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Y2 Pharmacology > Pharmacology of GORD > Flashcards

Pharmacology of GORD Flashcards

1
Q

give 3 NSAIDs

A

ibuprofen, naproxen, diclonefac

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2
Q

describe the primary mechanism of action for NSAIDs

A

inhibits cyclo-oxygenase, this is the rate limiting step for production of all prostanoids from arachidonic acid, thought that most wanted effects come from inhibition of COX2 whilst unwanted effects are from COX1 inhibition

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3
Q

prostanoids includes

A

prostaglandins and thromboxanes

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4
Q

what is the drug target for NSAIDs

A

cyclo oxygenase enzyme

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5
Q

what are common unwanted effects of NSAIDs

A

gastric irritation, ulceration and in extreme cases perforation, also reduced creatinine and possible nephritis, bronchoconstriction in susceptible individuals, skin rashes, other allergies, dizziness, tinnitus

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6
Q

in which patients is NSAIDs constricted for and why

A

asthma bc of the bronchoconstrictive effects

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7
Q

what are the adverse cardiovascular effects of NSAIDs

A

hypertension, stroke, MI may occur following prolonged use or in patients with pre-existing CV risk

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8
Q

prolonged analgesic abuse of NSAIDs over years is associated with what

A

chronic renal failure

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9
Q

what has aspirin use been linked with

A

a rare but serious post viral encephalitis (Reye’s syndrome) in children

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10
Q

what are the main uses for NSAIDs

A

analgesics (musculoskeletal pain, headache, dysmenorrhoea), antipyretics, anti inflammatories for chronic control of inflammatory disease

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11
Q

what else is aspirin used for

A

anti aggregatory agent to inhibit platelet aggregation in patient at risk of stroke or MI

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12
Q

what chronic inflammatory diseases are NSAIDs used to control

A

rheumatoid arthritis, OA)

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13
Q

give 2 Proton pump inhibitors

A

omeprazole, lansoprazole

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14
Q

what is the primary mechanism of action of PPIs

A

irreversible inhibitors of H+/K+ ATPase in gastric parietal cells, they are weak bases so accumulate in acid environment of canaliculi or parietal cells which concentrates action and prolongs it too

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15
Q

by how much is omeprasole’s action prolonged by

A

its plasma half life is 1h but single daily dose affects acid secretion for 2-3 days

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16
Q

by how much do PPIs inhibit basal and stimulated gastric acid secretion

A

by over 90%

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17
Q

what is the drug target for PPIs

A

H+/K+ ATPase (proton pump)

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18
Q

what are side effects of PPIs

A

headache, diarrhoea, bloating, abdominal pain, rashes
can also mask gastric cancer symptoms

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19
Q

what else does omeprazole do

A

inhibits cytochrome P2C19 and has been reported to reduce activity of eg clopidogrel when monitoring platelet function

20
Q

are PPIs pro drugs if so how are they metabolised

A

yes, at low pH converted into 2 reactive species which react with the sulphydryl groups in H+/K+ ATPase

21
Q

how are PPIs administered

A

orally but bc the degrade rapidly at low pH they are in capsules containing enteric coated granules

22
Q

what is ranitidine

A

H2 histamine receptor antagonist

23
Q

what is the primary mechanism of action of ranitidine

A

competitive antagonist of H2 receptors, so inhibit stimulatory action of histamine released from enterochromaffin like (ECL) cells on gastric parietal cells

24
Q

by how much do H2 receptor antagonists reduce gastric secretion

A

approx 60%

25
Q

what is the drug target for ranitidine

A

H2 receptor antagonist

26
Q

what are the side effects of H2 receptor antagonists

A

incidence is low, diarrhoea, dizziness, muscle pains, transient rashes

27
Q

what is cimetidine and what does it do

A

is a H2 receptor antagonist, inhibits cytochrome P450 and slows metabolism and potentiates the effect of a range of drugs including oral anticoagulants and tricyclic antidepressants

28
Q

how does the dosing for ranitidine work

A

plasma half life is 2-3h so taken twice daily

29
Q

what does it mean by ranitidine undergoes 1st pass metabolism

A

undergoes metabolism at specific location and decreases active drug’s conc upon reaching systemic circulation, for ranitidine there is 50% bioavailability

30
Q

what is paracetamol also known as

A

acetaminophen

31
Q

what is the primary mechanism of action of paracetamol

A

not totally clear
peripherally, may inhibit peroxidase enzyme
activation of descending serotonergic pathways possible via 5HT3 receptor activation
inhibits reuptake of endogenous endocannabinoids

32
Q

what does the peroxidase enzyme do

A

involved in conversion of arachidonic acid to prostaglandins

33
Q

how can the ability of paracetamol to inhibit peroxidase be blocked

A

if excessive levels of peroxide build up as is commonly seen in inflammation

34
Q

what would inhibition of the reuptake of endogenous endocannabinoids’ effect be

A

this would increase activation of cannabinoid receptors, which may contribute to activation of descending serotonergic pathways

35
Q

what are the drug targets for paracetamol

A

5HT3 receptors, cannabinoid reuptake proteins, peroxidase

36
Q

what are side effects of paracetamol

A

relatively safe

37
Q

what happens if u overdose on paracetamol

A

liver damage (less frequently renal damage too)
nausea vomiting, early features of poisoning (settles in 24h)
onset of right subcostal pain after 24h indicates hepatic necrosis

38
Q

paracetamol is taken for what

A

analgesia and as an anti pyretic, does not possess anti inflammatory activity

39
Q

how does stopping production of prostaglandins through COS by NSAIDs stop pain

A

prostaglandins sensitise peripheral nociceptors mediators (bradykinin and histamine) which causes pain
also indirectly prostaglandins mediate inflammation and so NSAIDs reduce this and thus pain

40
Q

how do NSAIDs cause gastric side effects

A

by blocking COX1 on gastric mucosal cells, this inhibits prostaglandin production and so inhibits prostaglandin mediated protection of gastric mucosa

41
Q

how do prostaglandins in gastric mucosal cells protect mucosa from acid

A

increase bicarbonate release, mucus production and blood flow

42
Q

what is the issue of taking both topical diclonefac gel and naproxen

A

bc diclonefac despite being tpocal can have systemic effects, they are both NSAIDs

43
Q

to manage adverse GI effects what should u prescribe if u want to give NSAIDs to someone with OA or RA or who is elderly

A

co prescribe PPI with NSAID

44
Q

what do you give to someone with low back pain, axial spondylarthritis, psoriatic arthritis and other peripheral spondylarthritides when u want to give NSAIDs

A

consider gastroprotection when prescribing NSAID

45
Q

what do u prescribe for those as high, moderate and mild risk of GI adverse vents when giving NSAIDs

A

for high - prescribe COX2 selective NSAID and PPI
for moderate - COX2 inhibitor alone, or NSAID plus PPI
for mild - non selective NSAID

46
Q

if u have osteoporosis why might not prescribe a PPI

A

PPIs known to increase risk of fracture, which is more likely if u have osteoporosis

47
Q

what is the mechanism behind PPIs increasing fracture risk

A

unclear but thought to be that calcium salt absorption is pH dependent so change in pH induced by PPIs might decrease this and so less calcium is available for bone

Y2 Pharmacology (8 decks)

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