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_Sem 4. CPT NOTES > S3 L2 Diuretics > Flashcards

S3 L2 Diuretics Flashcards

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1
Q

What are the main functions the kidney?

A
  1. Regulatory
    - Fluid balance
    - Acid-base balance
    - Electrolyte balance
  2. Excretory
    - Waste products
    - Drug elimination
    → Glomerular filtration
    → Tubular secretion
  3. Endocrine
    - Renin
    - Erythropoetin
    - Prostaglandins
    - 1α- calcidol
  4. Metabolism
    - Vit D
    - Polypeptides
    → Insulin
    - Drugs
    → Morphine
    → Paracetamol
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2
Q

Where do different drugs act on the renal tubule?

A
  1. Carbonic anhydrase inhibitors → PCT
  2. Osmotic diuresis → PCT and throughout
  3. SGLT2 inhibitors → PCT
  4. Loop Diuretic → TAL
  5. Thiazide → DCT
  6. Potassium sparing diuretics → DCT and CD
  7. Aldosterone antagonists → CD
  8. ADH antagonists → CD
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3
Q

Define:

  • Diuretics?
  • Natriuretic?
  • Aquaretic?
A

D- Increased production
N- Loss sodium in the urine
A- Loss of water without electrolytes

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4
Q

What do carbonic anhydrase inhibitors do?

A 
Prevent carbonic anhydrase working 
Stops conversion:
- CO2 + H2O ←→ H2CO3 ←→ H+ + HCO3-
Loss of NaCO3
→ 66% of filtered and 85% of NaHCO3 is normally reabsorbed in the proximal tubule 
Hypokalaemic metabolic acidosis
→ HCO3- excreted in urine 
→ Enhanced Na+ delivery to the CD, taken up by ENaC, K+ excreted into urine
Tolerance develops after 2-3 days
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5
Q

What are osmotic agents?

A

Mannitol

  • Can’t be reabsorbed
  • Increases the osmolality in the filtrate
  • Draw water out of cells
  • Reduced intracellular volume
  • Hypernatremia risk
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6
Q

What are SGLT2 inhibitors?

A 
Inhibit Na+ and glucose uptake in PCT
↑osmolality in the filtrate → water follows 
↑Plasma glucose 
↓Body weight
↓BP
↓Plasma uric acid
↓Glomerular hyperfiltration
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7
Q

How do loop diuretics work?

A

Inhibit the Na+/K+/2Cl- channel
- Loss of Na+ and H2O (25% of filtered reabsorbed)
- Hypokalemic metabolic alkalosis
→ Enhanced Na+ delivery to the CD, taken up by ENaC, K+ excreted into urine
- Increase Ca2+ loss
→ Normally K+ uptake and then K+ excreted, build up of +ve change forces Ca2+ and Mg2+ paracellularly

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8
Q

What do thiazide diuretics do?

A 
Block Na+/Cl- cotransporter
5% of filtered reabsorbed 
- Loss of Na+ and H2O
- Hypokalaemia metabolic alkalosis
- Increased Ca2+ reabsorption as Na+/ Ca2+ exchanger works in opposite direction- more Na+ brought out of plasma into cell, Ca2+ goes into plasma so then more Ca2+ reabsorbed - hypercalcaemia
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9
Q

How does aldosterone work?

A

Increase expression of ENaC and Na+/K+ ATPase in principle cells of the collecting duct

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10
Q

How do amiloride and spironolactone work?

A

Amiloride → ENaC channel blocker (potassium sparing)

Spironolactone → aldosterone blocker → stop ↑ENaC and ↑Na+/K+ ATPase expression therefore reducing Na+ uptake

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11
Q

How are amiloride ad spironolactone potassium sparing?

A

Only affect Na+ reabsorption

Reduced the activity of the Na+/ K+ ATPase resulting in less K+ being excreted

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12
Q

What are ADH antagonists?

A

Aquaretics- no affect on Na+ just water loss
1. Tolvaptan
ADH anatogonist
Diuretic but not natriuretic
Used to treat hyponatraemia (looks like low Na+ because of ↑H2O) (and prevent cyst enlargement in APCKD)
2. Lithium
- Treat bipolar disorder
- Inhibits action of ADH
- Need to keep up with water intake to avoid dehydration

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13
Q

How do the ADH antagonists work?

A

Tolvaptan block the ADH receptors
Lithium work on G protein along the cascade
Prevents insertion of aquaporin into the collecting duct
Preventing reabsorption of water

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14
Q

What other substance can have an diuretic action?

A

Alcohol- inhibits ADH release

Caffeine- ↑GFR and ↓tubular Na+ reabsorption

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15
Q

What are some of the adverse reactions that diuretics can cause?

A

Hypovolemia and hypotension
- Activate RAAS
- → AKI (hypoperfusion)
Electrolyte disturbance (Na+, K+, Mg2+ and Ca2+)- expect aquaretic
Metabolic Abnormalities (depends on individual drug)
Anaphylaxis/ photosensitivity, rash etc… rare

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16
Q

What are some of the common adverse drug reactions for thiazides?

A 
Gout → Uric acid reabsorption 
Hyperglycaemia 
Erectile dysfunction 
↑LDL ↑TG
Hypercalcaemia
17
Q

What are some of the common adverse drug reactions for frusemide?

A

Ototoxicity
Alkalosis - remove the H+
↑LDL ↑TG
Gout

18
Q

What are some of the common adverse drug reactions for spironolactone?

A

Hyperkalaemia - potassium sparing
Impotence
Painful gynaecomastia

19
Q

What are some of the common adverse drug reactions for bumetanide?

