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Bloc D - Renal > Jan4 M3-Antihypertensives, K and PO4 binders, Renally Cleared Drugs > Flashcards

Jan4 M3-Antihypertensives, K and PO4 binders, Renally Cleared Drugs Flashcards

1
Q

3 ways kidney affects CVS

A
  • EPO production: RBCs
  • ECF volume
  • TPR
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2
Q

three kinds of baroreceptors

A

arterial, cardiopulmonary, intrarenal

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3
Q

what intrarenal baroreceptors do

A

RAAS, GFR, salt and water reabsorption

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4
Q

what produces ADH

A

hypothalamus (not pituitary)

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5
Q

3 messages to renin production and which one is different

A
  • SS via beta adrenergic receptors
  • decreased P in renal arterioles
  • macula densa (this one can also decrease renin prod)
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6
Q

how macula densa communicates an increased flow

A

senses increased Na delivery, releases ATP (adenosine) which then decreases GFR and renin secretion

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7
Q

how macula densa communicates a decreased flow

A

drop in Na delivery, secretes NO and PGs, GFR and renin secretion increase

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8
Q

in the control of sodium excretion, what are drivers of Na excretion

A

dopamine, ECF conc of Na, ECF volume, natriuretic peptides

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9
Q

in the control of sodium excretion, what are drivers of Na retention

A

AT2, aldo, SS, ADH

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10
Q

why ACEi causes cough

A

ACE metabolizes kinins and substance P. kinins enhance production of PGs which may cause bronchial irritation and cough

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11
Q

only way to resolve ACEi cough side effect if present

A

stop this med and take ARB instead

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12
Q

less common side effects of ACEi

A
  • severe hypotension (if hypovolemic)
  • acute renal failure (if bilateral RAS)
  • hyperK
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13
Q

4 drug types in BP management

A
  • AT blockers (RAAS inhibitors)
  • Sympathoplegic agents
  • Direct vasodilators (like hydralazine)
  • Diuretics
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14
Q

anti htn drugs: choice in diabetic patient with proteinuria

A

RAAS inhibitors (AT blockers)

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15
Q

anti htn drugs: choice in patients with angina

A

beta blockers or CCB

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16
Q

anti htn drugs in HF

A

diuretic**,ARB, ACEi, beta blocker or hydralazine + nitrates

17
Q

anti htn drugs in BPH (benign prostatic hyperplasia)

A

a1 blockers

18
Q

5 classes of diuretics

A 
CA inhibitors
loop diuretics
thiazides
K-sparing diuretics
osmotic
19
Q

thiazides mode of action

A

block Na-Cl transporter in the DCT (5-7% reabso of Na note done)

20
Q

3 thiazides

A

indapamide, hydrochlorothiazide, metolazone

21
Q

thing that can influence effect of thiazides and loop diuretics

A

renal PG production, modified if taking NSAIDs

22
Q

side effect of thiazides (electrolytes)

A

hypokalemia and metabolic alkalosis

23
Q

3 mechanisms of hypoK and metabolic alkalosis as side effects in thiazides

A
  • increased Na to CT exchanged for K and H (CD for water..)
  • secondary hyperaldo
  • volume contraction
24
Q

other side effects of thiazides

A

hyponatremia, hyperuricemia, hyperglycemia, weakness-fatigue-parasthesias
changes in serum lipids

25
Q

loop diuretics are of choice in what 2 conditions

A

pulmonary edema and CHF

26
Q

2 mechanisms of loop diuretics and why are said to be potent

A
  • block Na-K-2Cl cotransporter in TAL (potent bc medullary interstitium not salty as a consequence
  • venous vasodilation by inducing production of PGs and NO in endoth cells to relax SM
27
Q

2 categories of loop diuretics, their drugs and why use the second

A
  • sulfonamides (furosemide, bumetanide, torsemide)

- nonsulfonamides (ethacrynic acid): for sulfonamide intolerant patients

28
Q

side effects of loop diuretics

A

hypokalemia, metabolic alkalosis (contraction), hyperuricemia, hypomagnesemia, ototoxicity

29
Q

how diuretics are handled by the body and consequence

A

kidneys secrete them actively. can develop resistance (transporters in the kidney change)

30
Q

reasons for diuretic resistance

A
  • high Na diets
  • CKD, aging
  • NSAIDs, low BP, low flow to the kidney
  • gut edema (less abso)
31
Q

K-sparing diuretics 2 different modes of action

A

MRA (nuclear receptor)

Na channel blockers in the CT and CD

32
Q

2 MRAs

A

spironolactone, eplerenone

33
Q

2 CT Na channel blockers

A

amiloride, triamterene

34
Q

CA inhibitors name and mode of ation

A

acetazolamide. no H + HCO3 produced so no Na-H exchange in PCT

35
Q

3 side effects of CAi

A

hyperchloremic MA
renal stones
renal potassium wasting

36
Q

osmotic diuretics: prototypic one and where acts mainly

A

mannitol. mainly PCT and DL

37
Q

side effects of mannitol (water and electrolytes)

A
  • volume expansion (prior to diuresis)
  • dehydration, hyperK and hyperNa
  • hypoNa: in renal failure (water not excreted)
38
Q

main side effect of k-sparing diuretics

A

hyperK

Bloc D - Renal (32 decks)

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