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Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

name 6 classes of drugs which act on the kidney

A

diuretics
vasopressin receptor agonists/antagonists
SGLT2 (sodium-glucose co-transporter 2 inhibitors)
uricosuric drugs (promote excretion of uric acid)
drugs for renal failure
drugs altering pH of urine

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2
Q

what do diuretics do?

A

increase urine flow, normally by inhibiting reabsorption o electrolytes (sodium) in nephron
enhance excretion of salt and water in conditions where increased volume of ECF (e.g oedema/tissue swelling)

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3
Q

what causes oedema?

A

imbalance between rate of secretion and absorption of interstitial fluid
- hydrostatic pressure in capillary (Pc)
hydrostatic pressure in interstitial fluid (Pi)
- oncotic pressure of plasma (Mp)
- oncotic pressure of interstitial fluid (Mi)

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4
Q

calculation for formation of interstitial fluid?

A

(Pc-Pi) - (Mp - Mi)

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5
Q

name 3 disease states which can increase Pc or decrease Mp

A

nephrotic syndrome
congestive heart failure
hepatic cirrhosis with ascites

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6
Q

what causes nephrotic syndrome?

A

disorder of glomerular filtration allowing for large proteins (mainly albumin) to appear in urine

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7
Q

is protein in the urine always abnormal?

A

no

small proteins can occur in urine after heavy exercise

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8
Q

how does decreased plasma oncotic pressure cause oedema/

A

decreased Mp > increased formation of interstitial fluid > reduced blood volume and CO > activation of the RAAS > aldosterone and angiotensin II cause Na+ and H2O retention > only salt and water added back, not protein so protein concentration in the blood is diluted > reduces plasma oncotic pressure even further and increases Pc > oedema

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9
Q

how does heart failure cause oedema?

A

reduced CO > renal hypoperfusion > activation of RAAS > blood volume expands and protein conc decreases > increased Pc and decreased Mp > oedema

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10
Q

how does cirrhosis cause ascites?

A

increased pressure at portal vein + decreased albumin production > loss of fluid into peritoneal cavity > oedema/ascites > RAAS activated

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11
Q

how do diuretics work (diagram)?

A

..

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12
Q

how is Na+ reabsorbed in the proximal tubule and what blocks this?

A

Na+/H+ exchange
blocked by carbonic anhydrase inhibitors (diuretics)
- site of 70% of sodium reabsorption

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13
Q

how is Na+ reabsorbed in the thick ascending limb of loop of henle and what blocks this?

A

triple co-transporter - Na+/K+/2Cl-

blocked by loop diuretics

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14
Q

how is sodium reabsorbed in the early distal tubule?

A

Na+/H+ exchange
- blocked by CA inhibitors
Na+/Cl- (mainly)
- blocked by thiazide diuretics

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15
Q

how is Na+ reabsorbed in the collecting tubule and duct?

A

Na+/K+ exchange

- blocked by potassium sparing diuretics

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16
Q

what type of diuretic can cause hypokalaemia?

A

any which increases reabsorption of Na+ in distal tubule (apart from potassium sparing ones)

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17
Q

a small inhibition of reuptake of NaCl can cause a large increase in Na+ excretion, true or false?

A

true

- as so much sodium is filtered

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18
Q

where do most diuretics act?

A

apical membrane of tubular cells

- therefore must enter the filtrate to act on these cells

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19
Q

how can diuretics enter the filtrate?

A

glomerular filtration (cant enter glomerular filtration if bound to large plasma proteins)
organic anion transporter (transport acidic drugs - thiazides and loops)
organic cation transporter (transport basic drugs - triamterene and amiloride)

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20
Q

secretion of diuretic into the filtrate allows what?

A

concentrate the diuretic in the filtrate (urine)

gives pharmacological selectiveness of the drug (makes sure it only works in renal system)

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21
Q

describe the organic anion transporter

A

basolateral and apical transport processes
basolateral
- anions enter cell against conc gradient in exchange for α-KG via OAT channels
- α-KG enters cell against conc gradient via NaDC3 transporter
apical membrane
- once in the cell, anion crosses to the lumen via multidrug resistance proteins 2 and 4 and BCRP via primary active transport
- anion crosses from the lumen via OAT4 channel in exchange for α-KG

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22
Q

name drugs which use anion transporter

A 
diuretics
simvastatin
penicillin
NSAIDs
endogenous urate
23
Q

how do diuretics increase acute gout risk?

A

impair ability to secrete urate out of the blood and into the urine (organic anion transporter)

24
Q

describe organic cation transporter

A

basolateral membrane
- organic cations enter cell via OCT2 channel driven by -ve potential, against conc gradient
apical membrane
- cation enters the lumen in rate limiting manner via electroneutral multidrug and toxin extrusion transporters (MATES) an active transport via MDR1

25
Q

what drugs use organic cation transporter?

