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pharm II exam 2 > Diuretics > Flashcards

Diuretics Flashcards

1
Q

How is sodium actively transported in the proximal tubule

A
  • apical
    • NHE: Na+/H+ exchange
  • basolateral
    • NaHCO3
    • NaCl
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2
Q

Where is calcium reabsorbed in the nephron? What hormones increases reabsorption?

A
  • distal convoluted tubule
  • parathyroid
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3
Q

anything less than what size is filtered in the glomerulus

A

< 43 kD

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4
Q

site of aldosterone action

A
  • principle cells in distal convuluted tubule and collecting duct
  • Na+/K+ ATPase
  • apical Na+ channel
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5
Q

what occurs in a-intercalated cells

A
  • reabsorb K+, secrete H+
  • H+ ATPase
  • H+,K+ ATP
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6
Q

Site of potassium secretion? Which drugs have an effect

A
  • secretion: distal tubules
    • Na+/K+ exchange
    • with or without aldosterone
    • can be modified by aldosterone-antagonists and K+ sparing diuretics
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7
Q

Thiazide diuretics have what effect on calcium

A

increase calcium reabsorption

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8
Q

loop diuretics have what effect on calcium

A

increase calcium and magnesium excretion

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9
Q

will weak bases in alkaline solution in the urine be more likely to be excreted or reabsorbed

A

weak bases in alkaline solution are less ionized -> more permeable -> less excretion

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10
Q

acids are secreted and reabsorbed via what mechanism

A

carrier dependent mechanism

  • * acidic drug will compete with uric acid for carrier and causes increase in uric acid -> gout
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11
Q

Name the carbonic anhydrase inhibitors

A
  • Acetazolamide
  • Dorzolamide
  • Brinzolamide
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12
Q

MOA of carbonic anhydrase inhibitors? site of action?

A
  • inhibits carbonic anhydrase
  • H2CO3 production is blocked: H2O + CO2 -> H2CO3
  • decreases H+ for exchange with Na+ resultin gin a increased Na+ and H2O loss
  • *site of action: proximal convoluted tubule
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13
Q

indications for using carbonic anhydrase inhibitors

A
  1. alkalinization of the urine (increase HCO3- in urine)
  2. glaucoma
    • topical: inhibition of bicarbonate transport in the eye and the choroid plexus -> decreases aqueous humor and CSF production
  3. alkalosis
    • metabolic
    • acute mountain sickness
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14
Q

diuretic effectiveness of carbonic anhydrase inhibitors

A

decreases in a several days

  • mechanism of drug is lack of H+ inside cell, but cells’ mitochondria will make H+
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15
Q

adverse effects of carbonic anhydrase inhibitors

A
  1. hypercholoremic metabolic acidosis
    • ​​Na+ loss is in the form of NaHCO3
  2. hypokalemia
    • increased presence of Na+ in lumen -> increases Na+/K+ exchange in DCT
  3. hyperuricemia
    • competing for uric acid secretion
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16
Q

contraindications of carbonic anhydrase inhibitors

A
  • hepatic cirrhosis
    • (decreased ammonia excretion)
  • sulfonamide hypersensitivity
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17
Q

name the loop diuretics

A
  • Furosemide (lasix)
  • Bumetanide
  • Torsemide
  • Ethacrynic acid
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18
Q

MOA of loop diuretics

A
  1. blocks the NKCC2 transporter in the thick ascending limb
  2. induce kidney Prostaglandins
    • decreases salt transport in kidney
    • vasodilation
      • renal and systemic
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19
Q

indications: loop diuretics

A
  • CHF
  • pulmonary edema
    • relieve pulmonary congestion by increasing systemic venous capacitance
    • PGI reduces preload to the heart thus reducing BP in the RV which reduces pulmonary pressure
  • hypercalcemia
    • decrease reabsorption of Mg2+ and Ca2+ by reducing the K+ gradient
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20
Q

adverse effects of loop diuretics

A
  • hypokalemic metabolic alkalosis
    • induce K+ and H+ loss
  • hypochloremia
    • direct loss of Cl- by pump inhibition
  • hypocalcemia and hypomagnesemia
  • hyperuricemia
  • irreversible ototoxicity
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21
Q

which diuretic has the worse ototoxicity?

