Pharmacology Flashcards

1
Q

What is the mechanism of mannitol?

A

Osmotic diuretic

Increase tubular fluid osmolarity, producing increased urine flow

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2
Q

What is the clinical use of mannitol?

A

Shock

Drug overdose

Treat increased intracranial/intraocular pressure

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3
Q

Toxicity of mannitol

A

Pulmonary edema

Dehydration

Contraindicated in anuria, CHF

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4
Q

Mechanism of acetazolamide

A

Carbonic anhydrase inhibitor

Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3- stores

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5
Q

Clinical use of acetazolamide

A

Glaucoma

Urinary alkalinization

Metabolic alkalosis

Altitude sickness

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6
Q

Toxicity of acetazolamide

A

Hyperchloremic metabolics acidosis

Neuropathy

NH3 toxicity

Sulfa allergy

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7
Q

Mechanism of furosemide

A

Sulfonamide loop diuretic

Inhibits cotransport system (Na+, K+, 2 Cl-) of thick ascending limb of loop of Henle

Abolishes hyperotnicity of medulla, preventing concentration of urine

Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs

Increase Ca2+ excretion

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8
Q

Clinical use of furosemide

A

Edematous states

  • CHF
  • Cirrhosis
  • Nephrotic syndrome
  • Pulmonary edem

HTN

Hypercalcemia

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9
Q

Toxicity of furosemide

A

Ototoxicity

Hypokalemia

Dehydration

Allergy

Nephritis

Gout

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10
Q

Mechanism of ethacrynic acid

A

Phenoxyacetic acid derivative (Not a sulfonamide)

Essentially same action as furosemide

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11
Q

Clinical use of ethacrynic acid

A

Diuresis in patients allergic to sulfa drugs

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12
Q

Toxicity of ethacrynic acid

A

Similar to furosemide

Can cause hyperuricemia

Never use to treat gout

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13
Q

Mechanism of hydrochlorothiazide

A

Thiazide diuretic

Inhibits NaCl reabsorption in early distal tubule, reducing concentrating capacity of the nephron

Decreases Ca2+ excretion

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14
Q

Clinical use of hydrochlorothiazide

A

HTN

CHF

Idiopathic hypercalciuria

Nephrogenic diabetes insipidus

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15
Q

Toxicity of hydrochlorothiazide

A

Hypokalemic metabolic alkalosis

Hyponatremia

Hyperglycemia

Hyperlipidemia

Hyperuricemia

Hypercalcemia

Sulfa allergy

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16
Q

What are the K+ sparing diuretics?

A

Spironolactone

Triamterene

Amiloride

Eplerenone

17
Q

Mechanism of spironolactone

A

Competitive aldosterone receptor antagonist in the cortical collecting tubule

18
Q

Clinical use of K+ sparing diuretics

A

Hyperaldosteronism

K+ depletion

CHF

19
Q

Toxicity of K+ sparing diuretics

A

Hyperkalemia (can lead to arrhythmias)

Endocrine effects with aldosterone antagonists

20
Q
A
21
Q

How do diuretics affect urien NaCl?

A

Increases urine NaCl

serum NaCl may decrease as a result

22
Q

How do diuretics affect urine K+?

A

Increases K+

Serum K+ may decrease as a result

23
Q

Which diuretics lower blood pH?

A

Carbonic anhydrase

24
Q

Which diuretics increase blood pH?

A

Loop diuretics and thiazides

25
Q

How do loop diuretics affect urine Ca+?

A

Increase

Decreased paracellular Ca+ reabsorption → hypocalcemia

26
Q

How do thiazides affect urine Ca+?

A

Decrease

Enhanced paracellular Ca2+ reabsorption in proximal tubules and loop of Henle

27
Q

Name 3 ACE inhibitors

A

Captopril

Enalapril

Lisinopril

28
Q

Mechanism of ACE inhibitors

A

Inhibit angiotensin-converting enzyme, reducing levels of angiotensin II and preventing inactivation of bradykinin, a potent vasodilator

Renin release is increased due to loss of feedback inhibition

29
Q

Clinical use of ACE inhibitors

A

HTN

CHF

Diabetic renal disease

Prevent unfavorable heart remodeling as a result of chronic HTN

30
Q

Toxicity of ACE inhibitors

A

Cough

Angioedema

Taste changes

hypOtension

Pregnancy problems

Rash

Increased renin

Lower angiotensin II

Hyperkalemia

Avoid bilateral renal artery stenosis because ACE inhibitors significantly decrease GFR by preventing constriction of efferent arterioles

Increase in serum creatinine `