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Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what force drives water out of capillaries

A

hydrostatic pressure in the capillary (Pc)

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2
Q

what drives water into the capillary

A

oncotic pressure of plasma (derived from plasma proteins)

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3
Q

examples of diseases that increase Pc and decrease oncotic pressure of plasma

A

nephrotic syndrome
CHF
hepatic cirrhosis with ascites

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4
Q

what causes nephrotic syndrome

A

there is a disruption to filtration barrier causing proteins to leave circulation and enter the filtrate

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5
Q

classic urine presentation of proteinuria

A

frothy urine

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6
Q

how does CHF cause oedema?

A

there is reduced CO and renal hypoperfusion activating RAAS causing retention of Na+ and H2O

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7
Q

how does cirrhosis with ascites cause oedema

A

increased pressure in hepatic portal veins and decreased production of albumin (liver disease) causes loss of fluid into peritoneal cavity which activates RAAS due to reduced circulating volume-thrombosis danger

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8
Q

where is the triple co-transporter Na+/K+/2Cl- found?

A

thick ascending loop of Henle

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9
Q

which diuretic blocks the triple co-transporter?

A

loop diuretics

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10
Q

which (now obsolete) diuretic blocks Na+/H+ exchange?

A

carbonic anhydrase inhibitors (found in PCT and early DCT)

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11
Q

where is the Na+/Cl- co-transporter found?

A

early DCT

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12
Q

which diuretic blocks Na+/Cl- co-transport?

A

thiazide diuretics

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13
Q

where is Na+/K+ exchanger found?

A

collecting duct

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14
Q

what blocks the Na+/K+ exchanger?

A

potassium-sparing diuretics

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15
Q

to act diuretics must enter the filtrate by?

A
  • glomerular filtration (when not bound to large plasma proteins)
  • secretion by PCT
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16
Q

two transport processes in PCT that secrete diuretics into the filtrate?

A
  • organic anion transporters (OATs)

- organic cation transporters (OCTs)

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17
Q

what does OATs transport?

A

acidic/negatively charged molecules e.g. PAH, thiazides and loop

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18
Q

what do OCTs transport?

A

basic/ positively charged e.g. triamterene and amiloride

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19
Q

describe OA secretion

A
  • OA- enters the tubular cell from the blood in exchange for alpha-KG via OAT1,2,3
  • alpha-KG re-enters via NaDC3
  • OA- crosses to the filtrate via MRP2/4 and BCRP
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20
Q

describe OC secretion

A
  • OC+ enters the tubular cell via OCT2

- OC+ enters the lumen and filtrate via MATE or MDDR1

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21
Q

examples of loop diuretics

A

furosemide

bumetanide

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22
Q

what do loop diuretics bind to?

A

bind to Cl- on the triple co-transporter in PCT

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23
Q

action of loop diuretics

A

increased Na+ load is delivered to distal region of the nephron causing increased K+ loss with excretion of Ca2+ and Mg2+

also have a venodilator action

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24
Q

how do loop diuretics enter the filtrate?

A

strongly bind to plasma protein so enter via OAT

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25
Q

what are loop diuretics used in?

A 
acute pulmonary oedema
CHF
CKF (increase UO in AKF)
ascites
nephrotic syndrome
hypertension
acute hypercalcaemia
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26
Q

contra-indications of loop diuretics

A

severe hypovolaemia

dehydration

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27
Q

cautions with loop diuretics

A

hypokalaemia
hyponatraemia
hepatic encephalopathy
gout

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28
Q

adverse effects of loop diuretics

A
  • hypokalaemia (correct with potassium-sparing diuretics or supplements)
  • metabolic alkalosis (Na+/H+)
  • hypocalcaemia
  • hypomagnesemia
  • hypovolaemia
  • hyperuricaemia (competition between uric acid and loop)
  • dose related loss of hearing
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29
Q

which drugs does hypokalaemia increase toxicity of?

A 
digoxin
class III AADs
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30
Q

example of a thiazide diuretic

A

bendroflumethiazide

31
Q

what do thiazides bind to?

A

Cl- binding site on Na+/Cl- in early DCT

32
Q

action of thiazides

A

increase Na+ in collecting duct causing K+ loss and increased reabsorption of Ca2+ which causes diuresis

also vasodilation action

33
Q

how do thiazides enter the filtrate?

