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MB2: Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

positive pressures in peripheral capillaries

A

hydrostatic capillary pressure

oncotic pressure of interstitial fluid

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2
Q

pressures exerted on peripheral capillaries

A

hydrostatic pressure in interstitial fluid

oncotic plasma pressure

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3
Q

what conditions may lead to increased chances of oedema

A

nephrotic syndrome
hepatic cirrhosis and ascites
congestive heart failure

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4
Q

describe how nephrotic syndrome leads to oedema

A

large protein loss leads to decreased plasma oncotic pressure and so there is increased fluid in the interstitial space
decreases blood volume and leads to RAAS stimulation, fluid retention and further dilution of plasma proteins

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5
Q

describe how congestive heart failure leads to oedema

A

reduced CO and renal hypoperfusion stimulates RAAS

this leads to reduced plasma oncotic pressure and increased preload, worsening heart failure and leading to odema

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6
Q

describe how hepatic cirrhosis with ascites leads to oedema

A

increased pressure in hepatic portal vein and decreased albumin production leads to fluid loss into the peritoneal cavity
this increases capillary hydrostatic pressure and reduces capillary oncotic pressure

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7
Q

what channel do carbonic anhydrase inhibitors block and where

A

Na/H exchange in proximal convoluted tubule and early distal convoluted tubule

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8
Q

what channel do loop diuretics block and where

A

Na/K/2Cl cotransport in thick ascending limb of the loop of henle

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9
Q

what channel do potassium sparing diuretics block and where

A

Na/K exchange in collecting duct

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10
Q

what channel do thiazide diuretics block and where

A

Na/Cl cotransport in early distal convoluted tubule

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11
Q

what organic transporters transport acidic drugs

A

organic anion transporters

OAT

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12
Q

what organic transporters transport basic drugs

A

organic cation transporters

OCT

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13
Q

describe anion secretion in the proximal tubule

A

enter basolateral membrane by OAT1,2,3 and transported out of the apical membrane by BCRP and MRP

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14
Q

describe cation secretion in the proximal tubule

A

enter by OCT2 and enter lumen in a rate limiting step by MATES and MDR1

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15
Q

describe the specificity of OAT 1,2,3 and what drugs can interact

A 
diuretics 
statins 
penicillins 
NSAIDs
urate
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16
Q

describe the specificity of OCT2 and what drugs can interact

A 
diuretics 
atropine 
metformin
morphine 
catecholamines
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17
Q

describe the mechanism of action of loop diuretics

A

blocks triple cotransporter
prevents sodium uptake into interstitial fluid and prevents potassium recycling
this prevents Ca and Mg uptake and chloride
decreases osmolarity of interstitial fluid to lead to increased water loss

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18
Q

autosomal recessive mutations in the triple cotransporter lead to what

A

bartter syndrome

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19
Q

loop diuretics enter nephron by OCT/OAT?

A

OAT

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20
Q

clinical indications of loop diuretics

A 
acute hypercacaemia 
chronic heart failure 
CKD 
acute pulmonary oedema 
hepatic cirrhosis with ascites 
nephrotic syndrome 
refractory hypertension
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21
Q

contraindications to loop diuretics

A

dehydration/severe hypovolaemia

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22
Q

adverse effects loop diuretics

A 
hypokalaemia 
metabolic alkalosis 
hypocalcaemia, hypomagnaesmia 
dose related loss hearing 
hyperuricaemia 
hypovolaemia, hypotension
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23
Q

cautions loop diuretics

A

hypokalaemia, hepatic encephalopthy, gout, hyponatraemia

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24
Q

mechanism of action of thiazide diuretics

A

inhibition of Na/Cl cotransporter b binding to Cl site
increase load of Na delivered to collecting tubule
leads to K loss but increases Ca
vasodilator action

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25
Q

thiazide diuretics enter by OCT/OAT

A

OAT

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26
Q

mutations in the Na/Cl channel lead to ___ syndormw

A

gitelman

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27
Q

indication for thiazide diuretics

A 
mild heart failure 
hypertension 
severe resistant oedema 
renal stone disease
nephrogenic DI
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28
Q

contraindication to thiazide diuretics

A

hypokalaemia

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29
Q

caution for thiazide diuretics

A

hyponatraemia, gout

30
Q

adverse effects of thiazide diuretics

A 
hypokalaemia 
metabolic alkalosis 
hypovolaemia, hypotension 
mypomagnaesmia 
hyperuricaemia 
erectile dysfunction 
impaired glucose tolerance in DM
31
Q

describe how loop and thiazide diuretics lead to K loss

A

increased Na load caused by diuretics leads to increased uptake by other channels
there is charge separation, with excess -ve K let out of filtrate and +ve Na let into interstitium
depolarises luminal/BL membrane
causes increased K secretion, and this is washed away

32
Q

mechanism of action of amiloride and triamterine?

