Diuretics Flashcards

1
Q

What are diuretics

A

Drugs that increase rate of urine flow

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2
Q

What are natriuresis

A

Drugs that increase excretion of sodium

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3
Q

Main effect of diuretics

A

Decrease reabsorption of sodium and chloride

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4
Q

Clinical application of diuretic

A

Reduce extracellular fluid volume

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5
Q

Type of diuretics

A
Carbonic anhydride inhibitors
Loop diuretics 
Thiazide diuretics
Potassium sparing diuretics
Osmotic diuretics
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6
Q

Site of action of carbonic anhydrase inhibitors

A

Proximal convoluted tubule

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7
Q

Site of action of osmotic diuretics

A

Proximal convoluted tubule

Thin descending limb

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8
Q

Site of action of loop diuretics

A

Thick ascending limb

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9
Q

Sites of action of thiazide diuretics

A

Distal convoluted tubule

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10
Q

Site of action of potassium sparing diuretics

A

Cortical collecting tubule

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11
Q

Why is the enzyme carbonic anhydrase important

A

key role in sodium bicarbonate reabsorption and H+ secretion

breakdown of H2 CO3 -> co2 H2O in the lumen

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12
Q

What is the action of the carbonate anhydrase inhibitors

A

Inhibit both luminal and Cytoplasmic carbonic anhydrase Decreasing the absorption of sodium bicarbonate in the proximal tubule

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13
Q

Examples of carbonic anhydrase inhibitors

A

Acetazolamide
Dichlorphenamide
Methazolamide

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14
Q

How are carbonic Anhydraseinhibitors administered

A

Per os

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15
Q

In which segment of the proximal convoluted table are carbonic anhydrase inhibitors excreted

A

S2

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16
Q

Time needed for a change in urine pH after carbonic anhydrase inhibitors administration and time of action

A

Requires 30 to 120 minutes and persist for two hours

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17
Q

Should you reduce carbonic anhydrase inhibitors dose when there is renal insufficiency

A

Yes

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18
Q

Clinical uses of carbonic anhydrase inhibitors

A

Urine alkalinization
Glaucoma
Metabolic alkalosis

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19
Q

Carbonic anhydrase inhibitors unwanted effect

A

Metabolic acidosis due to chronic low bicarbonate
Potassium wasting
Paresthesia ,drowsiness, hypersensitivity reactions

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20
Q

Contra indication of carbonic anhydrase inhibitors

A

Patients with cirrhosis because of risk of. Hyperammonemia and. Hepatic encephalopathy

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21
Q

Mode of action of loop diuretics

A

Inhibition of sodium potassium chloride symporter at the thick ascending limb Preventing reabsorption of sodium potassium and chloride andWhich
also inhibit calcium and magnesium reabsorption

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22
Q

Loop diuretics examples

A
Furosemide 
Bumetanide 
Etacrynic acid 
 torsemide
Piretanide
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23
Q

