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Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Why are loop diuretics “K wasting”? 2 fold mechanism

A
  1. Inhibit ascending limb Na/K/2Cl co-transporter, thereby inhibiting reabsorption of 15% of filtered K load
  2. Inhibition of the Na/K/2Cl transporter decreases the passive following (reabsorption) of water; thus, more water remains in the tubule (increased tubular flow) which enhances K+ secretion in the distal segments via flow effects
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2
Q

Thiazide diuretic - Mechanism

A

Inhibit NaCl co-transporter in distal tubule; anti-hypertensive effect secondary to decreased plasma volume and decreased CO

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3
Q

Thiazides - Special considerations

A

Lose efficacy in later stages of CKD as less drug reaches the distal tubule; loop diuretics indicated at GFR < 30 ml/min

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4
Q

Spironolactone - Mechanism

A

Competitively inhibits the mineralocorticoid receptor from binding aldosterone, blocking the aldosterone-dependent up-regulation of Na/K exchange leading to reduced Na resorption and reduced K excretion

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5
Q

Eplerenone - Mechanism

A

Competitively inhibits the mineralocorticoid receptor from binding aldosterone

Binds more specifically than aldosterone

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6
Q

Mannitol - Mechanism, Uses, and Pharmacokinetics

A

Non-absorbed sugar, produces diuresis by elevating the osmolarity of the glomerular filtrate, decreasing tubular reabsorption of water

Used in management of elevated intracranial pressure

Administered IV

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7
Q

Acetazolamide - Mechanism, Pharmacokinetics, and Uses

A

Inhibits carbonic anhydrase in the proximal tubule; leads to sodium bicarbonate loss with increased loss of water

Oral administration

Used to treat metabolic alkalosis and acute mountain sickness

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8
Q

Loop Diuretics - Adverse Effects

A 
Hypokalemia
Hypomagnesemia
Hypocalcemia 
Uric acid retention (precipitation of gout attack) 
Metabolic alkalosis
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9
Q

Loop diuretics - 3 individual agents

A

Furosemide (Lasix) - most commonly used

Ethacrynic Acid - only non-sulfa containing loop or thiazide

Torsemide - improved bioavailability

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10
Q

3 pharmacological classes for treatment of HTN

A

ACEIs/ARBs
Calcium Channel Blockers
Diuretics

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11
Q

Beta blockers - Adverse Effects

A

Bradycardia
Bronchospasm
Glucose/lipid changes
Decreased libido

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12
Q

Alpha/Beta blockers

A

Labetalol

Carvedilol

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13
Q

Metoprolol vs. Atenolol - elimination

A

Metoprolol - renal and hepatic elimination

Atenolol - renal elmination only

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14
Q

Acetazolamide - Uses

A

Primarily used for metabolic alkalosis, acute mountain sickness; infrequently used as diuretic

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15
Q

Vasodilators - Mechanism

A

Induce release of NO, which induces arterial vasodilation

Hydralazine and minioxidil

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16
Q

Alpha 1 receptor blockers - Adverse Effects & Uses

A

Orthostatic hypotension, headache, peripheral edema

Primarily used in BPH

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17
Q

Loop diuretics - Mechanism

A

Inhibits the Na/K/2Cl co-transporter in the water-impermeable ascending Loop of Henle; this decreases the tonicity of the interstitium, thereby reducing the driving force on the reabsorption of water in the collecting duct

Leads to the excretion of 15-25% of filtered sodium

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18
Q

Thiazide - Adverse Effects

A 
Hypokalemia
Hyponatremia
Hypomagnesemia
Hyperglycemia and lipid abnormalities 
Hypercalcemia
Uric acid retention and precipitation of gout 
Metabolic alkalosis
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19
Q

Uses of spironolactone

A

Resistant HTN
Heart failure
Hyperaldosteronism

20
Q

Spironolactone - Adverse effects

A 
Hyperkalemia 
Gynecomastia (not seen with eplerenone)
21
Q

Sodium channel blockers diuretics - 2 examples

A

Amiloride

Triamterene

22
Q

Sodium channel blocker diuretics - Mechanism

A

Block reabsorption of Na+ in the distal tubule leading to decreased Na/water retention; less Na+ influx decreases the driving force on K+ secretion (K-sparing)

