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Pharm > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Which loop diuretic does not have a sulphonamide structure?

A

Ethacrynic acid

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2
Q

MOA of carbonic anhydrase inhibitors (CAIs)

A

When PCT lumen CA is inhibited, no H+ is formed in the cytosol and no Na+ and HCO3- is absorbed into the cells.
At the collecting tube, Na+ concentration is increased (because it was not absorbed at the PCT) and principle cells absorb it, while secreting K+ –> hypokalemia
The intercalated A cells of the collecting tube are unable to secrete H+ into the urine because CA is inhibited and so less NH4+ is excreted –> acidosis
On the basolateral membrane of the intercalated A cell, the bicarbonate/Cl- anti porter is inhibited, preventing Cl- excretion in the urine –> hyperchloremic acidosis

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3
Q

What are the uses of CAIs?

A

Glaucoma: oral acetazolamide or topical dorzolamide decrease aqueous humor formation
Urinary alkalization
Metabolic acidosis
Mountain sickness: above 3000m pt may have respiratory alkalosis (weak, dizziness, headache, insomnia) which can be treated with a CAI

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4
Q

ADR of CAIs

A

Hyperchloremic metabolic acidosis
Renal stones due to increased urine phosphate and Ca2+
Hypokalemia
Decreased urine NH4+ excretion, which can worsen hepatic coma
Cross-allergy with sulfonamide

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5
Q

When are CAIs contraindicated?

A

Hepatic encephalopathy

Sulfonamide allergy

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6
Q

MOA of loop diuretics

A

Na+/K+/2Cl- pump is inhibited at the thick ascending limb of LOH
Loss of 25% of Na+ in the urine
Lack of K+ in the cytosol leads to less K+ entering the lumen through leaky channels which inhibits the positive potential of the lumen that usually drives Mg2+ and Ca2+ reabsorption (via paracellular pathway) –> Mg2+ and Ca2+ are lost in urine
At the collecting tube, Na+ concentration is increased (because it was not reabsorbed at the TAL) and principle cells absorb it, while secreting K+ –> hypokalemia
The intercalated A cells of the collecting tube take back the lost K+ in exchange for H+ secretion –> blood alkalosis

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7
Q

Loop diuretics can be used for:

A 
Hyperkalemia 
Hypercalcemia
Acute renal failure
Acute heart failure
Hypertension emergency
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8
Q

Loop diuretics are contraindicated in:

A

Sulphonamide allergy

Acute gout

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9
Q

Which drugs are CAIs?

A

Acetazolamide

Dorzolamide

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10
Q

Which drugs are loop diuretics?

A

Furosemide
Bumetanide
Torsemide
Ethacrynic acid

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11
Q

ADR of loop diuretics

A

Hypokalemic metabolic alkalosis
Ototoxicity: worse if combined with aminoglycoside
Hyperuricemia: H+ competes with uric acid to be secreted (so increased H+ secretion leads to reduced uric acid secretion). As well, hypovolemia increases uric acid reabsorption in the PCT.
Hypomagnesemia
Cross-allergy with sulphonamide (except ethacrynic acid) –> skin rash

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12
Q

Thiazides MOA

A

Thiazides block the action of the Na+/Cl- cotransporter in the DCT –> 10% NaCl is lost in urine.
Na+ in the cytosol is reduced and so the Na+/Ca2+ anti porter on the basolateral membrane is activated by PTH leading to increased Ca2+ reabsorption.
At the collecting tube, Na+ concentration is increased (because it was not reabsorbed at the DCT) and principle cells absorb it, while secreting K+ –> hypokalemia
The intercalated A cells of the collecting tube take back the lost K+ in exchange for H+ secretion –> blood alkalosis

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13
Q

How can thiazides be used?

A

Hypertension: in the short term, they decrease BP. In the long term after about 6 months, they directly decrease vessel tension possibly due to K+ channel opening.
Kidney stone or hypercalciuria (Ca2+ is now in the blood, not the urine, so stones are less likely to form in the lumen)
Nephrogenic diabetes insipidus (unknown mechanism)
Chronic heart failure

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14
Q

ADR of thiazides

A

Hypokalemic metabolic alkalosis
Hyperuricemia: H+ competes with uric acid to be secreted (so increased H+ secretion leads to reduced uric acid secretion)
Hyperglycemia: hypokalemia decreases insulin release from the pancreas islet beta cells and impairs insulin sensitivity
Hyperlipidemia
Hyponatremia
Cross-allergy to sulphonamide

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15
Q

Thiazides are contraindicated in:

A

Sulfonamide allergy

Acute gout

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16
Q

Which are the most affective diuretics?

