Pharmacology Flashcards

(45 cards)

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?

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
What is the mechanism of action of triamterene and amiloride?
Triamterene and amiloride act by blocking Na+ channels in the cortical collecting tubule (ENaC).
26
What are the clinical uses for K+ sparing diuretics?
Hyperaldosteronism, K+ depletion, HF.
27
What are the side effects of K+ sparing diuretics?
Hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (e.g., gynecomastia, antiandrogen effects).
28
Which diuretics increase urine sodium? (possibly causing hyponatremia)
All diuretics except acetazolamide.
29
Which diuretics increase urine K+? (possibly causing hypokalemia). Why?
Loop diuretics, thiazide diuretics. | Increased distal sodium delivery, where sodium reabsorption is exchanged from K+ excretion
30
What is the effect of carbonic anhydrase inhibitors on blood pH?
Acidemia. Decreases bicarb reabsorption in the PCT.
31
What is the effect of loop diuretics on blood pH? How does this occur?
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
What is the effect of K+ sparing diuretics on blood pH?
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
What is the effect of thiazide diuretics on blood pH?
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
What is the effect of loop diuretics on Ca2+ ?
Increase urine Ca2+, due to decreased paracellular transport (hypocalcemia)
35
What is the effect of thiazide diuretics on Ca2+?
Enhanced Ca2+ absorption in DCT --> hypercalcemia.
36
What is the mechanism of ACEis?
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
What is the clinical use of ACEis?
Hypertension, HF, proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a result of chronic hypertension.
38
Why are ACEis used for slowing the progression of diabetic nephropathy?
Decr intraglomerular | pressure slows GBM thickening.
39
Toxicity of ACEis?
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
What is the mechanism of ARBs?
Selectively block binding of angiotensin II to AT1 receptor. Effects similar to ACE inhibitors, but ARBs do not increase bradykinin.
41
What is the clinical use of ARBs?
Hypertension, HF, proteinuria, or diabetic nephropathy with intolerance to ACE inhibitors (e.g., cough, angioedema).
42
What are the toxicities of ARBs?
Hyperkalemia,  renal function, hypotension; teratogen.
43
What is the mechanism of aliskiren?
Direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I.
44
What are the clinical uses of aliskiren?
HTN
45
What are the toxicities of aliskiren?
Hyperkalemia,  renal function, hypotension. Contraindicated in diabetics taking ACE inhibitors or ARBs.