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Flashcards in Pharmacology of Diuretics Deck (19):
1

1. Identify the sites along the nephron where the principal classes of diuretic drugs work.

acetazolamide (carbonic anhydrase inhibition) and osmotic agents (mannitol) in PCT

loop agents (furosemide) block NKCC in thick ascending limb

thiazides (HCTZ) block the Na/Cl channel in DCT

aldosterone antagonists block in the collecting duct

ADH antagonists block action of ADH in the collecting ducts

2

2. List three side effects of thiazide-class diuretic drugs whose mechanism you can explain and three side effects that can't explain.

1. postural hypertension
2. extreme sodium depletion
3. deplete total body potassium, cause hypokalemia
4. depletion of body Mg: tremors, twitches, cardiac arrhythmias, nausea and psychiatric concurs
5. renal failure aggravated (decrease blood volume and reduce GFR)

1. hyperuricema
2. decreased glucose tolerance
3. hyperlipidemia
4. reduce renal excretion of calcium
5. pancreatitis
6. sulfa allergy and sun sensitivity
7. hepatorenal syndrome
8. impotence

3

3. List three side effects of loop-class diuretic drugs whose mechanism you can explain and three side effects that can't be explained.

1. volume depletion, postural hypotension
2. profuse urination
3. deplete total body sodium and ADH secretion
4. low K+- muscle cramps and weakness, cardiac arrhythmias (esp with digitalis)
5. alkalosis (H+ is lost with K+ in DCT)
6. Mg and Ca are lost
7. threaten reduce by reducing material blood flow to utero placental unit

1. increased blood levels of uric acid, glucose and cholesterol (gout, DM and CAD)
2.reversible deafness
3. allergic retains, sensitize to sun burns (sulfa allergy)
4. induce pancreatitis
5. hepatorenal syndrome: liver and kidneys deteriorate quickly together

4

4. Describe the principal side effects of the potassium-sparring diuretics.

high serum potassium (hyperkalemia)- fatal, causing cardiac arrest, esp in patients with renal disease or DM, or patients taking ACE or ARB

gynecomastia, menstrual irregularities: anti-androgenic properties (increase estrogen)

high doses case nausea and other GI sym

5

5. State one combination of two diuretic drugs in which the combination increases the diuretic effect of either drug alone.

aldosterone antagonists can be use with thiazide drugs to min or prevent hypokalemia and hypmagnesemia more effectually than potassium supplements

thiazides and loops are ideal synergists with ACEI and ARBs

tihiazides and loops are also a good combination, potassium sparing diuretic is a logical 3rd addition

6

Amiloride

potassium-sparer

directly inhibit the mechanism where Na/K exchange takes place by blocking ENaC, working whether aldosterone is present, still reduces loss of K, Mg and protons
good tx. of Little's disease

take care of hyperkalemia, endocrine disturbances, nausea

7

Bumetanide

loop diuretic, better absorbed than furosamide and is more potent

work in ascending limb to inhibit Na/Cl reabsorption by blocking NKCC

"high ceiling" - max effect is large

inhibits reabsorption of Mg++ and Ca++ due to disturbed gradient

8

Eplerenone.

potassium-sparer
competitive inhibitor of aldosterone: reduce the activity of the sodium-potassium (magnesium and proton exchange site in the collecting duct)
reduce fibrosis of the heart and vessels
take care of hyperkalemia, endocrine disturbances, nausea

many less side effects than spirolactone

9

Furosemide.

loop diuretic (Lasix)
work in ascending limb to inhibit Na/Cl reabsorption via blocking NKCC

"high ceiling" - max effect is large

inhibits reabsorption of Mg++ and Ca++ due to disturbed gradient

limit ability to concentrate urine, destroy loop gradient

10

Hydrochlorothiazide

thiazide diuretic that increases sodium and water excretion by inhibiting Na/Cl cotransporter, protaglandins contribute to action, probably by causing vasodilation of renal vessels (blunted by NSAIDs)

"low ceiling"

thiazides eliminate the racial different in responsiveness to ACE-inhibitor

11

Spironolactone

potassium-sparer
(magnesium and proton exchange site in the collecting duct)
reduce fibrosis of the heart and vessels
competitive inhibitor of aldosterone
take care of hyperkalemia, endocrine disturbances, nausea

12

Triamterene

K sparring

directly inhibit the mechanism where Na/K exchange takes place by blocking ENaC, working whether aldosterone is present, still reduces loss of K, Mg and protons

13

List therapeutic uses for loop diuretics.

mobilize edema fluid
reduce arterial and venous blood pressure
palliate congestive heart failure
lower plasma K+ and Ca++ contraptions and reduce total body K+
increase plasma sodium concentration

14

Give conditions where a thiazide would be more or less effective than a loop.

thiazides are gentler, loops more brisk
thizides have better efficacy than loops in HTN
loops retain efficacy at low GFR unlike thiazides

15

How do diuretics effect edema?

shrink intravasulcar volume, hydrostatic pressure inside capillaries goes down and osmotic pressure goes up: reducing extra vascular fluid

16

Describe the mechanism of diuretics ability to reduce edema, and blood pressure immediate/long term

can reduce peripheral edema by reducing hydrostatic pressure and increasing oncotic pressure

in the short term thiazide have direct effect on veins, causing release of prostaglandins

unclear how it maintains low BP when long term volume compensation is complete (must include Na some how because Na ingestion negates effects)

17

What is the niche of mannitol?

seldom used to treat edema, heart failure or HTN

used to reduce edema in brain or eye

18

Give the unique benefits of
Chlorthalidone
Metalazone
Indapamide
Torasemide.

Chlorthaliadone- more efficacious then HCTZ
Metolazone: daily dosing
Indapamide- direct vasodilating, less hyperglycemia
Torsemide: lest potassium loss

19

Describe the drug interactions with :
lithium
NSAIDs
digitalis
antibiotics

thiazides reduce excretion of lithium
NSAIds reduce diuretic effectiveness
digitalis, increase hypokalemia
ototoxicity can be exaggerated with loop diuretics