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Clinical Pharmacology & Intro to Prescribing > Session 3: Diuretics & Drugs in Kidney Failure > Flashcards

Session 3: Diuretics & Drugs in Kidney Failure Flashcards

1
Q

Renal functions

A

Regulatory

Excretory

Endocrine

Metabolism

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2
Q

Regulatory functions.

A

Fluid balance

Acid-base balance

Electrolyte balance

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3
Q

Excretory functions

A

Waste products

Drug elimination

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4
Q

Endocrine functions

A

Renin

EPO

Prostaglandins

1-alpha calcidol

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5
Q

Metabolism functions

A

Vit D

Polypeptides (insulin)

Drugs (Morphine, paracetamol)

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6
Q

Give examples of drugs acting on renal tubules.

A

Carbonic anhydrase inhibitors (acetazolamide)

Osmotic diuretics

SGLT2 inhibitors

Loop diuretics

Thiazides

K+ sparing

Aldosterone antagonists

ADH antagonists

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7
Q

Definition of diuretic

A

Increased production of urine

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8
Q

Definition of natriuretic

A

Loss of sodium in urine

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9
Q

Definition of aquaretic.

A

Loss of water without electrolytes

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10
Q
A
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11
Q

Give an example of an aquaretic.

A

ADH antagonists

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12
Q

Give an example of an ADH antagonist.

A

Tolvaptan

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13
Q

Explain the action of tolvaptan.

A

Inhibits the V2 receptor which is suppose to cause transport of aquaporin to the apical membrane.

It is used to treat hyponatraemia and prevent cyst enlargement in APCKD.

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14
Q

Explain the action of lithium in the collecting duct.

A

Act on prinical cells as well but on the Gs causing the same outcome as Tolvaptan

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15
Q

Explain alcohol as an diuretic.

A

Inhibits ADH release

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16
Q

Explain caffeine as a diuretic.

A

Increased GFR and reduced tubular Na+ reabsorption

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17
Q

Generic adverse drug reactions of diuretics.

A

Hypovolaemia and hypotension

This activates RAAS and can lead to AKI.

Electrolyte imbalance

Metabolic abnormalities

Anaphylaxis/photosensitivity rash

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18
Q

Adverse drug effects of thiazides.

A

Gout

Hyperglycaemia

ED

LDL and TG increase

Hypercalcaemia

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19
Q

Adverse drug effects of Spironolactone

A

Hyperkalaemia

Impotence

Painful gynaecomastia

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20
Q

Adverse drug effects of furosemide

A

Ototoxicity

Alkalosis

LDL and TG increase

Gout

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21
Q

Adverse drug effects of Bumetanide

A

Myalgia

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22
Q
A
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23
Q

Examples of uses of diuretics.

A

Hypertension

Heart failure

Decompensated liver disease

Nephrotic syndrome

CKD

Oedema

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24
Q

Examples of drugs used in hypertension.

A

Thiazide diuretics

Spironolactone

Loop diuretics

ARBs

ACEi

CCBs

Beta-blockers

25
Q

Traditional treatment of HF

A

Loop diuretics

Spironolactone

ACEi/ARBs

Betablockers

26
Q

Novel treatment of HF

A

SGLT2-inhibitors

Tolvaptan

27
Q

Traditional treatment of decompensated liver disease

A

Spironolactone

Loop diuretics

28
Q

Novel treatment of decompensated liver disease

A

Tolvaptan

29
Q

Treatment of nephrotic syndrome

A

Loop diuretics

+/- thiazides

+/- K+ sparing/K+ supplements

30
Q

Lithium is used to treat bipolar disorder.

What is an unwanted side effect of lithium?

A

Inhibits action of ADH and causes dilute urine, increased free water clearance an raising serum sodium

31
Q

Treatment of CKD

A

The reduced GFR leads to salt and water retention

Therefore Loop diuretics are very good.

The alkalosis and potassium effects are also potentially beneficial.

Should avoid K+ sparing

32
Q

Why might furosemide not work in gut oedema?

A

The furosemide is not absorbed adequately orally in the gut.

33
Q

Why might furosemide not work in hypoalbuminaemia?

A

Because albumin is needed to carry the furosemide.

If there is no albumin to carry it is rendered more or less useless.

34
Q

Why is salt management important with diuretics?

