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Pharmacology > Pharmacology-Renal > Flashcards

Pharmacology-Renal Flashcards

(52 cards)

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1
Q

Name the drugs that work at the PCT:

A

mannitol, acetazolamide

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2
Q

Name the drugs that work at the Thick Ascending LOH

A

loop diuretics: furosemide, ethacrynic acid

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3
Q

Name the drugs that work at the DCT

A

hydrochlorothiazide

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4
Q

Name the drugs that work at the collecting duct

A

K+ sparing diuretics

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5
Q

name the K+ sparing diuretics:

A

spironolactone, eplerenone, amiloride, triamterine

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6
Q

Mannitol – mechanism

A
  • osmotic diuretic (increases tubular fluid osmolarity), increased urine flow
  • decreased intracranial and intraoccular pressure
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7
Q

Mannitol – site of action

A

PCT

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8
Q

Mannitol – use

A

Drug overdose, hydrocephaly, glaucoma

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9
Q

Mannitol – toxicity

A

pulmonary edema, dehydration

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10
Q

Mannitol – contraindications

A

anuria, CHF

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11
Q

Acetazolamide – mechanism

A
  • carbonic anhydrase inhibitor

- self-limited NaHCO3 diuresis and reduction in total-body HCO3- stores

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12
Q

Acetazolamide – site of action

A

PCT

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13
Q

Acetazolamide – use

A
  • Glaucoma
  • Urinary alkinization, metabolic alkalosis, alt. sickness
  • pseudotumor cerebri
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14
Q

Acetazolamide – toxicity

A
  • hyperchloremic metabolic acidosis
  • paresthesias
  • NH3 toxicity
  • sulfa allergy
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15
Q

Loop diuretics – names

A

furosemide, ethacrynic acid

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16
Q

Furosemide – type of loop diuretic

A

sulfonamide loop diuretic

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17
Q

Furosemide – mechanism

A
  • inhibits cotransport system (Na+, K+, 2Cl-) of thick ascending limb
  • abolishes hypertonicity of medulla, preventing [] of urine
  • Ca2+ excretion
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18
Q

What does furosemide stimulate the release of? effects?

A

PGE, vasodilatory effect on afferent arteriole

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19
Q

What is furosemide inhibited by?

A

NSAIDS

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20
Q

Furosemide – use

A

edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia

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21
Q

Furosemide – toxicity

Study These Flashcards
A 
OH DANG!
O - ototoxicity
H - hypokalemia
D - dehydration
A - allergy (sulfa)
N - nephritis (intersitial)
G - gout
22
Q

Ethacrynic acid – type of Loop diuretic

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A

phenoxyacetic acid derivative ** NOT A SULFA

23
Q

Ethacryic acid – action

Study These Flashcards
A

same as furosemide

24
Q

ethacrynic acid – use

Study These Flashcards
A

diuresis in patients allergic to sulfa drugs

25
Ethacrynic acid -- toxicity
similar to furosemide | CAN CAUSE HYPERURICEMIA -- NEVER USE TO TREAT GOUT!
26
Hydrochlorothiazide -- site of action
DCT
27
Hydrochlorothiazide -- mechanism
- Thiazide diuretic - (-) NaCl reabsorption in early DCT - reduces diluting capacity of the nephron - decrease Ca2+ excretion
28
Hydrochlorothiazide -- use
HTN, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus
29
Hydrochlorothiazide -- toxicity
- Hypokalemic metabolic alkalosis, Hyponatremia - (Hyper)GLUC: hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia - Sulfa allergy
30
K+ sparing diuretics -- names
SEAT -- Spironolactone, Ethacrynic acid, Amiloride, Triamterene
31
K+ sparing diuretics -- site of action
cortical collecting tubule
32
Spironolactone, Eplerenone -- mechanism
competetive aldosterone receptor antagonists
33
Triamterene, amiloride -- mechanism
Block Na+ channels
34
K+ sparing diuretics -- use
hyperaldosteronism, K+ depletion, CHF
35
K+ sparing diuretics -- toxicity
hyperkalemia -> arrhythmias
36
Spironolactone -- toxicity
endocrine effects (gynecomastia, antiandrogenic effects)
37
Diuretic induced electrolyte change: Urine NaCl
- increase in all diuretics | - NaCl in serum may decrease as a result
38
Diuretic induced electrolyte change: Urine K+
- increase in all diuretics except K+sparing | - serum K+ decrease as result
39
Diuretic induced electrolyte change: Decreased Blood pH
carbonic anhydrase inhibitors -- decrease HCO3- reabsorption K+ sparing -- aldosterone blockade prevent K+ and H+ secretion - hyperkalemia -> K+ entering all cels via H+/K+ exchanger so H+ exits and leads to more H+ in blood
40
Diuretic induced electrolyte change: Increased Blood pH
loops and thiazides via contraction alkalosis and paradoxical aciduria
41
Explain contraction alkalosis
volume contraction, leading to increased angiotensin II, therefore increased Na+/H+ exchange in PCT leading to increased HCO3- reabsorption
42
Explain paradoxical aciduria
- K+ loss leads to K+ exiting all cells (H+/K+ exchanger) in exchange for H+ entering cells - In low K+ state, H+ rather than K+ is exchanged for Na+ in cortical collecting tubule leading to alkalosis
43
Diuretic induced electrolyte change: increased Urine Ca2+
with loop diuretics: decrease paracellular Ca2+ reabsorption leading to hypocalcemia
44
Diuretic induced electrolyte change: decreased urine Ca2+
thiazides: enhanced paracellular Ca2+ reabsorption in proximal tubule and LOH
45
ACE inhibitors: names
captopril, enalapril, lisinopril (-pril)
46
Ace inhibitors: mechanism
(-)ACE -> decrease ATII, leading to decreased GFR by (-) constriction of efferent arterioles - renin increase because loss of feedback inhibition
47
ACE-I use
HTN, CHF, proteinuria, diabetic renal dz
48
ACE-I prevent what two things
unfavorable heart remodeling and diabetic nephropathy
49
ACE-I toxicity
"Captoprils CATCHH" Cough (prevent inactivation of bradykinin a potent vasodilator), Angioedema, Teratogen (fetal renal malformations), Creatinine increase (decrease GFR), Hyperkalemia, Hypotension
50
ACE-I contraindications
avoid in bilateral renal artery stenosis because ACE-I will further decrease GFR, leading to renal failure
51
ARB's: name
"-sartan" eg: losartan
52
ARB's -- toxicity difference with ACE-I
do not increase bradykinin so no cough or angioedema

Pharmacology (12 decks)

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