Eye Disorder-glucoma Flashcards
Aqueous humour
Secreted by cells of the epithelium then into POSTERIOR CHAMBER (behind iris)
Then drains from ANTERIOR chamber to blood stream
Intraocular pressure IOP
Determined by the vol of aqueous humour in ANTERIOR chamber of eye
Glaucoma (raised IOP)
^IOP caused by blockage of circulation / drainage of AH
Result: damage /impaired blood sup to optic nerve -> which is slowly destroyed (irreversible)
Types of glaucoma
Chronic (primary) open angle glaucoma
Acute angle closure glaucoma (need surgery)
Congenital glaucoma
Secondary glaucoma
Treat primary/open angle glucoma
Prostaglandin analogue (1st line)
Beta-blocking analogue (2nd line)
Alpha 2 agonist (3rd line)
Carbonic anhydrase inhibitor
Prostaglandins drugs
*ends with oprost
Latanoprost
Bimatoprost
Prostaglandin MOA
*glucoma asymptotic- adherence / compliance to drug is major problem
Reduce IOP by increasing uveoscleral outflow
Outflow ⬆️~ pressure ⬇️
Possibly due to
• activation of molecular transduction cascade
• ^ in biosynthesis of certain metallo-proteinases
• reduction of extracellular matrix within uveoscleral pathway
Prostaglandin AE
Applies to >1% pts
Irreversible increase in iris pigmentation
Darkening , lengthening , thickening of eyelashes
Eye irritation, blurred vision
Beta receptors
B1 - heart
B2 - smooth muscle of bronchioles, aterioles, visceral organs
B3 - adipose tissue
Adrenergic receptors
Alpha 1,2
Beta 1,2,3
Cholinergic receptors
Nicotinic
Muscarinic
B blocker (b receptor antagonist) MOA
Block B2 : reduce aqueous humour formation
⬇️production =⬇️ pressure
May also act on b2 on ciliary arteries and induce vasoC - further ⬇️ ptoduction
B blocker AE
Systemic related ..
But and prevent by use appropriately
• close eye and pressure on tear duct for 3min after instillation
• systemic absorption reduce by up to 70%
• drug stay in eye rather than system
B blocker drugs
*end with : olol
Timolol
Betaxolol
Timolo
Non selective blocker
B1-heart B2-bronchioles
Not used in pts with cardio /airway disease