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Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is the purpose of drugs that are used to alter the pH of the urine?

A

to change the rate of excretion of a substance of a substance

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2
Q

what does oedema result from?

A

an imbalance between the rate of formation and absorption of interstitial fluid

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3
Q

what does capillary pressure do?

A

drives water out of the capillary

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4
Q

what does capillary oncotic pressure do?

A

drives water into the capillary

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5
Q

what is capillary oncotic pressure mostly derived from?

A

from abundance of plasma protein particularly albumin

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6
Q

what are the 2 main factors of the startling forces that contribute to the formation of oedema?

A

capillary pressure and capillary oncotic pressure

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7
Q

changes in what factors result in an imbalance and formation of oedema?

A

a increase in capillary pressure and a decrease in oncotic pressure

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8
Q

what 3 diseases can cause oedema?

A
  1. the nephrotic syndrome
  2. congestive heart failure
  3. hepatic cirrhosis with ascites
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9
Q

what is the nephrotic syndrome?

A

involves a disorder of glomerular filtration, allowing protein (largely albumin) to appear in the filtrate - proteinuria

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10
Q

when can proteinuria be normal?

A

in conditions of intense exercise

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11
Q

what does urine with protein in it tend to look like?

A

very frothy

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12
Q

in nephrotic syndrome, what happens to the oncotic pressure?

A

it decreases

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13
Q

what affect does a decreased oncotic pressure have on interstitial fluid?

A

increased formation of interstitial fluid

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14
Q

what affect does an increased interstitial fluid have on blood volume and cardiac output?

A

decreases BV and CO

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15
Q

how does the decrease in blood volume and cardiac volume lead to odema?

A

activation of RAAS causes Na+ and water retention which causes an increase in capillary pressure and a decrease in oncotic pressure leading to odema

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16
Q

what causes the odema in hepatic cirrhosis?

A

increased pressure in the hepatic portal vein, combined with decreased production of albumin causes loss of fluid into the peritoneal cavity

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17
Q

what affect does aging have on the numbers of the nephrons?

A

decrease with age

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18
Q

what affect can pro-longed hypertension have on the number of renal nephrons?

A

can half the number

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19
Q

what does carbonic anhydrase inhibitors inhibit?

A

reabsorption of sodium at the Na+/H+ exhange in the proximal tubule

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20
Q

why are carbonic anhydrase inhibitors not used as dieuretics anymore?

A

they lose the their diuretic affect to due changes in bicarbonate levels in the body

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21
Q

what is the principle role of the thick ascending limb of the loop of Henle?

A

reabsorption of sodium, it is impermeable to water

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22
Q

what does loop diuretics block?

A

the triple co-transport (Na+/K+/2Cl-) on the thick ascending limb of the loop of Henle

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23
Q

what do thiazide diuretics block?

A

Na+/Cl- co-transport in distal convuluted tubule

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24
Q

where do potassium-sparing diuretics block?

A

Na+/K+ exchange in the collecting duct

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25
Q

what affect do potassium sparing agents have on the collecting tubule?

A

increase reabsorption of potassium

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26
Q

where is the site of action for almost all diuretics?

A

the apical membrane of tubular cells- the membrane facing the lumen

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27
Q

in what 2 ways can a diuretic enter the filtrate?

A
  • by glomerular filtration

- secretion via transport process in the proximal tubule

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28
Q

why can all diuretics no enter the filtrate by glomerular filtration?

A

a lot of diuretics are bound to plasma proteins

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29
Q

what is the only diuretic thats site of action is the basolateral membrane?

A

spironolactone

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30
Q

what are the 2 transport systems important in the transport of diuretics?

A
  • the organic anion transporters (OATs)

- the organic cation transporters (OCTs)

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31
Q

what do the OATs transport?

A

negatively charged or acidic drugs

32
Q

what do the OCTs transport?

A

postively charged drugs or basic drugs

33
Q

what makes diuretics selective?

A

they become more concentrated in the tubular fluid compared to their concentration in plasma

34
Q

how do organic anions (OA-) enter the cell at the basolateral membrane?

A

by either diffusion (if in uncharged state) but mostly in exchange for an alpa-ketoglutarate (alpha-KG) via OATs

35
Q

how is alpa-ketoglutarate transported into the cell?

A

against a concentration gradient via a sodium- dicarboxylate transporter

36
Q

how does OA- enter the lumen of the tubule?

A
  • at the apical membrane

- via either multidrug resistance protein 2 or OAT4 (in exchange for alpha-KG)

37
Q

how can thiazides cause hperuricaemia and gout?

