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Pharmacy Y3S1 > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

What is a common factor of glaucoma?

A

Acquired progressive nephropathy

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2
Q

What are the risk factors for glaucoma?

A 
High IOP (>21mmHg)
Family history
Race (Afro-Caribbean)
Systemic hypertension
CVD
Migraine
Previous occular disease
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3
Q

What are the types of glaucoma?

A

Primary
Secondary - occurs due to a secondary disorder
Open angle
Closed angle

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4
Q

Aims of antigaucoma treatment

A 
Reduce IOP <16-20mmHg
Sufficient duration of action (less needed)
Preserves visual field
No loss of effect over time
Compatible with other treatments
No topical or systemic side effects
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5
Q

Give examples of Prostaglandin analogues

A

Latanoprost
Travoprost
Tafluoprost

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6
Q

Give an example of a Prostamide analogue

A

Bimatoprost

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7
Q

Where are prostaglandins produced?

A

Most cells

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8
Q

Where/how is aqueous humour produced?

A

Produced in epithelial calls in ciliary muscles
The good blood supply via capillaries brings the fluid
Secreted by epithelial cells and round lens
In open angle - goes between iris and sclemm
At the crook of the angle there is the Trebecular Meshwork - 80% of the fluid flows through
Moves from the anterior to episcleral vein down a pressure gradient

Other route is the Uveoscleral Outflow - goes through cells of schlemm ad ciliary body which has more resistance so moves more slowly

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9
Q

What do the prostaglandin analogues act via?

A

PGF 2a receptor

A G-coupled receptor = when bound, PLC, DAG and IP3 activates

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10
Q

What is the mechanism of prostamide analogues?

A

Increase uveoscleral outflow by reducing resistance
Increases matrix metalloproteinases
Degrades collagen and extracellular matirx
Decreases resistance of ciliary muscle and sclera to increase outflow
Most likely via FP receptors and maybe some direct action on tribecular meshwork

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11
Q

What are the side effects of prostaglandin and prostamide analogues?

A

Red eyes on initial use
Increased pigmentation in iris, eyelashes and periocular skin
Eyelash growth
Precipitate/worsen cystoid macular oedema in aphakic eyes
Sensitivity to light
CI in pregnancy

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12
Q

What are the benefits are of Prostaglandins?

A

Pro-drugs (ester converted to acid before it can bind)
Long duration of action - OD at night
Efficacy - lower IOP by up to 35%
Good tolerability

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13
Q

How do beta receptors induce aqueous production?

A

B2 activation stimulates cAMP production (G-coupled so activates adenyl cyclase)
cAMP regulates ion transport in ciliary epithelium
Activates Na+K+2Cl- co-transporter in epithelial cells
Stimulates Cl- efflux in non-pigmentated epithelial cells
Efflux = osmostic gradient increase and increased humour production

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14
Q

What are the advantages of beta blockers?

A

Well tolerated
Rapid onset
Effective in 75% - lower IOP by 20-30%
Compatible with other drugs

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15
Q

What are the disadvantaged of beta blockers?

A

Can observe effects on the treated and untreated eye (systemic absorbance)
Systemic SE’s (CVD needs monitoring)
Efficacy declines over time

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16
Q

What are the side effects of beta blockers?

A

Systemic effects due to beta receptor location
Cardiovascular: hypertension, bradycardia, peripheral vasoconstriction, impotence
Bronchial: constricts bronchioles
Diabetic: Masks hypoglycemia

17
Q

How do carbonic anhydrase inhibitors work?

A

Inhibit carbonic anhydrase in ciliary epithelium which catalyses reaction to bicarbonates which are required for aqueous production (secreted into posterior chamber with fluid)
Reduces ion conc
Reduces fluid conc along gradient
Reduces vol of aq humour

18
Q

Give an example of a systemic CAI and when is it used?

A

Acetazolamide
Uses: Open angle glaucoma, secondary, peri-operatively in acute angle, when IOP highly elevated
Used in emergencies IV
(Side effects limit use)

19
Q

What are the side effects of systemic CAI’s?

A

Increased risk of allergy and blood disorders (sulfonamide derivative)
Many due to enzymes in body:
GIT, Diuresis, Acid-base disturbances, drowsiness/depression, parasthesias

20
Q

When are topical CAIs used?

A

With beta blockers or prostaglandin analogues

Alone when beta blockers are not tolerated

21
Q

What are the side effects of topical CAI’s?

A 
Burning/stinging when used
Blurred vision
Conjuctival hyperaemia
Transient myopathy
Blepharitis
Allergic conjuctivitis
Taste disturbances
Dry mouth 
Headache
22
Q

Where are the alpha receptors?

A

ciliary, conjuctival, corneal epithelium cells

23
Q

What are the effects of alpha adrenoceptor agonists?

A

No mydriasis
No vasoconstriction
Little effect on CV system as alpha selective

24
Q

What is the mechanism of alpha adrenoceptor agonists?

A 
Decreased secretion of aq:
Reduced cAMP 
Reduced ion transport
Reduced aqueous secretion
Reduced ultrafiltration (reduced bood flow and vasoconstriction)
Increased uveroscleral outflow

Neuroprotective?

25
Q

Give examples of alpha adrenoceptor agonists and describe them

A

Brimonidine: alpha 2 selective; rapid onset; peak 2 hours.
Apraclonidine: less selective; short term use (due to tachyphylaxis -rapid non sensitivity); used post surgery to prevent IOP rise after laser

26
Q

What are the side effects of alpha adrenoceptor agonists?

A

Local: Allergy, stinging, burning, blurred vision, photophobia
Systemic: Hypotension, drowsy, fatigue, dry mouth, taste disturbed

27
Q

Give an example of a parasympathomimetic

A

Pilocarpine

28
Q

What is the mechanism of parasympathomimetics?

A

Contracts just the ciliary muscle

Pulls scleral spur so Trabecular meshwork opens and outflow increases = reduced outflow

29
Q

How long do parasympathomimetics last?

A

About 6 hours

30
Q

How often do parasympathomimetics need to be used?

A

Four times a day

Pharmacy Y3S1 (14 decks)

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