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Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is the function of uricosuric drugs?

A

promote excretion of uric acid into the urine

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2
Q

what do diuretics do to urine volume?

A

increases urine volume

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3
Q

in what clinical conditions are diuretics used?

A

when there is excess interstitial fluid (oedema)

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4
Q

oedema results from an imbalance of what?

A

rate of interstitial fluid formation

rate of interstitial fluid absorption

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5
Q

what 2 starling forces when affected cause oedema?

A

increased capillary pressure

decreased capillary oncotic pressure

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6
Q

what is the main starling force which drives water out of the capillary?

A

capillary pressure

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7
Q

what is the main starling force which dries water into the capillary?

A

capillary oncotic pressure

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8
Q

what change in plasma content reduces capillary oncotic pressure?

A

reduced plasma proteins

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9
Q

what 3 main disease states cause oedema due to either increased capillary pressure or decreased oncotic pressure?

A
  • congestive heart failure
  • nephrotic syndrome
  • herpatic cirrhosis with ascites
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10
Q

what is nephrotic syndrome?

A

a disorder of glomerular filtration which allows protein (mainly albumin) to appear in the filtrate (proteinuria)

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11
Q

what is the apperance of urine with protein in it?

A

frothy

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12
Q

when can proteinuria be physiological?

A

intense periods of exercise

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13
Q

what does activation of the RAAS system do to Pc and COP starling forces and therefore what does this do to the oedema?

A

increases Pc
decreases COP

increases oedema

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14
Q

what does protein excretion in the urine do the rate of interstitial fluid formation?

A

increase rate of interstitial fluid

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15
Q

what drug type can be used to stop the cycle of oedema formation in nephrotic syndrome?

A

diuretics

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16
Q

why does congestive heart failure activate the RAS?

A

reduced cardiac output causes reduced pressure in afferent renal arteriole
activates RAS

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17
Q

why does ascites occur in hepatic cirrhosis?

A

increase capillary pressure in the portal vein

decrease oncotic pressure due to reduced production of albumin

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18
Q

why does ascites activate the RAS?

A

reduced circulating volume causes reduced pressure in the afferent renal arteriole activates RAS

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19
Q

what can longstanding hypertension do to the number of nephrons?

A

decrease

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20
Q

what diuretics work in the proximal convoluted tubule?

A

carbonic anhydrase inhibitors (no longer used)

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21
Q

what diuretics work in the thick ascending limb of the loop of henle?

A

loop diuretics

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22
Q

what diuretics work in the distal convoluted tubule?

A

carbonic anhydrase inhibitors (no longer used)

thiazide diuretics

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23
Q

what duretics work in the collecting tubule?

A

potassium-sparing diuretics

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24
Q

how do carbonic anhydrase inhibitor diuretics work?

A

block Na/H+ exchange transporter in the proximal convoluted tubule

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25
Q

how do loop diuretics work?

A

block Na/K/2Cl triple transporters in the thick ascending limb of the loop of henle

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26
Q

how do thiazide diuretics work?

A

block Na/Cl cotransporter on the distal convoluted tubule

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27
Q

how do potassium sparing diuretics work?

A

block ENaC or bind to aldosterone receptor and so prevent Na/K exchange transporter on the collecting tubule

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28
Q

compare thiazide and loop diuretics in terms of strength of diuresis?

A

thiazides have a milder diuresis

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29
Q

what is the main function of potassium-sparing diuretics?

A

for low serum potassium to prevent potassium excretion

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30
Q

what are the 2 important drug transport systems into the renal tubule?

A

organic anion transporters

organic cation transporters

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31
Q

what type of drugs do organic anion transporters transport?

A

acidic drugs

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32
Q

what type of drugs do organic cation transporters transporter?

A

basic drugs

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33
Q

how do organic anions enter the basolateral membrane of the tubular cells?

A

either diffusion

or via organic anion transporters

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34
Q

how do organic anion transporters work?

A

exchange organic ions for a-ketoglutarate (aKG)

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35
Q

how do organic anions enter the tubular fluid across the apical membrane?

A

either multidrug resistance protein 2 (MDRP2) or organic anion transporter (in exchange for aKG)

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36
Q

how do organic cations enter the basolateral membranes of the tubular cells?

A

either difusion

or via organic cation transporters

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37
Q

how do organic cation transporters work?

A

simple transporter

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38
Q

how do organic cations enter the tubular fluid across the apical membrane?

A

multidrug resistance protein 1 or OC+/H+ antiporter

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39
Q

why is gout a side effect of thiazide and loop diuretics?

A

thiazides and loop diuretics compete with uric acid for transport across the basolateral membrane via organic anion transporter, so lead to increased uric acid in the blood

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40
Q

where in the nephron are diuretics excreted into the tubular fluid?

A

proximal convoluted tubule

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41
Q

what site of the Na/K/2Cl triple transporter do loop diuretics bind to?

A

the Cl site

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42
Q

what does increased Na concentration of the filtrate in the distal tubules do to the excretion of K?

