Pharmacology Flashcards

1
Q

four sites of diuretic action in the nephron

A
  1. PCT
  2. thick ascending loop of Henle
  3. early DCT
  4. collecting duct
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2
Q

transporters in the PCT

A

Na+ (passive Cl- absorption)

Na+/H+ exchange

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3
Q

what blocks Na+/H+ exchange in the PCT and early DCT?

A

carbonic anhydrase inhibitors

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4
Q

what transporter is present in the thick ascending loop of Henle?

A

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

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5
Q

what blocks the Na+/K+/2Cl- co-transporter in the thick ascending loop of Henle?

A

loop diuretics

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6
Q

transporters in the early DCT

A

Na+/H+ exchange

Na+/Cl- co-transport

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7
Q

what blocks Na+/Cl- co-transporter in the early DCT?

A

thiazides

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8
Q

transporter present in collecting ducts

A

Na+/K+ exchange

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9
Q

what blocks Na+/K+ exchange in the collecting duct?

A

potassium-sparing diuretics

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10
Q

two ways diuretics can enter the filtrate?

A
  1. glomerular filtration

2. secretion

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11
Q

which drugs can enter the filtrate by glomerular filtration?

A

drugs not bound to large plasma proteins

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12
Q

two transport processes that secrete components into the filtrate

A
  1. organic anion transporters (OATs)

2. organic cation transporters (OCTs)

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13
Q

which drugs can enter the filtrate via OATs?

A

acidic/negatively charged

PAH, thiazides and loop

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14
Q

which drugs can enter the filtrate by OCTs?

A

basic/ positively charged

triamterene and amiloride

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15
Q

examples of loop diuretics

A

furosemide

bumetanide

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16
Q

action of loop diuretics

A

inhibit Na+/K+/2Cl- in PCT by binding to the Cl- site

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17
Q

what do loop diuretics cause excretion of?

A

Na+
K+
Ca2+
Mg2+

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18
Q

when are loop diuretics contra-indicated?

A

severe hypovolvaemia

dehydration

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19
Q

adverse of loop diuretics

A
hypokalaemia (use potassium-sparing diuretics)
metabolic alkalosis (Na+/H+ transporter)
hypocalcaemia
hypomagnesemia
hypovolaemia
hyperuricaemia
dose-related hearing loss
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20
Q

example of a thiazide diuretic

A

bendroflumethiazide

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21
Q

action of thiazide diuretics

A

inhibit Na+/Cl- binding to Cl- site in early DCT

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22
Q

what do thiazides cause in the body?

A

increases Na+ in the collecting duct causing K+ loss and reabsorption of calcium

23
Q

adverse of thiazides

A
hypokalaemia
metabolic alkalosis
hypovolaemia
hypomagnesemia (not calcium so used in elderly with OP)
hyperuricaemia
ED
impaired glucose tolerance in diabetes
24
Q

what receptors does aldosterone act on?

A

cytoplasmic receptors

25
Q

action of aldosterone

A

increases synthesis of a protein that activates ENaC and Na+/K+ATPase

26
Q

examples of potassium-sparing diuretics

A

spironolactone and eplerenone

27
Q

why do potassium-sparing diuretics have limited diuretic action?

A

modulated by aldosterone

28
Q

action of potassium-sparing diuretics

A

antagonists of aldosterone receptor so increase excretion of Na+ while decreasing excretion of K+

29
Q

action of amiloride and triamterene?

A

block luminal Na+ channels in collecting duct

30
Q

when are potassium-sparing diuretics contraindicated?

A

severe renal impairment
hyperkalaemia
Addison’s

31
Q

example of osmotic diuretic

A

mannitol

32
Q

how do osmotic diuretics enter the filtrate?

A

glomerular filtration

33
Q

where do osmotic diuretics act?

A

PCT

34
Q

when are osmotic diuretics used?

A

acutely raised ICP and IOP

prevention of acute hypovolaemia in renal failure to maintain UO

35
Q

adverse of osmotic diuretics

A

transient expansion of blood volume

hyponatraemia

36
Q

examples of CA inhibitors

A

acetazolamide

37
Q

action of CA inhibitors

A

increase excretion of HCO3-

38
Q

when are CA inhibitors used?

A

glaucoma
following eye surgery
dysuria to prevent uric stones

39
Q

example of a vaptan

A

tolvaptan

40
Q

action of vaptans

A

competitive antagonists of ADH receptors which causes excretion of water without accompanying Na+ loss as it acts in the collecting duct

41
Q

when are vaptans used?

A

SIADH to correct hyponatraemia

42
Q

where is glucose reabsorbed in the nephron? and which transporter?

A

PCT by SGLT2

43
Q

when does glucose appear in the urine?

A

concentration exceeds threshold

44
Q

example of SGLT2i

A

empagliflozin

45
Q

action of SLGT2i

A

excretion of glucose

weight loss

46
Q

adverse of SGLT2i

A

genital bacterial and fungal infections

47
Q

prostaglandins in the kidneys

A

PGE2

PGI2

48
Q

what do prostaglandins cause in the kidney?

A

vasodilation
loss of Na+
allowing adaption to hypoperfusion and maintenance of UO

49
Q

action of NSAIDs

A

inhibit COX and precipitate ARF in patients with low GFR

50
Q

what is involved in the triple whammy effect?

A

ACEI/ARB (efferent vasodilation)
diuretics
NSAIDs (afferent vasoconstriction)

51
Q

how is uric acid formed?

A

catabolism of purines

52
Q

what predisposes to gout?

A

high urate in serum

53
Q

action of probenecid and sulfinpyrazole

A

block reabsorption of urate in PCT

54
Q

action of allopurinol

A

stops urate synthesis