glaucoma

Question 1

what is galucoma?

Answer 1

is a group of eye diseases in which progressive damage to the optic nerve leads to impaired vision and, in a small proportion of people,
blindness.

Question 2

what are the characteristics of visual field defects?

Answer 2

arcuate scotomas, nasal steps, and altitudinal
loss.
Changes to the head of the optic nerve — including pathological cupping
– Nerve fibre layer defects.

Question 3

how can the head of the optic nerve become damaged?

Answer 3

combination of:
– IOP that is abnormally high — most common cause of damage.
– The blood supply to the optic nerve is compromised.
– There is a weakness in the optic nerve structure or fibres.

Question 4

define suspected glaucoma

Answer 4

is defined as changes in the optic
nerve head (optic disc) or visual field that suggest glaucomatous damage (regardless of the intraocular pressure).

Question 5

what is ocular hypertension?

Answer 5

Ocular hypertension is a condition defined by consistently or recurrently elevated intraocular pressure (greater than 21 mmHg) and no signs of glaucoma.

Question 6

what is the purpose of the aqueous humour?

Answer 6

the fluid created by the ciliary body in the posterior chamber

Question 7

what is the anterior chamber angle?

Answer 7

The space between the iris and pupil
behind and the cornea in front is called the anterior chamber. The anterior chamber angle is the structure formed where the iris and the cornea join the sclera (white of the eye) towards the outside of the eye.

Question 8

what is the purpose of the intraocular pressure?

Answer 8

Keeps the eye in the shape of a globe.

Question 9

how is the IOP maintained?

Answer 9

by the balance between production and outflow of aqueous humour.

Question 10

what can raised IOP cause?

Answer 10

an cause glaucoma by damaging the optic nerve.
– Intraocular pressure is normally around 10–21 mmHg, but it can be as high as 70 mmHg in acute angle closure glaucoma.

Question 11

how do drugs used to treat glaucoma work?

Answer 11

either reduce the production of aqueous humour, or increase its outflow.

Question 12

what are the 4 ways of characterising glaucoma?

Answer 12

• Age of onset: congenital, infantile, juvenile, or adult.
• Rate of onset: acute or chronic.
• Cause: Primary (no known cause)
  Secondary – causes include disease, drugs,
  developmental disorders (increase in IOP)
• Mechanism: Angle closure glaucoma v Open angle glaucoma.

Question 13

what is angle closure glaucoma?

Answer 13

the angle between the iris and the cornea is at least partially closed.

Question 14

what is the purpose of angle closure glaucoma?

Answer 14

This blocks the trabecular meshwork and
prevents drainage of intraocular fluid.
– As intraocular fluid continues to be
produced, the pressure within the eye
increases and the optic nerve is damaged.
Onset can be acute or chronic

Question 15

what is open angle glaucoma?

Answer 15

the angle between the iris and the cornea is open.
– Onset is usually insidious, and the course
chronic.
– Both eyes usually affected - signs of damage
may be worse in one eye.
– IOP is usually increased but can be within
normal range

Question 16

what is the prognosis of chronic open angle glaucoma without treatment?

Answer 16

• Will usually be asymptomatic until late in its
  course — visual field defects do not appear until most of the optic nerve fibres have been lost.

Question 17

what is the prognosis of open angle glaucoma with treatment?

Answer 17

• Most people with chronic open angle glaucoma will not go blind, although they
  will have some visual field defects.

Question 18

what is the prognosis for acute angle closure glaucoma?

Answer 18

Full recovery is likely for people
treated promptly Irreversible loss of vision is
more likely if there is:
* Delay in presenting for treatment.
* Delay in reducing intraocular
pressure to the normal range.
* Inability to maintain intraocular pressure within the normal range.

Question 19

how will patients with acute ACG present?

Answer 19

acute painful red eye
* Blurred vision
* Headaches or eye pain associated with nausea and seeing halos around lights; these symptoms typically occur in the evening and are relieved by sleeping.
* Use of adrenergic drugs (eg. phenylephrine) or an antimuscarinic drugs (eg. TCA’s)
* Semi-dilated and fixed pupil.
* Tender, hard eye.