A

Loop diuretics

17
Q

MOA of aldosterone antagonists

A

Bind to and block aldosterone receptor in the collecting tubule, reducing the expression of genes controlling synthesis of apical ENaC.
Less Na+ is reabsorbed into the cytosol, reducing the action of the basolateral Na+/K+ ATPase.
There is no loss of K+ –> hyperkalemia
Hyperkalemia reduces the action of the H+/K+ pump on the lumenal membrane of the intercalated A cells, inhibiting H+ excretion –> blood acidosis
Additionally, HCO3-/Cl- antiporter is inhibited in the intercalated A cell –> hyperchloremia

18
Q

Which potassium sparing diuretics are aldosterone antagonists?

A

Spironolactone

Eplerenone

19
Q

Which potassium sparing diuretics are direct ENaC inhibitors?

A

Amiloride

Triamterene

20
Q

MOA of ENaC inhibitors

A

Block ENaC channels in the collecting tubule.
Less Na+ is reabsorbed into the cytosol, reducing the action of the basolateral Na+/K+ ATPase.
There is no loss of K+ –> hyperkalemia
Hyperkalemia reduces the action of the H+/K+ pump on the lumenal membrane of the intercalated A cells, inhibiting H+ excretion –> blood acidosis
Additionally, HCO3-/Cl- antiporter is inhibited in the intercalated A cell –> hyperchloremia

21
Q

Uses of potassium sparing diuretics

A

Hypokalemia caused by loop diuretics and thiazides

Aldosteronism: Conn’s syndrome, cirrhosis, heart failure

22
Q

What special feature do spironolactone and eplerenone have in heart failure?

A

Decrease chronic heart failure mortality

23
Q

ADR of potassium sparing diuretics

A

Hyperkalemia (extreme caution needed when given along with an ACEI)
Hyperchloremic metabolic acidosis

24
Q

What is an ADR specific to spironolactone?

A

Gynecomastia, loss of libido and impotence in men due to it’s anti androgenic effects

25
Q

Mannitol MOA

A

Osmotic diuretic
Freely filtered in the glomerulus but poorly reabsorbed so it remains in the lumen and acts as an osmotic force pulling water into the lumen with it.
Major location of action is the PCT and descending LOH

26
Q

How is mannitol administered

A

IV injection

Does not cross BBB

27
Q

Mannitol is indicated in:

A

Cerebral edema
Glaucoma
Acute renal failure

28
Q

Effects of mannitol

A

Urine volume is increased within 3h to more than 50mL/h
Most filtered solutes will be excreted in larger amounts (especially Na+) because increased urine flow reduces the time of contact between electrolytes and the epithelium
Can reduce brain volume and intracranial pressure by osmotically extracting water from tissue into the blood

29
Q

Side effects of mannitol

A

ECF expansion prior to diureses (first 3h) so caution must be taken in heart failure
Dehydration, hperkalemia, hypernatremia
Hyponatremia

30
Q

ADH agonists MOA

A

ADH activates V2 receptors (Gs) –> increased cAMP causes insertion of additional aquaporin water channels into the luminal membrane of the tubule –> increased water reabsorption

31
Q

What are ADH and desmopressin used to treat?

A

Neurogenic diabetes insipidus

32
Q

MOA of ADH antagonists

A

Demeclocycline, lithium and conivaptan
Inhibit the action of ADH and therefore inhibit the insertion of aquaporins into the luminal membrane
Reduce water reabsorption

33
Q

What do ADH antagonists treat?

A

SIADH

34
Q

Which drug treats lithium-induced diabetes insipidus?

A

Amiloride

Blocks lithium reuptake into the collecting duct cells from the lumen because lithium has a similar structure to Na+

35
Q

Which drug treats nephrogenic diabetes insipidus?

A

Chlorothiazide

36
Q

Which drugs are used to treat kidney stones?

A

Thiazides (increase reabsorption of Ca2+

37
Q

Which drugs should NOT be used in kidney stones?

A

Loop diuretics

Pharm (7 decks)

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