Diuretics

Question 1

What drugs are used to treat acute closed angle glaucoma?

Answer 1

Carbonic anhydrase inhibitor and beta blocker

Question 2

Which 2 group of drugs should not be used with pt with closed angle glaucoma?

Answer 2

Anti M and alpha 1 agonist

Question 3

What are the 2 ways of treating glaucoma and what drugs are used?

Answer 3

Decrease aqueous production:
Beta blocker (Timolol)
Carbonic anhydrase inhibitor (acetazolamide) 
Increase drainage:
M3 agonist (pilocarpine)
Prostaglandin analog (latanoprost)
Mannitol

Question 4

What is AChE inhibitor’s affect on your blood vessel?

Answer 4

None (M3 is not innervated)

Question 5

When an organ/muscle doesn’t respond to indirect agonist but respond to direct agonist, what could be the reason behind that?

Answer 5

Denervation of the organ/muscle

Question 6

Why ganglionic blocker produce a significant tachycardia with NE?

Answer 6

NE has alpha 1 and beta 1 affect—>reflex bradycardia results from alpha 1 affect—>if block reflex—>unopposed beta 1 results in significant tachycardia

Question 7

For diuretics, hypokalemia goes with?

Answer 7

Alkalosis (K secretion is coupled with H secretion)

Question 8

Mannitol is contraindicated in ___ and ___ pt?

Answer 8

CHF and pulmonary edema

Question 9

How does carbonic anhydrase work?

Answer 9

Na/H antiporter transport H out to the urine—>H combine with HCO3- —>H2CO3—(carbonic anhydrase)—>CO2 and H2O—>CO2 goes into the cell—>combine with H2O—(carbonic anhydrase)—>H2CO3—>H + HCO3- —>HCO3- goes into the blood

Question 10

What is carbonic anhydrase side effect and what else does it treat besides HTN?

Answer 10

Metabolic acidosis/hyperchloremia (later Cl- reabsorption)/renal stone (due to alkaline urine)
acute mountain sickness

Question 11

Decrease in bicarb will always accompany with the increase of?

Answer 11

Cl-

Question 12

How is Na reabsorbed in the thick ascending limb of the kidney?

Answer 12

Na is absorbed with K+ and Cl- via Na/K/2Cl cotransporter—>create + potential along the luminal membrane—>facilitate Mg and Ca absorption between cells

Question 13

What are the electrolyte disturbance created by loop diuretics?

Answer 13

They block Na/K/2Cl contrasporter—>hypo Na/K/Cl/Mg/Ca
Alkalosis
Ototoxicity

Question 14

What are the loop diuretics?

Answer 14

Furosemide/torsemide/ethacrynic acid

Question 15

What is loop used for?

Answer 15

Pul edema/HF/hypercalcemia/HTN (thiazide is better)

Question 16

Which loop does not elicit sulfonamide sensitivity?

Answer 16

Ethacrynic acid

Question 17

Loop with ___ increase risk for ototoxicity?

Answer 17

Aminoglycoside

Question 18

Which 2 drugs do loop interact with?

Answer 18

Li—>decrease Li clearance

Digoxin—>increase digoxin toxicity from hypokalemia

Question 19

What are the diuretics that contain sulfonamide?

Answer 19

Carbonic anhydrase inhibitor/loop except for ethacrynic acid/thiazide

Question 20

Where and how does thiazide diuretics work?

Answer 20

Block Na/Cl cotransporter at early distal tubule

Question 21

What are some thiazide?

Answer 21

HCTZ (hydrochlorothiazide)/chlorthalidone/indapamide

Question 22

What is thiazide used for mainly?

Answer 22

HTN (#1 choice)/calcium stone/CHF/nephrogenic diabetes insipidus

Question 23

How does thiazide treat nephrogenic diabetes insipidus?

Answer 23

Use HCTZ—>lose Na—>proximal tubule reabsorb Na to compensate—>water follows—>increase water reabsorption

Question 24

What are the side effect of thiazide?

Answer 24

Hypokalemia and alkalosis/hypercalcemia/hyperglycemia/hyperglycemia/hyperlipidemia

Question 25

How does thiazide cause hyperglycemia?

Answer 25

Thiazide--->hypokalemia--->keep K channel open in beta cell of pancreas--->inhibit insulin release--->hyperglycemia

Question 26

Beta block and thiazide can treat HTN but they both cause?

Answer 26

Hyperlipidemia

Question 27

Which 2 types of diuretics cause hyperuricemia?

Answer 27

Loop and thiazide

Question 28

What is the most common cause of hypokalemia and metabolic alkalosis?

Answer 28

Loop and thiazide diuretics

Question 29

Why loop and thiazide cause hypokalemia and alkalosis?

Answer 29

Inhibit Na reabsorption--->kidney try to compensate by reabsorb more Na at principle cell of collecting duct--->Na is reabsorbed and K and H are secreted--->hypokalemia and alkalosis

Question 30

What is the most common cause of hyperkalemia?

Answer 30

Renal failure

Question 31

Where else does carbonic anhydrase work besides proximal tubule?

Answer 31

Intercalated cells of collecting duct--->secrete H

Question 32

What are the 2 kinds of K sparing diuretics?

Answer 32

Na channel blocker--->amiloride/triamterene | Aldosterone receptor blocker--->spironolactone/eplerenone

Question 33

How does Li cause nephrogenic diabetes insipidus? and what treats it?

Answer 33

Li gets into principle cell of collecting duct--->damage V2 receptor--->don't respond to ADH Amiloride treats Li induced nephrogenic diabetes insipidus

Question 34

What pH disturbance do carbonic anhydrase and K sparing agents have?

Answer 34

Metabolic acidosis

Question 35

Difference between spironolactone and eplerenone?

Answer 35

Eplerenone is not antiandrogen

Question 36

Paring with what HTN drugs with K sparing diuretics might cause hyperkalemia?

Answer 36

ACEI or ARB