pharmacology of chronic kidney disease Flashcards

1
Q

what are some examples of statins

A

simvastatin

artovastatin

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2
Q

what is the primary mechanism of action of statins

A

selective, competitive inhibitor of HMGCoa reductase which is enzymes responsible for converting hmgcoa to mevalonate in cholesterol synthesis pathway.
by reducing hepatic cholesterol synthesis, an upregulation of ldl receptors and increased hepatic uptake of ldl cholesterol from circulation occurs

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3
Q

what is the drug target of statins

A

HMGcoa reductase

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4
Q

what are the main side effects of statins

A

muscle toxicity can occur with all statins, however likelihood increases with higher doses and in certain patients at increased risk of muscle toxicity

constipation/ diarrhoea. and other gi symptoms

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5
Q

extra info on statins

A

effective at reducing risk of adverse cardiac events in people
all patients should be regularly followed up to monitor for hyperkalaemia and acute renal failure

co administration with potent 3a4 inhibitors may result in increased statin serum concentrations

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6
Q

what is the mechanism of action of statins

A

irreversible inactivation of cox enzyme. prevents oxidation of arachidonic acid to produce prostaglandins. reduction of thromboxane a2 in platelets reduces aggregation.
reduction of pge2 at sensory pain neurones reduces pain and sensation and in brain decreases fever

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7
Q

what is the target of aspirin

A

cyclooxygenase

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8
Q

what are some side effects of aspirin

A

dyspepsia
haemorrhage
in elderly patients avoid doses >160mg daily and co adminiter with ppi if past history of peptic ulcer

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9
Q

what dose of aspirin is most cost effective?

A

low dose aspirin - is most cost effective for prevention of secondary events of thrombosis

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10
Q

why is stomach lining effected by aspirin

A

blockade of cox1 in gastric mucosal cells reduces mucus/bicarbonate production which can expose stomach lining to acid

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11
Q

what is the mechanism of action of trimethoprim

A

direct competitor of enzyme dihydrofolate reductase. inhibits reduction of dihydrofolic acid to tetrahydrofolic acid, a necessary component for synthesising purines required for dna and protein production

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12
Q

what is the target of trimethoprim

A

dihydrofolate reductase

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13
Q

what are some side effects of trimethoprim

A

diarrhoea

skin reactions

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14
Q

why is trimethoprim often administered with sulfamethoxazole

A

in combination they block 2 steps in bacterial biosynthesis of essential nucleic acids and proteins

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15
Q

extra info on trimethoprim

A

need to monitor blood counts with long term use/in those at risk of folate deficiency.
also monitor serum electrolytes in patients at risk of developing hyperkalaemia

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16
Q

what is the mechanism of action of gentamicin

A

binds to bacterial 30s ribosomal subunit disturbing translation of mrna leading to formation of dysfunctional proteins

17
Q

target of gentamicin

A

30s ribosomal subunit

18
Q

side effects of gentamicin

A

ototoxicity and nephrotoxicity

19
Q

why is gentamicin ineffective against anaerobic bacteria

A

an aminoglycoside antibiotic. can pass through gram neg cell membrane in an oxygen dependant manner

20
Q

how is gentamicin most likely administered

A

intravenously (in hospital) for endocarditis, septicaemia, meningitis, pneumonia or surgical prophylaxis