furosemide metabolism

A

65% Excreted unchanged in urine

Rest conjugated to glucuronic acid

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24
Q

Metabolism of bumetanide and torse I de

A

Hepatic metabolism

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25
Loop diuretics have long or short half life
Short
26
What is the postdiuretic sodium retention effects
When there is decline of concentration of the loop diuretic there’s direct reabsorption of sodium occurring
27
Clinical uses of loop diuretics
``` Acute pulmonary edema chronic congestive heart failure Management of hypertension nephritic syndrome edema treatments associated with chronic renal insufficiency edema treatments Treatment of hepatic cirrhosis ```
28
Unwanted effects of loop diuretics
``` Hypokalemia Hypomagnesemia Hypocalcemia Ototoxicity Hyperuricemia Hyponatremia ```
29
Which of the loop diuretics mostly close ototoxicityf
Etacrynic acid
30
Loop diuretics contraindications
Patient allergic to sulfonamides should avoid loop diuretics with a sulfonamide base
31
Action of thiazide diuretics
Inhibits the sodium chloride symporter other distal convoluted tubule’s Increases excretion of sodium chloride and water
32
Examples of thiazide diuretics
``` Bendroflumethiazide Chlorothiazide Trichlormethiazide Hydrochlorothiazide Hydroflumethiazide Polythiazide ```
33
Examples of thiazides like diuretics
Indapamide Metolazone Quinethazone Chlorthalidone
34
Can you administer all thiazide per os
Yes
35
With which compound do thiazide diuretics compete with for secretion
Uric acid
36
Clinical uses of thiazide diuretics
Edema treatments in cases of. Congestive heart failure ,cirrhosis,nephritic syndrome
37
Unwanted effects of thiazide diuretics
Fatal Hyponatremia
38
thiazide diuretics contraindications
Patience hypersensitive to sulfonamides or congeners should avoid
39
What of action of potassium sparing diuretics
Reduced sodium reabsorption in the distal convoluted table and collecting tubules by antagonizing aldosterone and blocking sodium channels
40
Potassium sparing diuretics responsible for antagonizing aldosterone
Spironolactone | Eplerone
41
Potassium sparing diuretics responsible for blocking sodium channels
Amiloride | triamterene
42
Action of spironolactone
Block binding of aldosterone to its Cytoplasmic receptor -> Increases sodium excretion with chloride and water and decrees potassium secretion
43
Is spironolactone a strong or a weak diarrhetic
A weak diuretic
44
Amiloride and triamterene action
Decrease luminal membrane sodium permeability -> Increase excretion of sodium chloride and water , decreases potassium secretion
45
Where is s spironolactone absorbed
In the G.I. tract
46
Metabolism of spironolactone
Metabolized in the liver
47
What is Canrenone
An active metabolites of spironolactone with a long half-life of 16.5 hours
48
Is Amiloride poorly or well absorbed
Poorly
49
How is Amiloride excreted
By urinary excretion of unchanged drug
50
Time of action of Amiloride
Peaks at six hours | Duration of 24 hours
51
Is triamterene well or poorly absorbed in git
Well
52
Triamterene metabolism
Metabolized to active form 4hydroxytriamterene sulfate and excreted in urine
53
Action time of triamterene
Onset within two hours | duration of 12 to 16 hours
54
Clinical uses of potassium sparing diuretics
``` Hertz failure primary hyperaldosteronism( conns syndrome) Secondary hyperaldosteronism ```
55
Unwanted effects of potassium sparing diuretics
Hyperkalemia | Effect on steroid receptor causing gynecomastia ,impotence ,libido, menstrual irregularities
56
Contraindication of potassium sparing diuretics
Hyperkalemia patient
57
Osmotic diuretics mode of action
Retain water in luminal fluid and increased osmolarity of blood and renal filtrate
58
Osmotic diuretics examples
Glycerin isosorbide Mannitol urea
59
Murder of administration of osmotic diuretics
Parenterally
60
Is there a metabolism of osmotic diuretics
No
61
How long does it take to eliminate osmotic diuretics
30 to 60 minutes
62
Can you call uses of osmotic diuretics
Prophylaxis against acute renal failure treatment of raised intracranial pressure or cerebral edema raised intraocular pressure or glaucoma
63
Unwanted effects of osmotic diuretics
Increased extracellular fluid volume hyponatremia Dehydration Nausea headache vomiting
64
Why is there diuretics resistance
Increased sodium chlorite reabsorption downstream of segments of diuretic action Retention of sodium until next dose of diuretic when there is decline of diuretic concentration Compensatory mechanism through renin-angiotensin aldosterone system and SNS Decreased GI absorption and secretion into TUBULAR SITE leading to failure of drug to reach tubular sites
65
How do you manage diuretics resistance
Rule out diuretics noncompliance Reduce salt intake Increase diuretics dosage Inhibits different nephron sites through combination therapy Optimize treatment of underlying disorder Consider IV administration
66
What type of combination of diuretic it’s possible
Loop diuretics and thiazide | Potassium sparing + loop + thiazides
67
Which thiazides it is mostly used in combination with loop agents
Metolazone
68
Do you need potassium supplement Tatian in combination of metolazone with loop diuretics
Yes because of hypokalemia
69
When can you give a combination of potassium sparing plus loop and thiazide diuretics When should you avoid it
To prevent hypokalemia To avoid impatient with renal insufficiency