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2-Pharm Final > Diurectics > Flashcards

Diurectics Flashcards

1
Q

What do you need for heparin to work?

A

Antithrombin

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2
Q

What do diuretics block?

A

These drugs block sodium & chloride reabsorption at different sites in the nephron

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3
Q

What do diuretics increase?

A

Increases urinary sodium and water loss

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4
Q

What are diuretics used to treat? (6)

A

Used in treatment of HTN, heart failure, edematous states, hypercalcemia, renal dysfunction, & glaucoma

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5
Q

Review diuretics action at the nephron.

A
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6
Q

Where do Carbonic Anhydrase Inhibitors bind?

A

drugs bind to carbonic anhydrase in the proximal renal tubule

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7
Q

What do Carbonic Anhydrase Inhibitors result in?

A

results in decreased reabsorption of sodium, bicarbonate, & water (water & bicarbonate ion loss)

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8
Q

What is the functional unit of the kidney?

A

Nephron

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9
Q

What drugs are Carbonic Anhydrase Inhibitors?

A

acetazolamide

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10
Q

What are the clinical uses for Carbonic Anhydrase Inhibitors?

A

acetazolamide

  • decrease intraocular pressure in tx of glaucoma (decreases formation of aqueous humor
  • tx of idiopathic intracranial HTN (inhibits formation of CSF)
  • altitude sickness
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11
Q

What is the amount of sodium reabsorbed?

A
  • 2/3 at the proximal convoluted tubule
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12
Q

What are side effects of Carbonic Anhydrase Inhibitors?

A

Acetazolamide

  • metabolic acidosis (loss of bicarbonate ions)
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13
Q

What is the action of Loop Diuretics?

A

Acts by impairing the activity of the Na-K-2Cl transport protein in the ascending loop of Henle

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14
Q

How much of sodium is ascending reabsorbed at the loop of henle?

A

where 20% - 30% of Na is normally reabsorbed

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15
Q

What are we inhibiting with Loop Diuretics?

A

Inhibit reabsorption of sodium, potassium, & chloride

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16
Q

Loop diuretics are the most _____ diuretics

A

potent

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17
Q

What are the drugs of loop diuretics?

A

furosemide, torsemide, bumetanide, ethacrynic acid, azosemide

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18
Q

What is the formularies for Furosemide?

A

Oral or IV

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19
Q

What is the onset of Furosemide?

A

Fast onset of action; produces diuresis within 5-10 minutes

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20
Q

When is the peak effect of Furosemide?

A

peak effect 30 minutes

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21
Q

What is the duration of Furosemide?

A

duration of action 2 – 6 hours

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22
Q

What is the dose Furosemide in normal renal function?

A

With normal renal function, 40mg IV will produce maximal diuresis

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23
Q

What is the dose Furosemide in renal dysfunction?

A

With chronic renal insufficiency, 160mg – 200mg slow IV produces maximal diuresis, continuous infusion can also be considered instead of repeat bolus doses

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24
Q

What is the formularies of Bumetanide?

A

Can be given oral, IM, or IV

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25
Q

What is the potency of Bumetanide?

A

40 times more potent than furosemide

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26
Q

What is the clinical use of Loop Diuretics?

A

first-line therapy in patients w/fluid retention from heart failure; HTN; pulmonary edema; intracranial pressure

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27
Q

What is the most common side effect of Loop Diuretics?

A

hypokalemia

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28
Q

What are other side effects of Loop Diuretics?

A
  • Hypovolemia
  • Increase tissue concentrations of aminoglycosides enhancing nephrotoxicity
  • Potentiate nondepolarizing NMBDs
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29
Q

Patients allergic to ______ may exhibit cross-sensitivity to furosemide

A

sulfonamide drugs

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30
Q

Plasma concentrations of ____ may be acutely increased w/IV furosemide

A

lithium

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31
Q

Define components of hypokalemia and loop diuretics.

A

increases likelihood of digoxin toxicity

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32
Q

Define components of hypovolemia and loop diuretics.

A
  • should only be administered to patients w/normal or increased intravascular fluid volume
  • resulting hypotension can exacerbate renal ischemic injury
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33
Q

What do Thiazide Diuretics produce?

A

These drugs produce diuresis & Na loss by inhibiting reabsorption of Na & chloride ions in distal convoluted tubule; block Na-chloride cotransporter/water

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34
Q

What is urinary excretion of Thiazide Diuretics?