A

increases K excretion

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43
Q

why do loop diuretics cause hypokalaemia?

A

block Na reabsorption so increase Na concentration in the distal tubules, this increases the Na+ exchange for K+ so more K+ is excreted

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44
Q

what channels in the distal and collecting tubules does Na pass into? (these are heavily regulated by aldosterone)

A

ENaC

epithelial Na channels

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45
Q

how do loop diuretics indirectly effect the blood pressure?

A

venodilator action

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46
Q

why are loop diuretics used in chronic heart failure?

A

reduce circulating volume

47
Q

why are loop diuretics used in acute chronic kidney failure?

A

maintain urine output in a vastly reduced kidney blood supply

48
Q

can loop diuretics be used in hyper or hypo-calcaemia in order to bring serum Ca to the normal levels?

A

hypercalcaemia

49
Q

in what condition can diuretic resitance to loop diuretics occur and why?

A

nephrotic syndrome

-binds to proteins within the urine and so cant bind to triple cotransporter

50
Q

what do loop diuretics do to serum potassium?

A

reduce it - hypokalaemia

51
Q

why should you be careful using loop diuretics with digoxin or class III anti-dysrhythmic drugs? (potassium channel blockers)

A

because hypokalaemia increases toxicity of these drugs

52
Q

loop and thiazide diuretics cause a shift in acid-base balance, what is this shift and why is it cause?

A

metabolic alkalosis

due to increase Na in the distal tubules so increased H+ (and K) secretion (through Na/H antiporter)

53
Q

what do loop diuretics do to serum calcium and serum magnesium?

A

decrease serum calcium

decrease serum magnesium

54
Q

what site in the Na/Cl channel on the distal tubule to thiazide diuretics bind to and therefore block?

A

Cl- site

55
Q

what are the main loop diuretics in use?

A

furosemide and bumetanide

56
Q

what are the main thiazide diuretics in use?

A

bendroflumethiazide

hydrochlorothiazide

57
Q

how do thiazide diuretics cause hypokalaemia

A

block Na reabsorption so increase Na concentration in the distal tubules, this increases the Na+ exchange for K+ so more K+ is excreted

58
Q

what do thiazide diuretics do to serum calcium and serum magnesium?

A

increases serum calcium

decreases serum magnesium

59
Q

how do thiazide diuretics indirectly contribute to antihypertensive effects?

A

vasodilatory action

60
Q

what are the main 2 reasons for thiazide diuretic use?

A

mild heart failure

hypertension

61
Q

why can thiazides be used for renal stone disease (nephrolithiasis)?

A

decreases Ca excretion and so discourages Ca stone formation

62
Q

which type of diuretic can help increase responsiveness of nephron to ADH? (in nephrogenic diabetes insipidus)

A

thiazides

63
Q

why must you be cautious about using thiazide diuretics in type 1 or 2 diabetics?

A

impaired glucose tolerance

64
Q

what are the 2 types of potassium sparing diuretics/

A

aldosterone antagonists

ENaC inhibitors

65
Q

what type of potassium sparing diuretics are amiloride and tiamterene?

A

ENaC inhibitors

66
Q

what type of potassium sparing diuretics are spironolactone and eplerenone?

A

aldosterone antagonists

67
Q

what system can counteract the effect of thiazide and loop diuretics?

A

RAS

due to reduced BP

68
Q

what is the function of potassium-sparing diuretics when added to a loop or thiazide diuretic?

A

increases effect of diuretic (by blocking aldosterone)

prevents hypokalaemia

69
Q

what 4 conditions are aldosterone antagonists used in?

A
  • heart failure
  • primary hyperaldosteronism (Conn’s)
  • resistant essential hypertension
  • secondary hyperaldosteronism (due to hepatic cirrhosis with ascites)
70
Q

how do osmotic diuretics enter the nephron?

A

glomerular filtration

71
Q

how do osmotic diuretics work?

A

increase osmoarity of the filtrate so reduce the reabsorption of water

72
Q

how do osmotic diuretics secondarily decrease Na reabsorption?

A

cause an increase in volume of filtrate and so there is a decreased Na conc and so a decreased electrochemical gradient for Na to follow

73
Q

when are osmotic diuretics used? (specifically for effect on kidney)

A

prevention of acute hypovolaemic renal failure by maintaining urine flow

74
Q

how are osmotic diuretics administered?

A

IV

75
Q

why can osmotic diuretics be used in raised intracranial and raised intraocular pressure?

A

so polar that the solute cannot enter the eye or brain but increased plasma osmolarity extracts water from these compartments

76
Q

why does osmotic diuresis occur in hyperglycaemia?

A

glucose transporters (SGLT1 and SGLT2) limits are exceeded so glucose remains in the filtrate, this increased osmolarity decreases reabsorption of water

77
Q

why can patients with cardiovasculat problems experience hypotension due to iodine-based radiocontrast dyes?