23
Q

Sodium channel blocker diuretics - Adverse effects

A

Hyperkalemia
Hyperuricemia
Glucose intolerance in diabetes

24
Q

ACE Inhibitors - Mechanism

A

Inhibits angiotensin converting enzyme (ACE), blocking the conversion of angiotensin I to angiotensin II; reduces angiotensin II-mediated vasoconstriction and stimulation of aldosterone release; also blocks degradation of bradykinin

25
Q

ACEIs - Adverse effects

A

Cough
Hyperkalemia
Mild increase in serum creatinine; contraindicated with b/l renal artery stenosis
Contraindicated in pregnancy

26
Q

Angiotensin II Receptor Blockers (ARBs)

A

Irreversibly blocks the actions of angiotensin II at its receptor, preventing vasoconstriction and aldosterone release

27
Q

ARB - Adverse Effects

A

Hyperkalemia
Mild increase in serum creatinine; contraindicated in bilateral rental artery stenosis
Contraindicated in pregnancy

Does not cause cough

28
Q

Dihydropyridine CCBs - 3 examples

A

Amlodipine
Felodipine
Nifedipine

29
Q

DHPs - Mechanism

A

Block L-type Ca2+ channels, causing arterial vasodilation which lowers peripheral vascular resistance; selective for vascular smooth muscle over cardiac tissue (no significant effect on chronotropy or inotropy)

30
Q

Non-dihydropyridines - 2 examples

A

Verapamil

Diltiazem

31
Q

DHPs - Adverse Effects

A

Peripheral edema
Reflex tachycardia
Flushing
Headache

32
Q

NDHPs - Mechanism

A

Block L-type Ca2+ channels, causing vasodilation and decreased peripheral vascular resistance; equally selective for cardiac and vascular L-type Ca2+ channels, also causing negative chronotropic and inotropic effects

33
Q

NDHPs - Adverse Effects

A

Conduction defects; contraindicated in 2nd or 3rd degree heart block
Nausea
Headache

34
Q

Selective Beta 1 Blockers 2 examples & Pharmacokinetics

A

Atenolol - eliminated by the kidney

Metoprolol - eliminated by the liver

35
Q

Non-selective Beta-1/Beta-2 blockers - 2 examples

A

Propanalol

Timolol

36
Q

Beta / alpha blockers - 2 examples & mechanism

A

Carvedilol
Labetalol

Block beta receptors on heart, decreasing CO; also block alpha receptors on vascular smooth muscle, causing arterial vasodilation and decreased peripheral resistance

37
Q

Hydralazine

A

Direct vasodilator

Stimulate release of NO, which interferes with intracellular Ca2+ release causing peripheral vasodilation of arterioles

38
Q

Minoxidil

A

Direct vasodilator

K+ channel opener; causes hyperpolarization of smooth muscle cells

39
Q

Direct vasodilator - Adverse effects

A 
Reflex tachycardia 
Reflex activation of RAAS leading to Na/H2O retention
Headache
Anorexia
Nauseavomiting
Diarrhea
40
Q

Alpha 1 blockers - 3 examples

A

Prazosin
Terazosin
Doxazosin

41
Q

Alpha 1 blockers - Mechanism & Uses

A

Selectively block alpha-1 adrenergic receptors causing decreased SVR; particularly strong effect on alpha-1 receptors in the prostatic stroma, decreasing urethral resistance and relieving obstruction

Most often used in symptomatic BPH

42
Q

Alpha-1 blocker Adverse Effects

A

Orthostatic HTN
Headache
Peripheral edema

43
Q

Classes of immunosuppression meds

A 
Calcineurin inhibitor (Cyclosporine, Tacrolimus) 
Proliferation inhibitor (MMF, Sirolimus) 
Predisone
44
Q

Calcineurin inhibitors

A

Ex: Cyclosporine, Tacrolimus

Prevents NFAT-mediated T-cell clonal expansion

Adverse effects (Cyclosporine): Nephrotoxicity, gout, HTN, hyperlipidemia

45
Q

Proliferation Inhibitors - Transplant Meds

A

MMF, mTOR inhibitors (Sirolimus)

Inhibit purine synthesis

Adverse effects: leukopenia, anemia

46
Q

Prednisone - Adverse Effects

A

HTN
Hyperlipidemia
Cataracts
Weight gain

Renal (13 decks)

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