A

many drugs compete with organic ion transporter and thiazides compete with uric acid here, can lead to increase of uric acid

38
Q

how do organic cations (OC+) enter at the basolateral membrane?

A

by diffusion or OCT

39
Q

what drives both diffusion and transport by OCT of OC+ at the basolateral membrane?

A

negative potential of cell interior and it is against a concentration gradient

40
Q

how does OC+ enter the lumen?

A

at apical membrane, enters lumen via either multidrug resistance protein 1 or OC+/H+ antiporters (OCTN)

41
Q

example of an osmotic diuretic?

A

mannitol IV

42
Q

how do osmotic diuretics enter the nephron?

A

by glomerular filtration

43
Q

what affect does osmotic diuretics have on the osmolarity of the filtrate?

A

increase the osmolility

44
Q

what does an increase in the osmolality of the filtrate oppose?

A

the absorption of water in parts of the nephron that are freely permeable to water

45
Q

where is the major site of action for osmotic diuretics?

A

proximal tubule

46
Q

what is the secondary action of osmotic diuretics?

A

decrease in sodium reabsorption

47
Q

when are osmotic diuretics used for their effect on the kidney?

A

in prevention of acute hypovolaemic renal failure to maintain urine flow

48
Q

what extra-renal problem can osmotic diuretics used for?

A

in acutely raised ICP and IOP.

49
Q

how do osmotic diuretics work to help raised ICP and IOP?

A

solute does not enter the eye or brain but increased plasma osmolality extracts water from these compartments

50
Q

in what state can osmotic diuresis happen?

A

in hyperglycaemia

51
Q

what iatrogenic reason can cause osmotic diuresis?

A

as a consequence of the use of iodine-based radiocontrast dyes in imaging

52
Q

2 types of DI?

A
  • neurogenic DI

- nephrogenic DI

53
Q

how is neurogenic DI treated?

A

with desmopressin

54
Q

what is desmopressin?

A

synthetic analogue of vasopressin with V2 receptor selectivity

55
Q

why is it important that desmopressin is selective to V2 receptors?

A

to avoid V1 receptor being activated and causing an increase in BP

56
Q

where are V1 receptors present?

A

on vascular smooth muscle

57
Q

what is the problem in nephrogenic DI?

A

inability of the nephron to respond to vasopressin

58
Q

what do aquaretics do?

A

act as competitive antagonists of vasopressin receptors

59
Q

what do V1A receptors mediate?

A

vasoconstriction

60
Q

what do V2 receptors mediate?

A

water reabsorption in collecting tubule

61
Q

how do V2 receptors mediate water reabsorption at collecting tubule?

A

by transporting aquaporins from the cytoplasm onto the apical membrane

62
Q

what does blockage of V2 receptors cause?

A

excretion of water without accompanying sodium loss

63
Q

give an example of a V2 antagonist?

A

tolvaptan

64
Q

what is tolvaptan used in the treatment of?

A

SIADH to correct hyponatraemia

65
Q

where is SGLT1 expressed?

A

in both the kidney and the intestine

66
Q

where is SGLT2 expressed?

A

confined to the proximal tubule

67
Q

how is reabsorption of glucose facilitated at the apical membrane?

A

secondary active transport

68
Q

how is reabsorption of glucose facilitated at the basolateral membrane?

A

facilitated diffusion

69
Q

what is the affinity and capacity of SGLT2?

A

low affinity and high capacity

70
Q

what is the affinity and capacity of SGLT1?

A

high affinity and low capacity

71
Q

inhibition of SGLT2 mimics what condition?

A

familial renal glucosuria

72
Q

examples of SGLT2 inhibitors?

A

canagliflozin, dapagliflozin, empagliflozin

73
Q

what are the major prostaglandins synthesised by the kidney? what part of the kidney synthesizes them?

A

PGE2 - medulla and PGI2 - glomeruli

74
Q

under normal conditions, prostaglandins have little effect upon RBF and GFR, when do they gain importance and what do they cause?

A

under conditions of vasoconstriction or decreased effective arterial blood volume, where they cause compensatory vasodilation

75
Q

in what 2 ways do prostaglandins affect GFR?

A
  • a direct vasodilator effect upon the afferent arteriole

- releasing renin

76
Q

what do NSAIDS inhibit?

A

COX

77
Q

in what conditions can NSAIDS precipitate acute renal failure?

A

in conditions where renal blood flow is dependent upon vasodilator prostaglandins ( cirrhosis of liver, heart failure, the nephrotic syndrome)

Renal (10 decks)

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