Anti-inflammatory and Anti-allergy drugs Flashcards
(39 cards)
What are the inflammatory stages?
Arachidonic acid is made from membrane phospholipids by Phospholipase A2 enzyme.
Leukotrines are made from arachidonic acid by Lipoxygenase enzyme and Prostanoids are made by Cyclo-oxygenase enzyme (COX).
Prostacyclin, Prostaglandins and Thromboxane are made from Prostanoids.
What part of the inflammatory stage do corticosteroids inhibit?
Phospholipase A2 enzyme - arachidonic acid is not made and therefore neither are leukotrines or prostaglandins
What reaction does Prostaglandin E cause?
Vasodilation (so redness, warmth and oedema)
Fever
Tissue sensitivity (pain and irritation)
What is the result of corticosteroids (what is reduced?)
Vasodilation reduced, so redness, warmth and oedema reduce
Fibroblast proliferation reduced (results in less collagen deposition so reduced scarring)
What are the indications for using corticosteroids?
Reduce inflammation when substantial but non-infectious (e.g. uveitis, blunt trauma)
Post-operative prophylactic treatment to reduce inflammation (e.g. cataract op)
What are the contraindications for using corticosteroids?
Red eye with an unknown cause - if infected corticosteroids could mask inflammatory signs as well as reduce immune response (making infection worse)
‘Steroid responders’ - IOP increase when on steroids
What forms does Prednisolone come in and what is it?
Corticosteroid
Pred forte 1% w/BC
0.5% w/BC
0.5% minims
How often should Prednisolone be administered?
Every 1-2 hours
What are the ADRs for corticosteroids?
Increased IOP (up to 8mmHg)
Immunosuppression
Infectious signs masking
Retarded wound healing
Steroid cataract
Steroid glaucoma
Corneal thinning
What form does Betamethasone come in, what is it and how often should it be administered?
Corticosteroid
Bethesol 0.1% w/BC
Every 1-2 hours
What forms does Dexamethasone come in, what is it and how often should it be administered?
Corticosteroid
Maxidex 0.1% w/BC
Maxitrol 0.1% w/neomycin and polymixin B
Minims
4-6x daily
What form does Fluoromethalone come in, what is it and how often should it be administered?
Corticosteroid
0.1% w/BC
Hourly for first 24-48 hours, then 2-4x daily
Which part of the inflammatory stages do NSAIDs affect?
Inhibit Cyclo-oxygenase enzymes (COX), preventing Prostaglandin synthesis
Older inhibit both COX 1 and 2
Newer only inhibit COX 2
What is the difference between COX 1 and 2?
COX 1: produces prostaglandins as part of normal homeostasis and is present in all cells
COX 2: produces prostaglandins as part of an inflammatory reaction and so only present in inflamed cells
What are the main effects of NSAIDs?
Reduction of vasodilation (so redness, warmth and oedema)
Anti-pyretic (reduces fever)
Analgesic (reduces pain)
What might an older NSAID which targets both types of COX cause and why?
GI tract issues (e.g. ulcer)
Due to inhibition of COX 1, so homeostasis is affected (prostaglandins are protective in GI wall, secretions become more acidic without them)
What are the indications for NSAIDs?
Post-op for cataracts to prevent inflammation and CMO
Argon laser trabeculoplasty to prevent inflammation
Seasonal allergic conjunctivitis
AC inflammation and corticosteroids contraindicated
What are the contraindications for NSAIDs?
Aspirin sensitivity
GI tract issues
Anticoagulant meds
What is Diclofenac and what is it available as?
NSAID
Voltarol 0.1% single-use drops
What is Flurbiprofen and what is it available as?
NSAID
Ocufen 0.03% single-use drops
What is Keterolac and what is it available as?
NSAID
Acular 0.5% multidose drops
Give some examples of systemic NSAIDs.
Ibuprofen
Aspirin
Diclofenac
How do mast cells release mediators?
Activated by IgE binding of 2 or more allergens on cell surface, then releases mediators by degranulation (mediators inside mast cell in granules)
What is Mast cell stabiliser’s mode of action?
Release of mediators prevented (no degranulation)
If some already released, no effect on these but will prevent further inflammation