Pharmacology

Question 1

Mannitol is a ____ diuretic

Answer 1

Osmotic

Question 2

Mannitol mechanism?

Answer 2

Increased tubular fluid osmolarity–>
Increased urine flow–>
Decreased intracranial/intraocular pressure

Question 3

Mannitol clinical use?

Answer 3

Drug Overdose

Elevated intracranial/intraocular pressure

Question 4

Mannitol Toxicity?

Answer 4

Pulmonary Edema

Dehydration

Question 5

Mannitol is contraindicated in what?

Answer 5

Annuria

CHF

Question 6

Acetozolamide is a _________ inhibitor.

Answer 6

Carbonic anhydrase

Question 7

Acetozolamide mechanism?

Answer 7

Self limited NaHCO3 diuresis–>

Reduction in total body HCO3 stores

Question 8

Acetozolamide clinical use?

Answer 8

Glaucoma
Urinary alkalinazation
Metabolic alkalosis
Altitude sickness
pseudotumor cerebri

Question 9

Acetozolamide toxicity?

Answer 9

Hyperchloremic Metabolic Acidosis
Paresthesia
NH3 toxicity
Sulfa allergy

Question 10

Furosemide is a _____ diuretic

Answer 10

Sulfonamide loop

Question 11

Furosemide inhibits _________ of __________

Answer 11

Cotransporter system (Na, K, 2Cl)
Thich ascending LOH

Question 12

Furosemide abolishes _______ of medulla, preventing ________ of urine.

Answer 12

Hypertonicity

Concentration

Question 13

Furosemide stimulates _____ release which has a _________ on the afferent arteriole

Answer 13

PGE

vasodilatory

Question 14

Furosemide leads to _______ excretion

Answer 14

Increased calcium

Question 15

Furosemide clinical uses?

Answer 15

Edematous states:
CHF
Cirrhosis
Nephrotic syndrome
Pulmonary edema

HTN
Hypercalcemia

Question 16

Furosemide toxicity?

Answer 16

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

Question 17

Ethacrynic acid is a ______ derviative

Answer 17

Phenoxyacetic acid

Question 18

Ethacrynic acid has the same action as _________.

Answer 18

Furosemide

Question 19

Ethacrynic acid clinical use?

Answer 19

Diuresis in patients who are allergic to Sulfa drugs

Question 20

Ethacrynic acid toxicity?

Answer 20

Similar to furosemide

esp. hyperuricemia (don’t use for gout)

Question 21

Hydrochlorothiazide is a ________ diuretic

Answer 21

Thiazide

Question 22

Hydrochlorothiazide mechanism?

Answer 22

Inhibits NaCl reabsorption in early DT–>

Reduces diluting capacity of nephron

Question 23

Hydrochlorothiazide causes _________ excretion

Answer 23

Decreased Ca

Question 24

Hydrochlorothiazide Clinical use?

Answer 24

HTN
CHF
Idiopathic hypercalciuria
nephrogenic diabetes insipidus

Question 25

Hydrochlorothiazide toxicity?

Answer 25

hypokalemic metabolic alkalosis hyponatremia Sulfa allergy ``` HyperGLUC: hyperglycemia hyperlipidemia hyperuricemia hypercalcemia ```

Question 26

K+ sparring diuretics include what?

Answer 26

Spironolactone, eplerenone, Triamtere, Amiloride

Question 27

What is Spironolactone and eplerenones mechanism?

Answer 27

Competitive alosterone receptor antagonists in the CCT

Question 28

What is Triamterene and amilorides mechanism?

Answer 28

Blocks Na channels in the CCT

Question 29

K+ sparring diuretics clinical use?

Answer 29

Hyperaldosteronism K+ depletion CHF

Question 30

K+ Sparring diuretics toxicity?

Answer 30

- Hyperkalemia (arrhythmias) | - Edocrine effects with spironolactone (gynecomastia, antiandrogen effects)

Question 31

How do diuretics effect urine NaCl?

Answer 31

Increase it in all diuretics (may cause low serum NaCl)

Question 32

How do diuretics effect urine K?

Answer 32

Increase it in all but K+ sparring diuretics (may cause low serum K)

Question 33

What happens to urine Ca with loop diuretics?

Answer 33

Increases: Decreased paracellular Ca reabsorption--> hypocalcemia

Question 34

What happens to urine Ca with thiazides?

Answer 34

Decreases: | Enhanced paracellular Ca reabsorption in PT and LOH

Question 35

What diuretics cause acidemia?

Answer 35

- CA inhibitors (decrease HCO3 reabsorption) | - K+Sparing (aldosterone blockade prevents K and H secretion )

Question 36

What else about diuretics causes acidemia?

Answer 36

Hyperkalemia--> K+enters all cells via H/K exchanger--> More H+ exiting cells

Question 37

What diuretics cause alkalemia?

Answer 37

Loop diuretics | Thiazides

Question 38

What are the mechanisms that Loop diuretics and thiazides cause alkalemia?

Answer 38

Volume Contraction | K+ Loss

Question 39

What is volume contraction?

Answer 39

"Contraction Alkalosis" Increased ATII--> Increased Na/H exchange in PT--> Increased HCO3 reabsorption

Question 40

How does K+ loss lead to Alkalosis?

Answer 40

K+Loss--> K+ exits cells via H/K exchanger--> Increased H entering cells

Question 41

In low K states, _______ rather than _______ is exchanged for Na in the CCT, leading to ____ and ________

Answer 41

H+, K+, alkalosis, Paradoxical aciduria

Question 42

What are the ACE Inhibitors?

Answer 42

Captopril, Enalapril, Lisiopril

Question 43

What is the ACE inhibitor mechanism?

Answer 43

Inhibit ACE--> Decreased ATII--> Decreased GFR via prevention of constriction of eff arteriole

Question 44

With ACE I, levels of _______ increase as a result of __________.

Answer 44

Renin, Loss of feedback inhibition

Question 45

Inhibition of ACE also prevents ________ of _______, a potent vasodilator.

Answer 45

Inactivation, Bradykinin

Question 46

ARBs have similar effects to ACE I, but do not increase________ and thus do not cause ______ or _______

Answer 46

Bradykinin Cough Angiodedema

Question 47

ACE I clinical use?

Answer 47

HTN CHF Proteinuria Diabetic renal disease

Question 48

ACE I can also prevent unfavorable ________ as a result of chronic ________.

Answer 48

Heard remodeling | HTN

Question 49

ACE I toxicity?

Answer 49

``` CATCHH Cough Angioedema Teratogen Creatinine increase (decrease GFR) Hyperkalemia Hypotension ```

Question 50

Avoid ACE I in ______

Answer 50

Bilateral renal artery stenosis

Question 51

Why should you avoid ACE I in bilateral renal artery stenosis?

Answer 51

Further decrease GFR--> | renal failure