Diuretics & PBL Drugs

Question 1

Acetazolamide MOA/location/main AE

Answer 1

Carbonic Anhydrase inhibitor
PCT
NaHCO3 excretion, loss of HCO3 –> Causes acidosis

Question 2

Mannitol MOA/location

Answer 2

Osmotic diuretic: inc. tubular fluid osmolarity –> pull water into tubule –> inc. urine flow
PCT

Question 3

Loop diuretics MOA/location

Answer 3

Inhibit NKCC (N, K, 2Cl)
Thick ascending limb of LOH
Cannot reabsorb Na, 2Cl back –> do not hyperconcentrate medulla insterstitium–> water doesn’t follow –> excrete more urine
Stimulate PGE release –> vasodilate afferent arteriole –> inc. GFR –> excrete more urine
Inc. Ca++ excretion (don’t have Na+ to power reabsorption)

Question 4

loop diuretics adverse effects

Answer 4

OH DANG!
Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout

Question 5

thiazide diuretics names

Answer 5

chlorthalidone, hydrochlorothiazide

Question 6

thiazides MOA/location

Answer 6

inhibit NaCl reabsorption in early DCT –> decrease diluting capacity of nephron
Decrease Ca++ excretion

Question 7

thiazides AE

Answer 7

Hypokalemia, metabolic acidosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy

Question 8

K+ sparing diuretics examples

Answer 8

spironolactone, eplerenone

triamterine, amiloride

Question 9

spironolactone, eplerenone MOA and location

Answer 9

competitive aldosterone receptor antagonists in cortical collecting duct

Question 10

triamterine amiloride MOA and location

Answer 10

Block Na+ channels in cortical collecting duct

Question 11

K+ sparing diuretics AE

Answer 11

Hyperkalemia –> arrhythmias

endocrine effects w/ spironolactone

Question 12

When use TMP-SMX

Answer 12

acute cystitis when resistance rates < 20% and not used in last 3 months
first line female (and uncomplicated male - but usually have prostatitis, then use fluoros)

Question 13

when use nitrofurantoin

Answer 13

first line female (w/ bactrim) - do NOT use in pyelonephritis

Question 14

concerns with using fluroquinolones in UTI

Answer 14

Resistance, broad spectrum –> C diff

Tendon rupture

Question 15

MEchanism for thiazides to decrease BP

Answer 15

decrease blood volume AND decrease resistance (major method) - open K+ channels –> increase K+ –> decrease Ca++ in smooth muscle –> decrease contraction

Question 16

mechanism for thiazides to cause hyperglycemia

Answer 16

suppress insulin release (sulfonylureas) - bind SUR on K channel controlling insulin release - open channel, hyperpolarize cell

Question 17

loop diuretics names

Answer 17

furosemide, bumetanide

Question 18

thiazide diuretics names

Answer 18

chlorthalidone, hydrochlorothiazide, metalazone

Question 19

diuretics used to decrease kidney stones

Answer 19

thiazides (hypouricuria, hyperuricemia though)

Question 20

K+ sparing diuretics - aldosterone inhibitors names

Answer 20

spironolactone, epleronone

Question 21

K+ sparing diuretics - inhibit Na/K/H exchange - names

Answer 21

amiloride

triamterene

Question 22

ADH name and its congener

Answer 22

Vasopressin = natural hormone
Desmopressin = synthetic congener

Question 23

indications ADH

Answer 23

central DI

bedwetting

Question 24

abx w/ some activity as an ADH antagonist

Answer 24

Demecocycline

- would act as an ADH diuretic

Question 25

allopurinol MOA

Answer 25

blocks formation of uric acid by inhibiting xanthine oxidase (for gout)

Question 26

probenacid, sulfinpyrazone MOA

Answer 26

inhibits renal organic acid transporter to facilitate excretion of uric acid --> reduce gout risk

Question 27

colchicine MOA

Answer 27

microtubule inhibitor with anti-inflammatory properties

Question 28

4 types of insulin

Answer 28

ultra-rapid (fast-acting) regular nph (intermediate) long-acting (glargine)

Question 29

names of fast-acting insulin

Answer 29

insulin aspart ***insulin lispro insulin glulisine "ultra-rapid"

Question 30

NPH human insulin =

Answer 30

intermediate acting

Question 31

names of long-lasting insulin

Answer 31

insulin glargine | insulin detemir

Question 32

why insulin lispro so fast

Answer 32

quickly dissociates from hexamer form to monomers which are active at IR

Question 33

why insulin glargine long lasting

Answer 33

insoluble so forms micro-precipitates which release constant amounts of insulin to give constant blood level

Question 34

ultra-rapid insulin onset, peak, duration

Answer 34

15 min 2 hours 4 hours

Question 35

regular insulin onset, peak, duration

Answer 35

30 min 3 hours 6 hours

Question 36

NPH insulin onset, peak, duration

Answer 36

2 hours 6.5 hours 17 hours

Question 37

insulin glargine onset, peak, duration

Answer 37

1.5 hours 9 hours 22 hours