drug management Flashcards

1
Q

what are they symptoms of glaucoma

A

optic nerve damage, visual field loss, eventual blindness

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2
Q

risk factors

A

high IOP >21, family history, race, systemic hypertension, cvd, migraine, previous ocular disease.

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3
Q

what is the cause of glaucoma

A

impaired drainage of aqueous humour

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4
Q

where are the sites of aqueous outflow

A

trabecular meshwork, sclera and ciliary body.

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5
Q

what are the main Aims of antiglaucoma treatment

A

to reduce IOP to <16-20, preserves visual field, compatibility with other treatments and no topical or systemic se.

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6
Q

how is prostaglandins involved in aq humour outflow

A

it decreased IOP

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7
Q

which receptors do the prostaglandin analogues act via

A

FP receptors

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8
Q

where are FP receptors present

A

ciliary body, muscle and sclera, trabecular meshwork

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9
Q

3 examples of prostaglandin analogues

A

latanaprost, tafluprost, travoprost

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10
Q

what is the moa of prostamide analogues

A

FP receptor agonist. increases uveoscleral and trabecular outflow

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11
Q

how is IOP lowered

A

increase in uvoscleral outflow and reduced resistance by degradation of collagen and extracellular metric and decreases resistance of ciliary muscle and sclera

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12
Q

side effects of prostaglandin and prostamide analogues

A

red eye, eyelash growth, sensitivity to light

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13
Q

why can’t prostaglandin and prostamide analogues be used in pregnancy

A

effects on cell division

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14
Q

how do beta blockers decrease aqueous humour production

A

blocks cAMP production which prevents ion transport in the ciliary epithelium preventing aqueous humour production due to lack of osmotic gradient.

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15
Q

what are the disadvantaged of using beta blockers to decrease IOP

A

effects are seen on untreated eye too, systemic se are also observed

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16
Q

what are the side effects of beta blockers

A

vasoconstriction, bronchoconstriction, masks hypoglycaemia

17
Q

how do carbonic anhydrase inhibitors lower IOP

A

carbonic anhydrase catalysis the formation of bicarbonate which is required for aq secretion.

18
Q

what formulation do carbonic anhydrase inhibitors come in

A
  • systemic - serious se incl. gi problems, drowsiness and depression (enzyme also in the parts of the body) therefore only in when IOP is very highly elevated and for short term use only
  • topical
19
Q

how would you decrease the side effects of CAIs

A

modify acetazolamide to allow corneal absorption ( lipid sol)

20
Q

combination treatments

A

CAIs+ beta blockers

CAIs+ prostaglandin analogues

21
Q

side effects of topical CAIs

A

blurred vision, burning, stinging

22
Q

what is the mechanism of adrenoceptor agonists

A

similar to beta blockers. decrease cAMP and mom transport and aq secretions ALSO
reduces blood flow and vasoconstriction.

23
Q

what is an example of an adrenoceptor agonist

A

brimonidine

24
Q

side effects of adrenoceptor agonists

A

stinging, burning, blurred vision, hypotension, fatigue, dry mouth

25
Q

what is the moa of a parasympathomimetics (pilocarpine)

A

contracts ciliary muscle, opens trebecular meshwork and increasing outflow decreasing IOP

26
Q

what precent decrease of IOP does prostaglandin analogues provide

A

35%

27
Q

what percent decrease in IOP do CAIs provide

A

20%

28
Q

what percent decrease in IOP do beta blockers provide

A

20-30%