A
  • Ethacrynic acid
  • don’t give with aminoglycosides
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22
Q

Contraindications/precautions: Loop diuretics

A
  • sulfonamide hypersensitivity
  • drug interactions
    • COX inhibitors (NSAIDs, ASA) may interfere with loop diuretics actions where PGI synthesis is required (vasodilation)
    • aminoglycosides: increase ototoxicity
    • Lithium
    • Digoxin
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23
Q

All loop diuretics have a sulfonamide hypersensitivity except

A

ethacrynic acid

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24
Q

List the thiazide diuretics

A
  • Hydrochlorothiazide
  • Chlorothiazide
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25
Q

list the compounds that are related to thiazide diuretics

A
  • chlorthalidone
  • metolazone
  • quinethazone
  • indapamide
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26
Q

MOA of thiazide diuretics

A
  • inhibit Na+ reabsorption at the distal convoluted tubule
    • inhibit the NCC (Na+-Cl- co-transporter)
    • this effect is dependent on PGI synthesis
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27
Q

Thiazides are the DOC for what two conditions

A
  • HTN
  • CHF
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28
Q

indications for thiazide diuretics

A
  • HTN, CHF
  • Nephrolithiasis (kidney stone)
    • decrease Ca2+ in the urine
  • Nephrogenic diabetes insipidus
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29
Q

Which diuretic is responsible for an increase in ATP-dependent K+ channel opening? What are the effects?

A
  • Thiazide diuretic
  • causes hyperpolarization of cell membranes
    • beneficial effects: relaxation of smooth muscle -> vasodilation
    • adverse effects: reduced insulin secretion
30
Q

which diuretic causes reduced insulin secretion? How?

A
  • thiazide
  • increases ATP-dependent K+ channel opening
    • beta cells in pancreas are hyperpolarized and causes decrease in insulin release
31
Q

thiazide effect on calcium

A
  • decrease Ca2+ excretion
    • increase acitivity of PTH dependent Ca2+ channels
    • an increase in luminal Na+ -> increases cell membrane potential -> increased Ca2+ reabsorbtion
32
Q

What is unique of indapamide in terms of how it is excreted

A

indapamide is excreted by biliary system, therefore is useful in patients with renal insufficiency

33
Q

adverse effects of thiazide

A
  • Hypokalemic metabolic alkalosis
    • induce K+ and H+ loss at the distal exchange sites for Na+
    • cause plasma volume contraction -> stimulates aldosterone -> encourages potassium loss
  • Hyperuricemia
    • they are acids and compete for uric acid excretion
  • Hypomagnesemia
  • Hyperglycemia
  • elevated serum lipid levels (except indapamide)
    • due to decreased insulin levels
34
Q

all thiazides cause elevated serum lipid levels except

A

indapamide

35
Q

Contraindications/Precautions of thiazide diuretics

A
  • sulfonamide hypersensitivity
  • CI in Diabetics
    • due to hyperglycemia
  • acute gouty attacks
  • Hypercalcemia
  • Blood Dyscrasias
  • Necrotizing vasculitis
  • lithium toxicity
36
Q

what is unique about Metolazone

A
  • able to produce diuresis in patients with a reduced GFR
    • (i.e < 20mL/min)
    • most thiazides don’t work at low GFR
37
Q

name three things that are unique about indapamide

A
  • causes pronounced vasodilation
  • does not increase plasma lipids
  • metabolized in the liver
38
Q