A

Urinary excretion of Na, chloride, & K ions; also stimulate reabsorption of Ca in distal convoluted tubule

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35
Q

What are drugs of Thiazide Diuretics?

A

HCTZ, chlorthalidone, metolazone

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36
Q

What is the first line use of Thiazide Diuretics?

A
  • First-line therapy for essential HTN by decreasing extracellular fluid volume & peripheral vasodilation
  • tx of calcium-containing renal calculi (stimulate Ca reabsorption)
37
Q

What is the components of Chlorthalidone?

A

longer acting, reduces risk of major cardiovascular events

38
Q

What are side effects of Thiazide Diuretics?

A
  • Hypokalemia, hypochloremia, metabolic alkalosis
  • cardiac arrhythmias d/t hypokalemia or hypomagnesemia, hypercalcemia (esp in pts receiving Ca or Vit. D supp)
39
Q

hypokalemia may predispose pts to ______

A

dig toxicity

40
Q

What are side effects of Thiazide Diuretics?

A
  • Potentiation of nondepolarizing NMBDs
  • Potentiate lithium toxicity (promote lithium reabsorption)
  • Hyperglycemia in diabetic pts
  • Hyperlipidemia
41
Q

Must consider _________ status in patients receiving thiazide diuretics & scheduled for surgery

A

fluid volume

42
Q

Patients w/ ________ may demonstrate cross-reactivity to thiazide & loop diuretics

A

Patients w/sulfa allergy may demonstrate cross-reactivity to thiazide & loop diuretics

43
Q

What is the relationship of thiazide diuretics and diabetic patients?

A

Hyperglycemia in diabetic pts (esp when used in combo w/beta blockers)

44
Q

What do Osmotic Diuretics result in?

A
  • Osmotic diuretics result in increased plasma & renal tubular fluid osmolality which results in osmotic diuresis
45
Q

Where do Osmotic Diuretics act?

A

Act primarily at proximal renal tubules & loop of Henle

46
Q

What is the osmotic drugs in clinical use?

A

mannitol

47
Q

What is the cellular effects of Osmotic Diuretic: Mannitol?

A

Increases plasma osmolarity & draws fluid from intracellular to extracellular spaces

48
Q

What does Osmotic Diuretic: Mannitol expand?

A

Acute expansion of intravascular fluid volume

49
Q

What pt population is Osmotic Diuretic: Mannitol poorly tolerated?

A

may be poorly tolerated in patients w/borderline cardiac function

50
Q

What are the clinical uses of Osmotic Diuretic: Mannitol?

A
  • Acute management of elevated ICP
  • tx of glaucoma
  • used during cardiac & major vascular surgery for renal protection
51
Q

What are the renal protection effects of mannitol?

A
  • Renal protection effects:
    • osmotic diuresis that forces casts & necrotic debris out of renal tubules
    • vasodilation of renal vasculature by release of prostaglandins which improves renal blood flow/protect kidneys from acute failure following renal tubular necrosis
    • oxygen-free radical scavenger property may prevent cellular injury
52
Q

What are side effects of Osmotic Diuretic: Mannitol?

A
  • May cause hypernatremia from water diuresis
  • May cause pulmonary edema
  • May cause hypovolemia, hypokalemia, plasma hyperosmolarity
53
Q

increased intravascular volume with Osmotic Diuretic: Mannitol in pts w/__________

A

poor LV function

  • increase risk of pulmonary edema
54
Q

Where do Potassium-Sparing Diuretics act?

A

Act on the renal collecting ducts

55
Q

NSAIDs block what?

A

Prostaglandins and this can be bad for the kidneys

56
Q

What are the two groups off Potassium-Sparing Diuretics?

A

pteridine analogues & aldosterone receptor blockers

57
Q

What are the effects of pteridine anaglogues Potassium-Sparing Diuretics?

A

prevent Na reabsorption

58
Q

What are pteridine anaglogues Potassium-Sparing Diuretics drugs?

A

triamterene & amiloride

59
Q

What is the MOA of Aldosterone antagonists Potassium-Sparing Diuretics?

A

prevent synthesis & activation of aldosterone-dependent Na-K-ATPase pump which decrease Na reabsorption without increased K excretion

60
Q

What are the drugs of Aldosterone antagonists Potassium-Sparing Diuretics?

A
  • spironolactone
  • eplerenone
  • used w/thiazide diuretic
61
Q

What are the clinical uses of Potassium-Sparing Diuretics??