A

block apical Na channel to decrease reabsorption in late distal and collecting duct

33
Q

absorption of potassium sparing diuretics is by OAT/OCT

A

OCT

34
Q

mechanism of action of spironolactone/eplerenone

A

compete with aldosterone binding to intracellular receptors to prevent aldosterone action
increase Na excretion and decrease K excretion

35
Q

indication for potassium sparing diuretics

A

heart failure
primary hyperaldosteronism
refractory essential hypertension
secondary hyperaldosteronism

36
Q

contraindication to potassium sparing diuretics

A

severe renal impairment
hyperkalaemia
addisons disease

37
Q

describe the mechanism of action of IV mannitol

A

enters nephron by filtratiob and is not reabsorbed

causes increased urine osmolarity so decreases water reabsorption as well as Na reabsorption

38
Q

indication for IV mannitol

A

urgent management of raised ICP/IOP

39
Q

adverse effects of IV mannitol

A

hyponatraemia

blood volume expansion

40
Q

besides use of mannitol, what other examples of osmotic diuresis may occur

A

hyperglycaemia, due to saturation of glucose reabsorption

iodine contrast in imaging

41
Q

describe the action of carbonic anhydrase inhibitors

A

increase excretion of bicarb with N, K, H to cause alkaline diuresis and metabolic acidosis

42
Q

indication of carbonic anhydrase inhibitors

A 
no longer as diuretic 
lower IOP in glaucoma and surgery 
prophylaxis altitude sickness 
infantile epilepsy 
salicylate poisoning, cystitis, preventing uric acid stones
43
Q

what aquaporin is inserted on the apical membrane

A

AP4

44
Q

what aquaporin is secreted on the basolateral membrane

A

AP2/3

45
Q

true/false - alcohol stimulates ADH

A

false

46
Q

true/false - nicotine stimulates AD

A

true

47
Q

what drugs inhibit the action of vasopressin

A

vaptans
lithium
demeclocycline

48
Q

mechanism of action of desmopressin?

A

analogue of vasopresisn with V2 receptor selectivity to avoid increase in BP

49
Q

what ADH receptor mediates vasoconstriction and what mediates H2O reabsorption

A

V1A - vasoconstriction

V2 - H20 reabsorption

50
Q

mechanism of action of tolvaptan

A

V2 antagonist, used in hypervolaemia hyponatramia and SIADH

51
Q

mechanism of action of SGLT2i

A

inhibits SGLT2 and so there is osmotic diuresis of glucose and water in urine

52
Q

describe the effect that prostaglandins have on GFR

A

cause vasodilation of afferent arteriole and stimuilate renin to produce ATII to constrict the efferent arteriole

53
Q

describe the effect that NSAIDs have on prostaglandins

A

inhibit COX so can precipitate acute renal failure when blood flow is dependent on prostaglandins

54
Q

a combination of what drugs is particularly detrimental and can cause AKI

A

ACEI, diuretic, NSAID

55
Q

Drugs that cause renal injury?

A 
tacrolimus 
NSAIDs
diuretics 
ACEI/ARB
cocaine
56
Q

clue to hyperkalaemia in ECG

A

T wave bigger than R wave in all leads is abnormal

57
Q

what drugs have a narrow therapeutic index

A 
theophylline 
warfarin
lithium
digoxin
levothyroxine 
gentamicin
vancomicin
phenytoin
cyclosporin
carbamazepine
58
Q

what is the most effective way to find adverse drug reactions

A

drug development

59
Q

what is the least effective way to find adverse drug reactions

A

phase IV

60
Q

adverse drug reactions are almost always due to phase___

A

1

61
Q

how can allopurinol lead to stephens johnson syndrome

A

hypersensitivity within HLAB5801

62
Q

type A drug interactions?

A

augmented effect and dose dependent, drug/drug, drug/food or drug/disease

63
Q

type B drug interactions? examples?

A 
bizarre and idiosyncratic 
dose independent 
halothane and hepatic necrosis 
chloramphenicol and bone marrow aplasia 
drug rash
64
Q

type C drug interactions and example

A

chronic
steroid cushings
NSAID hypertension

65
Q

type D drug interactions and example

A

delayed
craniofacial abnormalities in isotrentinoin
secondary malignancies

66
Q

type E drug interactions and example

A

end of treatment
rebound angina from stopping BB
steroid withdrawal and addisonian crisis

67
Q

type F drug interactions

A

failed therapy

68
Q

examples of dose dependent type A reactions

A

AKI precipitated due to diuretics/ACEI and hypotension

ATN due to gentamicin, aspirin

69
Q

examples of drug/disease type A reactions

A

NSAIDs can worsen heart failure
constipation worsened by CCB or anticholinergics
beta blockers and asthma

70
Q

examples of drug/drug type A reactions

A

statins/macrolide
ACEI and SU
clopidogrel and PPI

71
Q

examples of drug/food type A reactions

A

grapefruit juice and statins
st johns wort and antidepression
banana, orange, green leafy veg and K sparing diuretics
dairy and poultry and abx, thyroid meds, digoxin, diuretics

MB2: Renal (11 decks)

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