A

OATs

34
Q

clinical indications for thiazides

A
  • hypertension (mild HF)
  • severe resistant oedema
  • renal stone disease (reduces Ca2+)
  • nephrogenic DI
35
Q

contra-indications and cautions of thiazides

A

hypokalaemia
hyponatremia
gout

36
Q

adverse effects of thiazides

A 
hypokalaemia
metabolic alkalosis
hypovolvaemia
hypomagnesemia
hyperuricaemia
ED
impaired glucose tolerance in diabetes
37
Q

on what receptors does aldosterone act?

A

via cytoplasmic receptors

38
Q

action of aldosterone

A

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

39
Q

why do spironolactone and eplerenone have limited diuretic action?

A

modulated by aldosterone

40
Q

action of spironolactone and eplerenone

A

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

41
Q

action of amiloride and triamterene

A

block luminal Na+ channels in collecting duct

42
Q

how do potassium sparing diuretics enter the nephron

A

OCT in PCT

43
Q

clinical indications of potassium-sparing diuretics

A
  • in conjunction with diuretics that cause potassium loss (alone cause hyperkalaemia)
  • heart failure
  • primary aldosteronism (Conn’s) and secondary (cirrhosis and ascites)
  • resistant hypertension
44
Q

contra-indications of potassium-sparing diuretics

A

severe renal impairment
hyperkalaemia
Addisons

45
Q

example of osmotic diuretic

A

mannitol

46
Q

where does mannitol act

A

PCT

47
Q

how does mannitol enter the filtrate?

A

glomerular filtration

48
Q

clinical indications of mannitol

A
  • prevent acute hypovolaemia renal failure to maintain UO

- acutely raised ICP and IOP

49
Q

adverse of mannitol

A

transient expansion of blood volume and hyponatraemia

50
Q

causes of osmotic diuresis

A

mannitol
hyperglycaemia
iodine radiocontrast dyes

51
Q

examples of carbonic anhydrase inhibitors

A

azetazolamide

52
Q

clinical uses of carbonic anhydrase inhibitors

A 
no longer used as diuretics
glaucoma
following eye surgery (reduce IOP)
prophylaxis of altitude sickness
infantile epilepsy
53
Q

when is alkalising the urine useful?

A

dysuria
prevention of uric stones
excretes weak acids

54
Q

how to alkalinise the urine

A
  • citrate salts (generate HCO3- in Krebs)

- carbonic anhydrase inhibitors

55
Q

substances that inhibit ADH

A

lithium
demeclocycline
vaptans

56
Q

example of vaptan

A

tolvaptan

57
Q

action of tolvaptan

A

competitive antagonist of ADH receptors which causes excretion of water (but not Na+)

58
Q

what is tolvaptan used in?

A

SIADH

59
Q

when can glucose appear in the urine

A

diabetes when glucose concentration exceeds renal threshold (11mmol)

60
Q

example of SGLT2i

A

empagliflozin

61
Q

action of SGLT2i

A

excretes glucose
decreases HbA1c
weight loss

62
Q

adverse of SGLT2i

A

genital bacterial and fungal infections

63
Q

where is SGLT2 found?

A

PCT

responsible for reabsorption of glucose (against gradient with Na+ symport)

64
Q

examples of prostaglandins synthesised by the kidney

A

PGE2 (medulla)

PGI2 (glomeruli)

65
Q

action of prostaglandins

A

vasodilation

loss of Na+

66
Q

when is synthesis of prostaglandins enhanced?

A 
ischaemia
trauma
angiotensin II
ADH
bradykinin
67
Q

when do prostaglandins have the largest effect

A

when there is vasoconstriction or hypovolaemia as vasodilates afferent arteriole and releases renin (angiotensin II vasoconstricts efferent) allowing kidneys to maintain UO

68
Q

examples of NSAIDs

A

aspirin
naproxen
diclofenac

69
Q

action of NSAIDs

A

inhibit COX and precipitate ARF in patients with low GFR e.g. bilateral RAS or hypovolaemia

70
Q

describe the triple whammy effect

A

combination of ACEI/ARB, diuretic and NSAID

71
Q

how is uric acid formed?

A

catabolism of purines

72
Q

what does high urate in the serum predispose to?

A

gout

73
Q

what blocks reabsorption of urate in PCT?

A

probenecid

sulfinpyrazole

74
Q

action of allopurinol

A

stops urate synthesis

Renal (54 decks)

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