A
  • tx of essential HTN (in combo w/thiazides) – prevents thiazide-induced hypokalemia & hypomagnesemia
  • promotes diuresis in patients w/edema & fluid overload asso/w hyperaldosteronism such as liver cirrhosis, nephrotic syndrome, & heart failure
62
Q

What is the effect of spironolactone with ACE-I?

A

spironolactone w/ ACE-I in tx of heart failure decreases CV morbidity & mortality

63
Q

What are the side effects of Potassium-Sparing Diuretics?

A

hyperkalemia (especially when combined w/ACE-Is or ARBs or w/NSAIDS)

64
Q

What do Dopamine Receptor Agonists result in?

A

These drugs result in natriuresis & increased renal blood flow via action on renal tubular dopamine-1 (D1) receptors

65
Q

Where is the activation of Dopamine Receptor Agonists? What does it cause?

A

Activation of D1 receptors in proximal renal tubule & loop of Henle increases cyclic AMP production resulting in inhibition of the Na-H exchange & Na-K-ATPase pump

66
Q

What do D1 receptors also mediate?

A

increased renal blood flow & increased GFR

67
Q

What is an example of D receptor agonists?

A

fenoldopam

  • fast-acting IV antihypertensive used in short-term treatment of severe HTN
  • administration results in increased renal blood flow & decreased SVR
68
Q

What is the metabolism divisions of lipoprootein?

A

exogenous & endogenous pathways

69
Q

What are the exogenous pathway of Lipidoprotein metabolism?

A

Exogenous pathway: processing of dietary fats, cholesterol, & lipid-soluble vitamins

70
Q

What are the endogenous pathway of Lipidoprotein metabolism?

A

hepatic cholesterol synthesis & its distribution to peripheral tissues

71
Q

What lipoproteins increased risk of cardiovascular disease?

A

Increased plasma concentration of total & LDL cholesterol

72
Q

What lipoproteins reduce the risk of atherosclerosis & CV events?

A

Higher HDL cholesterol levels

73
Q

What is the characteristics of lipoproteins and CAD?

A

Lowering plasma concentrations of total & LDL cholesterol w/ drugs decreases risk of cardiac events in patients with and without CAD

74
Q

Lipid-lowering agents are used to treat ___________

A

hyperlipidemia

75
Q

What is an example of Lipid-Lowering Agents?

A

Statins

76
Q

What are statins MOA?

A

Statins are competitive inhibitors of HMG-CoA reductase, the enzyme that catalyzes cholesterol biosynthesis within the liver

77
Q

What do Lipid-Lowering Agents: Statins cause?

A
  • Cause decreased cholesterol synthesis and increased LDL uptake by liver resulting in decreased LDL concentration
  • also cause increase in HDL
78
Q

What is the metabolism of Lipid-Lowering Agents: statins?

A

Hepatic metabolism – CYP3A4

79
Q

What drugs are Lipid-Lowering Agents: statins?

A

atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin

80
Q

What do Lipid-Lowering Agents: Statins stabilize?

A

Stabilize atherosclerotic plaques

81
Q

What is the properties of Lipid-Lowering Agents: Statins?

A

Antiinflammatory, antioxidant, & vasodilatory properties

82
Q

What are the skeletal muscle effects of Statins?

A
  • Statin-related myotoxicity (skeletal muscles)
    • myalgia
    • myositis
    • CPK can range between mild and extreme elevations
    • rhabdomyolysis
83
Q

Severe statin muscle-related adverse events secondary to _______

A

drug interactions

84
Q

What are the drug interactions that cause statin-Statin-related myotoxicity (skeletal muscles)?

A

Drug interactions with agents that are also metabolized by hepatic CYP450 system

85
Q

What drugs are most frequently associated with Myopathy?

A

most frequent w/ atorvastatin, simvastatin, lovastatin

86
Q

What are the CYP3A4 inhibitors that can effect statin levels?

A

CYP3A4 inhibitors (warfarin, protease inhibitors, macrolide antibiotics, azole antifungals) may increase concentration of statins & lead to myopathy

87
Q

___________ does not increase incidence of statin-induced myopathy

A

Succinylcholine

88
Q

What does hepatic dysgunctioon with statins manifest as?

A

manifests as plasma aminotransferase elevation

89
Q

What are the two primary side effects of Statins?

A
  • Statin-related myotoxicity (skeletal muscles)
  • Hepatic dysfunction

2-Pharm Final (10 decks)

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