A

the dyes are filtered but not reabsorbed so increase osmolarity of the filtrate, so reduce water reabsorption and increased water is excreted
these patients already have a low cardiac output so reduced volume can send them into hypotension

78
Q

carbonic anhydrase inhibitors shift the pH into what? and why?

A

metabolic acidosis

due to increase HCO3- excretion

79
Q

even though carbonic anhydrase inhibitors are not used as diuretics any more, what are their 3 clinical uses?

A

glaucoma/following eye surgery
prophylaxis of altitude sickness
infantile epilepsy

80
Q

how do carbonic anhydrase inhibitors reduce intraocular pressure in glaucoma?

A

suppress formation of aqueous humour

81
Q

what does alkalinising the urine do to the excretion of weak acids and why?

A

increases excretion

because alkaline pH favours ionised form of acid which cannot be reabsorped

82
Q

what is neurogenic diabetes insipidus treated with?

A

desmopressin

a vasopressin analogue

83
Q

what benefit does treating diabetes insipidus with desmopressin have over vasopressin?

A

desmopressin is selective for V2 receptor activity, so doesn’t stimulate V1 which would cause increased blood pressure
(vasopressin stimulates V1)

84
Q

what is nephrogenic diabetes indispidus usually caused by?

A

mutations in V2 receptor gene

AVPR2

85
Q

what does lithium do to the action of vasopressin on the kidney?

A

inhibits

-nephrogenic diabetes inspidus

86
Q

compare diuretics to aquaretics?

A

diuretics- Na loss with accompanying water loss

aquaretics- water loss with no Na loss

87
Q

what is the function of aquaretics/vaptans?

A

competitive antagonists of vasopressin receptors (AVPR2) to prevent aquaporin stimulation –>
increased water excretion

88
Q

compare diuretics and aquaretics in terms of what happens to plasma Na con?

A

diuretics do not change plasma Na conc

aquaretics increase plasma Na conc

89
Q

what drug can be used in the syndrome of inappropriate anti-diuretic hormone secretion?

A

tolvaptan

an aquaretic

90
Q

why is tolvaptan used in the syndrome of inappropriate anti-diuretic hormone syndrome?

A

causes loss of water to correct hyponatraemia

91
Q

what vasopresin receptor is found in the vascular smooth muscle?

A

V1a

92
Q

what vasopressin receptor is found in the basolateral membrane of the renal tubular cells?

A

V2

93
Q

what vasopressin receptor is tolvaptan selective for?

A

V2

94
Q

where in the nephron is most affected by osmotic diuretics?

A

proximal tubule

95
Q

where is SGLT1 found?

A
  • in the S2/3 segments of the proximal convoluted tubule of the kidneys
  • small intestine
96
Q

where is the SGLT 2 found?

A

in the S1 segment of the proximal conoluted tubule of the kidneys

97
Q

compare the percentages of glucose reabsorption in the PCT via SGLT1 and SGLT2?

A

SGLT1 - 10%

SGLT2- 90%

98
Q

reabsorption of glucose via SGLT1 and SGLT2 on the apical is through what mechanism?

A

secondary active transport

99
Q

reabsorption of glucose on the basolateral membrane is through what mechanism?

A

facilitated diffusion using GLUT

100
Q

compare SGLT1 and SGLT2 in terms of affinity and capacity for glucose?

A

SGLT1- high affinity, low capacity

SGLT2- low affinity, high capacity

101
Q

familial renal glucosuria is caused by what?

A

dysfunction of SGLT2

102
Q

what is the most common side effects of SGLT2 inhibitors?

A

increased genital bacterial and fungal infections

due to sugar in urine

103
Q

are SGLT2 inhibitors dependent or independent of insulin?

A

independent

104
Q

what are the major prostaglandins synthesised in the kidney?

A

PGE2

PGI2

105
Q

where in the kidney is PGE2 synthesised?

A

medulla

106
Q

where in the kidney is PGI2 synthesised?

A

glomeruli

107
Q

what do PGE2 and PGI2 do to the vascular smooth muscle?

A

vasodilation

108
Q

PGE2 and PGI2 are synthesised by the kidney in response to which 5 stimuli?

A 
ischamie
mechanical trauma
angiotensin II
ADH
bradykinin
109
Q

when do prostaglandins produced by the kidneys become important?

A

under conditions of vasoconstriction or decreased arterial blood volume

110
Q

why are prostaglandins produced by the kidneys important in conditions of vasoconstriction or decreased blood volume?

A

compensatory vasodilation to maintain GFR and urine output

111
Q

which 2 important molecules cause the production of prostaglandins?

A

COX 1

COX 2

112
Q

why may NSAIDS precipitate acute renal failure (reduced GFR)?

A

reduce prostaglandin vasodilator affect and so further reduce renal blood flow and GFR

113
Q

what drug combination must you avoid in the kidneys?

A

ACEI/ARB
and diuretic
and NSAIDs
‘triple whammy’

114
Q

what does a triple whammy cause? (ACEI/ARB, diuretic and NSAID)

A

increased chance of renal failure (due to poor renal perfusion)

Renal (6 decks)

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