10 - HTN - Nephrologist's approach Flashcards

1
Q

hallmark of renal pathology due to HTN

A

glomerulosclerosis

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2
Q

how does kidney damage from HTN further contribute to worsening HTN?

A

inc peripheral resistance due to vascular damage > inc RAAS and SYNS
tubular atrophy and glomerulosclerosis > Na retention due to inability to excrete Na load

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3
Q

main consequence of salt sensitive HTN

A

lose sensitivity of regulatory process

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4
Q

etiologies of RAS

A

atherosclerosis (60-80% of cases) - old guys, mostly proximal 1/3 of main renal artery
fibromuscular dysplasia (20-40%) - young women, distal 2/3 and branches
neurofibromatosis
vasculitis
radiation

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5
Q

Goldblatt’s hypothesis about acquired renal injury

A

primary renal microvascular dz > renal ischemia > oxidative stress > inflammatory cells > Na retention > HTN

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6
Q

what happens when only one renal artery is stenosed?

A

inc in aldosterone > hypokalemia

other kidney can maintain normal blood volume due to pressure natriuresis at this stage

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7
Q

phases of RAS

A

acute - RAAS and SYNS stim. volume normal due to pressure natriuresis in nl kidney. BP elevated due to vasconstriction and inc CO

transitional - more sensitive to ATII and SNS, expanded volume, still treatable w/ reversal of stenosis

chronic - HTN w/ normal or slightly inc RAAS and SNS. HTN no longer treatable after stenosis removal, nl kidney gets damaged from high pressure

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8
Q

bilat renal stenosis makes ____ dependent HTN

A

volume

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9
Q

clinical presentation of RAS

A

severe HTN in previously well controlled pt
flash pulm edema
renal failure w/ ACEis

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10
Q

what happens when you add ACEis to a person w/ bilateral RAS?

A

kidney failure - removes contraction of efferent arteriole, so now GFR is even further reduced

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11
Q

tx of RAS

A
control BP as well as possible
stop smoking
lipid lowering drugs
anti platelet drugs
surgical tx
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12
Q

5 P’s of pheochromocytoma

A
pressure
pain (HA)
perspiration
palpitation
pallor
(paroxysms are 6th P)
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13
Q

pheo rule of 10

A
10%:
extra adrenal
occur in children
familial
bilat or multiple
recur
malignant
discovered incidentally
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14
Q

best biochem tests for dx of pheos

A

Urine catecholamines + metanephrines

plasma metanephrines

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15
Q

tx of pheo

A

alpha and beta adrenergic blockers (phentolamine and propanolol)
surgery

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16
Q

primary hyperaldosteronism presentatino

A

hypokalemia and metab alkalosis

17
Q

tx of primary hyperaldosteronism

A

spironolactone or eplerenone

adrenalectomy