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Flashcards in Diuretics Deck (32):
1

Describe sodium reabsorption at the PCT

Na+/K+ ATPase brought sodium into the interstitium.
Na+/H+ exchanger brought sodium into the intracellular compartment from the tubular lumen.

2

Role of Carbonic Anhydrase

CA associates H+ with CO2 to form Carbonic Acid. Carbonic acid diffuses into the intracellular compartment where CA again converts Carbonic acid to CO2 and H2O. H2O is then reabsorbed into the interstitium along with the other solutes.
CA finally converts H2O and CO2 into H+ and HCO3-.

3

Name the CA-inhibitor

Acetazolamide

4

Acetazolamide MOA

Inhibits carbonic anhydrase. HCO3-1 and Na+ remain in the tubular lumen. Water is also unable to be reabsorbed.

5

Does Acetazolamide cause metabolic acidosis or alkalosis?

Acidosis b/c HCO3- is unable to be reabsorbed.

6

Acetazolamide treatment?

Decreases intraoccular pressure
Decreases production of CSF.
Prevent mountain sickness.

7

Acetazolamide adverse effects

Hypokalemia
Type II renal tubular acidosis
Calcium phosphate stones.
Sulfa allergy.

8

Mannitol MOA

Osmotic diuresis

9

Mannitol treatment?

Decreases intracranial and intraocular pressure

10

Mannitol adverse effects.

Expanded extracellular volume causing pulmonary edema.
Hyponatremia.
Exacerbate heart failure

11

Explain reabsorption at the Loop of Henle

Na+/K+ ATPase reabsorbs sodium into the interstitium.
The Na/K/2Cl transporter brings these ions into the intracellular compartment.

12

Is the the ascending limb of the loop of Henle permeable to water?

No, this segment is called the diluting segment.

13

Name the loop diuretics

Furosemide
Ethacrynic Acid

14

Furosemide MOA

Inhibits the N/K/Cl co-transporter

15

Loop diuretics promote the excretion of what ions and why?

Mg and Ca

These are excreted because diuretics lower the positive charge w/in the tubular lumen

16

Connection b/w loop diuretics and prostaglandins?

Induce the expression of COX-2 thereby increasing production of prostaglandins.
Prostaglandins dilate the afferent arteriole and cause an increased excretion of salt.

17

Loop diuretics treatment?

1st line for acute symptomatic HF
Pulmonary edema
Liver failure
Hypertension

18

Loop diuretics adverse effects?

Ototoxicity
Sulfa allergy
Interstitial nephritis
Hyperuricemia
Alkalosis

19

Reabsorption at the DCT

Na/K ATPase drive sodium into the interstitium.
Na/Cl co-transporter drives these ions into the intracellular compartment.
PTH regulates the active reabsorption of calcium at the DCT

20

Name Thiazide diuretics

Hydrochlorothiazide
Chlorthalidone

21

Thiazide diuretics MOA

Inhibit the NCC and promote the excretion of sodium and chloride.
Enhanced reabsorption of Ca++

22

Thiazide treatment?

Hypertension
Symptomatic treatment of HF
Nephrogenic diabetes insipidus
Prevent calcium stones

23

Thiazide adverse effects

Hypercalcemia
Hyperlipidemia
Hyperglycemia
Hyperuricemia
Increased lithium
Hyperkalemia
Hypernatremia
Sulfa allergy
Alkalosis

24

Name the K+ sparing diuretics

Triamterene
Spirinolactone
Amiloride
Eplerenone

25

Reabsorption at the collecting duct

Aldosterone exerts its effects here.
Contains principal cells.
Na/K ATPase brings sodium into the interstitium.
ENaC reabsorbs Na+ from the tubular lumen.
K+ is excreted
Alpha-intercalated cells excrete H+ via the H+ ATPase

26

Amiloride MOA

Inhibit ENaC, thus inhibiting reabsorption of Na+

27

Triamterene MOA

Inhibits ENaC

28

Eplerenone MOA

Mineralocorticoid receptor antagonist, thus inhibiting the effects of Aldosterone

29

Spirinolactone MOA

Mineralocorticoid receptor antagonist

30

Eplerenone and Spirinolactone treatment

1* or 2* Hyperaldosteronism

31

K+ Sparing diuretics treatment

Heart failure
Prevent myocardial remodeling
Nephrogenic DI
Liddle's Syndrome

32

K+ Sparing diuretics adverse effects

Hyperkalemia
Acidosis
Type 4 renal tubular acidosis
Inhibition of testosterone synthesis
Polycystic ovarian syndrome causing symptoms of androgen excess
Gynecomastia
Impotence