what ist he first sign of diabetic renal disease?
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microalbuminuria with normal or increased GFR
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At what point do diabetic develop renal disease?
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about 15 yrs after diagnosis of diabetes
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What is the course of diabetic nephropathy?
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microalbuminuria, overt proteinuria, progressive decline in GFR
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What do microscopic lesions of diabetic renal disease look like?
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enlarged glomeruli with diffuse thickening of GBM, nodular/diffuse increase in mesangleial matrix and glomerulosclerosis
afferent and efferent arteiolar hyalinization with accompanying arteriosclerosis of larger vessels |
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Which vessels are hyalinized in hypertension?
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afferent, not efferent arteriole
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What groups are associated with worse kidney disease?
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AAs, low birth weight at term birth
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What do you give to diabetics for hypertension?
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ACEI, ARBs
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What are the mechanisms of prophylactic anti-hypertensives?
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angiotensin inhibition, extracellular matrix accumulation in hypertension
inhibiting angiotensin II may block matrix production and augment matrix degradation |
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What do the microscopic lesions of systemic sclerosis look like?
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fibrinoid necrosis acutely, organizing as intimal proliferation, proliferation of endothelial cells involving arterioles and interlobular arteries, glomeruli show ischemic collapse
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Which vessels are involved in idiopathic malignant hypertension?
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smaller vessels
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What is the kidney injury in atherosclerosis?
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narrowing at the origin of the renal artery, can cause acute renal failure due to ischemia if significant narrowing bilaterally
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Who gets fibromuscular dysplasia?
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younger women
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What are the lesions in fibromuscular dysplasia?
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intimal, medial, perimedial fibroplasia, some with aneurysms
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What causes cholesterol embolization?
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emboli of atheromatous plaque material, occludes interlobular arteries
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How do kidney cholesterol emboli present?
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acute renal failure, mimics vasculitis
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What is thrombotic microangiopathy?
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vascular lesion of endotehlial injury with fibrin thrombi in several clinical settings, including HUS, presenting as acute renal failure
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What causes hemolytic uremic syndrome?
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e. coli verotoxin
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Waht does E. coli verotoxin do?
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damages endothelium, causes microthrombi to be formed
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What are the systemic manifestations of HUS?
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hemolysis, decreased platelets, diarrhea
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Who gets HUS?
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children
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What do the microscopic lesions of HUS look like?
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glomerulus and afferent arteiole contain fibrin thrombi, swelling of capillary wall, inflammatory cell interposition give double contour appearance in chronic phase
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What is preeclampsia?
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hypertension, proteinuria, edema, decreased GFR in the third trimester, usually with first pregnancy
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What is eclampsia?
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preeclampsia plus seizures
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What is the pathologenesis of preeclampsia?
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placental ischemia, endothelial cell injury and vasoconstriction, could be due to VEGF
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What do the microscopic lesions of preeclampsia look like?
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glomerular endothelial swelling
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What do the lesions of vasculitis look like?
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necrotizing, crescentic glomerular lesions, varying involvement of other vessels, rapidly progressive glomerulonephritis
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What do lesions of polyarteritis nodosa look like?
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large arteries with segmental irregular nodose lesions with necrosis and inflammation in GI, liver, heart, CNS, kidney
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What does polyarteritis microsocopic form look like?
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glomeruli and small vessel involvement
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