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Renal - Pharmacology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the site of action of mannitol?

A

proximal tubule

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2
Q

What is the mechanism of mannitol?

A

Osmotic diuretic. Incr tubular fluid osmolarity, Incr urine flow.

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3
Q

What are the clinical uses of mannitol?

A

Drug overdose, elevated intracranial/intraocular

pressure.

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4
Q

What are the side effects of mannitol?

A

Pulmonary edema, dehydration.

Contraindicated in anuria, HF.

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5
Q

What is the site of action of acetazolamine?

A

Proximal tubule

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6
Q

What is the mechanism of action of acetazolamide?

A

Carbonic anhydrase inhibitor. Causes self-limited NaHCO3

diuresis and decreases total body bicarb stores.

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7
Q

What are the clinical uses of acetazolamide?

A

Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor
cerebri.

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8
Q

What are the side effects of acetazolamide?

A

Hyperchloremic metabolic acidosis,
paresthesias, NH3
toxicity, sulfa allergy.

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9
Q

What class of drugs are bumetanide and torsemide?

A

Loop diuretics

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10
Q

What is the mechanism of action of loop diuretics?

A
  1. Inhibit cotransport
    system (Na+/K+/2Cl−) of thick ascending limb of loop of Henle. 2. Abolish hypertonicity of
    medulla, preventing concentration of urine.
  2. Stimulate PGE release (vasodilatory effect
    on afferent arteriole); inhibited by NSAIDs.
    4. Increase Ca 2+ excretion. Loops Lose Ca2+.
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11
Q

What are the clinical uses of loop diuretics?

A

Edematous states (HF, cirrhosis, nephrotic
syndrome, pulmonary edema), hypertension,
hypercalcemia.

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12
Q

What are the side effects of loop diuretics?

A

Ototoxicity, Hypokalemia, Dehydration, Allergy
(sulfa), Nephritis (interstitial), Gout.
(OH DANG!)

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13
Q

What is the site of action of ethacrynic acid?

A

thick ascending loop

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14
Q

What is the mechanism of action of ethacrynic acid?

A

Phenoxyacetic acid derivative (not a
sulfonamide). Essentially same action as
furosemide.

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15
Q

What is the clinical use of ethacrynic acid?

A

Diuresis in patients allergic to sulfa drugs.

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16
Q

What are the side effects of loop diuretics?

A

Similar to furosemide; can cause

hyperuricemia; never use to treat gout.

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17
Q

What class of drug is chlorthalidone?

A

Thiazide diuretic

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18
Q

What class of drug is hydrochlorothiazide?

A

Thiazide diuretic

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19
Q

What is the site of action of thiazide diuretics?

A

DCT

20
Q

What is the mechanism of action of thiazide diuretics?

A

Inhibit NaCl reabsorption in early DCT
, decr diluting capacity of nephron. Incr Ca
2+ excretion.

21
Q

What is the clinical use of thiazide diuretics?

A

Hypertension, HF, idiopathic hypercalciuria,

nephrogenic diabetes insipidus, osteoporosis.

22
Q

What are the side effects of thiazide diuretics?

A

Hypokalemic metabolic alkalosis,
hyponatremia, hyperGlycemia,
hyperLipidemia, hyperUricemia,
hyperCalcemia. Sulfa allergy.

(hyperGLUC)

23
Q

What is the side of action of K+ sparing diuretics?

A

collecting duct

24
Q

What is the mechanism of action of spironolactone and eplerenone?

A

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

25
Q

What is the mechanism of action of triamterene and amiloride?

A

Triamterene and amiloride
act by blocking
Na+ channels in the cortical collecting tubule (ENaC).

26
Q

What are the clinical uses for K+ sparing diuretics?

A

Hyperaldosteronism, K+ depletion, HF.

27
Q

What are the side effects of K+ sparing diuretics?

A

Hyperkalemia (can lead to arrhythmias),
endocrine effects with spironolactone (e.g.,
gynecomastia, antiandrogen effects).

28
Q

Which diuretics increase urine sodium? (possibly causing hyponatremia)

A

All diuretics except acetazolamide.

29
Q

Which diuretics increase urine K+? (possibly causing hypokalemia). Why?

A

Loop diuretics, thiazide diuretics.

Increased distal sodium delivery, where sodium reabsorption is exchanged from K+ excretion

30
Q

What is the effect of carbonic anhydrase inhibitors on blood pH?

A

Acidemia. Decreases bicarb reabsorption in the PCT.

31
Q

What is the effect of loop diuretics on blood pH? How does this occur?

A

Alkalemia.

1) volume contraction –> AT2 –> Greater Na+/H+ exchange in PCT, greater bicarb reabsorption.
2) K+ loss leads to K+ exiting all cells (via H+/K+ exchanger), driving H+ into cells and out of blood
3) In low K+ state, H+ rather than K+ is exchanged for Na+ in cortical collecting tubule –> alkalosis with paradoxical aciduria

32
Q

What is the effect of K+ sparing diuretics on blood pH?

A

Acidemia.
Aldo blockade prevents K+ secretion and H+ secretion. Additionally, hyperkalemia leads to K+ entering all cells (via K+/H+ exchanger) in exchange for H+ leaving

33
Q

What is the effect of thiazide diuretics on blood pH?

A

Alkalemia. Same mechanism as loop diuretics; Contraction alkalosis, K+ loss leading to K+ cell exit/H+ cell entry, and low K+ state leading to H+ exchange instead of K+ in collecting tubule.

34
Q

What is the effect of loop diuretics on Ca2+ ?

A

Increase urine Ca2+, due to decreased paracellular transport (hypocalcemia)

35
Q

What is the effect of thiazide diuretics on Ca2+?

A

Enhanced Ca2+ absorption in DCT –> hypercalcemia.

36
Q

What is the mechanism of ACEis?

A

Inhibit ACE , Decr AT II Ž, decr GFR by preventing
constriction of efferent arterioles. Levels
of renin incr as a result of loss of feedback
inhibition. Inhibition of ACE also prevents
inactivation of bradykinin, a potent vasodilator.

37
Q

What is the clinical use of ACEis?

A

Hypertension, HF, proteinuria, diabetic
nephropathy. Prevent unfavorable heart
remodeling as a result of chronic hypertension.

38
Q

Why are ACEis used for slowing the progression of diabetic nephropathy?

A

Decr intraglomerular

pressure slows GBM thickening.

39
Q

Toxicity of ACEis?

A

Cough, Angioedema (contraindicated in C1
esterase inhibitor deficiency), Teratogen (fetal
renal malformations),  Incr Creatinine (decr GFR),
Hyperkalemia, and Hypotension. Avoid in
bilateral renal artery stenosis, because ACE
inhibitors will further  decr GFR Ž –> renal failure.

40
Q

What is the mechanism of ARBs?

A

Selectively block binding of angiotensin II to AT1
receptor. Effects similar to ACE inhibitors, but
ARBs do not increase bradykinin.

41
Q

What is the clinical use of ARBs?

A

Hypertension, HF, proteinuria, or diabetic nephropathy with intolerance to ACE inhibitors (e.g.,
cough, angioedema).

42
Q

What are the toxicities of ARBs?

A

Hyperkalemia, renal function, hypotension; teratogen.

43
Q

What is the mechanism of aliskiren?

A

Direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I.

44
Q

What are the clinical uses of aliskiren?

A

HTN

45
Q

What are the toxicities of aliskiren?

A

Hyperkalemia, renal function, hypotension. Contraindicated in diabetics taking ACE inhibitors
or ARBs.

Renal - Pharmacology (1 decks)

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