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SUM '20 - Pharm II > diuretics > Flashcards

diuretics Flashcards

1
Q

what are diuretics commonly used for

A

HTN

heart failure

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2
Q

diuretics sit of action

A

upstream of the collecting duct. =hyponatremia, hypokalemia and metabolic alkalosis.

in collecting duct result in hyperkalemia and metabolic acidosis

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3
Q

what class of drugs is Acetazolamide

A

prototype of a class of sulfonamide drugs that- avidly bind to the enzyme carbonic anhydrase

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4
Q

what type of inhibition does acetazolamide produce

A

noncompetitive inhibition of the enzyme activity

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5
Q

in normal circumstances- what is the carbonic anhydrase enzyme responsible for in the renal tubule

A

NA+/H+ exchanger- allowing absorption of NA in exchange for secretion of H+ into the renal tubule

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6
Q

in normal circumstances what happens to bicarb and H in the proximal renal tubule

A

they combine to form carbonic acid

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7
Q

what does the carbonic anhydrase enzyme do to H2C03

A

catalyzes it into C02 and water

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8
Q

c02 diffuses readily into the tubular cells where cytoplasmic carbonic anhydrase catalyses the reverse reaction leading to

A

Hc03- and absorption of HC03

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9
Q

carbonic anhydrase inhibitors do what

A

inhibit carbonic anhydrase in the proximal renal tubule by this class of diuretics results in decreased reabsorption of Na, HC03, an water

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10
Q

who do we adjust acetazolamide dosing for

A

renal patients and the elderly

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11
Q

acetazolamide blocks what in the proximal tubule

A

membrane bound and cytoplasmic carbonic anhydrase in the proximal tubule-preventing na and HC03 absorption

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12
Q

***acetazolamide acid base imbalance

A

alkaline urine and metabolic acidosis

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13
Q

***acetazolamide increase in delivery of sodium to the distal tubules leads to

A

k loss

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14
Q

how is acetazolamide effective in the treatment of glaucoma

A

high concentration of carbonic anhydrase enzyme in the ciliary processes, inhibition of the enzyme activity by acetazolamide results in decreased formation of aqueous humor and consequently a decrease in intraocular pressure.

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15
Q

acetazolamide what does it do to ICP

A

cerebral spinal fluid formation is inhibited by acetazolamide- treatment for idiopathic intracranial hypertension.

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16
Q

if acetazolamide does not decrease ICP-what treatment should occur

A

placement of ventriculoperitoneal shunt to reduce elevated ICP

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17
Q

acetazolamide produces metabolic acidosis- what might it do to the respiratory drive

A

it may stimulate the respiratory drive in patients who are hyperventilating in a compensatory response to respiratory alkalosis- such as in altitude sickness

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18
Q

hypoxia at high altitudes is counteracted by hyperventilating which results in respiratory alkalosis resulting in ventilation depression. what can we give to reverse this hypoventilaiton

A

acetazolamide induced metabolic acidosis can reverse hypoventilation.

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19
Q

***The loss of bicarbonate ions necessary to buffer carbon dioxide may result in the exacerbation of respiratory acidosis in patients with COPD leading to CNS depression

A

.

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20
Q

Side Effects of Acetazolamide:

A

Fatigue
Decreased appetite
Depression
Paresthesia (could be secondary to metabolic acidosis)

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21
Q

LOOP DIURETICS

A

Furosemide, Torasemide, Azosemide, Bumetanide and Ethacrynic acid

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22
Q

loop diuretics Inhibit reabsorption of

A

NA, K, CL

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23
Q

where do loop diuretics work in the nephron

A

thick ascending limb of the loop of henle

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24
Q

the thick ascending limb of the loop of henle- is impermeable to water and accounts for the reabsorption of how much filtered na

A

20-30%

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25
Q

Diuretics in general and loop diuretics in particular are 1st line therapy for what patients

A

patients with fluid retention resulting form heart failure

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26
Q

what is a common side effect of all loop diuretics

A

ototoxicity

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27
Q

why dont we use ethacrynic acid

A

no longer in use due to increased incidence of ototoxicity and nausea and vomiting

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28
Q

furosemide % protein bound to albumin

A

90%

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29
Q

furosemide PO absorption varies 10-100% with average bioavailability of what %

A

50%

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30
Q

glomerular filtration and renal tubular secretion account for what percent of furosemide excretion

A

50-60%

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31
Q

furosemide remaining 40-50% is

A

conjugated to glucuronide in the kidneys

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32
Q

elimination furosemide half life

A

1-2 hours resulting in short duration of action

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33
Q

furosemide rapid onset producing diuresis is within

A

5-10 minutes of administration

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34
Q

peak effect of furosemide

A

30 minutes

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35
Q

duration of furosemide

A

2-6hrs

36
Q

normal renal function furomsedie dose

A

40mgIV

37
Q

what happens to the furosemide dose in renal insufficiency patients

A

increase dose

38
Q

max diuresis can be achieved with IV bolus of furosemide- what mg?
push slow d/t?

A

160-200mg

give slowly to avoid tinnitus

39
Q

will doses larger than 200 of furosemide increase natriuresis

A

no

40
Q

bumetanide bioavailability

A

80-100% after PO administration

41
Q

bumetanide administration routes

A

IV, PO, IM

42
Q

bumetanide how many more times potent than furosemide

A

40 x more potent

43
Q

torasemide metabolism

A

mostly by liver

44
Q

patients with liver failure receiving torsemide will have an increase drug delivery to which organ

A

kidneys

45
Q

torasemide is how much more potent as furosemide

A

2x

46
Q

torsemide duration of action

A

longer duration of action with plasma 1/2 life 3-4 hours thus once a day dosing

47
Q

comparing furosemide to torsemide which is better for heart failure

A

Treatment with torasemide was found to decrease readmissions related to heart failure when compared to furosemide.1

48
Q

what diuretic lowers calcium.

