10/15

Question 1

long-term diuretic administrarion

Answer 1

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

Question 2

thiazide diuretic MOA

Answer 2

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

Question 3

thiazide like diuretics

Answer 3

chlorthalidone, indapamide, metolazone

Question 4

any drugs that inc Na delivery to collecting tubule ___

Answer 4

will cause K wasting

Na tries to come back in, K goes out

Question 5

thiazide toxicities

Answer 5

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

Question 6

clinical uses of diuretics

Answer 6

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

Question 7

thiazides CI

Answer 7

sulfa allergy

Question 8

loop diuretics examples

Answer 8

furosemide, bumetanide, ethacrynic acid

Question 9

loop diuretics MOA

Answer 9

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

Question 10

loop diuretic toxicites

Answer 10

dehydration, hypokalemia, ototoxicity, hyperuricemia, hypomagnesemia

Question 11

loop CI

Answer 11

sulfa allergy

Question 12

diuretics that act in the collecting tubule

Answer 12

amilioride and triamterine

Question 13

amilioride and triamterine MOA

Answer 13

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

Question 14

amilioride and triamterine uses

Answer 14

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

Question 15

amilioride and triamterine toxicites and CI

Answer 15

hyperkalemia, hyperchloremic metabolic acidosis

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

Question 16

diuretics that act in the collecting tubule

Answer 16

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

Question 17

spiranolactone actions

Answer 17

blocks production of Na channels (aldosterone action)

inhibits 5a reductase

Question 18

clinical uses of spiranolactone

Answer 18

HTN or CHT w other diurects

Question 19

spiranolactone toxicities and CI

Answer 19

hyperkalemia, gynecocomastia, impotence, BPH

CI: K+ supplements, ACEI, chronic renal insufficiency

Question 20

eplerenone actions

Answer 20

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

Question 21

eplerenone toxicities and CI

Answer 21

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

Question 22

renin is responsible for

Answer 22

converting angiotensinogen to angiotensin I (not active)

Question 23

Ang I is rapidly converted to ___ by ___

Answer 23

ang II by ACE

Question 24

ANG II 2 actions

Answer 24

• vasoconstriction -> inc PVR

- aldosterone release -> inc Na and water retention

Question 25

ARBs place in RA system

Answer 25

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

Question 26

spironolactone and eplerenone place in RA system

Answer 26

blocks aldosterone actions (inc Na and water retention)

Question 27

ACEI place in RA system

Answer 27

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

Question 28

aliskiren place in RA system

Answer 28

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

Question 29

ang II works on __ receptors

Answer 29

AT1

Question 30

AT1 receptors are located:

Answer 30

in the BV, brain, adrenal, kidney and heart | activation of these receptors increases BP

Question 31

3 pathways that control renin release

Answer 31

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

Question 32

ACEI overview

Answer 32

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

Question 33

sulfhydryl-containing ACEI

Answer 33

captopril (Capoten) active site inhibitor short half life (

Question 34

dicarboxyl-containing ACEI

Answer 34

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

Question 35

phosphate-containing ACEI

Answer 35

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

Question 36

uses of ACEI

Answer 36

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

Question 37

ACEI AE

Answer 37

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

Question 38

ACEI drug drug interactions

Answer 38

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

Question 39

ACEI CI

Answer 39

pregnancy - ANG II needed for normal growth and function | high doses CI in pts with renal insufficiency

Question 40

ARB overview

Answer 40

the "sartans" losartan (Cozaar) Valsartan (Diovan)

Question 41

ARB actions

Answer 41

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)

Question 42

ACEI primarily excreted through hepatic metabolism

Answer 42

moexipril (use w compromised renal fxn)

Question 43

ARB uses

Answer 43

HTN, CHF, diabetic nephropathy, stroke prophylaxis

Question 44

ARB AE

Answer 44

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

Question 45

renin inhibitors

Answer 45

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