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Pharmacology II Exam 2 (Lauren) > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Thiazide diuretics (increase/decrease) calcium reabsorption

A

Increase

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2
Q

Loop diuretics (increase/decrease) calcium and magnesium excretion

A

Increase

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3
Q

What effect do acidic drugs have on uric acid excretion?

A

They compete for excretion with uric acid, so they may cause hyperuricemia —> gout

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4
Q

What are the 3 Carbonic Anhydrase Inhibitors?

A

Acetazolamide (Diamox)

Dorzolamide (Trusopt) eyedrop

Brinzolamide (Azopt) eyedrop

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5
Q

What is the MOA of Carbonic Anhydrase Inhibitors?

A
  1. Block Carbonic Anhydrase enzyme
  2. Prevents production of bicarb
  3. H+ can’t exchange with Na+ in the urine so more Na+ and H2O are lost in the urine
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6
Q

What are the 3 indications for Carbonic Anhydrase Inhibitors?

A
  1. Glaucoma- decreases aqueous humor and CSF
  2. Alkalinization of the urine (more bicarb in urine)
  3. Alkalosis (metabolic and respiratory/Acute Mountain Sickness)

(WOW WHY ISN’T HTN OR EDEMA ON HERE????? ISNT THIS THE DIURETIC LECTURE!!??)

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7
Q

How long do Carbonic Anhydrase Inhibitors work as diuretics?

A

Only a few days

Reason we don’t use it as a diuretic

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8
Q

Weak bases are (more/less) ionized in alkaline environments

A

Less ionized.

Which makes it easier for them to diffuse across membranes

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9
Q

What are the adverse effects of Carbonic Anhydrase Inhibitors?

A

Hyperchloremic Metabolic Acidosis

Hypokalemia

Hyperuricemia

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10
Q

Why do CA Inhibitors cause hyperchloremic metabolic acidosis?

A

The Na+ loss is in the form of NaHCO3, not NaCl.

=you’re losing bicarb

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11
Q

Why do CA inhibitors cause hypokalemia?

A

More Na+ is in the lumen which causes an increased Na/K exchange further down the line

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12
Q

Why do CA inhibitors cause hyperuricemia?

A

They are acids and compete for uric acid secretion

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13
Q

What are the 4 Loop Diuretics?

A

Furosemide (Lasix)

Bumetanide

Torsemide

Ethacrynic Acid

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14
Q

What is the MOA of Loop Diuretics?

A
  1. Block NKCC2 cotransporter
  2. Induce kidney prostaglandins which decreases salt reabsorption
  3. Vasodilation- due to the prostaglandins
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15
Q

What are the indications for Loop Diuretics?

A

Heart Failure

Pulmonary Edema

Peripheral Edema

Hypercalcemia

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16
Q

How do loop diuretics relieve pulmonary congestion?

A

By increasing systemic venous capacitance

NOT because of fluid loss!!!**

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17
Q

What are the adverse effects of loop diuretics?

A

Hypokalemic metabolic alkalosis (induces K+ and H+ loss)

Hypocalcemia and hypomagnesemia

Hyperuricemia (loops are acids)

Irreversible ototoxicity**

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18
Q

Which loop diuretic is the worst at causing ototoxicity?

A

Ethacrynic acid**

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19
Q

What other drug will make the ototoxicity of loop diuretics even worse?

A

Aminoglycosides

Streptomycin, tobramycin, neomycin, amikacin, gentamycin in case you forgot

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20
Q

Which loop diuretic is NOT a sulfonamide and is OK for patients with Sulfa allergies?

A

Ethacrynic acid***

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21
Q

What other drug should not be combined with loop diuretics due to the risk of fatal hypokalemia?

A

Digoxin

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22
Q

What makes ethacrynic acid (Edecrin) different from the other loop diuretics?

A

It is not a sulfonamide derivative

It has the highest risk of ototoxicity

*100% chance this is on the test

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23
Q

Your patient has profound edema and your choices are Lasix and Ethacrynic Acid. Which one should you use?

A

Use lasix unless he has a sulfa allergy

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24
Q

What are the 2 thiazides and the 4 compounds released to thiazides?

A

Thiazides:
Hydrochlorothiazide

Chlorothiazides

Related compounds:
Chlorthalidone
Metolazone
Quinethazone
Indapamide

(You have to know the related compounds too)

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25
Q

What is the MOA of thiazide diuretics?

A

Inhibition of sodium reabsorption at the early distal tubule.

Also increases ATP-dependent K+ channel opening which hyperpolarizes membranes=vasodilation (as well as decreased insulin release because these K+ channels are in the pancreas too)

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26
Q

What are the indications of thiazides?

A

Hypertension

Heart failure

27
Q

What are the effects of thiazides causing increased ATP-dependent K+ channel opening?

A

Vasodilation

Reduced insulin secretion***** (pancreas also uses those ATP dependent K+ channels)BAD THING

28
Q

What effect do thiazides have on Calcium reabsorption?

A

Increased calcium reabsorption

29
Q

How could thiazides help prevent kidney stones?

A

They increase calcium reabsorption= less calcium in the urine

30
Q

Which thiazide drug is NOT metabolized by the kidneys?

A

Indapamide

***

31
Q

Which thiazide has the longest duration of action due to its slow absorption?

