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FA - Renal > Renal - Pharmacology > Flashcards

Renal - Pharmacology Flashcards

Pg. 546-549 in First Aid 2014 Pg. 499-502 in First Aid 2013 Sections include: -Diuretics: site of action -Mannitol -Acetazolamide -Loop diuretics -Ethacrynic acid -Hydrochlorothiazide -K+-sparing diuretics -Diuretics: electrolyte changes -ACE inhibitors

1
Q

Draw a nephron, labeling the tubules and depicting the reabsorption and/or secretion of the following substances in each of the tubules: (1) Ca2+ (2) 2Cl- (3) Mg2+ (4) K+ (5) Na+ (6) H2O (7) NaHCO3 (8) H+ (9) NaCl. Now, label the site of action for each of the following diuretics: (1) Acetazolamide (2) ADH antagonists (3) Loop diuretics (4) Mannitol (5) Potassium-sparing diuretics (6) Thiazides.

A

See p. 546 in First Aid 2014 or p. 499 in First Aid 2013 for visual

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2
Q

What is the mechanism of mannitol? Include its major effect and 3 effects that follow from that.

A

Osmotic diuretic, increase tubular fluid osmolarity, producing increased urine flow, decrease intracranial/intraocular pressure

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3
Q

What are 2 things for which mannitol is used clinically?

A

(1) Drug overdose (2) Elevated intracranial/intraocular pressure

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4
Q

What are 2 toxicities associated with mannitol?

A

(1) Pulmonary edema (2) (Intravascular) dehydration

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5
Q

What are 2 clinical contexts/conditions in which mannitol is contraindicated?

A

(1) Anuria (2) CHF

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6
Q

What is the mechanism/drug type of acetazolamide? What are 2 related effects that stem from this mechanism?

A

Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3- stores.

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7
Q

What are 5 things for which acetazolamide is clinically used?

A

(1) Glaucoma (2) Urinary alkalinization (3) Metabolic alkalosis (4) Altitude sickness (5) Pseudotumor cerebri

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8
Q

What are 4 toxicities associated with acetazolamide?

A

(1) Hyperchloremic metabolic acidosis (2) Paresthesias (3) NH3 toxicity (4) Sulfa allergy; Think: “‘ACID’azolamide causes ACIDosis”

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9
Q

Name two loop diuretics. What kind of loop diuretic is each.

A

(1) Furosemide: Sulfonamide loop diuretic (2) Ethacrynic acid: Phenoxyacetic acid derivative (not a sulfonamide)

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10
Q

What is the mechanism of loop diuretics (e.g., furosemide, ethacrynic acid)? What are 3 effects of this mechanism?

A

Inhibits cotransport system (Na+, K+, 2Cl-) of thick ascending limb of loop of Henle; (1) Abolishes hypertonicity of medulla, preventing concentration of urine (2) Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs. (3) Increase Ca2+ excretion; Think: “Loops Loose calcium”

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11
Q

Which effect of loop diuretics (e.g., furosemide, ethacrynic acid) do NSAIDs inhibit?

A

Loop diuretics stimulate PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs.

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12
Q

What are 3 clinical uses for furosemide?

A

(1) Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema) (2) Hypertension (3) Hypercalcemia

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13
Q

What are 6 toxicities associated with furosemide?

A

(1) Ototoxicity (2) Hypokalemia (3) Dehydration (4) Allergy (sulfa) (5) Nephritis (interstitial) (6) Gout; Think: “OH DANG!”

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14
Q

What is a clinical use for ethacrynic acid?

A

Diuresis in patients allergic to sulfa drugs

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15
Q

How do the toxicities of ethacrynic acid relate to those of furosemide? What is one contraindication of ethacrynic acid, and why?

A

Similar to furosemide (OH DANG); can cause hyperuricemia; never use to treat gout

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16
Q

What kind of diuretic is hydrochlorothiazide? What is its mechanism? What are 2 effects of this mechanism?

A

Thiazide diuretic. Inhibits NaCl reabsorption in early distal tubule, (1) reducing diluting capacity of the nephron. (2) Decreasing Ca2+ excretion.

17
Q

What are 5 clinical uses for hydrochlorothiazide?

A

(1) Hypertension (2) CHF (3) Idiopathic hypercalciuria (4) Nephrogenic diabetes insipidus (5) Osteoporosis

18
Q

What effect does furosemide/ethacrynic acid versus hydrochlorothiazide have on calcium?

A

LOOP DIURETICS: Increase Ca2+ excretion; HYDROCHLOROTHIAZIDE: Decrease Ca2+excretion

19
Q

What are 7 toxicities associated with hydrochlorothiazide?

