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Y3 Patient sem 1 > Drugs used for glaucoma > Flashcards

Drugs used for glaucoma Flashcards

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1
Q

What are the risk factors for glaucoma?

A
  • high IOP (>21mmHg)
  • family history of glaucoma
  • race (African more likely to develop)
  • systemic hypertension
  • cardiovascular disease
  • migraine
  • previous ocular disease
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2
Q

What is normal IOP?

A

12-16 mmHg

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3
Q

What is the cause of glaucoma?

A

Impaired drainage of aqueous humour - pressure of fluid in the eye builds up and exerts a greater pressure inside the eye (increased IOP)

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4
Q

What are the 2 types of glaucoma?

A
  • Primary
  • Secondary (from another eye condition)
  • can also be divided into open and closed angle - this lecture focuses on drugs that treat OPEN angle, closed angle tends to be treated with surgery
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5
Q

Where is aqueous humour produced?

A

In epithelial cells of the ciliary muscle (large blood supply helping it to flow and be secreted out)

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6
Q

What is meant by open angle?

A

Angle between iris and sclera

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7
Q

What is presented at the open angle?

A

Trabecular meshwork of cells

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8
Q

What features does the trabecular meshwork have that allows aqueous humour to flow through?

A
  • lots of spaces between cells allowing humour flow
  • flows due to pressure in the anterior chamber being higher than in the episceral vein
  • allows 80% of aqueous humour to flow
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9
Q

What is another route of aqueous humour outflow?

A

Uveoscelral outflow route - bypasses trabecular meshwork and goes through the cells of the scelra and ciliary body

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10
Q

Why is the Uveoscleral route less preferred to the trabecular route?

A

Cells of the sclera and ciliary body are more tightly packed together, meaning there is more resistance and pressure compared to the ‘holey’ trabecular meshwork.
Travels much more slowly

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11
Q

What are the aims in antiglaucoma treatment?

A
  • reduce IOP <16-20 mmHg
  • drug to have sufficient duration of action
  • provides:
    • Preservation of visual field
    • No loss of effect over time (lifetime treatment)
    • Compatibility with other treatments
    • No topical or systemic side effects
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12
Q

What causes neuropathy and damage to vision?

A

high IOP

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13
Q

What patient compliance do eye drops have?

A

LOW - inconvenient, multiple uses per day, cause temporary blurred vision

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14
Q

What is the first line treatment for glaucoma?

A

Prostaglandin and prostamide analogues

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15
Q

What features does prostaglandin E have?

A

Has great control in production of aqueous humour - however is very unstable and breaks down quickly so cannot be used

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16
Q

What prostaglandin is used as a drug ?

A

Prostaglandin F2alpha and its analogues.

It is an acid, less unstable than E

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17
Q

What are the analogues of Prostaglandin F2alpha?

A
  • Latanoprost
  • Travoprost
  • Tafluoprost

*ESTERS - more stable, less charged, last longer in formulation. Unique mechanism to decrease IOP

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18
Q

What is the analogue of Prostamide F2alpha?

A

Bimatoprost

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19
Q

Where are prostaglandins produced?

A

Naturally in most cells

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20
Q

What roles do prostaglandins play?

A

Decrease IOP - most efficacious

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21
Q

Where do the Prostaglandin analogues act?

A

Via the FP receptor

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22
Q

What reaction needs to happen in order for the prostaglandin analogues to be able to work on the FP receptor?

A

The ester analogues need to be converted back to acids (converted by esterases in the cornea)
*this means the ester analogues are PRODRUGS

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23
Q

What type of receptor is the FP receptor?

A

G-protein-coupled receptor (G-alpha-q), so when analogues bind, it causes activation of phospholipase C , which will increase diacyl glycerol and triphosphate within tissue.

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24
Q

Where are FP receptors present?

