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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
list the compounds that are related to thiazide diuretics
* chlorthalidone * metolazone * quinethazone * indapamide
26
MOA of thiazide diuretics
* **inhibit Na+ reabsorption** at the distal convoluted tubule * inhibit the **NCC** (Na+-Cl- co-transporter) * this effect is dependent on PGI synthesis
27
Thiazides are the DOC for what two conditions
* HTN * CHF
28
indications for thiazide diuretics
* **HTN, CHF** * **Nephrolithiasis** (kidney stone) * decrease Ca2+ in the urine * **Nephrogenic diabetes insipidus**
29
Which diuretic is responsible for an **increase in ATP-dependent K+ channel opening**? What are the effects?
* Thiazide diuretic * causes hyperpolarization of cell membranes * beneficial effects: relaxation of smooth muscle -\> vasodilation * adverse effects: reduced insulin secretion
30
which diuretic causes reduced insulin secretion? How?
* thiazide * increases ATP-dependent K+ channel opening * beta cells in pancreas are hyperpolarized and causes decrease in insulin release
31
thiazide effect on calcium
* **decrease Ca2+ excretion** * increase acitivity of PTH dependent Ca2+ channels * an increase in luminal Na+ -\> increases cell membrane potential -\> **increased Ca2+ reabsorbtion**
32
What is unique of indapamide in terms of how it is excreted
indapamide is excreted by biliary system, therefore is useful in patients with renal insufficiency
33
adverse effects of thiazide
* **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
all thiazides cause elevated serum lipid levels except
indapamide
35
Contraindications/Precautions of thiazide diuretics
* sulfonamide hypersensitivity * CI in **Diabetics** * due to hyperglycemia * acute gouty attacks * Hypercalcemia * Blood Dyscrasias * Necrotizing vasculitis * lithium toxicity
36
what is unique about Metolazone
* able to produce **diuresis in patients with a reduced GFR** * (i.e \< 20mL/min) * most thiazides don't work at low GFR
37
name three things that are unique about indapamide
* causes pronounced vasodilation * does not increase plasma lipids * metabolized in the liver
38
What are the two classes of potassium sparing diuretics
* aldosterone antagonists * direct inhibitors of Na+ flux
39
What is the major use of potassium sparing diuretics
* 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
name the aldosterone antagonist
* spironolactone * Eplerenone
41
MOA of spironolactone
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
indications of spironolactone
* edema associated with CHF, cirrhosis, nephrotic syndrome * most effective: treating **hyperaldosteronism**
43
adverse effects of spironolactone
* hyperkalemia * Gynecomastia
44
contraindications/precautions: spironolactone
* hyperkalemia * chronic renal insufficiency * liver damage
45
which drug is a selective aldosterone receptor antagonist (SARA)
Eplerenone
46
what is unique about Eplerenone
* has spironolactone effects but **decreases the incidence of endocrine related side effects**
47
Eplerenone metabolized by
CYP3A4: many drug interactions
48
Name the potassium sparing diuretics that are direct inhibitors of Na+ flux
* Amiloride * Triamterene
49
MOA of Amiloride and Triamterene
* inhibit Na+/K+ ion exchange mechanism independent of aldosterone * MOA * directly inhibit aldosterone sensitive Na+ channel * leads to decrease in K+ excretion
50
indications of Amiloride and Triamterene
* combination with K+ losing diuretics
51
what is the only diuretic class that does not cause hyperuricemia
Amiloride and Triamterene: they are not acids
52
DOC: Li+ induced diabetes insipidus
Amiloride
53
adverse effects of Amiloride and Triamterene
* Hyperkalemia
54
Contraindications: Amiloride and Triamterene
* don't use in burn patients -\> they are already hyperkalemic -\> arrhythmias
55
List the osmotic diuretics
* mannitol * Isosorbide * Glycerin * Urea
56
route of admission of osmotic diuretics
IV only!! * if given orally -\> diarrhea
57
MOA of osmotic diuretics
* filtered but not reabsorbed by the kidneys * keeps water in tubules
58
indications for osmotic diuretics
* prophylaxis of acute renal failure * decrease intraoccular pressure * decrease intracranial pressure * protect kidney
59
excessive administration of osmotic diuretics can cause
* extracellular volume expansion * pulmonary edema in CHF * excessive cellular dehydration
60
What is Desmopressin
ADH agonist
61
indications of desmopressin
* treats symptoms of central diabetes insipidus
62
List the ADH antagonists
* Conivaptan * Tolvaptan * Demeclocycline, Lithium (use of these has been discontinued with development of vaptans)
63
MOA of Conivaptan
* non-peptide V1 and V2 receptor antagonist * increase Na+ concentrations and increase free H2O clearance
64
indications of Conivaptan
* treatment of euvolemic or hypervolemic hyponatremia in hospitalized patients * euvolemic: ex: SIADH, hypothyroidism
65
route of admission of Conivaptan
IV only
66
adverse effects of Conivaptan
hypokalemia
67
contraindication of Conivaptan
* hyponatremia associated with **hypovolemia**
68
What is unique about Tolvaptan
* similar to conivaptan except * V2 receptor antagonist * administered orally
69
MOA of demeclocycline
blocks V2 receptor 2nd messenger system -\> nonspecific -\> many side effects
70
order of the expected maximum diuretic effect
* loop \>\> thiazide \>\> CA inhibitors \>\> K+ sparing

pharm II exam 2 (9 decks)

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