Pharmacological aspects of Immunology Flashcards
Mechanism of action of NSAIDs
-aspirin
Blocks cycloxygenase pathway
-irreversibly binds enzyme to prevent prostaglandin synthesis
Role of COX 1 enzyme
Constitutive expression- all tissues
Stomach, Kidney, Platelets, Vascular endothelium
Inhibition → anti-platelet activity, side effects
Role of COX 2 enzyme
Induced in inflammation (IL-1)
Injury, infection, neoplasia
Inhibition → analgesia and anti-inflammatory actions
Role of COX 3 enzyme
CNS only
Inhibited specifically by paracetamol → antipyretic and analgesic actions
Limitations of Aspirin
- GI toxicity
- Tinnitus – mechanism obscure, usually reversible
- Reye’s syndrome (fulminant hepatic failure in children)
Class of drug of Clopidogrel and dipyrimidole
Non-NSAID antiplatelet drugs
Paracetamol
- No anti-inflammatory effect as no binding to COX 1 and 2
- No GI toxicity
- Analgesic/anti-pyretic
- overdose
Paracetamol metabolism
overdose can lead to hepatic necrosis
NSAID GI toxicity
- loss of prostaglandins
- these normally decrease acid production, Increase mucus production,
- Increase blood supply
What is the biggest risk factor for GI bleed?
Previous GI bleed
What causes NSAID nephrotoxicity?
- Decreaed GFR
- Na+ retention
- Hyperkalaemia
- Papillary necrosis
Give examples of NSAIDs in order of increasing potency
Ibuprofen, Naproxen, Diclofenac, Indometacin
Side effects of aspirin in an asthmatic
bronchospasm
Predominant endogenous glucocorticoid
- Cortisol (hydrocortisone)
- Steroids reduce immune activation by altering gene expression in numerous cell types, including T cells, B cells and cells of the innate immune system. Their onset of action is delayed and they must be taken regularly