What are the two classes of potassium sparing diuretics

A
  • aldosterone antagonists
  • direct inhibitors of Na+ flux
39
Q

What is the major use of potassium sparing diuretics

A
  • they are weak diuretics by themselves
  • used in combination with other K+ loosing drugs to minimize K+ loss and minimize alkalosis by other diuretics
40
Q

name the aldosterone antagonist

A
  • spironolactone
  • Eplerenone
41
Q

MOA of spironolactone

A
  1. competitive inhibitor of aldosterone
    • promotes the excretion of Na+ and retention of K+ at the collecting tube
      • less Na+ channels
      • blocked Na+ conductance -> hyperpolarized cell -> decreased K+ excretion
      • decrease Na+-K+ ATPase activity -> decreases K+ secretion and excretion
42
Q

indications of spironolactone

A
  • edema associated with CHF, cirrhosis, nephrotic syndrome
  • most effective: treating hyperaldosteronism
43
Q

adverse effects of spironolactone

A
  • hyperkalemia
  • Gynecomastia
44
Q

contraindications/precautions: spironolactone

A
  • hyperkalemia
  • chronic renal insufficiency
  • liver damage
45
Q

which drug is a selective aldosterone receptor antagonist (SARA)

A

Eplerenone

46
Q

what is unique about Eplerenone

A
  • has spironolactone effects but decreases the incidence of endocrine related side effects
47
Q

Eplerenone metabolized by

A

CYP3A4: many drug interactions

48
Q

Name the potassium sparing diuretics that are direct inhibitors of Na+ flux

A
  • Amiloride
  • Triamterene
49
Q

MOA of Amiloride and Triamterene

A
  • inhibit Na+/K+ ion exchange mechanism independent of aldosterone
    • MOA
      • directly inhibit aldosterone sensitive Na+ channel
      • leads to decrease in K+ excretion
50
Q

indications of Amiloride and Triamterene

A
  • combination with K+ losing diuretics
51
Q

what is the only diuretic class that does not cause hyperuricemia

A

Amiloride and Triamterene: they are not acids

52
Q

DOC: Li+ induced diabetes insipidus

A

Amiloride

53
Q

adverse effects of Amiloride and Triamterene

A
  • Hyperkalemia
54
Q

Contraindications: Amiloride and Triamterene

A
  • don’t use in burn patients -> they are already hyperkalemic -> arrhythmias
55
Q

List the osmotic diuretics

A
  • mannitol
  • Isosorbide
  • Glycerin
  • Urea
56
Q

route of admission of osmotic diuretics

A

IV only!!

  • if given orally -> diarrhea
57
Q

MOA of osmotic diuretics

A
  • filtered but not reabsorbed by the kidneys
  • keeps water in tubules
58
Q

indications for osmotic diuretics

A
  • prophylaxis of acute renal failure
  • decrease intraoccular pressure
  • decrease intracranial pressure
  • protect kidney
59
Q

excessive administration of osmotic diuretics can cause

A
  • extracellular volume expansion
    • pulmonary edema in CHF
    • excessive cellular dehydration
60
Q

What is Desmopressin

A

ADH agonist

61
Q

indications of desmopressin

A
  • treats symptoms of central diabetes insipidus
62
Q

List the ADH antagonists

A
  • Conivaptan
  • Tolvaptan
  • Demeclocycline, Lithium (use of these has been discontinued with development of vaptans)
63
Q

MOA of Conivaptan

A
  • non-peptide V1 and V2 receptor antagonist
  • increase Na+ concentrations and increase free H2O clearance
64
Q

indications of Conivaptan

A
  • treatment of euvolemic or hypervolemic hyponatremia in hospitalized patients
    • euvolemic: ex: SIADH, hypothyroidism
65
Q

route of admission of Conivaptan

A

IV only

66
Q

adverse effects of Conivaptan

A

hypokalemia

67
Q

contraindication of Conivaptan

A
  • hyponatremia associated with hypovolemia
68
Q

What is unique about Tolvaptan

A
  • similar to conivaptan except
    • V2 receptor antagonist
    • administered orally
69
Q

MOA of demeclocycline

A

blocks V2 receptor 2nd messenger system -> nonspecific -> many side effects

70
Q

order of the expected maximum diuretic effect

A
  • loop >> thiazide >> CA inhibitors >> K+ sparing

pharm II exam 2 (9 decks)

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