A 
diuretics 
atropine
metformin
morphine
procainamide
catecholamines
26
Q

…

A

blocks triple transporter > low intracellular Na+ > drives reabsorption of Na+

27
Q

…

A

…

28
Q

what are the 2 principle loop diuretics and how do they work in general terms?

A

furosemide
bumetanide
inhibit the triple transporter by binding to the Cl- site and thus

29
Q

what is the impact of inhibiting the triple transporter?

A

decrease tonicity of medulla interstitium
prevent dilution of filtrate in thick ascending limb
increase load of Na+ delivered to distal nephron causing K+ loss
increased excretion of calcium and magnesium
causes 15-25% of filtered Na+ to be excreted

30
Q

what additional action of loop diuretics can be helpful in acute pulmonary oedema before the diuretic action kicks in?

A

venodilator action

31
Q

which loop is better in heart failure?

A

bumetonide

32
Q

pharmacokinetics of loop diuretics?

A

absorbed by GI tract (subject to variation in CHF)
bind to plasma protein
enter nephron via OAT

33
Q

indications for loop diuretics?

A

reduce salt and water overload associated with cardiac/renal failure, cirrhosis or nephrotic syndrome
to increase urine volume in AKI
treat hypertension
to reduce acute hypercalcaemia

34
Q

how may nephrotic syndrome affect loop diuretic action?

A

reduce effectiveness

drug binds to high amount of protein in urine

35
Q

contraindications for loop diuretics?

A

severe hypovolaemia or dehydration

use with caution in hypokalaemia/hyponatraemia, hepatic encephalopathy and gout

36
Q

side effects of loop diuretics?

A

low electrolyte states (including metabolic alkalosis due to H+ secretion)
hypovolaemia/hypotension
hyperuricaemia (gout)
dose-related hearing loss

37
Q

where is the triple transporter found in the nephron?

A

thick ascending limb of loop of henle

38
Q

what do thiazide diuretics block?

A

sodium chloride co-transporter

39
Q

principle thiazide and thiazide-like diuretics?

A 
bendroflumethiazide
thiazide like
- chlortalidone
- indapamide
- metolazone
40
Q

what do thiazide like diuretics do?

A

inhibit Na+/Cl- co-transporter by binding to Cl- site and therefore
- prevent dilution of filtrate/urine in early distal tubule
- increase load of Na+ delivered to collecting tubule causing K+ loss
- increased reabsorption of calcium
causes up to 5% of filtered Na+ to be secreted (modest diuresis)

41
Q

additional action of thiazides?

A

vasodilator action

- benefit in hypertension

42
Q

pharmacokinetics of thiazides?

A

well absorbed from GI tract

enter nephron via OAT mechanism

43
Q

indications for thiazides?

A

mild heart failure
hypertension (indapamide or chlotalidone)
severe resistant oedema
renal stone disease (reduced Ca2+ excretion discourages Ca2+ stone formation- less calcium in urine so less likely to precipitate out)
nephrogenic diabetes (reduced ADH response in collecting ducts)

44
Q

contraindications for thiazides?

A

hypokalaemia

use with caution - hyponatraemia, gout

45
Q

side effects of thiazides?

A 
hypokalaemia
metabolic alkalosis
hypovolaemia/hypotension
hypomagnesia (not hypocalcaemia)
hyperuricaemia (gout)
erectile dysfunction
impaired glucose tolerance
46
Q

which diuretic is best to use in elderly person with osteoporosis and why?

A

thiazide

- don’t cause loss of calcium

47
Q

function of aldosterone?

A

acts via cytoplasmic receptors to increase reabsorption of Na+ in the late distal and collecting tubule via increasing ENac (sodium) channel and Na+/K+ ATPase

48
Q

how does aldosterone affect potassium?

A

increased Na+ reabsorption = increased K+ excretion

49
Q

how does Na+ reabsorption cause K+ excretion?

A

charge separation makes lumen more -ve and depolarizes the luminal/basolateral membrane
this causes an increased driving force of K+ across the luminal membrane leading to enhanced secretion of K+ (Sgk1 increases ROMK K+ channel numbers in apical membrane)
secreted K+ is washed away by increased urinary flow rate that also indirectly activates the ROMK channel leading to development of hypokalaemia

50
Q

name 4 potassium diuretics?

A

amiloride
triamterene
spironolactone
eplerenone

51
Q

how do amiloride and triamterene work?

A

enter nephron via organic cation transport system in proximal tubule and block apical sodium channels in collecting tubules and decrease Na+ reabsorption

52
Q

how does spironolactone and eplerenone work?

A

enter cell via basolateral membrane and compete with aldosterone for binding to intracellular cytoplasmic receptors preventing the actions of steroid described previously

  • increase Na+ excretion
  • decrease K+ excretion
53
Q

indications for potassium sparing diuretics?

A 
given in conjunction with other agents that cause potassium loss (as they cause hyperkalaemia)
...
.
.
.
54
Q

contraindications of potassium sparing diuretics?

A

//

Renal (34 decks)

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