diuretics Flashcards

1
Q

what are diuretics commonly used for

A

HTN

heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what class of drugs is Acetazolamide

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what type of inhibition does acetazolamide produce

A

noncompetitive inhibition of the enzyme activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

they combine to form carbonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does the carbonic anhydrase enzyme do to H2C03

A

catalyzes it into C02 and water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

who do we adjust acetazolamide dosing for

A

renal patients and the elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

***acetazolamide acid base imbalance

A

alkaline urine and metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

k loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

acetazolamide what does it do to ICP

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

if acetazolamide does not decrease ICP-what treatment should occur

A

placement of ventriculoperitoneal shunt to reduce elevated ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Side Effects of Acetazolamide:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

LOOP DIURETICS

A

Furosemide, Torasemide, Azosemide, Bumetanide and Ethacrynic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

loop diuretics Inhibit reabsorption of

A

NA, K, CL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

where do loop diuretics work in the nephron

A

thick ascending limb of the loop of henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Diuretics in general and loop diuretics in particular are 1st line therapy for what patients
patients with fluid retention resulting form heart failure
26
what is a common side effect of all loop diuretics
ototoxicity
27
why dont we use ethacrynic acid
no longer in use due to increased incidence of ototoxicity and nausea and vomiting
28
furosemide % protein bound to albumin
90%
29
furosemide PO absorption varies 10-100% with average bioavailability of what %
50%
30
glomerular filtration and renal tubular secretion account for what percent of furosemide excretion
50-60%
31
furosemide remaining 40-50% is
conjugated to glucuronide in the kidneys
32
elimination furosemide half life
1-2 hours resulting in short duration of action
33
furosemide rapid onset producing diuresis is within
5-10 minutes of administration
34
peak effect of furosemide
30 minutes
35
duration of furosemide
2-6hrs
36
normal renal function furomsedie dose
40mgIV
37
what happens to the furosemide dose in renal insufficiency patients
increase dose
38
max diuresis can be achieved with IV bolus of furosemide- what mg? push slow d/t?
160-200mg | give slowly to avoid tinnitus
39
will doses larger than 200 of furosemide increase natriuresis
no
40
bumetanide bioavailability
80-100% after PO administration
41
bumetanide administration routes
IV, PO, IM
42
bumetanide how many more times potent than furosemide
40 x more potent
43
torasemide metabolism
mostly by liver
44
patients with liver failure receiving torsemide will have an increase drug delivery to which organ
kidneys
45
torasemide is how much more potent as furosemide
2x
46
torsemide duration of action
longer duration of action with plasma 1/2 life 3-4 hours thus once a day dosing
47
comparing furosemide to torsemide which is better for heart failure
Treatment with torasemide was found to decrease readmissions related to heart failure when compared to furosemide.1
48
what diuretic lowers calcium.
In the presence of symptomatic hypercalcemia, furosemide may be used to lower the plasma concentration of calcium by stimulating urine output
49
what combination decreases ICP most effectively.
A combination of furosemide and mannitol is more effective in decreasing ICP than either drug alone
50
Side Effects: loop diuretics
Normally manifest as abnormalities of fluid and electrolyte balance Hypokalemia; Digitalis Toxicity Hyperuricemia: rarely clinically significant Potential hyperglycemia not as likely as thiazides
51
braking phenomenon
Acute or chronic treatment of patients with diuretics, including loop diuretics, may result in tolerance to the diuretic effect
52
Side Effects: look diuretics relating to aminoglycosides
enhances he possible nephrotoxic effects of these antibotics
53
side effects - loop diuretics and non depolarizing neuromuscular blockers
potentiate non depolarizing neuromuscular blockade
54
loop diuretics cephalosporin
Cephalosporin nephrotoxicity may also be increased by furosemide
55
furosemide cross sensitivity
Cross sensitivity may exist when allergic to sulfonamides
56
furosemide and lithium reaction
An acute increase in lithium plasma concentrations with IV administration of furosemide in perioperative period
57
furosemide- ototoxicity
Ototoxicity is either transient or permanent; is a rare reaction and is dose dependent.
58
HCTZ and thiazide drugs
chlorthalidone and indapamide
59
thiazide diuretics what are they used for
most often used for long term treatment of hypertension in which the combination of diuresis, natriuresis, and vasodilation are synergistic
60
what is the second most frequently prescribed antihypertensive med with other antihypertensives
HCTZ
61
thiazide diuretics may be used to mobilize edema associated with what three organ dysfunction
renal hepatic cardiac dysfunction
62
thiazide diuretics less common use is
management of DI and hypercalcemia
63
are thiazide diuretics readily absorbed PO?
yes
64
HCTZ bioavailability and protein bound
60-70% bioavailability extensively protein bound.
65
thiazides are eliminated unchanged by the kidneys- except indapamide which is metabolized how
by the liver
66
thiazide diuretics half life
8-12 hours
67
thiazide diuretic with the longest elimination half life of 50-60 hrs
chlorthalidone
68
how effective is thiazide diuretics in renal patients
markedly decrease effectiveness
69
with the exception of metolazone. thiazide diuretics have what effect on severe renal insufficiency
ineffective in renal insufficiency- use loop diuretics
70
electrolyte excretion with thiazide diuretics
kaliuresis may accompany sodium and magnesium ion loss
71
with the loss of potassium and magnesium- thiazide diuretics may present with cardiac
dysrhythmias
72
side effects of thiazide diuretics
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
preop orthostatic hypotension suggest
low circulation of fluid volume
74
what is the only osmotic diuretic in use
mannitol
75
where does mannitol work
proximal real tubule and loop of henle are the principle site of action
76
how is osmotic diuretics cleared
from plasma by glomerular filtration
77
mannitol is a scavenger of free radicals which may prevent?
Is a scavenger of oxygen-free radicals, which may prevent cellular injury
78
Mannitol Clinical Uses:
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
Mannitol Clinical Uses:
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
in the setting of acute tubular necrosis- what can mannitol be used to prevent
Can be used to prevent perioperative kidney failure in the setting of acute tubular necrosis
81
patients with LV dysfunction may not tolerated mannitol leading to
pulmonary edema
82
what medication is a better choice to treat high ICP in patients with LV dysfunction
furosemide
83
in renal dysfunction mannitol is not filtered and will cause
In renal dysfunction mannitol is not filtered and will cause increase in the intravascular volume
84
Prolonged use of Mannitol may cause:
Hypovolemia Electrolyte disturbances Hypokalemic hypochloremic alkalosis Plasma hyperosmolarity due to excessive excretion of water and Na+
85
NOT INCLUDED_potassium sparing diuretics
potassium sparing diuretics