Drugs in Glaucoma Flashcards
what is glaucoma?
blanket term for a variety of conditions
- differenet features
- different mechanisms
- not just one typical disease affects everyone who suffers
the common factory is acquired progessive neuropathy if left untreared
- optic nerve damage
- visual field loss
- eventual blindness
what are the risk factors of glaucoma/
- normally asymptomatic, no warning signs
- high IOP >21mmHg (normal is 12-16)
- family history
- afro caribbean are more at risk
- systemic hypertension
- migraines
- previous ocular disease or surgery
- usually due to impaired drainage of the aqueous humour
where is aqueous humour produced?
cilliary muscle is the outer most part of the epithelial cells and has a large blood supply which makes up the aqueous humour.
it goes round the lens and into the side.
meshwork of cells means there are spaces for the aqueous humour to flow
what do we look for in antiglaucoma treatment?
- reduction in occular pressure <16-20mmHg depending on patient
- anything under 21 should reduce risk of neuropathy
- drug needs to have sufficient duration of action to increase patient compliance
- compatability with other treatments
- no side effects
- no loss of vision over time
- keeps vision as best as it can be
what are the first line treamtents for glaucoma?
prostaglandin f2 alpha
prostamide f2 alpha
what is prostagladin E/
this controls the production of aqueous humour, but it is very unstable and breaks down rapidly
what is prostglandin f2 alpha?
abit more stable, so this is what they design drugs on
- analogues are all esters whereas it is an acid. this increases stability of the drug and gives it a longer duration of action on the eye
what are prostagladins used for in the eye?
they are produced naturally in most cells not just within the eyes involved wirh - aquous humour outflow - first choice clinically - unique mechansim of decreasing IOP
how do prostagladin analogues work?
they act via the PGF2a receptor - they need to be converted back to the acid form from the ester form.
the analoguse are the pro-drug
they are g-coupled receptors
what are examples of prostaglandin analogues?
latanoprost, tafluprost and travoprost
- all pro drugs
- long duration of action
- greatest efficacy of the drugs available
- lowers IOP by 35%
- not too many side effects
what are prostamide analogues?
- increase uveoscleral and trabecular outflow
- not a pro drug
- effiacy, tolerability and side effects are the same as prostaglandin
what are the side effects of prostaglandin?
- red eye of initial use
- increase pigmentation in iris and eyelashes
- can increase eyelash growth, but sometimes you only do it to one eye
- sensitivity to light
- contraindicated in pregnancy
what is the second line treatment of glaucoma?
beta receptor induced aqueous production
how do beta receptors work?
b2 activation stimulates cAMp production, this causes an increase in ion transport across the cell
when there is an efflux of ions into the posterior chamber, it increase osmotic gradient and more fluid is filtered so increase in aqeuous humoiur
BETA BLOCKERS PREVENT THIS and decrease the production
what is the mechanism of action of beta blockers?
• Decreased ion concentration
• Decreased fluid along osmotic gradient
• Decreased volume of aqueous humour
• Better balance of production and drainage
Different angle to treat glaucoma – prevent the amount of aqueous humour to be produced so there is less to be drained out
what are the advantages of beta blockers/
- well tolerated
- rapid onset
- effective in 75% of patients, lower IOP 20-30%
what are the disadvantages of beta blockers?
- can observe effects on treated and untreated eye - systemic absorption
- CVD patients have problems
- efficacy declines over time
- twice daily - poorer patient compliance
what are the side effects of beta blockers
- generally systemic
- cardiovascular, bradycardia, hypotension
- contraindicated in heart block
- diabetic
- constricts bronchiolea
what are the fixed dose combinations?
Different classes of drugs have additive effects – as they have different mechanisms. If you put a prostaglandin and a beta blocker together you might not get a decrease of 65% but it will be higher then one by itself
what are the advantages of a fixed dose combination?
- better patient compliance
- reduced exposure to preservatives
- avoids washout effects
- decreased cost of treatment
- decreased cost to patient
what are carbonic anhydrase inhibitors?
third line treatment
The only time you would use a carbonic anhydrase is if the other two drops were not suitable for some reason.
ONLY USED FOR EMERGENCIES
how do carbonic anhydrases inhibitors work?
This enzyme catalyses the following reaction
CO2 + H2O H2CO3 H+ + HCO3-
The bicarbonate ions tend to be excreted out into posterior chamber and when this happens you get fluid following these ions
This means if we can stop the bicarbonate ions from forming we can reduce aqueous humour production
what is an example of a CAi?
Acetazolamide
- not absorbed topically
- not particularly lipophilic
- short term use only
what are the side effects of Acetazolamide?
Increased risk of allergy and blood disorders because is has sulphonamide group attached
Enzyme present throughout body -kidney blood and lungs also within the CNS
Gastrointestinal problems –Diuresis
Acid / base balance disturbances
Drowsiness, depression
Parasthesias