A

Because diuretics will not work properly if there is a large intake of salt constantly.

35
Q

Management of refractory oedema

A

Check salt intake to see if sodium excretion is necessary

Give IV furosemide if gut oedema is likely.

Find the minimum effective dose and give repeated bolus or infusion

36
Q

Briefly explain Bartter’s and Gitelman syndrome.

A

Bartter cause NKCC2 to not work properly and patients will exhibit the same signs and symptoms as being on loop diuretics.

Gitelman cause NaCl to not work properly and patients will exhibit the same signs and symptoms as being on thiazide diuretics.

37
Q

Briefly explain Liddle’s syndrome

A

Increased function of ENaC leading to similar sympoms and signs as being on amiloride.

38
Q

Explain action of a carbonic anhydrase inhibitor such as acetazolamide.

A

Inhibits H2O and CO2 to be converted into H+ and HCO3-.

The H+ is then supposed to be transported out into the lumen in exchange for Na+ via the Na+/H+ antiporter.

39
Q

Side effects of carbonic anhydrase inhibitors.

A

Loss of NaHCO3

Hypokalaemic metabolic acidosis (Due to loss of HCO3- as well as reabsorption of Na+ in CD in exchange for K+ being excreted)

Renal stones

40
Q

Why is acetazolamide not commonly used as a diuretic?

When is it used instead?

A

Because the patient will quickly build tolerance to the drug and it will not have any effect.

It’s used instead in glaucoma, altitude sickness and rare cases of epilepsy

41
Q

Explain action of mannitol.

A

Works like an osmotic agents and pulls H2O into the lumen.

42
Q

Side effects of mannitol

A

Loss of water

Reduced intracellular volume

Hypernatraemia

Allergic reactions

43
Q

When is mannitol used?

A

To reduce high intracerebral pressure

44
Q

Explain the action of SGLT2 inhibitors.

A

Causes inhibition of SGLT2 leading to Na+ and glucose not to be absorbed.

This leads to the macula densa to absorb Na+ and Cl- and via tubuloglomerular feedback it causes vasoconstriction of the afferent arteriole. This is preferential in cases of glomerular hyperfiltration.

45
Q

Effects of SGLT2 inhibitors.

A

Lowered plasma glucose

Loss of weight

Lowered BP

Lowered plasma uric acid

Lowered glomerular hyperfiltration

46
Q

Explain the action of loop diuretics.

A

Blocks the NKCC2 cotransporter.

This leads to Na+ not being reabsorbed in the same amounts.

47
Q

Side effects of loop diuretics.

A

Loss of Na+ and water

Hypokalaemic metabolic alkalosis

Increased Ca2+ loss

48
Q

Explain why you might get hypocalcaemia in loop diuretics.

A

Because since K+ is no longer be reabsorbed ROMK will stop working which is supposed to create a positive luminal membrane that is the driving force for reabsorption of Ca2+ and Mg2+

49
Q

Explain the action of thiazide diuretics.

A

Block the NCCT (Na+/Cl- cotransporter)

50
Q

Side effects of thiazide diuretics.

A

Loss of Na+ and water

Hypokalaemic metabolic alkalosis

Increased Ca2+ reabsorption

51
Q

Explain why hypercalcaemia might occur in thiazide diuretics.

A

Less Na+ reabsorbed. This leads to more Na+ secreted from interstitium to tubule cell in order to compensate for the loss of Na+. A transporter exchanging Ca2+ for Na+ on the basolateral membrane is responsible for this. This leads to more Ca2+ going into interstitium.

52
Q

Usage of loop diuretics.

A

Oedema and hypertension in advanced CKD

53
Q

Usage of Thiazides and thiazide-like diuretics.

A

Hypertension

54
Q

Use of amiloride.

A

Low potassium where diuretic required.

55
Q

Side effects of amiloride

A

Hyperkalaemia

56
Q

Usage of spironlactone

A

HF

Ascites

Hypertension

Hyperadrenalism

57
Q

Side effects of spironolactone

A

Hyperkalaemia

Gynaecomastia

58
Q

Usage of ADH antagonist such as tolvaptan.

A

Hyponatraemia

59
Q

Side effects of tolvaptan

A

Hypernatraemia

Deranged liver function

Clinical Pharmacology & Intro to Prescribing (24 decks)

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