Adverse Drug Reactions Flashcards
(65 cards)
What is the key difference between ADRs and Side Effects?
difficult to distinguish
SEs may be good or bad
ADRs are bad
What is a key safety concept for prescribing?
benefits must outweigh drawbacks
What is the beneficial SE of old anti-histamines (give eg.)?
sedation, OTC sleep medication
promethazine
What is the adverse effect of old anti-histamines (give eg.)?
sedation for allergy
promethazine
What must you do when prescribing to patients?
indicate 2-3 common or key SEs
What is the most important ADR?
NSAIDs: GI bleeding, renal impairment, wheezing
What is the second most important ADR?
Diuretics: hypotension (incl. postural: falls - encourage not too give up too rapidly), electrolyte imbalances (thiazide-like: hypokalaemia)
What is the third most important ADR?
Warfarin (bleeding + drug interactions)
What are the last 4-10 ADRs?
ACEIs/ATRAs (renal disfunction, measure eGFR during)
Antidepressants + lithium -in bipolar, narrow TW
Beta-blockers (avoid in asthma as risk of bronchospasm)
Opioids
Digoxin
Prednisolone
Clopidogrel (GI bleeding)
What are type A ADRs?
Augmented response
dose-related
predictable
usually managed by dose adjustment
How can u predict a dry mouth?
inhibition of saliva such as in anti-muscarinic drugs, blurred vision, constipation due to slower GI, urinary retention
How can you predict oesophageal erosion?
bisphosnates
osteeoporisis
corrosive
What is the most ADR of NSAIDs?
ulcerogenic effects
what else alongside NSAIDs can be associated with peptic damage/ulceration?
corticosteroids, esp. when co-prescribed with NSAIDs
low-dose aspirin also carries 3-fold risk
What anti-platelet drug may also cause GI bleeding?
clopidogrel
What NSAID has the lowest incidence of GI SEs?
ibuprofen
How do NSAIDs work?
inhibit production of prostaglandins (which contribute to inflammatory response, fever and pain)
prostaglandins are synthesized from arachnoid acid by COX action
COX1: always expressed in most cells, COX2 induced in inflammed tissues
different isoforms have diff fucntions in diff tissues
levels normally low but go up drastically in acute inflammation
What is the difference between selective and non-selective NSAIDs?
non-selective, inhibit both COX-1 and COX-2
COX-2 selective
what do all non-selective NSAIDs, except aspirin act as?
reversible COX inhibitors, compete with AA for binding to the enzyme
aspirin covalently modifies and permanently destroys COX enzymes
Where is the irreversible action of aspirin most notable?
blood platelets
cannot synthesize new COX enzymes as have no nucleus
enzyme inactivated = no production of Thromboxane A2 and hence no platelet aggregation for lifespan of platetels
aspirin is therefoe a potent anti-thrombotic agent
Can aspirin be taken with other non-selective NSAIDs?
no or at least 2 hours after aspirin as will compete with aspirin for common binding site on platelets COX-1
What are the contraindications of aspirin?
being anti-thrombotic, aspirin prolongs bleeding and is contra-indicated in patients with bleeding risks or hemorrhagic disorders
Why do NSAIDs cause GI irritation
COX-1-dependent prostaglandins suppress gastric acid secretion and help maintain gastric mucosal barrier, providing protection to the stomach lining because non-selective NSAIDs inhibit COX-1, they may cause gastric irritation, peptic ulcer disease and GI bleeding
How can GI damage be reduced?
- paracetamol for analgesia
- identify patients at risk eg. 65+, ulcer history, H.Pylori infection
- prophylaxis with PPI
- give in combo with misoprostol