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Renal > Drugs acting on the kidneys > Flashcards

Drugs acting on the kidneys Flashcards

1
Q

What are diuretics?

A

agents that increase urine output through causing a net electrolyte and water loss

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2
Q

What do the organic anion transporters transport?

A

acidic drugs eg thiazides and loop agents

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3
Q

What do organic canion transporters tranposrt?

A

basic drugs

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4
Q

Where do loo/p diuretics work

A

ascending loop of Henle

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5
Q

What transporter do loop diuretics inhibit?

A

Na/K/2Cl cotransporter

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6
Q

Where do thiazides work?

A

DCT

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7
Q

Where does spironolactone work?

A

collecting duct

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8
Q

Why do loop diuretics cause hypokalaemia?

A

increase the load of sodium to DCT which results in compensatory mechanisms to get sodium back in exchange for potassium

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9
Q

What other electrolyes are depleted with looop diuretics?

A

calcium and magnesium

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10
Q

What action do loop diuretics have on blood vessels?

A

venodilator

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11
Q

What acid-base abnormality can be cause by loop diuretics?

A

metabolic alkalosis

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12
Q

What are the adverse effects of loop diuretics?

A

hypokalaemia; hypomagnesaemia; hypocalcaemia; hyperglycaemia; hyperuricaemia; hearing loss; hypovolaemia

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13
Q

Why do loop diuretics cause hearing loss?

A

there are the same cotranporters in endolymph

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14
Q

What transporter do thiazides work on?

A

bind to Na/Cl symprter

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15
Q

What effect do thiazides have on calcium?

A

increase reabsorption of calcium

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16
Q

Why are thiazides not as potent as loops?

A

because by DCT lots of sodium has already been reabsorbed

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17
Q

What effect do thiazides have on vessels?

A

vasodilator

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18
Q

What are the uses of thiazides?

A

mild HF; HT; nephrolithiasis (hypercalciuria); nephrogenic DI

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19
Q

Are thiazides and loops effective in renal failure?

A

loops are, thiazides arent

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20
Q

What extrarenal metabolic disturbances do thiazides cause?

A

hyperglycaemia and hyperlipidaemia

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21
Q

What are the side effects of thiazides?

A

postural hypotension; metabolic alkalosis; hypokalaemia; hyponatraemia; hypomagnesaemia; hypercalcaemia; hyperuricaemia; low blood counts; impotence; pancreatitis; cholestasis; pneumonitis; photosensitivity

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22
Q

What does risk of hypokalaemia depend on?

A

duration of action of the drugs

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23
Q

Which type of diuretic is less likely to cause hypokalaemia?

A

loop- shorter duration of action

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24
Q

Waht are teh signs of hypokalaemia?

A

weaknss; myalgia, fatigue, arrhythmias

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25
Q

How do loop diuretics cause metabolic alkalosis?

A

The increased sodium at the DCT causes the DCT to increase sodium reabsorption using Na/H transports and Na/K transports leading to hypokalaemia and alkalsis, the loss of chloride also leads to loss of anions so body gets more bicarb to replace

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26
Q

What is the main problem associated with loop and thiazides?

A

cause secondary hyperaldosteronism

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27
Q

What is the use of potassium sparing diuretics?

A

although weak diuretics on their own they blunt the secondary hyperaldosteronism with other diuretics so are useful in adjucts

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28
Q

What is the action of amiloride and triamterene?

A

block the apical sodium channel to decrease sodium reabsorption

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29
Q

What is the action of spironolactone and eplerone?

A

compete with aldosterone

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30
Q

What type of receptor does spironolactone compete with aldosterone for?

A

intracellular receptors

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31
Q

What does the competitive antagonism of spironolactone cause?

A

decreased gene expression and reduced synthesis of a protein mediator that activates sodium channels in the apical membrane and decrease the numebrs of sodium potassium pumps in the basolateral membrane

32
Q

How do amiloride and triamteren enter the nephron?

A

via organic cation tranport system in the PT- basic drugs

33
Q

What is the active metabolite of spironolactone?

A

canrenone

34
Q

What is the difference between amiloride and traimterene?

A

although amilordie is 10x more potent, triamterene is better absorbed fro mthe GI tract

35
Q

What hormonal disturbances does spironolactone cause?

A

gynaecomastia, impotence and menstrual irregularities

36
Q

When are there increased risk of hyperkalaemia assocaited with sprionolactone?