A
  • Predominantly Ciliary body & muscle, sclera
  • Iris sphincter
  • Trabecular meshwork cells (few present)
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25
What characteristics do the prostaglandin analogues have?
- prodrugs (need to be converted) - long duration of action (once daily preparation at night) - Greatest efficacy - can lower IOP up to 35% - well tolerated
26
Where do the Prostamide analogues act?
On FP receptors as well, however also work on more specific prostamide analogues present in higher concentrations in trabecular meshwork (better action)
27
What do prostamide analogues do?
Increase Uveoscleral and trabecular meshwork outflow
28
Is the prostamide analogue a prodrug?
- NO - minor metabolism to bimatoprost acid | - Potent FP receptor agonist
29
What is the efficacy and tolerability of the prostamide analogue?
Same as for prostaglandin analogues
30
What is the mechanism of action for lowering IOP with prostaglandin/prostamide analogues ?
- As FP receptors are highly expressed on ciliary body and scelra, we can increase uveoscleral outflow - Once receptors are stimulated, intracellular signalling causes a change in the structure of these cells - more enzymes are introduces (matrix metalloproteinases) to break down collagen and structure of scelral cells (to make more mesh-like) - When we get a decrease in collagen in the extracellular matrix, we get a decrease in structure, meaning more flexibility and less resistance of ciliary muscle to increase outflow aqueous humour flowing through cells
31
What do matrix metalloproteinases do?
Break down collagen and structure of sceral cells to make more holey
32
What are the side effects of prostaglandin/prostamide analogues?
- Red eye (initial usage) - vasodilation - Increase pigmentation in iris, eyelashes & periocular skin (darker eyelashes) - Eyelash growth Precipitate or worsen cystoid macular oedema in aphakic eyes (rare) - Sensitivity to light (rare) - Contraindicated in pregnancy (can induce labour) - Theoretical general effect on cell division
33
Does glaucoma affect both eyes?
NO - usually only one, but drug side effects can affect both eyes
34
What is the second line of glaucoma treatment?
Beta 2 receptor blockers
35
What does B2 activation stimulate?
cAMP production (Gs coupled; activated adenylate cyclase)
36
What does cAMP do?
- INCREASES ion transport in cells in ciliary epithelium - cAMP activates Na+K+2Cl- cotransporter in pigmented epithelial cells - cAMP stimulates Cl- efflux in non-pigmented epithelial cells
37
What happens when we have a greater efflux of ions across epithelial cells into the posterior chamber? (caused by b2 receptors)
- cause an osmotic gradient - more fluid will flow into the posterior chamber and therefore more aqueous humour production *BLOCKING this with b2 blockers will prevent/reduce aqueous humour production
38
What do B2 blockers do?
- Reduce aqueous humour production by blocking Na+K+2Cl- cotransporter, meaning a reduction of ions coming IN to non pigmented cells and a reduction of ions going OUT into the posterior chamber - This reduces humour volume flowing along gradient - reduced production and reduced drainage of aqueous humour
39
What are the advantages of beta blockers?
- Very well tolerated - Rapid onset of action - Effective in ~75% of patients - Lower IOP by 20-30% - Compatible with other drugs
40
What are the disadvantages of beta blockers?
- Can observe effects on treated AND untreated eye (systemic absorption) - Systemic side effects - Efficacy declines over time (doesn't work as well as prostaglandin anagloues for chronic treatment)
41
How often are beta blockers administered?
At least Twice daily or once daily with certain preparations
42
What are the side effects of beta blockers?
- Generally systemic - Cardiovascular (b2 receptors location) - Bradycardia, hypotension, peripheral vasoconstriction, impotence - Contraindicated in heart block, heart failure - Bronchial - Constricts bronchioles - Contraindicated in asthma & chronic obstructive airways disease - Diabetic - Masks hypoglycemia
43
Are beta receptors used in glaucoma treatments specific?
NO, nonspecific, block b1 receptors too
44
What are fixed dose combinations?
- Multiple drugs with different mechanisms can be used at the same time to have additive effects. - Both drugs are formulated into one 'drop' ("FIXED")
45
What are the advantages of fixed dose combinations?
