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Renal Step 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Mannitol is a ____ diuretic

A

Osmotic

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2
Q

Mannitol mechanism?

A

Increased tubular fluid osmolarity–>
Increased urine flow–>
Decreased intracranial/intraocular pressure

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3
Q

Mannitol clinical use?

A

Drug Overdose

Elevated intracranial/intraocular pressure

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4
Q

Mannitol Toxicity?

A

Pulmonary Edema

Dehydration

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5
Q

Mannitol is contraindicated in what?

A

Annuria

CHF

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6
Q

Acetozolamide is a _________ inhibitor.

A

Carbonic anhydrase

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7
Q

Acetozolamide mechanism?

A

Self limited NaHCO3 diuresis–>

Reduction in total body HCO3 stores

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8
Q

Acetozolamide clinical use?

A 
Glaucoma
Urinary alkalinazation
Metabolic alkalosis
Altitude sickness
pseudotumor cerebri
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9
Q

Acetozolamide toxicity?

A

Hyperchloremic Metabolic Acidosis
Paresthesia
NH3 toxicity
Sulfa allergy

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10
Q

Furosemide is a _____ diuretic

A

Sulfonamide loop

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11
Q

Furosemide inhibits _________ of __________

A 
Cotransporter system (Na, K, 2Cl)
Thich ascending LOH
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12
Q

Furosemide abolishes _______ of medulla, preventing ________ of urine.

A

Hypertonicity

Concentration

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13
Q

Furosemide stimulates _____ release which has a _________ on the afferent arteriole

A

PGE

vasodilatory

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14
Q

Furosemide leads to _______ excretion

A

Increased calcium

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15
Q

Furosemide clinical uses?

A 
Edematous states:
CHF
Cirrhosis
Nephrotic syndrome
Pulmonary edema

HTN
Hypercalcemia

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16
Q

Furosemide toxicity?

A 
OH DANG!
Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout
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17
Q

Ethacrynic acid is a ______ derviative

A

Phenoxyacetic acid

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18
Q

Ethacrynic acid has the same action as _________.

A

Furosemide

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19
Q

Ethacrynic acid clinical use?

A

Diuresis in patients who are allergic to Sulfa drugs

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20
Q

Ethacrynic acid toxicity?

A

Similar to furosemide

esp. hyperuricemia (don’t use for gout)

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21
Q

Hydrochlorothiazide is a ________ diuretic

A

Thiazide

22
Q

Hydrochlorothiazide mechanism?

A

Inhibits NaCl reabsorption in early DT–>

Reduces diluting capacity of nephron

23
Q

Hydrochlorothiazide causes _________ excretion

A

Decreased Ca

24
Q

Hydrochlorothiazide Clinical use?

A

HTN
CHF
Idiopathic hypercalciuria
nephrogenic diabetes insipidus

25
Q

Hydrochlorothiazide toxicity?

A

hypokalemic metabolic alkalosis
hyponatremia
Sulfa allergy

HyperGLUC:
hyperglycemia
hyperlipidemia
hyperuricemia
hypercalcemia
26
Q

K+ sparring diuretics include what?

A

Spironolactone, eplerenone, Triamtere, Amiloride

27
Q

What is Spironolactone and eplerenones mechanism?

A

Competitive alosterone receptor antagonists in the CCT

28
Q

What is Triamterene and amilorides mechanism?

A

Blocks Na channels in the CCT

29
Q

K+ sparring diuretics clinical use?

A

Hyperaldosteronism
K+ depletion
CHF

30
Q

K+ Sparring diuretics toxicity?

A
  • Hyperkalemia (arrhythmias)

- Edocrine effects with spironolactone (gynecomastia, antiandrogen effects)

31
Q

How do diuretics effect urine NaCl?

A

Increase it in all diuretics (may cause low serum NaCl)

32
Q

How do diuretics effect urine K?

A

Increase it in all but K+ sparring diuretics (may cause low serum K)

33
Q

What happens to urine Ca with loop diuretics?

A

Increases:
Decreased paracellular Ca reabsorption–>
hypocalcemia

34
Q

What happens to urine Ca with thiazides?

A

Decreases:

Enhanced paracellular Ca reabsorption in PT and LOH

35
Q

What diuretics cause acidemia?

A
  • CA inhibitors (decrease HCO3 reabsorption)

- K+Sparing (aldosterone blockade prevents K and H secretion )

36
Q

What else about diuretics causes acidemia?

A

Hyperkalemia–>
K+enters all cells via H/K exchanger–>
More H+ exiting cells

37
Q

What diuretics cause alkalemia?

A

Loop diuretics

Thiazides

38
Q

What are the mechanisms that Loop diuretics and thiazides cause alkalemia?

A

Volume Contraction

K+ Loss

39
Q

What is volume contraction?

A

“Contraction Alkalosis”
Increased ATII–>
Increased Na/H exchange in PT–>
Increased HCO3 reabsorption

40
Q

How does K+ loss lead to Alkalosis?

A

K+Loss–>
K+ exits cells via H/K exchanger–>
Increased H entering cells

41
Q

In low K states, _______ rather than _______ is exchanged for Na in the CCT, leading to ____ and ________

A

H+, K+, alkalosis, Paradoxical aciduria

42
Q

What are the ACE Inhibitors?

A

Captopril, Enalapril, Lisiopril

43
Q

What is the ACE inhibitor mechanism?

A

Inhibit ACE–>
Decreased ATII–>
Decreased GFR via prevention of constriction of eff arteriole

44
Q

With ACE I, levels of _______ increase as a result of __________.

A

Renin, Loss of feedback inhibition

45
Q

Inhibition of ACE also prevents ________ of _______, a potent vasodilator.

A

Inactivation, Bradykinin

46
Q

ARBs have similar effects to ACE I, but do not increase________ and thus do not cause ______ or _______

A

Bradykinin
Cough
Angiodedema

47
Q

ACE I clinical use?

A

HTN
CHF
Proteinuria
Diabetic renal disease

48
Q

ACE I can also prevent unfavorable ________ as a result of chronic ________.

A

Heard remodeling

HTN

49
Q

ACE I toxicity?

A 
CATCHH
Cough
Angioedema
Teratogen 
Creatinine increase (decrease GFR)
Hyperkalemia
Hypotension
50
Q

Avoid ACE I in ______

A

Bilateral renal artery stenosis

51
Q

Why should you avoid ACE I in bilateral renal artery stenosis?

A

Further decrease GFR–>

renal failure

Renal Step 1 (6 decks)

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