A

with used with potassium suppements and ACEi/ARBs

37
Q

Where is the carbonic anhydrase enzyme present?

A

renal tubules; gastric mucosa; pancreas, eye, brain and RBCs

38
Q

What is the actions of CA inhibitiors?

A

increase excretion of bicarbonate with sodium, potassium and water

39
Q

What can CAi result in?

A

alkaline diuresis; hypokalarmia and metabolic acidosis

40
Q

What are carbonic anhydrase inhibitors used for?

A

glaucoma; acute mountain sickness;

41
Q

What is the name of osmotic diuretics?

A

mannitol

42
Q

What is the major site of action in the kidneys of mannitol?

A

proximal tubule

43
Q

How is mannitol given?

A

IV

44
Q

How does mannitol get into the tubule?

A

freely filtered at the glomerulus

45
Q

What are the pharmacology properties of mannitol?

A

pharmacologically inert; not metabolised in the body; does not enter cells

46
Q

What are osmotic diuretics used for?

A

raised ICP and IOP; prevention of impending acute renal failure

47
Q

What type of receptor does ADH work on?

A

GPCR

48
Q

What do V1 receptors do?

A

vasconstriction

49
Q

What do V2 receptors do?

A

vasodilatory; increase water reaborption in renal CD

50
Q

What are aquaretics/vaptans?

A

competitive antagonsits of vasopressin receptors

51
Q

What do vasopressin receptor antagonists cause?

A

electrolyte free aquaresis; reduce urine osmolality; raise seum Na

52
Q

What is the main SE of osmotic diuretics?

A

hyponatraemic headache

53
Q

What is the main SE of aquaretics/ vaptans?

A

increased thirst

54
Q

What is the MOA of mannitol?

A

The presence of a nonreabsorbable solute such as mannitol prevents the normal absorption of water by interposing a countervailing osmotic force. As a result, urine volume increases. The increase in urine flow rate decreases the contact time between fluid and the tubular epithelium, thus reducing sodium as well as water reabsorption.

55
Q

How are prostaglandins formed?

A

from the fatty acid arachidonic acid in membrane phospholipids by the COX enzymes

56
Q

Which COX enzyme is mainly active during inflammation?

A

COX2

57
Q

What are hte PGs important in the kidneys?

A

PGE2 and PGI2

58
Q

What is the function of PGs in the kidney?

A

they are vasodilators and so increased renal blood flow and eGFR; increase water, Na and K excretion

59
Q

When are PGs most important?

A

in angiotensin induced vasoconstriction in volume deleted states

60
Q

When is renal blood flow dependent upon vasodilator prostaglandins?

A

CHF; cirrhosis and nephrotic syndrome

61
Q

What is the effect of NSAIDs?

A

tend to retain salt and water by inhibiting COX and PG synthesis

62
Q

What is the triple combination of drugs that can cause serious renal problems?

A

ACEi + diuretic + NSAID

63
Q

What is the difference between the action of uricosuric agents vs allopurinol?

A

allopurinol inhibits urate synthessis whereas uricosuric drugs reduce reabsorption of urate

64
Q

How do uricosuric agents reduce reabsorption of urate?

A

block the active transport of organic acids

65
Q

Who are uricosuric agents unsuitable for use in?

A

patients with renal impairment of hx of renal stones

66
Q

Why must high doses of uricosuric agents be given rather than low dose?

A

at low dose, uricosuric agents block urate secretion- increasing blood urate levels

67
Q

Give examples of uricosuric agents?

A

probenecid; sulfinpyrazole

68
Q

What uricosuric agent may be used in mild renal impairment?

A

benzbromarone

69
Q

What other drugs have mild uricosuric properties?

A

losartan and fenofibrate

70
Q

What should patients be told to do when started on a uricosuric agent?

A

increase fluid intake to 2-3 litres daily

71
Q

What drugs antagonise uricosuric drugs in the proximal ubule?

A

aspirin and other salicylates

72
Q

Gvie examples of SGLT2 inhibitors?

A

dapaglilofzin and empagliflozin

73
Q

What drugs cause uricaemia?

A

thiazides and loops

74
Q

How do SGLT work?

A

transport glucose against a conc gradient by coupling it to sodium influx

75
Q

What are the effects of SGLT2 inhibitors?

A

excretion of glucose, decrease in HbA1c and weight loss (calorific loss and mild osmotic diuresis); increased genital infections

Renal (33 decks)

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