Diuretics Flashcards

1
Q

What are 5 classes of diuretic? [5]

A

Carbonic anhydrase inhibitors
Thiazide
Loop
Potassium sparing diuretics
Osmotic diuretics

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

Where do carbonic anhydrase inhibitors work? [1]

MoA of CA inhibitors?

A
  • CA inhibitors work at PCT
  • Causes more HCO3-, H+ & Cl- excreted in urine
  • Get less CO2 and water in cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which of the following is the most effective type of diuretic?

Carbonic anhydrase inhibitors
Thiazide
Loop
Potassium sparing diuretics
Osmotic diuretics

A

Which of the following is the most effective type of diuretic?

Carbonic anhydrase inhibitors
Thiazide
Loop: e.g. Frusemide
Potassium sparing diuretics
Osmotic diuretics

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

Where do loop diuretics work? [1]

How do they work? [1]

A

Loop diuretic: work at thick ascending limb

MoA:
- Block NaKCl2 transporter (competing with Cl- for binding site)
- Less Na into tubular cell: less Na into blood / more Na excreted in urine
- Results in less K+ reabsorbed
- Causes decreased Ca2+, Mg2+ absorption via paracellular transport

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

Explain two AEs of using loop diuretics? [3]

A

Hypokalemia: directly blocks K reabsorption through blockage of NaKCl2

Dehydration

Kidney stones: due to retained Ca in urine

Deafness

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

Thiazide diuretics work in which location of nephron? [1]

MoA of thiazide diuretics? [1]

A

Thiazide diuretics: work at DCT

MoA: Blocks Na/Cl transporter

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

Explain how thiazide diuretics impact K+ levels

A

Cause hypokalaemia:

  • Thiazied diuretics block Na/Cl transporter at DCT
  • Na is delivered to CD, where absorbed by ENaC channels
  • This causes the aldosterone-sensitive Na/K pump to increase Na reabsorption in the principal cells
  • This exchange increases Na transfer into the interstitium and increases K transfer into the collecting tubules and lumen.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the two type of K sparing diuretics? [2]

Name two examples of each xx [4]

A

Epithelial Na Channel antagonists
* Amiloride
* Triamterene

Aldosterone antagonists:
* Spironolactone
* Eplerenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where do potassium sparing diuretics, such as spironolactone or eplerenonework in nephron? [1]

MoA? [1]
How do they ensure K+ reabsorption? [1]

A

Spironolactone and eplerenone work at CD

Both: aldosterone antagonists (Na/K transporter)

Because Na doesn’t get reabsorbed into blood, K doesn’t have to be excreted in exchange

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

Where do Epithelial Na Channel antagonists
potassium sparing diuretics, like Amiloride or Triamterene work in the nephron? [1]

MoA? [1]
How do they ensure K+ reabsorption? [1]

A

Collecing Duct / Distal tubule

Work by blocking urine lumen side Na+ transporter: stops Na+ reabsorption; driving force for K+ secretion is eliminated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a osmotic diuretic and which is the most clinically important? [2]

A

Any osmotically active molecule that is freely filtered in the glomerulus, and is not reabsorbed by the tubules, stopping water reabsorption

Most important clinical osmotic diuretic: Mannitol

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

What is Acetazolamide mainly used for? [1]

A

Mountain sickness: try and reverse resp. alkalosis by creating metabolic acidosis (by increasing HCO3- excretion)

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

What are AEs of CA inhibitors like Acetazolamide? [3]

A

Metabolic acidosis
Sedation
Sulphonamide antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is clinical use of thiazide diuretic? [1]

Why? [2]

A

Antihypertensive:
reduces plasma volume and peripheral resistance

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

AEs of thiazide diuretics? [3]

A

Hypokalaemia: K+excretion is enhanced due to the increase in Na+delivered to the distal tubule.

Hypercalcaemia: Ca2+excretion is decreased via a poorly understood mechanism

Hyponatraemia (particularly in old people)

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

Explain AEs of thiazide diuretics? [5]

A

Hypokalaemia: K+excretion is enhanced due to the increase in Na+delivered to the distal tubule / CD, where Na is reabsorped at expense of K+

Hypercalcaemia: Ca2+excretion is decreased via a poorly understood mechanism

Hyponatraemia (particularly in old people)

Hyperglycaemia: inhibits insulin secretion slightly

Hypercholesterolaemia: unknown mech

17
Q

Thiazide diuretics cause increase excretion of which electrolytes? [2]

18
Q

Clinical use of loop diuretics? [3]

A
  • Most potent diuretic

Also for:
* HTN
* Heart failure
* Volume overload from CKD

19
Q

Loop diuretics cause increase excretion of which electrolytes? [4]

A

K+, Na+, H20, Ca, Mg.

20
Q

Explain how loop diuretics maintain renal blood flow

A

.Loop diuretics block the Na+, K+, Cl-symporter in the macula densa.

As a result the tubuloglomerular feedback mechanism is blocked

. Because of this loop diuretics maintain renal blood flow.

21
Q

Why can loop diuretics cause kidney stones?

A

Loop diuretics cause increase Ca2+ excretion: increases chances

22
Q

What are clinical uses of aldosterone inhibitors? [4]

A

Hyperaldosteronism (Conns)
Heart failure
Hypokalaemia (from other diuretics)
Cirrhosis

23
Q

AEs of aldosterone inhibitors? [3]

A

Hyperkalaemia
Hyperkalaemia –> can lead to cardiac arrythmias and death
Hyperkalaemia
Gynecomastia (not eplerenone)
Hyponatraemia (Cirrhosis)

24
Q

Why do aldosterone inhibitors lead to hyperkalaemia?

A

Na not excreted, so K kept

25
Clinical uses of amiloride?
**Heart failure** **Hypokalaemia** (from other diuretics) Co-amilofruse Co-amilozide Cirrhosis
26
AEs of amoliride? [2]
**Hyperkalaemia** Hyponatraemia
27
When would you use osmotic diuretic clinically? [1]
**Clinical use:** * Cerebral odema AEs: * Transient fluid overload: **pulmonary odema** * If using glucose: **DKA/HHS** * If using urea: **Disequilibrium syndrome**
28
When should you not use diuretics ! [5] key
When **hypotensive** When **dehydrated** When **hypokalaemic** (Loop/Thiazide) When **hyperkalaemic** (Amiloride, aldosterone antagonists) **Post surgery**, with a poor **urine output**
29
Explain MoA of SGLT-2 inhibitors
Normally SGLT2 allows Na AND glucose to be reabsorbed at PCT Blocking SGLT2 causes more Na to be delivered to macula densa: here it causes glomerulus afferent arteriole constriction, which normalises GFR. Also causes glucose to be excreted in urine
30
Effects of SGLT2 inhibitors? [5]
**Glycosuria**: weight loss, reduction in blood glucose, HbA1c reduced **Uric acid reduced** **Natuiresis**: fall in BP **Reduced hyperinfiltration**: reduced albuininuria **Reversible reduction in GFR**
31
Cardio protective effects of SGLT-2 inhibitors?