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Z YEAR 2 Pharm > GORD Core Drugs > Flashcards

GORD Core Drugs Flashcards

(49 cards)

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1
Q

What are examples of NSAIDs?

A
  • ibuprofen
  • naproxen
  • diclofenac
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2
Q

What do NSAIDs inhibit?

A

enzyme cyclo-oxygenase (COX)

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3
Q

What does COX do?

A

rate-limiting step for the production of all prostanoids (prostaglandins & thromboxanes) from the parent arachidonic acid

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4
Q

What do prostanoids do?

A

act through a large number of prostanoid receptors to produce a highly complex array of actions

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5
Q

What are the anti-inflammatory actions, and probably most of the analgesic & antipyretic actions, of the NSAIDs related to?

A

Inhibition of COX-2

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6
Q

What are the unwanted effects of NSAIDs due to?

A

Inhibition of COX-1

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7
Q

What is the drug target of NSAIDs?

A

cyclo-oxygenase (COX) enzyme

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8
Q

What are the main side effects of NSAIDs?

A
  1. gastric irritation
  2. ulceration
  3. bleeding
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9
Q

What can NSAIDs cause in extreme cases?

A
  • perforation
  • reduced creatinine clearance and possible nephritis
  • bronchoconstriction in susceptible individuals (contraindicated in asthma)
  • Skin rashes and other allergies
  • dizziness
  • tinnitus
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10
Q

What may occur with prolonged use or in patients with existing CV risk with NSAIDs?

A

adverse cardiovascular effects (hypertension, stroke, MI)

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11
Q

What happens with prolonged analgesic abuse over a period of years?

A

chronic renal failure

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12
Q

What has been aspirin been linked to?

A

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

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13
Q

When are NSAIDs used as analgesic?

A

relief of mild to moderate pain (e.g. musculoskeletal pain, headache, dysmenorrhoea)

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14
Q

When are NSAIDs used as an antipyretic?

A

reduce fever

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15
Q

When are NSAIDs used for their anti-inflammatory properties?

A

chronic control of inflammatory diseases (e.g. rheumatoid arthritis, osteoarthritis)

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16
Q

When is aspirin used?

A

anti-aggregatory agent to inhibit platelet aggregation in patients who are at risk of stroke or myocardial infarction

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17
Q

How commonly were these drugs prescribed in the West London area in 2020?

A
  1. ibuprofen (48th), naproxen (45th), diclofenac (92nd)
  2. omeprazole (5th) and lansoprazole (10th)
  3. Ranitidine (37th)
  4. Paracetamol (14th)
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18
Q

What are examples of proton pump inhibitors (PPIs)?

A

omeprazole, lansoprazole

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19
Q

What do PPIs inhibit?

A

irreversible inhibitors of H+/K+ ATPase in gastric parietal cells

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20
Q

What are PPIs? Why do they last long?

Study These Flashcards
A
  1. weak bases and accumulate in the acid environment of the canaliculi of the parietal cells
  2. concentrates their actions there and prolongs their duration of action
21
Q

How effective are PPIs?

Study These Flashcards
A
  1. omeprazole plasma half-life approx. 1 h
  2. single daily dose affects acid secretion for 2-3 days)
  3. PPIs inhibit basal and stimulated gastric acid secretion by >90%.
22
Q

What is the drug target of PPIs?

Study These Flashcards
A

H+/K+ ATPase (‘proton pump’)

23
Q

What are the uncommon unwanted side effects of PPIs?

Study These Flashcards
A
  • headache
  • diarrhoea
  • bloating
  • abdominal pain
  • rashes
24
Q

What can the use of PPIs mask?

Study These Flashcards
A

symptoms of gastric cancer

25
What can omezrapole reduce the activity of?
1. Omeprazole is an inhibitor of cytochrome P2C19 | 2. has been reported to reduce the activity of e.g. clopidogrel, when platelet function is monitored
26
What happens to PPIs at low pH?
- PPIs are pro-drugs - At low pH 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
27
How are PPIs given?
orally but degrade rapidly at low pH so administered as capsules containing enteric-coated granules
28
What are examples of Histamine (H2) receptors antagonist?
ranitidine
29
How do H2 receptor antagonists work?
1. competitive antagonists of H2 histamine receptors (structural analogues of histamine) 2. inhibit the stimulatory action of histamine released from enterochromaffin-like (ECL) cells on the gastric parietal cells
30
How effective are H2 receptor antagonists?
nhibit gastric acid secretion by approximately 60%
31
What are the targets of H2 receptor antagonists?
Histamine H2 receptors
32
Are side effects of histamine H2 receptor antagonists?
no
33
What are the main side effects of H2 receptor antagonists?
1. Diarrhoea 2. dizziness 3. muscle pains 4. transient rashes
34
What does cimetidine affect?
(but not other H2 antagonists) 1. inhibits cytochrome P450 2. may retard the metabolism 3. potentiate the effects of a range of drugs incl. oral anticoagulants and TCAs
35
What is the dosage of ranitidine like?
1. plasma half-life approx. 2-3 h – well tolerated so twice daily dosing effective 2. 1st pass metabolism (50% bioavailability) 3. low dose over-the-counter formulations available from pharmacies for short term use without prescription
36
What is paracetamol also known as?
acetaminophen
37
What is the mechanism of paracetamol?
- largely restricted to nervous tissue but its mechanism of action is unclear 1. both a central and peripheral action possibly involving interaction with a COX-3 isoform (inhibition of PG synthesis), cannabinoid receptors or the endogenous opioids 2. Interactions at 5HT & adenosine receptors have also been proposed.
38
What is the drug target of paracetamol?
Not yet well defined. COX-3 isoform?
39
What are the side effects of paracetamol?
1. very safe drug with few side-effects at therapeutic dose. 2. does not cause gastric irritation 3. occasional allergic skin reactions
40
What does an overdose of paracetamol cause?
hepatotoxicity
41
Is paracetamol anti-inflammatory?
not an NSAID as it has little anti-inflammatory activity
42
What can paracetamol help with?
good analgesic for mild-to-moderate pain and also has antipyretic activity
43
Are there restrictions on paracetamol sale?
Legal restrictions on sales of paracetamol have significantly reduced the number of fatalities from overdose in the UK although, regrettably, ingestion of large amounts of paracetamol remains a common method of suicide
44
Do PGs cause pain?
NO
45
How come COX causes pain?
-COX produces prostaglandins (PG) -PGs do not directly cause pain themselves, but they sensitise peripheral nociceptors mediators (bradykinin and histamine) which causes pain -NSAIDs inhibit COX
46
How do PGs in gastric mucosal cell protect the acid?
- increase bicarbonate release - increase mucus production - increase blood flow
47
Can topical drugs cause systemic side effects?
YES
48
Why does ratinidine and H2 not cause fractures but PPIs do?
Not sure
49
How does H2 histmaine receptors work?
1. ↓ acid production from parietal cell 2. Histamine receptors ↑ acid production via cAMP dependent activation of H+/K+ ATPase 3. The damaged mucosal barrier leaves stomach wall exposed to acid  symptoms pain 4. ↓ acid production, ↓ corrosive nature of environmen

Z YEAR 2 Pharm (9 decks)

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