- Patient compliance – only need to use 1 drop - Reduce exposure to preservatives (which can damage the eye with long term use) - Avoids washout effect of use of 2nd drop - Decreases cost of treatment - Decreases cost to patient – one prescription charge
46
What is used as a 3rd line treatment in glaucoma?
Carbonic anhydrase inhibitors
47
What preparations are available for carbonic anhydrase inhibitors?
systemic and topical use (systemic use limited to emergencies)
48
What do carbonic inhibitors do?
Inhibit carbonic anhydrase in ciliary epithelium
49
Where is the carbonic anhydrase enzyme expressed and why does this have bad effects?
Expressed in many major organs - blocking it has significant systemic side effects
50
What reaction does carbonic anhydrase catalyse?
CO2 + H2O H2CO3 H+ + HCO3-
51
Where are HCO3- (bicarbonate) ions excreted?
Into the posterior chamber, and when this happens, fluid follows these ions
52
Therefore what effect does blocking the reaction catalysed by carbonic anhydrase have do?
Reduces aqueous formation and secretion, lowering IOP
53
What systemic Carbonic anhydrase inhibitor is available?
Acetazolamide (not absorbed topically)
54
What is Acetazolamide used in?
Open angle secondary glaucoma and peri-operatively in acute angle closure glaucoma (when IOP very highly elevated) - side effects limit use - short term use only (can be injected as a one off in emergencies)
55
What are the side effects of Acetazolamide?
- Sulfonamide derivative (Increased risk of allergy and blood disorders) - Enzyme present throughout body - Gastrointestinal problems - Diuresis - Acid / base balance disturbances - Drowsiness, depression - Parasthesias HOWEVER, unlikely to get systemic side effects is administered directly to the eye
56
How are carbonic anhydrase inhibitors made more specific, and what are examples of topical CAIs?
Make more selective – CA-2 enzyme Led to Dorzolamide and brinzolamide (analogues) Good lipid solubility
57
What are topical CAIs used with?
- Used in conjunction with beta blockers OR prostaglandin analogues
58
How much reduction in IOP is seen with CAIs?
20% - less efficacious than other mechanisms
59
What are the side effects of topical CAIs?
- Transient burning, stinging (acidic drop) - pH brinzolamide drops 7.5 - pH dorzolamide drops 5.6-6.0 - Blurred vision, conjunctival hyperaemia, transient myopia, blepharitis, allergic conjunctivitis - Taste disturbances, dry mouth, headache
60
What is the 4th line treatment for glaucoma?
Alpha 2 adrenoceptor agonists
61
Where are alpha 2 receptors expressed?
On the ciliary, conjunctival and corneal epithelial cells
62
What are the advantages of alpha 2 adrenoceptors?
- No mydriasis - No vasoconstriction - Little effect on CV system (because they are alpha 2 selective) - very few side effects
63
What is the mechanism for alpha 2 adrenoceptors?
- Decrease secretion of aqueous - Decreases cAMP (Gi coupled; inactivates adenylate cyclase) - Decreases ion transport – decrease in osmotic gradient and therefore aqueous humour - Decreases aqueous secretion - Decreases ultrafiltration – less fluid being filtered through from capillaries (reduced blood flow, vasoconstriction) - Increases uveo-scleral outflow - Neuroprotective? Optic nerve, retinal ganglion cells
64
What are examples of alpha 2 adrenoceptors ?
- Brimonidine - Selective for a2 receptors - Rapid onset with peak effect in ~2hours - Apraclonidine - Less selective for a2 receptors Short term use due to tachyphylaxis - Used post surgery to prevent rise in IOP following laser surgery
65
What are the side effects and contra-indications for alpha2 adrenoceptors?
- Local Allergy, stinging / burning Blurred vision, photophobia - Systemic Hypotension Drowsiness, fatigue Dry mouth, taste disturbances Tend to only be used pre/post surgery
66
What is the last class of drug used in glaucoma?
Parasympathomimetics
67
What is an example of a Parasympathomimetics?
Pilocarpine
68
What is the mechanism of pilocarpine?
Acts at M3 receptors (muscarinic agonist), binds to M3 and ciliary muscle contracts - pulls scleral spur which opens up trabecular meshwork - allows more drainage to occur by reduction in resistance
69
How long does pilocarpine work for?
Effects last for 6 hours (cyclical reduction) | - not an ideal drug - needs to be used at least 4 times a day

Y3 Patient sem 1 (22 decks)

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