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Kidney physiology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

What is the underlying principle of a diuretic drug?

A

Increase rate of urine production

Increase presence of osmotically active particles in the urine

Water follows

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2
Q

What two classes of diuretic is there?

A

Osmotic

Naturiuetics

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3
Q

What underpins an osmotic diuretic?

A

Injected intravenously. Raises the osmotic pressure of the urine and draws additional water into it.

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4
Q

What underpins a naturiuetic diuretic?

A

Increase the amount of sodium in the urine, and water is excreted along with the extra sodium.

Often target pumps that reabsorb Na+

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5
Q

What are the three key types of naturiuetics?

A

Loop diuretic
Thiazide diuretic
Potassium sparing diuretic

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6
Q

What are the three key therapeutic objectives of diuretics?

A

Reduce ECV (thus lower afterload and reduce strain on failing heart)
Reduce oedema
Vasodilate

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7
Q

Why are diuretics good for treating heart failure?

A

Decrease afterload (lower ECV, vasodilation)

Reduce preload (reduced venous return due to venodilation)

Starling curve pushed back into normal range

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8
Q

What are key side effects of diuretics?

A

Hypotension
Increases sympathetic drive
Electrolyte disturbances

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9
Q

Why do diuretics cause hypotension?

A

Reduce ECV and some vasodilate

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10
Q

Why do diuretics raise sympathetic drive?

A

Activated baroreceptor reflex due to hypotension

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11
Q

What is the main electrolyte disturbance that diuretics cause?

A

Potassium loss

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12
Q

Which two types of diuretic cause potassium loss?

A

Loop diuretics and thiazides

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13
Q

Why do diuretics cause potassium loss?

A

Increased Na/KATPase activity

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14
Q

What two factors upregulate the Na/KATPase leading to potassium loss?

A

Increased sodium in the distal nephron (diuretic) leads to additional sodium being reabsorbed in CD Na/KATPase, K+ lost to urine

Diuretic drug activates the juxtaglomerular apparatus - renin release. Renin leads to release of aldosterone -increase in activity of the Na/K-ATPase

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15
Q

Which diuretic is more potent thus leading to greater potassium loss?

A

Loop

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16
Q

What is an example of a commonly used loop diuretic?

A

Furosemide

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17
Q

Why do loop diuretics have a short 1/2 life?

A

They are actively excreted in the proximal tubule as well as being filtered at the glomerulus

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18
Q

What is the principle action of loop diuretics like furosemide?

A

Inhibit the Na/K/2Cl transporter (NKCC2) in the thick ascending limb of the loop of Henle

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19
Q

Why does blocking of NKCC2 by furosemide result in diuresis?

A

Reduction of sodium absorption in the loop

More sodium is delivered to the distal tubule; reducing the osmotic gradient for water reabsorption in the collecting duct.

Osmotic potential of the interstitium is lower than usual, reducing the potential for water absorption in the collecting duct.

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20
Q

What function other than diuresis do loop diuretics have?

A

Vasodilation

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21
Q

Which vessels vasodilate in response to furosemide?

A

Systemic resistance arterioles
Renal resistance arterioles
Vasa recta

22
Q

Why does vasodilation of the vasa recta increase diuresis?

A

Results in washing out of the interstitium, lowers osmotically active substances, less water reabsorbed

23
Q

Why does vasodilation of the renal resistance vessels increase diuresis?

A

Increased GFR, potentially increases diuresis

24
Q

Is inhibition of NKCC2 the main reason behind loop diuretics causing hypokalemia?

A

No

25
Q

Why is inhibition of NKCC2 not the main reason behind loop diuretics causing hypokalemia?

A

Most of the K+ pumped out of lumen by NKCC2 leaks back.

Instead the potassium is lost at the distal tubule

26
Q

Are thiazide less or more potent than loop diuretics?

A

Less

27
Q

What is a key example of a thiazide?

A

Bendroflumethiazide

28
Q

Where do thiazides act?

A

DCT

29
Q

What do thiazide diuretics inhibit?

A

NCC on the apical surface of DCT epithelia

30
Q

What action does NCC have?

A

Movement of Na+ and Cl- coupled across the apical membrane

31
Q

Why does inhibition of NCC by thiazide drugs cause diuresis?

A 
More sodium (and Cl-) remains in the lumen.
Less water is reabsorbed
32
Q

Thiazide and loop diuretics have the opposite effect on Ca2+ excretion. What is it?

A

Loop diuretics increases excretion of Ca2+

Thiazide diuretics reduce excretion of Ca2+

33
Q

What is the principle action of potassium sparing diuretics?

A

Aldosterone antagonists

34
Q

What two ways can postassium sparing diuretics act?

A

Antagonise mineralocorticoid receptors

Block ion channels such as ENaC inhibits sodium reabsorption

35
Q

Which drug is an example of a potassium sparing diuretic that antagonises mineralocorticoid receptors?

A

Spironolactone

36
Q

Which drug is an example of a potassium sparing diuretic that blocks ENaC?

A

Amiloride

37
Q

When are potassium sparing diuretics used (3 examples)?

A

When aldosterone levels are elevated by disease (reduced renal perfusion, hypertension, raised sympathetic drive)

When aldosterone levels are elevated in a compensatory response to diuretic therapy: the diuresis activates the juxtaglomerular apparatus, which releases renin and causes the production of aldosterone

Reduce risk of hypokalemia

38
Q

What niche example often requires use of osmotic diuretics?

A

Cerebral oedema

39
Q

What is the only currently used osmotic diuretic?

A

Mannitol

40
Q

What is the mechanism of action of an osmotic diuretic?

A

An osmotic diuretic is infused into the blood (through a venous cannula).

It should (temporarily) increase the osmotic pressure of the plasma, causing water to move out of the inflamed area and into the blood.

Filtered at the glomerulus and so it moves from the blood into the urine , taking water with it

Prevents reabsorption in the proximal tubule, by increasing the osmotic potential within the lumen and so opposing the movement of water out of the lumen.

41
Q

Why is it essential for mannitol to be filtered at the glomerulus?

A

So it moves from the blood into the urine, taking water with it and so effectively clearing the water from the inflamed area into the urine.

42
Q

What substances can act as endogenous osmotic diuretics in disease?

A

Glucose (diabetes mellitus)

Protein (glomerulonephritis)

43
Q

What substance can act as a weak diuretic?

A

Acetazolamide

44
Q

What does acetazolamide do?

A

Inhibit carbonic anhydrase

45
Q

How does acetazolamide act as a diuretic?

A

Excretion of sodium bicarbonate and sodium chloride

46
Q

Why is acetazolamide weak and ‘self-limiting’?

A

Loss of bicarbonate leaves the patient with an acidaemia, and so the amount of bicarbonate being filtered falls as the patient becomes more acidaemic.

47
Q

What drug can inhibit ACE?

A

Captopril

48
Q

Which one of the following describes the main site of action of osmotic diuretics?

A

Proximal convoluted tubule

49
Q

What are aldosterone antagonists?

A

Potassium sparing diuretics

50
Q

What is diuresis vs anti-diuresis, how to know instantly?

A

Diuretic - increase urine production and lower ECV DIURESIS

Anti-diuresis - increase ECV and smaller urine production, ADH (AQP channels)

Kidney physiology (7 decks)

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