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Year 2 - BRS > 1.12 - Pharmacology of GORD (core drugs) > Flashcards

1.12 - Pharmacology of GORD (core drugs) Flashcards

1
Q

What classes of drugs are involved in GORD? (4)

A
  • NSAIDs (increase GORD)
  • proton pump inhibitors (PPIs)
  • histamine (H2) receptor antagonists
  • paracetamol (AKA acetaminophen)
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2
Q

What are some examples of NSAIDs? (3)

And what NSAID can be used for peptic ulcer?

A
  • ibuprofen
  • naproxen
  • diclofenac

Celecoxib - COX-2 specific

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3
Q

What is the primary mechanism of action of NSAIDs?

A
  • inhibit the enzyme cyclo-oxygenase (COX) which is the rate-limiting step for the production of all prostanoids (prostaglandins and thromboxanes) from arachidonic acid
  • prostanoids act through a large number of prostanoid receptors to produce a highly complex array of actions
  • COX-2 inhibition leads to anti-inflammatory, analgesic and antipyretic effects
  • unwanted side effects due to COX-1 inhibition reducing PGs (PGs increase HCO3-, mucus production, blood flow, inhibit acid production)
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4
Q

What is the drug target for NSAIDs?

A

Cyclo-oxygenase (COX) enzyme

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5
Q

What are the main side effects of NSAIDs? (8)

A
  • gastric irritation, ulceration, bleeding
  • gastric perforation (extreme)
  • reduced creatinine clearance and possible nephritis
  • chronic renal failure in prolonged analgesic abuse over years
  • bronchoconstriction in susceptible individuals (contraindication in asthma)
  • skin rashes & allergies, dizziness, tinnitus
  • adverse cardiovascular effects (hypertension, stroke, MI) may occur with prolonged use/pre-existing CV risk
  • aspirin linked with rare but serious post-viral encephalitis (Reye’s syndrome) in children
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6
Q

What are the main uses of NSAIDs? (4)

A
  • analgesics for relief of mild to moderate pain (e.g. MSK pain - osteoarthritis, headache, dysmenorrhoea)
  • antipyretics to reduce fever
  • anti-inflammatory drugs for control of chronic inflammatory diseases e.g. RA, OA
  • aspirin only: anti-aggregatory agent to inhibit platelet aggregation in stroke/MI risk patients
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7
Q

What are some examples of PPIs? (2)

A
  • omeprazole
  • lansoprazole
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8
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 and accumulate in the acid environment of the canaliculi of the parietal cells
  • this concentrates their actions there and prolongs their duration of action
  • omeprazole plasma half-life is approx. 1hr but single daily dose affects acid secretion for 2-3 days
  • PPIs inhibit basal and stimulated gastric acid secretion by >90%
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9
Q

What is the drug target of PPIs?

A

H+/K+ ATPase (proton pump)

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10
Q

What are the main side effects of PPIs?

A
  • uncommon:
    • headache
    • diarrhoea
    • bloating
    • abdominal pain & rashes
  • use of PPIs may mask gastric cancer symptoms
  • omeprazole is an inhibitor of cytochrome P2C19 and has been reported to reduce the activity of e.g. clopidogrel, when platelet function is monitored
  • increased fracture risk
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11
Q

What is some extra information about PPIs? (2)

A
  • PPIs are pro-drugs which at low pH are converted into 2 reactive species which react with sulphydryl groups in the H+/K+ ATPase responsible for transporting H+ ions out of the parietal cells
  • generally given orally but degrade rapidly at low pH so given as capsules of enteric-coated granules
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12
Q

What is an example of a histamine (H2) receptor antagonist?

A

Ranitidine

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13
Q

What is the primary mechanism of action of H2 antagonists?

A
  • competitive antagonists of H2 histamine receptors (structural analogues of histamine)
  • inhibit stimulatory action of histamine released from enterochromaffin-like (ECL) cells on gastric parietal cells
  • inhibit gastric acid secretion by 60%
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14
Q

What is the drug target of H2 antagonists?

A

Histamine H2 receptor

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15
Q

What are the main side effects of H2 antagonists?

A
  • side effect incidence is low
  • diarrhoea, dizziness, muscle pains and transient rashes have been reported
  • cimetidine (not other H2 antagonists) inhibits cytochrome P450 and may retard metabolism and potentiate effects of a range of drugs including oral anticoagulants and TCAs
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16
Q

What is some extra information about H2 antagonists? (3)

A
  • ranitidine plasma half-life is 2-3 hours and well tolerated so 2x daily dose is effective
  • undergo 1st pass metabolism (50% bioavailability)
  • low dose OTC formulations available from pharmacy for short term use without prescription
17
Q

What is the main mechanism of action of paracetamol (acetaminophen)?

A
  • still not totally clear
  • at peripheral sites, may inhibit a peroxidase enzyme involved in converting arachidonic acids to prostaglandins (involves COX)
    • the ability of paracetamol to inhibit peroxidase can be blocked if excessive levels of peroxide build up (common in inflammation)
  • activation of descending serotonergic pathways possibly via 5HT3 receptor activation
  • inhibits reuptake of endogenous endocannabinoids, which would increase activation of cannabinoid receptors - may contribute to activation of descending pathways
18
Q

What is the drug target of paracetamol?

A
  • unclear:
    • peroxidase
    • 5HT3 receptors
    • cannabinoid reuptake proteins
19
Q

What are the main side effects of paracetamol?

A
  • relatively safe drug with few common side effects
  • overdose can lead to:
    • liver damage and less frequently renal damage
    • nausea and vomiting are early features of poisoning (settle in 24h)
    • onset of right subcostal pain after 24h indicates hepatic necrosis
20
Q

What is some extra information about paracetamol? (3)

A
  • anti-pyretic and analgesic
  • NOT anti-inflammatory
  • many medications contain paracetamol, must be careful not to OD
21
Q

How do NSAIDs have an analgesic effect?

A
  • NSAIDs inhibit COX, which produces prostaglandins
  • PGs do not directly cause pain but sensitise peripheral nociceptor mediators (bradykinin and histamine) which causes pain
  • NSAIDs inhibit this
  • indirect effect on pain too - PGs mediate inflammation, and hence NSAIDs will reduce inflammation
22
Q

How do NSAIDs have adverse effect on the stomach?

A
  • non-selective so also target COX 1 (unintended –> side effect)
  • acts on gastric mucosal cells to inhibit PG production and hence inhibition of PG-mediated protection of gastric mucosa
  • PGs increase HCO3- release, mucus production and blood flow
23
Q

For patients with osteoarthritis etc and requiring an NSAID for the pain, what can you co-prescribe to reduce risk of GI adverse events?

A

PPI

24
Q

How might PPIs increase fracture risk?

A

Mechanism of action unclear, but absorption of calcium salts is pH dependent, so the change in pH induced by PPIs might be responsible for a reduction in absorption and decrease in calcium available for bone

Year 2 - BRS (84 decks)

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