Renal Pharmacology Flashcards
(50 cards)
1
Q
mannitol–mechanism
A
- osmotic diuretic
- increase tubuar fluid osmolarity –> increase urine flow, decrease intracranial/intraocular pressure
2
Q
mannitol–use
A
- drug overdose
- elevated intracranial/intraocular pressure
3
Q
mannitol–toxicity
A
- pulmonary edema
- dehydration
4
Q
what are contraindications for mannitol?
A
- anuria
- HF
5
Q
acetazolamide–mechanism
A
- carbonic anhydrase inhibitor
- causes self limited NaHCO3 diuresis and decrease in total body HCO3- stores
6
Q
acetazolamide–use
A
- glaucoma
- urinary alkalinization
- metabolic alkalosis
- altitude sickness
- pseudotumor cerebri
7
Q
acetazolamide–toxicity
A
- proximal renal tubular acidosis
- paresthesias
- NH3 toxicity
- sulfa allergy
- “ACIDazolamide causes ACIDosis”
8
Q
name the 4 loop diuretics
A
- furosemide
- bumetanide
- torsemide
- ethacrynic acid
9
Q
furosemide, bumetanide, torsemide–mechanism
A
- inhabit contransport system (Na/K/2Cl) of thick ascending limb of loop of Henle
- abolishes hypertonicity of medulla which prevents concentration of urine
- increase Ca2+ excretion
- Loops Lose Ca2+
10
Q
furosemide, bumetanide, torsemide–what type of loop diuretic?
A
- sulfonamide loop diuretic
11
Q
what does furosemide, bumetanide, torsemide stimulate and what is the effect?
A
- stimulates the release of PGE
- vasodilatory effect on afferent arteriole
12
Q
what is furosemide, bumetanide, torsemide inhibited by?
A
NSAIDs
13
Q
furosemide, bumetanide, torsemide–use
A
- edematous states
- HF
- cirrhosis
- nephrotic syndrome
- pulmonary edema
- hypertension
- hypercalcemia
14
Q
furosemide, bumetanide, torsemide–toxicity
A
-
OH DANG
- Ototoxicity
- Hypokalemia
- Dehydration
- Allergy (sulfa) and Metabolic Alkalosis
- Nephritis (interstitial)
- Gout
15
Q
ethacrynic acid–mechanism
A
- nonsulfonamide inhibitor of cotransport system (Na/K/2Cl) of thinck ascending limb of loop of Henle
16
Q
ethacrynic acid–use
A
- diuresis in patients allergic to sulfa drugs
17
Q
ethacrynic acid–toxicity
A
- similar to furosemide
- more ototoxic
- “Loop earrings hurt your ears”
- more ototoxic
- hyperuricemia
- never use to treat gout
18
Q
name the diuretics that work at the PCT:
A
- mannitol
- acetazolamide
19
Q
name the diuretics that work at the loop of Henle:
A
- furosemide
- bumetanide
- torsemide
- ethacrynic acid
20
Q
name the diuretics that work at the DCT:
A
- hydrochlorothiazide
- chlorthalidone
- metolazone
21
Q
name the diuretics that work at the collecting duct:
A
- K+ sparing diuretics
- spironolactone
- eplerenon
- triamterene
- amiloride
22
Q
name the thiazide diuretics:
A
- hydrochlorothiazide
- chlorthalidone
- metolazone
23
Q
hydrochlorothiazide, chlorthalidone, metolazone–mechanism
A
- inhibit NaCl reabsorption in early DCT –> decrease diluting capacity of nephron
- decrease Ca2+ excretion
24
Q
hydrochlorothiazide, chlorthalidone, metolazone–use
A
- hypertension
- HF
- idiopathic hypercalciuria
- nephrongenic diabetes insipidus
- osteoporosis
25
hydrochlorothiazide, chlorthalidone, metolazone--toxicity
* hypokalemic metabolic alkalosis
* hyponatremia
* hyper**G**lycemia
* hyper**L**ipidemia
* hyper**U**ricemia
* hyper**C**alcemia
* Hyper**GLUC**
* sulfa allergy
26
name the potassium sparing diuretics
* **S**pirinolactone and eplerenone
* **T**riamterene
* **A**miloride
* "the K+ **STA**ys"
27
spironolactone and eplerenone--mechanism
* (K+ sparing)
* spironolact**ONE** and epleren**ONE** are competitive aldoster**ONE** receptor antagonists in cortical collecting tubule
28
