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RUSVM Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What are diuretic drugs typically used to treat?

A

Edema (localized or generalized0

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2
Q

What are the main classes of diuretic drugs?

A 
Osmotic diuretic 
Loop direct 
Thiazides diuretics 
Potassium -sparking 
Carbonic-anhydrase inhibitor
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3
Q

What is the MOA of osmotic diuretics?

A

Filtered at glomerulus and poorly reabsorbed in nephron -> water stays in nephrons with the drug -> urine volume increased

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4
Q

what is the osmotic diuretic?

A

Mannitol

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5
Q

How is mannitol administered?

A

IV (can crystallized at room temp)

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6
Q

Does mannitol enter the CNS or eye?

A

Nope

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7
Q

What drug is used to manage acute cerebral edema and acute glaucoma?

A

Mannitol

Osmotically draws water out of these compartment back to the circulating blood

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8
Q

When is use of mannitol contraindicated?

A

If BBB or BOB is disrupted and mannitol enters this compartment –> worsen edema

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9
Q

What is the MOA of loop diuretics?

A

Inhibit Na/K/2Cl cotransporter at the luminal membrane of the tick ascending Loop of Henle

Sodium is not reabsorbed -> water stays in the nephron –> increased urine

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10
Q

Loops diuretics inhibit reabsorption of _________ and increases _______ loss, in addition to its effect on sodium and water.

A

Ca and Mg; K and H

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11
Q

What is the drug of choice to treat pulmonary edema/acute pulmonary edema ?

A

Furosemide

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12
Q

What drugs is used for treatment of exercise induced pulmonary hemorrhage in horse?

A

Furosemide

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13
Q

What diuretic drug would be useful in treatment of hypercalcemia ?

A

Furosemide

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14
Q

What are adverse effects to furosemide use?

A

Fluid and electrolyte imbalances (cats more sensitive than dog)
Chronically -> metabolic ALKALOSIS, hypocalcemia, hypomagnesium, hyponatermia, hyperuricemia
Ototoxicity (esp in cats)

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15
Q

When is use of furosemide contraindicated?

A

Dehydrated patients

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16
Q

What is the MOA of thiazide diuretics

A

Inhibiting Na/Cl symporter in the early part of the distal convoluted tubule -> less Na and Cl reabsorption -> less water reabsorbed -> diuretics

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17
Q

Which has more diuretic effect, thiazide or loop diuretic?

A

Loop diuretic (25% of water reabsorption in the loop vs 5% in distal convoluted tubule j

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18
Q

Are thiazide diuretics potassium wasting or potassium sparing?

A

Potassium wasting -> can lead to hypokalemia

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19
Q

What are side effects of this aside diuretics?

A

Inhibit conversion of proinsulin to insulin -> hyperglycemia

Fluid and electrolyte imbalances (less severe than furosemide )

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20
Q

T/F: furosemide and hydrochlorothiazide decrease calcium absorption, therefore hypercalcemia can be a side effect

A

F

Furosemide decreases calcium -> hypocalcemia

Hydrochlorothiazide increase calcium -> hypercalcemia

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21
Q

What drug can be used to treat edema, treat nephrogenic diabetes insipidus, and manage calcium oxalate urolithiasis?

A

Hydrochlorothiazide

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22
Q

What are precautions to using hydrochlorothiazide ?

A

Fluid and electrolyte imbalances
Dehydration
Hyponatermia, hypokalemia, hypomagnesemia, hyperuricemia, metabolic ALKALOSIS

Hypercalcemia
Hyperglycemia

23
Q

Spironolactone is what type of drug?

A

Potassium-sparing diuretic

24
Q

What is the MOA of spironolactone?

A

Reduce aldosterone-mediated Na/K exchange in late distal convoluted tubule -> Na/Cl loss and K reabsorption

25
Q

What drug is sometimes used to manage ascites or treat mineralocortocoid producing tumors?

A

Spironolactone

26
Q

What are precautions to using spironolactone ?

A

Can lead to HYPERkalemia especially if used in combination with ACE inhibitors

Metabolic ACIDOSIS

Block androgens
Block mineralocorticoids

27
Q

In what patients is spironolactone contraindicated?