A

In the presence of symptomatic hypercalcemia, furosemide may be used to lower the plasma concentration of calcium by stimulating urine output

49
Q

what combination decreases ICP most effectively.

A

A combination of furosemide and mannitol is more effective in decreasing ICP than either drug alone

50
Q

Side Effects: loop diuretics

A

Normally manifest as abnormalities of fluid and electrolyte balance
Hypokalemia; Digitalis Toxicity
Hyperuricemia: rarely clinically significant
Potential hyperglycemia not as likely as thiazides

51
Q

braking phenomenon

A

Acute or chronic treatment of patients with diuretics, including loop diuretics, may result in tolerance to the diuretic effect

52
Q

Side Effects: look diuretics relating to aminoglycosides

A

enhances he possible nephrotoxic effects of these antibotics

53
Q

side effects - loop diuretics and non depolarizing neuromuscular blockers

A

potentiate non depolarizing neuromuscular blockade

54
Q

loop diuretics cephalosporin

A

Cephalosporin nephrotoxicity may also be increased by furosemide

55
Q

furosemide cross sensitivity

A

Cross sensitivity may exist when allergic to sulfonamides

56
Q

furosemide and lithium reaction

A

An acute increase in lithium plasma concentrations with IV administration of furosemide in perioperative period

57
Q

furosemide- ototoxicity

A

Ototoxicity is either transient or permanent; is a rare reaction and is dose dependent.

58
Q

HCTZ and thiazide drugs

A

chlorthalidone and indapamide

59
Q

thiazide diuretics what are they used for

A

most often used for long term treatment of hypertension in which the combination of diuresis, natriuresis, and vasodilation are synergistic

60
Q

what is the second most frequently prescribed antihypertensive med with other antihypertensives

A

HCTZ

61
Q

thiazide diuretics may be used to mobilize edema associated with what three organ dysfunction

A

renal
hepatic
cardiac dysfunction

62
Q

thiazide diuretics less common use is

A

management of DI and hypercalcemia

63
Q

are thiazide diuretics readily absorbed PO?

A

yes

64
Q

HCTZ bioavailability and protein bound

A

60-70% bioavailability extensively protein bound.

65
Q

thiazides are eliminated unchanged by the kidneys- except indapamide which is metabolized how

A

by the liver

66
Q

thiazide diuretics half life

A

8-12 hours

67
Q

thiazide diuretic with the longest elimination half life of 50-60 hrs

A

chlorthalidone

68
Q

how effective is thiazide diuretics in renal patients

A

markedly decrease effectiveness

69
Q

with the exception of metolazone. thiazide diuretics have what effect on severe renal insufficiency

A

ineffective in renal insufficiency- use loop diuretics

70
Q

electrolyte excretion with thiazide diuretics

A

kaliuresis may accompany sodium and magnesium ion loss

71
Q

with the loss of potassium and magnesium- thiazide diuretics may present with cardiac

A

dysrhythmias

72
Q

side effects of thiazide diuretics

A

Hypercalcemia especially if on supplements
Potentiate NDMB by producing hypokalemia
Effectiveness is decreased when patient is taking NSAIDS
Potentiates lithium toxicity
May cause glucose intolerance and aggravate glucose control in diabetics
May aggravate hyperlipidemia
Patients with sulfa allergy may demonstrate cross-reactivity to these classes of diuretics

73
Q

preop orthostatic hypotension suggest

A

low circulation of fluid volume

74
Q

what is the only osmotic diuretic in use

A

mannitol

75
Q

where does mannitol work

A

proximal real tubule and loop of henle are the principle site of action

76
Q

how is osmotic diuretics cleared

A

from plasma by glomerular filtration

77
Q

mannitol is a scavenger of free radicals which may prevent?

A

Is a scavenger of oxygen-free radicals, which may prevent cellular injury

78
Q

Mannitol Clinical Uses:

A

Primarily used in the acute management of elevated ICP and in treatment of glaucoma
Exerts effect within 10-15 minutes
Peak effect at 30-45 minutes
Duration of 6 hours

79
Q

Mannitol Clinical Uses:

A

Effect on ICP is dose dependent: larger dose may last longer
Large doses up to 2g/kg and repeated administration can result in metabolic derangements
Intact blood-brain barrier is necessary for cerebral effects of Mannitol
Non-intact blood-brain barrier may enter the brain, drawing fluid with it and causing worsening cerebral edema
Rebound increase in ICP may occur following mannitol use

80
Q

in the setting of acute tubular necrosis- what can mannitol be used to prevent

A

Can be used to prevent perioperative kidney failure in the setting of acute tubular necrosis

81
Q

patients with LV dysfunction may not tolerated mannitol leading to

A

pulmonary edema

82
Q

what medication is a better choice to treat high ICP in patients with LV dysfunction

A

furosemide

83
Q

in renal dysfunction mannitol is not filtered and will cause

A

In renal dysfunction mannitol is not filtered and will cause increase in the intravascular volume

84
Q

Prolonged use of Mannitol may cause:

A

Hypovolemia
Electrolyte disturbances
Hypokalemic hypochloremic alkalosis
Plasma hyperosmolarity due to excessive excretion of water and Na+

85
Q

NOT INCLUDED_potassium sparing diuretics

A

potassium sparing diuretics

SUM '20 - Pharm II (30 decks)

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