A

(1) Hypokalemic metabolic acidosis (2) Hyponatremia (3) HyperGlycemia (4) HyperLipidemia (5) HyperUricemia (6) HyperCalcemia (7) Sulfa allergy; Think: “HyperGLUC(emia)”

20
Q

What are 4 examples of K+-sparing diuretics?

A

(1) Spironalactone and (2) eplerenone (3) Trimaterene (4) Amiloride; Think: “The K+ STAys”

21
Q

What is the mechanism of sprinolactone? What other diuretic shares this mechanism?

A

Spironolactone and eplerenone are competitive aldosterone receptor antagonists in the cortical collecting tubule

22
Q

What is the mechanism of triamterene? What other diuretic shares this mechanism?

A

Triamterene and amiloride act at the same part of the tubule by blocking Na+ channels in the CCT

23
Q

Again, what are 4 examples of K-+sparing diurectics? What are 3 clinical uses for K+-sparing diuretics?

A

(1) Spironalactone and (2) eplerenone (3) Trimaterene (4) Amiloride; Think: “The K+ STAys”; (1) Hyperaldosteronism (2) K+ depletion (3) CHF

24
Q

What are 2 toxicities associated with K+-sparing diuretics?

A

(1) Hyperkalemia (can lead to arryhythmias) (2) Endocrine effects with spironolactone (e.g., gynecomastia, antiandrogen effects).

25
Q

What is the effect of nearly all diuretics on urine NaCl? What side effect may this have? Name a diuretic that is an exception to the norm in the case of urine NaCl effect.

A

All diuretics except acetazolamide increase urine NaCl; Serum NaCl may decrease as a result

26
Q

What are 2 diuretics that increase urine K+? What side effect may this have?

A

Increase with loop and thiazide diuretics; Serum K+ may decrease as a result

27
Q

Name 2 diuretics/renal drugs that decrease blood pH, causing acidemia, and briefly describe their mechanism behind this.

A

Decrease blood pH (acidemia): (1) Carbonic anhydrase inhibitors - decrease HCO3- reabsorption. (2) K+ sparing - Aldosterone blockade prevents K+ secretion and H+ secretion. Additionally, hyperkalemia leads to K+ entering all cells (via H+/K+ exchange) in exchange for H+ exiting cells

28
Q

Name 2 diuretic/renal drugs the increase blood pH, causing alkalosis. Also, briefly describe 3 mechanisms behind this.

A

Increase blood pH (alkalemia): (1) Loop diuretics and (2) thiazides cause alkalemia through several mechanisms: (1) Volume contraction –> increase AT II –> increase Na+/H+ exchange in proximal tubule –> increase HCO3- reabsorption (“contraction alkalosis”) (2) K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells (3) In low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule, –> alkalosis and “paradoxical aciduria”

29
Q

What 2 diuretics/renal drugs affect urine Ca2+? What are those effects, and what are the mechanisms behind them?

A

Increase Urine Ca2+ with loop diuretics: decrease paracellular C2+ reabsorption –> hypocalcemia; Decrease Urine Ca2+ with thiazides: Enhanced paracellular Ca2+ reabsorption in distal tubule

30
Q

What are 3 examples of ACE inhibitors?

A

(1) Captopril (2) Enalapril (3) Lisinopril

31
Q

What is the mechanism of ACE inhibitors? What effects does this have on GFR, renin, and unrelated metabolism?

A

Inhibit angiotensin-converting enzyme (ACE) –> decrease angiotensin II –> decrease GFR by preventing constriction of efferent arterioles; Levels of renin increase as a result of loss of feedback inhibition; Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator

32
Q

What drugs have effects similar to ACE inhibitors? How do they differ from ACE inhibitors?

A

Angiotensin II receptor blocks (-sartans) have effects similar to ACE inhibitors but do not increase bradykinin –> no cough or angioedema.

33
Q

What are 4 clinical uses for ACE inhibitors?

A

(1) Hypertension (2) CHF (3) Proteinuria (4) Diabetic renal disease

34
Q

What prevention do ACE inhibitors provide in the context of chronic hypertension?

A

Prevent unfavorable heart remodeling as a result of chronic hypertension

35
Q

What are 6 toxicities associated with ACE inhibitors?

A

(1) Cough (2) Angioedema (3) Teratogen (fetal renal malformations) (4) Creatinine increase (decrease GFR) (5) Hyperkalemia (6) Hypotension; Think:” Captopril’s CATCHH”

36
Q

In what condition/context are ACE inhibitors contraindicated, and why?

A

Avoid in bilateral renal artery stenosis, because ACE inhibitors will further decrease GFR –> renal failure

FA - Renal (13 decks)

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