A

Addison’s disease (hypoadrenocorticism) -> blocks mineralocorticoids

28
Q

What type of drug in amiloride?

A

Potassium-sparing diuretics

29
Q

What is the MOA of amilordie ?

A

Block Na reabsorption in distal convoluted tubule and in the collecting duct -> Na blocked -> reduced the net driving force for K secretion

30
Q

What are cautions to using amiloride?

A

HYPERkalemia

Metabolic acidosis

31
Q

What drug is a carbonic anhydrase inhibitor?

A

Acetazolamide

32
Q

What is the MOA of acetazolamide?

A

Reversible inhibition of carbonic anhydrase (CA) in proximal convoluted tubule and collecting duct -> inhibit exchange of Na for H

33
Q

What is the main use of carbonic anhydrase inhibitors

A

Decrease aqueous humor production in eye -> decrease IOP for treatment of glaucoma

34
Q

What are the topical carbonic anhydrase inhibitors used for glaucoma treatment?

A

Dorzolamide
Brinzolamide
Sulfonamides derivatives

35
Q

When should acetazolamide not be used ?

A

Significant renal/hepatic disease

Hypoadrenocorticism, hyponatremia, hypokalemia, or hyperchloremic acidosis, other electrolyte imbalances

36
Q

Acetazolamide can increase ammonia levels. What drug can bind these ions for excretion?

A

Lactulose

37
Q

Explain RAAS

A

Low BP or hyponatremia-> renin (juxtaglomular cells) -> covert angiotensinogen to angiotensin I -> vasoconstriction and aldosterone release -> aldosterone increase water reabsorption

38
Q

How is renin secretion inhibited?

A

Local or systemic hypertension

Antigotenin II (pos feedback)
ADH, increased Na
B-adrenergic blockers

39
Q

What is the function of angiotensin II ?

A

Vasoconstriction

Stimulate aldosterone secretion
Positive feedback to inhibit renin

40
Q

What are the ACE- inhibitors?

A

Enalaril

Benazepril

41
Q

How are enalapril and benazepril administered?

A

Oral

42
Q

How are Enalapril and Benazepril excreted?

A

Enalapril - 95% at kidney

Benazepril - 45% kidney and 55% liver

43
Q

What are the indications to using ACE-inhibitors?

A

Secondary physiological effects of chronic heart failure

Systemic hypertension

Protein losing neuropathy

44
Q

What are cautions to using ACE inhibitors

A

In animals with renal insufficiency> lower doses

Not in critically ill renal failure patients

Monitor

Hyperkalemia

45
Q

What is the action of ADH in the body?

A

Normally secreted in response to decreased vascular volume -> work on V2 receptors in collecting ducts -> increase water reabsorption through aquaporins -> increase vascular volume

46
Q

What are the two types of diabetes insipidus?

A

Central ->. Decreased secretion of ADH (pituitary)

Nephrogenic -> ADH is secreted but kidney is not responding

47
Q

What is the hallmark of diabetes insipidus?

A 
PU/PD 
Hyposethenuric urine (more dilute than plasma)
48
Q

What do we use to treat central DI?

A

Desmopressin - synthetic ADH analog

49
Q

What can be used in a dose-dependent manner to increase plasma factor VIII to manage von Willebrands disease?

A

Desmopressin

50
Q

How is desmopressin administered?

A

Topically on conjunctiva

51
Q

Can desmopressin be administered orally?

A

Yes. But is broken down in GI tract -> low oral bioavailability -> dose needs to be much higher if given orally

52
Q

Do you do a water deprivation test to determine central vs neprhogenic DI?

A

NO

Dr. BOOTS SAYS NO!

53
Q

How can you determine central vs nephrogenic DI?

A

Give desmopressin

  • > concentrated urine = central
  • > still no concentration = nephrogenic
54
Q

How do you treat nephron DI?

A

Thiazides diuretics (hydrochlorothiazide) -> help reduce clinical symptoms (polyuria) upregulate aquaporin in collecting duct

RUSVM Pharmacology (18 decks)

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