Step 1 - Pharm - Renal Drugs

Front 1

This diuretic creates an osmotic diuresis

Back 1

Mannitol

Front 2

This diuretic is used to treat shock and drug overdose

Back 2

Mannitol

Front 3

This drug is used to lower intracranial and intraocular pressure

Back 3

Mannitol

Front 4

This diuretic is contraindicated in anuria and CHF

Back 4

Mannitol

Front 5

This diuretic can cause pulmonary edema and dehydration

Back 5

Mannitol

Front 6

MOA of acetazolamide

Back 6

Carbonic anhydrase inhibitor

Front 7

This diuretic causes self-limited NaHOC3 diuresis, and reduction in total-body HCO3 stores

Back 7

Acetazolamide

Front 8

This diuretic causes a hyperchloremic metabolic acidosis

Back 8

Acetazolamide (HCO3 is lost which means [H]plasma is increasing)

Front 9

This diuretic is used in glaucoma

Back 9

Acetazolamide

Front 10

This diuretic is used to alkalinize the urine (as for the treatment of kidney stones in cystinuria)

Back 10

Acetazolamide

Front 11

This diuretic is used to treat altitude sickness

Back 11

Acetazolamide

Front 12

Side effects of acetazolamide

Back 12

Hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy

Front 13

These diuretics cause sulfa allergy

Back 13

Acetazolamide, thiazide, furosemide

Front 14

This diuretic can cause NH3 toxicity

Back 14

Acetazolamide

Front 15

This diuretic inhibits the NA/K/2Cl pump of the ascending limb

Back 15

Furosemide

Front 16

This diuretic abolishes the hypertonicity of the medulla, thereby preventing concentration of urine

Back 16

Furosemide

Front 17

This diuretic increases Ca excretion

Back 17

Furosemide
(vs Thiazide, which increases Ca reabsorption)

Front 18

This diuretic is used to treat edema (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension and hypercalcemia

Back 18

Furosemide

Front 19

Side effects of furosemide

Back 19

Ototoxic, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout
("OH DANG")

Front 20

This diuretic can cause interstitial nephritis and gout

Back 20

Furosemide

Front 21

This loop diuretic is not a sulfonamide

Back 21

Ethacrynic acid

Front 22

Clinical use of ethacrynic acid

Back 22

Diuresis in patients with sulfa allergies; it is a loop diuretic and works the same as furosemide

Front 23

Unlike furosemide, ethacrynic acid can be used in patients with these conditions

Back 23

Hyperuricemia/acute gout, patients with sulfa allergies

Front 24

This diuretic inhibits NaCl absorption in the early distal tubule, reducing diluting capacity of the nephron

Back 24

Hydrochlorothiazide

Front 25

This diuretic decreases calcium excretion

Back 25

Hydrochlorothiazide

Front 26

This diuretic reduces diluting capacity of nephron

Back 26

Hydrochlorothiazide

Front 27

This diuretic reduces concentrating capacity of nephron

Back 27

Furosemide

Front 28

This diuretic is used to treat idiopathic hypercalciuria (ie, calcium kidney stones)

Back 28

Hydrochlorothiazide

Front 29

This diuretic is used to treat recurrent kidney stones in cystinuria

Back 29

Acetazolamide

Front 30

This diuretic is used to treat nephrogenic DI

Back 30

Hydrochlorothiazide

Front 31

This diuretic can cause hyponatremia

Back 31

Hydrochlorothiazide

Front 32

These diuretics are sulfa drugs

Back 32

Furosemide, hydrochlorothiazide, acetazolamide

Front 33

Hydrochlorothiazide causes increased levels of these

Back 33

Hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia
("HyperGLUC")

Front 34

These diuretics work on the proximal tubules

Back 34

Mannitol, acetazolamide

Front 35

These diuretics work on the thick ascending limb

Back 35

Furosemide, ethacrynic acid

Front 36

This diuretic works on the distal tubule

Back 36

Hydrochlorothiazide

Front 37

These diuretics work on the collecting tubules

Back 37

Spironolactone, triamterne, amiloride, eplerenone (K-sparing)

