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
Traditional treatment of HF
Loop diuretics Spironolactone ACEi/ARBs Betablockers
26
Novel treatment of HF
SGLT2-inhibitors Tolvaptan
27
Traditional treatment of decompensated liver disease
Spironolactone Loop diuretics
28
Novel treatment of decompensated liver disease
Tolvaptan
29
Treatment of nephrotic syndrome
Loop diuretics +/- thiazides +/- K+ sparing/K+ supplements
30
Lithium is used to treat bipolar disorder. What is an unwanted side effect of lithium?
Inhibits action of ADH and causes dilute urine, increased free water clearance an raising serum sodium
31
Treatment of CKD
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
Why might furosemide not work in gut oedema?
The furosemide is not absorbed adequately orally in the gut.
33
Why might furosemide not work in hypoalbuminaemia?
Because albumin is needed to carry the furosemide. If there is no albumin to carry it is rendered more or less useless.
34
Why is salt management important with diuretics?
Because diuretics will not work properly if there is a large intake of salt constantly.
35
Management of refractory oedema
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
Briefly explain Bartter's and Gitelman syndrome.
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
Briefly explain Liddle's syndrome
Increased function of ENaC leading to similar sympoms and signs as being on amiloride.
38
Explain action of a carbonic anhydrase inhibitor such as acetazolamide.
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
Side effects of carbonic anhydrase inhibitors.
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
Why is acetazolamide not commonly used as a diuretic? When is it used instead?
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
Explain action of mannitol.
Works like an osmotic agents and pulls H2O into the lumen.
42
Side effects of mannitol
Loss of water Reduced intracellular volume Hypernatraemia Allergic reactions
43
When is mannitol used?
To reduce high intracerebral pressure
44
Explain the action of SGLT2 inhibitors.
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
Effects of SGLT2 inhibitors.
Lowered plasma glucose Loss of weight Lowered BP Lowered plasma uric acid Lowered glomerular hyperfiltration
46
Explain the action of loop diuretics.
Blocks the NKCC2 cotransporter. This leads to Na+ not being reabsorbed in the same amounts.
47
Side effects of loop diuretics.
Loss of Na+ and water Hypokalaemic metabolic alkalosis Increased Ca2+ loss
48
Explain why you might get hypocalcaemia in loop diuretics.
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
Explain the action of thiazide diuretics.
Block the NCCT (Na+/Cl- cotransporter)
50
Side effects of thiazide diuretics.
Loss of Na+ and water Hypokalaemic metabolic alkalosis Increased Ca2+ reabsorption
51
Explain why hypercalcaemia might occur in thiazide diuretics.
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
Usage of loop diuretics.
Oedema and hypertension in advanced CKD
53
Usage of Thiazides and thiazide-like diuretics.
Hypertension
54
Use of amiloride.
Low potassium where diuretic required.
55
Side effects of amiloride
Hyperkalaemia
56
Usage of spironlactone
HF Ascites Hypertension Hyperadrenalism
57
Side effects of spironolactone
Hyperkalaemia Gynaecomastia
58
Usage of ADH antagonist such as tolvaptan.
Hyponatraemia
59
Side effects of tolvaptan
Hypernatraemia Deranged liver function