A

Myalgia - pain or tenderness in one or more muscles of the body

20
Q

How do the drug interact with each other?

A

ACEi and K+ sparing → hyperkalaemia - cardiac problems
Aminoglycoside + loop diuretics → ototoxicity and nephrotoxicity
Digoxin + thiazide and loop → Hypokalaemia - increased digoxin binding and toxicity
B-blockers + thiazide → hyperglycaemia, hyperlipidaemia, and hyperuricaemia
Steroids + thiazide + loop → Hypokalaemia
Lithium + thiazide + loop → Lithium toxicity (thiazides), reduced lithium levels (loop)
Carbamazepine + thiazide + loop → Increased risk of hyponatraemia

21
Q

What are the uses of diuretics?

A 
Hypertension 
Heart failure 
Decompensated liver disease
Nephrotic syndrome
Chronic kidney disease
22
Q

What diuretics are used to treat hypertension?

A

Thiazide diuretics
Spironolactone → secondary hypertension, Liddle syndrome (ENaC channels are always on), inhibits aldosterone preventing expression of ENaC channels
Loop diuretic - accommodation downstream (compensated for)
(ACEi/ ARBs and B blockers also used)

23
Q

How is heart failure treated?

A 
Traditional 
- Loop Diuretics 
- Spironolactone 
(- ACEi/ ARB + B blockers)- not diuretics 
Novel 
- SGLT-2 inhibitors 
- Tolvaptan
24
Q

What is secondary hyperalodersteonism?

A

Body trying to compensate for things that have gone wrong
Arterial ↓BP - either due to hypovolemia (trauma associated) or HF- sense hypovolemia because heart not pumping very well + blood flow is reduced but actually volume is normal or ↑
Activate RAAS and sympathetic system to ↑ Volume= fluid overload- need diuretics

25
Q

What is decompensated liver disease treatment?

A

Similar to HF- detects effective fluid volume has decreased BUT because everything has gone leaky (not in blood stream) due to decrease albumin levels from liver
Traditional
- Spironolactone
- Loop Diuretics
Novel
- Tolvaptan - prevent aquaporins insertion + water reabsorption

26
Q

What is nephrotic syndrome?

A

Kidney function is normal but loose albumin in the urine so loose oncotic pressure hence fluid leaks into tissue- secondary aldosteronism

  • Loop diuretics needed
  • (+/-) Thiazides
  • (+/-) Potassium sparing diuretic/potassium supplements
27
Q

What is chronic kidney disease?

A

Glomerular doesn’t function as well → Loose nephrons
↓GFR leads to salt and water retention
Loop Diuretics
Alkalosis and kalliuretic (↓remove K+) effects potentially beneficial
Generally avoid K+ sparing diuretics
- Role for SGLT2 inhibitors in the future - reduce speed of kidney damage

28
Q

What is diuretic resistance?

A

Initially starts off really well - loose loads of fluids
Then gradually the kidney accommodates
Upregulation of channels further downstream

29
Q

What affects diuretic delivery to the renal tubule?

A

Different parts of the absorption and metabolism can be affected…
1. Gut wall- need to absorb tablet- oedema- don’t absorb all the renal tablet
2. Blood- needs to bind to albumin to be transported- need enough albumin
3. Uptake into PCT epithelial cell - Actively transported via OATs (apical 1 or 3, basolateral 4)
4. PCT lumen
Patients actually need a lot more frusemide to get it to where it is actually needed

30
Q

What is the importance of salt in the diet?

A

Drugs to reduce salt
Need to ensure you reduce salt in the diet
Problem- hedonistic behaviour - loose salt become thirsty and crave salt

31
Q

What is refractory oedema?

A

Get rid of salt and water
Body detect loss
Reabsorbs it further down the nephron

32
Q

How is refractory oedema managed?

A

Check salt intake- 24hours sodium excretion if necessary
Give fruosemide IV if gut oedema likely
Find minimum effective dose
Give repeated bolus or infusion (short t1/2)

33
Q

What is the mechanism for managing BP?

A 
↓BP and BV
Baroreceptors and kidney detect
↑CO, vasoconstriction, thirst, ↑NaCl and water reabsorption 
↑ECF volume 
↑BP
34
Q

How should diuretics be used to increase effectiveness?

A

Used in combination

35
Q

Why is there a difference in electrolyte balance between thiazide and loop diuretics?

A

Thiazide→ disrupt the electrolyte balance more than loop diuretics, acts on the isosmotic part of the kidney, so inhibiting it has less effect on tonicity- less effect on NaCl and K+ so less effect on water
Loop diuretics→ ascending limb, Na+ reabsorbed helps concentrate the medulla and maintain counter current mechanism, high osmolality in the medulla- water, urea absorption due to hypertonic interstitium

36
Q

What is Bartter’s and Gitelman’s syndrome?

A

Bartter’s syndrome → Blockage of Na+/K+/2Cl- channels
Gitelman’s syndrome → Blockage of Na+/Cl- channel
No reabsorption of these electrolytes so no reabsorption of water
Results in hypotension

37
Q

What is Liddle’s syndrome?

A

Syndrome results from increased function
Increased ENaC
Results in hypertension

38
Q

Give a brief summary of the diuretics and what they are used for?

A

Carbonic anhydrase inhibitors → glaucoma, altitude sickness
Osmotic diuretics → reduce high intracerebral pressure
Loop diuretics → oedema (+/- hypertension in advanced CKD)
Thiazides and thiazide-like → hypertension
Potassium sparing diuretics → low potassium where diuretic required
Aldosterone antagonists → HF, ascites, hypertension, hypoadrenalism
ADH antagonists → Hyponatraemia

_Sem 4. CPT NOTES (26 decks)

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