Front 38

These are the K-sparing diuretics

Back 38

Spironolactone, triamterne, amiloride, eplerenone
("The K STAEs")

Front 39

This diuretic is a competitive aldosterone receptor blocker

Back 39

Spironolactone

Front 40

These diuretics block Na channels in the cortical collecting tubule

Back 40

Triamterne, amiloride

Front 41

This diuretic is used in hyperaldosteronism

Back 41

Spironolactone

Front 42

Side effect of K-sparing diuretics

Back 42

Arrhythmia (caused by hyperkalemia, which most importantly affects automaticity)

Front 43

Side effect of spironolactone

Back 43

Gynecomastia, antiandrogen effects; arrhythmia (as with all K-sparing diuretics, due to hyperkalemia)

Front 44

Effect of diuretics on urine NaCl

Back 44

All diuretics increase urine NaCl

Front 45

Effect of diuretics on urine potassium

Back 45

All except for the K-sparing diuretics increase urine potassium

Front 46

Effect of diuretics on blood pH

Back 46

Carbonic anhydrase inhibitors (acetazolamide) and K-sparing diuretics cause acidemia. Loop and thiazide diuretics cause alkalemia

Front 47

Mechanism by which K-sparing diuretics cause acidemia

Back 47

Hyperkalemia leads to K entering cells in exchange for H leaving cells

Front 48

Mechanism by which CA inhibitors cause acidemia

Back 48

Direct result of decreased HCO3 reabsorption

Front 49

Mechanisms by which loop and thiazide diuretics cause alkalemia

Back 49

(1) Volume contraction: increased AT II leads to increased Na/H exchange in the proximal tubule, causing increased HCO3
(2) Hypokalemia (K leaves cells and enters blood, H leaves blood and enters cells)
(3) Not enough K to exchange with Na in principal cells, therefore H is exchanged (and lost) instead

Front 50

Define "paradoxical aciduria"

Back 50

Unexpected acidic urine in the setting of a patient with metabolic alkalosis. It occurs in hypokalemia. There is not enough K to be exchanged for Na in the principal cells, so H is exchanged for Na instead, leading to alkalosis. Na is reabsorbed, H is excreted.

Front 51

Effect of diuretics on urine Ca

Back 51

Increased by loop diuretics, decreased by thiazides.
Loop diuretics abolish the lumen-positive potential, decreasing paracellular Ca reabsorption and causing hypocalcemia/hypercalcinuria. Thiazides block luminal Na/Cl cotransport in the distal tubule, thus increasing the Na gradient leading to more Na/Ca exchange; Na leaves and Ca enters, causing hypercalcemia/hypocalcinuria

Front 52

Effect of ACE inhibitors on renin levels

Back 52

Renin increases, since there is a loss of feedback inhibition

Front 53

MOA of losartan

Back 53

Angiotensin II receptor blocker (does not cause cough)

Front 54

Cause of cough in ACE inhibitor therapy

Back 54

Increased level of bradykinins (ACE, the enzyme, inhibits kinin; thus remove ACE and kinin levels rise)

Front 55

Actions of bradykinin

Back 55

Vasodilation, increased vessel permeability, pain

Front 56

Side effets of ACE inhibitors

Back 56

Cough, angioedema, proteinuria, taste changes, hypotension, pregnancy problems (fetal renal damage), rash, increased renin, low angiotensin II, hyperkalemia
("CAPTOPRIL")

Front 57

ACE inhibitors should be avoided in these patients

Back 57

Patients with renal artery stenosis. ACE inhibitors will cause a decrease in angiotensin II, which normally acts to constrict efferent arterioles to preserve renal function. If efferents don't constrict, the kidney can't compensate for the fall in RPF due to RAS, thus GFR falls.