triamterene and amiloride--mechanism
* (K+ sparing)
* act at the same part of the tubule by blocking Na+ channels in the cortical collecting tubule
29
K+ sparing diuretics--use
* hyperaldosteronism
* K+ depletion
* HF
* hepatic ascites (spironolactone)
* nephrongenic DI (amiloride)
30
K+ sparing diuretics--toxicity
* hyperkalemia--can lead to arrhythmias
* endocrine effects with spironolactone
* gynecomastia
* antiandrogen effects
31
diuretic induced electrolyte change: urine NaCl
* inc with all diuretics
* strength varies on potency of diuretic effect
* serum NaCl may decrease as a result
32
diuretic induced electrolyte change: urine K+
* inc especially with loop and thiazide diuretics
* serum K+ may dec as a result
33
diuretic induced electrolyte change: decreased blood pH (acidemia)
* carbonic anhydrase inhibitors
* decrease HCO3- reabsorption
* K+ sparing:
* aldosterone blockade prevents K+ secretion adn H+ secretion
* hyperkalemia --\> K+ entering all cells via H/K exchanger in exchange for H exiting cells
34
diuretic induced electrolyte change: increase in blood pH (alkalemia)
* loop diuretics and thiazides cause alkalemia through severeal mechanisms:
* volume contraction --\> increase AT II --\> increase Na/K exchange in PCT --\> inc HCO3- reabsorption
* "contraction alkalosis"
* K+ loss leads to K+ exiting all cells (via 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 --\> alkalosis and "paradoxical aciduria"
35
diuretic induced electrolyte change: urine Ca2+
* increase with loop diuretics:
* decrease paracellular Ca2+ reabsorption --\> hypocalcemia
* decrease with thiazides:
* enhanced Ca2+ reabsorption
36
name the angiotensin converting enzyme inhibitors
* captopril
* enalapril
* lisinopril
* ramipril
37
ACE inhibitors--mechanism
* inhibit ACE --\> decrease AT II --\> decrease GFR by preventing constriciton of efferent arterioles
* increase renin due to loss of negative feedback
* inhibition of ACE also prevent inactivation of bradykinin, a potent vasodilator
38
ACE inhibitors--use
* HTN
* HF (dec mortality)
* proteinuria
* diabetic neuropathy
39
what are 2 things that ACE inhibitors can prevent?
* unfavorable heart remodeling
* diabetic neuropathy
* increase intraglomerular pressure, slows GBM thickening
40
ACE inhibitors--toxicity
* "Captopril's **CATCHH**"
* **C**ough
* **A**ngiodema
* due to increased bradykinin
* **T**eratogen
* fetal renal malformation
* increased **C**reatinine
* decrease GFR
* **H**yperkalemia
* **H**ypotension
41
what are contraindications for ACE inhibitors?
* CI esterase inhibitor deficiency
* bilateral renal artery stenosis
42
why are ACE inhibitors contraindicated in bilateral renal artry stenosis?
* b/c ACE inhibitors further decrease GFR --\> renal failure
43
name the 3 Angiotensin II receptor blockers (ARBs)
* losartan
* candesartan
* valsartan
44
Angiotensin II Receptor Blockers--mechanism
* selectively block binding of angiotensin II to AT1 receptor
* effects similar to ACE inhibitors
* but ARBs do not increase bradykinin
45
Angiotensin II Receptor Blockers--use
* HTN
* HF
* proteinuria
* diabetic neuropathy with intolerance to ACE inhibitors
* ie. cough, angioedema
46
Angiotensin II Receptor Blockers--toxicity
* hyperkalemia
* decrease GFR
* hypotension
* teratogen
47
Aliskiren--mechanism
* direct renin inhibitor
* blocks conversion of angiotensinogen to angiotensin I
48
Aliskiren--use
* hypertension
49
Aliskiren--toxicity
* hyperkalemia
* decrease GFR
* hypotension
50
what is a contraindication for aliskiren?
* patients already taking ACE inhibitors or ARBs
