Материал: 2016_Kaplan_USMLE_Step_1_Lecture_Notes_Pharmacology

Chapter 1 λ Diuretics

Chapter Summary

λDiuretics are used to treat HTN, heart failure, edema, renal dysfunction, hypercalcemia, renal stones, glaucoma, and mountain sickness. In addition to their diuretic action, the loop and thiazide diuretics also cause vasodilation.

λFigure III-1-1 illustrates the water and ion exchange occurring in the various segments of a renal tubule and the site of action of the different classes of diuretics.

λThe positive and negative effects of IV mannitol, an osmotic diuretic, are discussed.

λCarbonic anhydrase inhibitors (e.g., acetazolamide) act in the proximal tubule to decrease absorption of Na+ and bicarbonate. The mechanisms involved are summarized in Figure III-1-2. The clinical uses and adverse affects are listed.

λLoop diuretics (e.g., furosemide) inhibit the Na+/K+/2Cl– cotransporter on the luminal membrane of the thick ascending loop. The mechanisms causing their diuretic actions (Figure III-1-3) and their clinical uses and adverse effects are discussed.

λThe thiazides (e.g., hydrochlorothiazide) inhibit the Na+/Cl– cotransporter on the luminal membrane of the distal convoluted tubule. The mechanisms leading to their diuretic actions (Figure III-1-4) and their clinical uses and adverse effects are discussed.

λSpironolactone, amiloride, and triamterene are K+-sparing, weak diuretics that act at the collecting tubule and duct level. The mechanisms leading to their diuretic actions (Figure III-1-5) and their clinical uses and adverse effects are discussed.

λTable III-1-1 summarizes the mechanisms of action, the urinary electrolyte patterns, and the resultant blood pH associated with administration of the various classes of diuretics.

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Section III λ Cardiac and Renal Pharmacology

ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACEIs)

AND ANGIOTENSIN-RECEPTOR BLOCKERS (ARBs)

λDrugs:

−ACEIs: captopril, lisinopril (and other “−prils”)

ºBlock formation of angiotensin II

ºResulting in prevention of AT1-receptor stimulation

º↓ aldosterone, vasodilation

ºACEIs prevent bradykinin degradation

−ARBs: losartan (and other “−sartans”)

ºBlock AT1 receptors

ºSame results as ACEIs on BP mechanisms

ºARBs do not interfere with bradykinin degradation

−Renin inhibitor: Aliskiren

ºBlocks formation of angiotensin I

ºSame results as ACEIs on BP mechanisms

ºAliskiren does not interfere with bradykinin degradation

λUses:

−Mild-to-moderate hypertension (all)

−Protective of diabetic nephropathy (ACEI/ARBs)

−CHF (ACEI/ARBs)

λSide effects:

−Dry cough (ACEIs)

−Hyperkalemia

−Acute renal failure in renal artery stenosis

−Angioedema

λContraindication: pregnancy

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