Renal-Pharmacology Flashcards

1
Q

What is Mannitol?

A

an osmotic diuretic that increased tubular fluid osmolarity, thus increasing urine flow and decreasing intracranial/intraocular pressure

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2
Q

What are the clinical uses of Mannitol?

A

drug OD, elevated intracranial/ocular pressure

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3
Q

What are the AEs of Mannitol?

A

pulmonary edema

dehydration

contraindictaed in anuria, HF

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4
Q

What is Acetazolamide?

A

Carbonic anhydrase inhibitor that causes self-limited NaHCO3 diuresis and decreased total body HCO3- stores

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5
Q

What are the clinical uses of Acetazolamide?

A

glaucoma,

urinary alkalinzation

metaboic alkalosis

altitude sickness

pseudotumor cerebri

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6
Q

What are the AEs of Acetazolamide?

A

herpchloremia metabolic acidosis

paresthesias

NH3 toxicity

sulfa allergy

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7
Q

What are the loop diuretics?

A

Furosemide, bumetanide, torsemide

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8
Q

How do loop diuretics work?

A

sulfonamide loop diuretics that inhibit cotransport NaK2Cl in the thick ascending limb of Henle

this eliminated the hypertonicity of the medulla, preventing urine concentration and stimulates PGE release (vasodilatory effect on the afferent arterioles) and increased Ca2+ loss

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9
Q

What drugs block loop diuretics release of PGE?

A

NSAIDs

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10
Q

What are the clinical uses of loop diuretics?

A

edematous states (hF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia

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11
Q

What are the AEs of loop diuretics?

A

OH DANG!

ototoxicity

hypokalemia

dehydration

allergy (sulfa)

Nephritis (interstitial)

Gout

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12
Q

What is Ethacrynic Acid?

A

phenoxyacetic acid derivative (not a sulfonamide)- essentially same action as furosemide for induction of diuresis in pts allergic to sulfa drugs

Toxicities are similar to furosemide; can cause hyperuricemia; never use to tx gout

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13
Q

What are the thiazide diuretics?

A

Chlorthalidone, Hydrochlorohiazide

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14
Q

How do thiazide diuretics work?

A

they inhibit Nacl reabsorption in the early DCT

also decrease Ca2+ excretion/loss

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15
Q

What are the clinical uses of thiazide diuretics?

A

HTN

HF

idiopathic hypercalciuria

nephrogenic dabetes insipidus

osteoporosis

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16
Q

What are the AEs of thiazide diuretics?

A

hypokalemia metabolic alkalosis

hyponatremia

hyperGlycemia, hyperLipidemia hyperUricemia, hyperCalcemia

sulfa allergy

17
Q

What are the K+ sparing diuretics?

A

Spironolactone and eplerenone

Trimterene and Amiloride

18
Q

What are Spironolactone and eplerenone?

A

competitive aldosterone receptor antagonists in the cortical CT

19
Q

What are Triamterene and Amiloride?

A

ENaC channel blockers

20
Q

What are the clinical uses of K+-sparing diuretics?

A

hyperaldosteronism, K+ depletion, HF

21
Q

What are the AEs of K+-sparing diuretics?

A

hyperkalemia (can lead to arrhyhtmias)

endocrine effects with spironolactone (e.g. gynecomastis, antiandrogen effects, spironolactone bodies-below)

Spironolactone bodies Long-term administration of spironolactone gives the histologic characteristic of spironolactone bodies in the adrenal cortex. Spironolactone bodies are eosinophilic, round, concentrically laminated cytoplasmic inclusions surrounded by clear halos in preparations stained with hematoxylin and eosin

22
Q

What urine NaCl changes are seen with diuretics?

A

icnreased with all except acetazolamide; serum NaCl may decrease as a result

23
Q

What urine K+ changes are seen with diuretics?

A

increased with loop and thiazide diuretics; serum K+ may decrease as a result

24
Q

What blood pH changes are seen with diuretics?

A

acidemia with: CA inhibitors (Decreased HCO3- reabsorption), K+ sparing diuretics (aldosterone blockade prevents K+ secretion and H+ secretion). Additionally hyperkalemia lead to K+ entering cells in exchnage for H+

Alkalemia with: loop diuretics and thiazides via volume contraction (increased AT II leading to increased NaH exchange action in the PCT, resulting in increased HCO3- reabsorption), hypokalemia promotes inward shift of H+, and in low K+ states, H+ rather than K+ is exchanged for Na+ in the cortical CT

25
Q

What urine Ca2+ changes are seen with diuretics?

A

increased with loop diuretics via decreased paracellular Ca2+ reabsorption

decreased with thiazides via enhanced Ca2+ reabsorption in the DCT

26
Q

What are some ACEIs?

A

Captopril, Enalapril, Lisinopril, and Ramipril

27
Q

How do ACEIs work?

A

they inhibit ACE (which converts AT I to II), this decreased GFR by preventing constriction of efferent arterioles.

Renin levels increase as a result of loss of feedback inhibiton

28
Q

Inhibition of ACE also prevents inactivation of ______, a potent vasodilator

A

bradykinin

29
Q

What are the uses of ACEIs?

A

HTN, HF, proteinuria,

diabetic nephropathy (slows GBM thickening but decreasing intraglomerular pressure)

prevent unfavorable heart remodeling as a result of chronic HTN

30
Q

What are the AEs of ACEIs?

A

CATCHH

Cough

Angioedeama (contraindicated in C1 esterase inhibitor deficiency)

Teratogen (fetal renal malformations)

elevated creatinine (decreased GFR)

Hyperkalemia

Hypotension

31
Q

What are the ARBs?

A

Losartan, Candesartan, Valsartan, etc. (effects similar to ACEis, but ARbs do not increase bradykinin)

32
Q

What are the clinical uses of ARBs?

A

HTN, HF, proteinuria, or diabetic nephropathy with intolerance to ACEIs (e.g. those with cough, angioedema, poorly controlled)

33
Q

What are the AEs of ARBs?

A

hyperkalemia

decreased renal function

hypotension

teratogen

34
Q

What is Aliskiren?

A

direct renin inhibitor, blocks conversion of angiotensinogen to angiotension I for tx of HTN

35
Q

What are the AEs of Aliskiren?

A

Hyperkalemia

decreased renal function

hypotension

contraindicated in diabetics taking ACEIs or ARBs