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module 2a > 10/15 > Flashcards

10/15 Flashcards

1
Q

long-term diuretic administrarion

A

HR and CO = unchanged
TPR = dec (mechanism unknown)
plasma volume = dec or unchanged
plasma renin activity = inc

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2
Q

thiazide diuretic MOA

A

acts in distil convoluted tubule, blocks Na/Cl symport (from urine), Na stays in urine, water stays in urine
Ca reabsorption
may open Ca activated K channels leading to vasodilation
decrease in peripheral resistance may result from negative Na balance

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3
Q

thiazide like diuretics

A

chlorthalidone, indapamide, metolazone

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4
Q

any drugs that inc Na delivery to collecting tubule ___

A

will cause K wasting

Na tries to come back in, K goes out

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5
Q

thiazide toxicities

A

hypokalemia, hyperuricemia, hypercalcemia, impaired carbohydrate tolerance, hyperlipidemia, hyponatremia, ED

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6
Q

clinical uses of diuretics

A

HTN, edema, CHF, kidney disease, hepatic cirrhosis, hypercalcemia, diabetes insipidus

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7
Q

thiazides CI

A

sulfa allergy

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8
Q

loop diuretics examples

A

furosemide, bumetanide, ethacrynic acid

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9
Q

loop diuretics MOA

A

inhibit the Na/K/2Cl cotransporter in the thick ascending limb
K+ is still transported to urine, drives Ca2+ and Mg2+ to be reabsorbed because of charge difference
-in pts w normal renal fxn, thiazides are more effective antihypertensives

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10
Q

loop diuretic toxicites

A

dehydration, hypokalemia, ototoxicity, hyperuricemia, hypomagnesemia

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11
Q

loop CI

A

sulfa allergy

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12
Q

diuretics that act in the collecting tubule

A

amilioride and triamterine

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13
Q

amilioride and triamterine MOA

A

inhibit Na channels in the apical membrane of collecting tubule
reduced Na entry into these cells reduces K excretion (sparing)

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14
Q

amilioride and triamterine uses

A

amilioride - adjunct treatment w thiazide or loop in CHF or HTN
triamterene - edema associated w CHF, hepatic cirrhosis, nephrotic syndrome or hyperaldosteronism, does not lower BP alone

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15
Q

amilioride and triamterine toxicites and CI

A

hyperkalemia, hyperchloremic metabolic acidosis

CI: K+ supplements, ACEI, kidney stones (triamterene)

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16
Q

diuretics that act in the collecting tubule

A

aldosterone antagonists
aldosterone enters cell of collecting duct and transcribes proteins (AIP) that inc Na reabsorption
-spiranolactone (aldactone)
-eplerenone

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17
Q

spiranolactone actions

A

blocks production of Na channels (aldosterone action)

inhibits 5a reductase

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18
Q

clinical uses of spiranolactone

A

HTN or CHT w other diurects

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19
Q

spiranolactone toxicities and CI

A

hyperkalemia, gynecocomastia, impotence, BPH

CI: K+ supplements, ACEI, chronic renal insufficiency

20
Q

eplerenone actions

A

selective antagonism of MC receptor in kidney, heart, BVs and brain

21
Q

eplerenone toxicities and CI

A

hyperkalemia, hypertriglycemia
CI: K+ supplements, K+ sparing diuretics, ACEI, chrionic renal insufficiency, DM w microalbuminuria, CYP450 3A4 inhibitors

22
Q

renin is responsible for

A

converting angiotensinogen to angiotensin I (not active)

23
Q

Ang I is rapidly converted to ___ by ___

A

ang II by ACE

24
Q

ANG II 2 actions

A
  • vasoconstriction -> inc PVR

- aldosterone release -> inc Na and water retention

25
Q

ARBs place in RA system

A

block ANG II from binding (no vasoconstriction or aldosterone secretion)

26
Q

spironolactone and eplerenone place in RA system

A

blocks aldosterone actions (inc Na and water retention)

27
Q

ACEI place in RA system

A

inhibit ACE (no ANG I -> ANG II, no bradykinin inactivation (vasodilation))

28
Q

aliskiren place in RA system

A

inhibits renin (angiotensinogen will not be converted to ANG I)

29
Q

ang II works on __ receptors

A

AT1

30
Q

AT1 receptors are located:

A

in the BV, brain, adrenal, kidney and heart

activation of these receptors increases BP

31
Q

3 pathways that control renin release

A
  • nacl reabsorption at macula densa
  • BP in pre-glomerular vessels
  • activation of B1 adrenergic receptors on juxtula glomerulur cells
32
Q

ACEI overview

A

“prils”
sulfhydryl-containing (captopril (Capoten))
dicarboxyl-containing (enalorpil (Vasotec))
phosphorus-containing (Cosinopril sodium (Monopril))

33
Q

sulfhydryl-containing ACEI

A

captopril (Capoten)
active site inhibitor
short half life (

34
Q

dicarboxyl-containing ACEI

A

enalapril (Vasotec):pro-drug, requires hydrolysis of ethyl ester to form diacid form (enalaprilat), 11 hour half life, parenteral availability
lisinopril (Prinvil, Zestril): active molecule, 12 hour half life

35
Q

phosphate-containing ACEI

A

fosinopril (Monopril): prodrug, requires cleavage by hepatic esterases to the active form (fosinoprilat), 11.5 hour half life

36
Q

uses of ACEI

A

HTN, left ventricular systolic dysfunction, myocardial infarction, diabetic neuropathy

37
Q

ACEI AE

A

hypotension, dry cough, hyperkalemia, acute renal failure, skin rash (captopril), angioedema

38
Q

ACEI drug drug interactions

A

Antacids: reduce bioavailability
NSAIDS: reduce effectiveness (interfere w bradykinin mediated vasodilation)
K+ supplements: hyperkalemia
digoxin and lithium: increased levels

39
Q

ACEI CI

A

pregnancy - ANG II needed for normal growth and function

high doses CI in pts with renal insufficiency

40
Q

ARB overview

A

the “sartans”
losartan (Cozaar)
Valsartan (Diovan)

41
Q

ARB actions

A

do not effect bradykinin
selectively block effects on ANG II (pressor effects, stimulation of NE system, secretion of aldosterone, effects on renal vasculature, growth-promoting effects of cardiac and vascular tissue)

42
Q

ACEI primarily excreted through hepatic metabolism

A

moexipril (use w compromised renal fxn)

43
Q

ARB uses

A

HTN, CHF, diabetic nephropathy, stroke prophylaxis

44
Q

ARB AE

A

hypotension, hyperkalemia, teratogenic potential (2nd or 3rd trimester)

45
Q

renin inhibitors

A

aliskiren
direct inhibition of renin (dipeptide like mimetic)
SE: diarrhea
CI: pregnancy and nursing

module 2a (13 decks)

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