Renal Pharmacology Flashcards

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1
Q

What type of diuretic is mannitol?

A

Osmotic diuretic (it’s a sugar that pulls water into tubules)

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2
Q

Where is mannitol’s site of action?

A

Proximal convoluted tubule and descending LOH

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3
Q

Describe mannitol’s mechanism

A

Increase tubular fluid osmolarity and increase urine flow. Decrease intracranial/intraocular pressure

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4
Q

What clinical circumstances use Mannitol?

A

Drug overdose, elevated intracranial/intraocular pressure (head trauma)

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5
Q

What are some adverse effects of mannitol?

A

Pulmonary edema, dehyrdration

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6
Q

What are contraindications for mannitol?

A

Anuria, CHF, active cerebral hemorrhage

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7
Q

Where does Acetazolamide function?

A

PCT

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8
Q

Describe the mechanism of Acetazolamide

A

Carbonic anhydrase inhibitor in the PCT. Decreases NaHCO3 synthesis and thus decreases total body HCO3- stores

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9
Q

What clinical uses does Acetazolamide have?

A

Glaucoma (decrease aqueous humor production), urinary alkalinzation, metabolic alkalosis, altitude sickness, pseudotumor cerebri

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10
Q

What are adverse effects of Acetazolamide

A

Proximal Renal Tubular Acidosis (Type 2), Paresthesias, NH3 toxicity (more NH3 is retained), sulfa allergy

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11
Q

List three common Loop diuretics (FuTor Bum)

A

Furosemide, Bumetanide, Torsemide

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12
Q

Describe the mechanism of loop diuretics (where they act, what they do)

A

Act on Thick Ascending LoH. Inhibit Na/K/2Cl cotransporter. Abolish hypertonicity, preventing concentration of urine. Stimulate PGE release (vasodilate AA). Increase Ca+2 excretion

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13
Q

When are loop diuretics used?

A

Edematous states (HF, cirrhosis, nephrotic syndrome, pulm edema), hypertension, hypercalcemia

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14
Q

Adverse Effects of Loop diuretics (OH DANG A)

A
Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout 
Alkalemia
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15
Q

When do you use Ethacrynic acid?

A

When a patient needs loop diuretic but has sulfa allergy

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16
Q

What are the adverse effects of Ethacrynic acid?

A

Similar to furosemide but more ototoxic

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17
Q

Where do thiazide diuretics act?

A

Distal convoluted tubule

18
Q

Mechanism of thiazide diuretics (HCTZ, chlorthalidone, metolazone)

A

Inhibit NaCl reabsorption in DCT. Inhibit Ca+2 excretion.

19
Q

Clinical use of Thiazide diuretics

A

Hypertension, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis

20
Q

Adverse effects of thiazide diuretics (HyperGLUC)

A

Hypokalemic metabolic acidosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia. Sulfa allergy

21
Q

List three potassium-sparing diuretics (The K+ STAys)

A

Spironolactone and eplerenone; Triamterene, Amiloride

22
Q

Mechanism of spironolactone and epleronone?

A

competitive aldosterone receptor antagonists in cortical collecting tubule

23
Q

Mechanism of Triamterene and Amiloride

A

Block Na+ channels in cortical collecting tubule

24
Q

Clinical use of K+-sparing diuretics

A

Hyperaldosteronism, K+ depletion, HF, hepatic ascites (spironolactone), nephrogenic DI (amiloride)

25
Q

Adverse effects of K+sparing diuretics

A

Hyperkalemia (arrythmias), endocrine effects with spironolactone (gynecomastia, antiandrogen effects)

26
Q

How does ATII act on the PCT?

A

Increases Na/H+ exchange, leading to increased HCO3- reabsorption (contraction alkalosis)

27
Q

Describe paradoxical aciduria with loop and thiazide diuretics

A

K+ loss leads to K+ depleted state. In cortical collecting tubule, H+ (rather than low K+) is exchanged for Na+ leading to alkalosis and paradoxical aciduria

28
Q

Describe the mechanism of ACEIs

A

Inhibition of ACE and conversion of AI to AII. Acts on efferent arterioles. Decreases AII, leads to increase of renin due to loss of negative feedback. Prevents inactivation of bradykinin so increased vasodilation

29
Q

What is the effect of ACE inhibitors on GFR?

A

Decreased GFR

30
Q

Clinical use of ACE inhibitors (-prils)

A

Hypertension, heart failure (decreases mortality), proteinuria in diabetic neuropathy. Prevents unfavorable heart remodeling as a result of chronic hypertension

31
Q

Which electrolyte abnormalities do you get with loop diuretics?

A

Hypokalemia, metabolic alkalosis and hypocalcemia

32
Q

Which electrolyte abnormalities do you get with thiazide diuretics?

A

Hyponatremia, Hypokalemia, metabolic alkalosis, Hypercalcemia

33
Q

Which electrolyte abnormalities do you get with Acetazolamide?

A

Metabolic acidosis, hypokalemia

34
Q

Which electrolyte abnormalities do you get with K+ sparing diuretics?

A

Hyperkalemia, metabolic acidosis

35
Q

What are common side effects of chlorthalidone?

A

Muscle weakness, cramps and possible rhabdomyolysis

36
Q

Which medications help with reducing progression to renal failure in patients with diabetes?

A

ACE inhibitors

37
Q

Why do ACEIs lead to coughing?

A

Inhibit degradation of bradykinin

38
Q

Which antiviral can cause renal calcium and magnesium wasting (leading to hypocalcemia and hypomagnesemia)?

A

Foscarnet

39
Q

Chlorthalidone is what type of diuretic

A

Thiazide

40
Q

Hypercholesterolemia and hyperglycemia occur with use of thiazide diuretics due to

A

decreased insulin secretion and increased insulin resistance

41
Q

Hyperuricemia with use of thiazide diuretics occurs because

A

of increased reabsorption in PT due to decreased renal blood flow

42
Q

Best diuretics for patients in heart failure (increased RAAS, audible S3)

A

Aldosterone-inhibitors (Spironolactone or eplerenone)