A

Chlorthalidone** this apparently makes it the ~preferred~ thiazide

32
Q

What are the sided effects of thiazides?

A

Hypokalemic metabolic alkalosis (induce K+ and H+ loss, and causes volume contraction= aldosterone secretion and more K+ loss)

Hyperuricemia

Magnesium loss

HYPERGLYCEMIA

Elevated serum lipid levels (except indapamide)

33
Q

Which class of diuretics is NOT ok to give to patients with Type II diabetes?

A

Thiazides

They decrease insulin release and increase glucose intolerance

34
Q

Why do thiazides cause elevated lipid levels?

A

Because they decrease insulin release

Impedes the usage of glucose for energy, so lipid stores get activated

35
Q

How is indapamide different from the other thiazides?

A
  • excreted by biliary system in addition to kidneys, so its useful for patients with bad kidneys
  • does not elevate lipid levels
36
Q

If a patient is on lithium, what class of diuretics can he not take?

A

Thiazides- aggravate lithium toxicity

37
Q

What are the contraindications/precautions to thiazides?

A

Sulfa allergy

NSAID use may decrease action

Hypokalemia can cause Digitalis toxicity

DIABETES (contraindication**)

Hyperuricemia (may cause gout)

38
Q

Can thiazides work in patients with low GFR?

A

Only Metolazone. All others are useless in a low GFR

39
Q

What are the 2 unique thiazides?

A

Metolazone- works at low GFR

Indapamide- doesn’t increase lipids and is metabolized by liver and kidneys 50/50

40
Q

Do loop diuretics work if a patient has a low GFR?

A

YES

41
Q

Are potassium sparing diuretics strong or weak diuretics?

A

Weak. They are used in combo with thiazides or loops.

42
Q

What are the 4 potassium sparing diuretics?

A

Amiloride (Midamor)

Triamterene (Dyrenium)

Aldosterone antagonists:
Spironolactone (Aldactone)

Eplerenone (Inspra)

43
Q

What is the MOA of spironolactone?

A

Competitive inhibitor of aldosterone**

(Less Na+ channels in the late distal tubule and collecting duct bringing Na+ in from urine, so less K+ will be excreted into the urine=
Leads to decreased K+ excretion)

44
Q

What is the most effective drug for treating hyperalodteronism

A

Spironolactone

45
Q

How does spironolactone affect men and women differently?

A

Women- cures hirsutism 🧔🏼->👩🏼

Men- gynecomastia 🥥🥥

(Due to spironolactone being an androgen receptor antagonist)
*****this is definitely gonna be on the test)

46
Q

What are the indications for spironolactone?

A

Edema

Hyperaldosteronism

Eliminate need for K+ supplements for patients on loops or thiazides

Hirsutism

47
Q

What are the adverse effects of spironolactone?

A

Gynecomastia

Hyperkalemia (especially when combined with ACE/ARBs)

NOT TOO BAD

48
Q

What is the difference between Eplerenone and spironolactone?

A

Won’t cause Gynecomastia in men

More drug interactions since its metabolized by CYP3A4

49
Q

True or False:

Amiloride and Triamterene depend on aldosterone

A

False

They are independent of aldosterone

50
Q

What is the MOA of Amiloride and Triamterene?

A

Directly inhibit the aldosterone sensitive Na+ channel (ENaC)

Leads to decreased K+ excretion

51
Q

What is the main use for Amiloride and Triamterene?

A
  • Combination with K+ losing diuretics

- Amiloride is the DOC for Lithium induced diabetes insipidus

52
Q

What is the only class of diuretics that are not acids, and will not cause hyperuricemia

A

Amiloride and Triamterene

53
Q

What is the only serious toxicity of Amiloride and Triamterene?

A

Hyperkalemia

54
Q

Who can NOT have potassium-sparing diuretics?

A

Burn patients (have hyperkalemia)

55
Q

What are the 4 osmotic diuretics?

A

Mannitol

Isosorbide

Glycerin

Urea

56
Q

How are osmotic diuretics administered?

A

IV only!!

If you take them orally you get diarrhea 💩

57
Q

What is the MOA of osmotic diuretics?

A

Keep water in the tubules and causes diuresis

58
Q

What are the indications of osmotic diuretics?

A

Prevents acute renal failure (keeps water flowing through tubules if flow is getting dangerously low)

Decrease intraocular pressure before eye surgery

Decrease intracranial pressure

Protect kidney against nephrotoxic substances

59
Q

What are the adverse effects of osmotic diuretics?

A

Dehydration

Large doses cause ECF volume expansion- cellular dehydration and pulmonary edema in heart failure

60
Q

Who can NOT have osmotic diuretics?

A

People in heart failure

Because they can cause pulmonary edema via an ECF volume expansion i don’t remember the physiology of this

61
Q

what is the only ADH agonist we talked about

A

Desmopressin

It is synthetic ADH

62
Q

Desmopressin (synthetic ADH) can be used to treat (central/nephrogenic) diabetes insipidus

A

Central*****

63
Q

What are the ADH antagonists?

A

Conivaptan

Tolvaptan

Lithium NOT ON TEST

Demeclocycline NOT ON TEST

64
Q

What class of diuretics have the strongest diuretic effect?

A

Loops

Pharmacology II Exam 2 (Lauren) (9 decks)

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