Question 20

what is emergency management of acute ACG?

Answer 20

– One drop of pilocarpine 2% in blue eyes/ pilocarpine 4% in brown eyes
– Followed by a single dose of oral acetazolamide 500 mg

Question 21

what is the management of acute ACG in secondary care?

Answer 21

Topical and IV drugs to reduce intra-occular pressure and analgesia.
– Definitive treatment is surgery (often laser surgery) to allow aqueous humour to flow from the posterior chamber into the anterior chamber.

Question 22

what are the risk factors for Chronic OAG?

Answer 22

• Raised intraocular pressure -the main treatable risk factor for chronic
  open angle glaucoma
• Age - prevalence increases steeply with age.
• Family history - risk is increased when a first-degree relative has
  glaucoma.
• Ethnicity - more common in people of black African origin
• Corticosteroids - The use of oral, inhaled, or high-potency topical
  corticosteroids has been associated with increased risk of glaucoma
  …………….corticosteroids increase the resistance to outflow of the aqueous
  humour………Most common with eye drop preparations!
• Myopia - People who are short-sighted are more likely to develop
  glaucoma and more likely to develop it at a younger age; the risk increases
  with severity of myopia
• Diabetes mellitus

Question 23

how do you manage chronic OAG?

Answer 23

treatment based on the
person’s age, IOP, and central corneal thickness.
– Offer a topical prostaglandin analogue to people with IOP of 24 mmHg or more if they are at risk of visual impairment within their lifetime

Question 24

what is the treatment for early/moderate COAG?

Answer 24

where treatment is indicated - a topical prostaglandin analogue is
recommended first line.

Question 25

what is the treatment for advanced COAG?

Answer 25

Surgery with augmentation — chemotherapy (mitomycin C
or 5-fluorouracil) augments surgery by modifying wound
healing.
– Topical prostaglandin analogues, and other topical
intraocular pressure-lowering agents.
– Laser treatment (trabeculectomy).

Question 26

how do topical prostaglandin analogues work?

Answer 26

Lower IOP by increasing uveoscleral outflow
and hence increasing the outflow of aqueous
humour.

Question 27

what are some examples of topical prostaglandin analogues?

Answer 27

– Latanoprost /Travoprost/Bimatoprost drops.

Question 28

what are some combination products for topical prostaglandin analogues?

Answer 28

– Bimatoprost and timolol — Ganfort®.
– Latanoprost and timolol — Xalacom®.
– Travoprost and timolol — DuoTrav®.

Question 29

what are the local adverse effects of topical prostaglandin analogues?

Answer 29

– Increased brown pigmentation in the iris - more
noticeable if mixed-coloured iris
– Increased pigmentation of peri-ocular skin.
– Darkening, thickening, and lengthening of the eyelashes.
– Blepharitis/Dry eyes.
– Ocular pain and irritation.

Question 30

what are the systemic effects of topical prostaglandin analogues?

Answer 30

– Dyspnoea/Exacerbation of asthma.
Dizziness/Arthralgia/Myalgia/Iritis/Headache/Photophobia
.

Question 31

how do topical BB work?

Answer 31

Lower IOP by reducing aqueous production

Question 32

give and example of a topical beta-blocker and how it works?

Answer 32

timolol is also available as Long-acting once daily preparations — Nyogel®
/Timoptol®-LA
once/ twice daily

Question 33

what are the local adverse effects associated with topical beta-blockers?

Answer 33

burning, stinging, pain, itching, redness, dry eyes, allergic reactions to the active drug or preservatives.

Question 34

what are the systemic adverse effects with topical beta-blockers?

Answer 34

More likely with high doses for prolonged periods.
Bradycardia/Bronchoconstriction/Worsening of circulatory disorders/Sleep disturbances/Hallucination/Fatigue.

Question 35

how do topical sympathomimetics work?

Answer 35

Reduce IOP by decreasing aqueous production
and increasing aqueous drainage.

Question 36

what is an example of a topical sympathomimetics?

Answer 36

Brimonidine tartrate 0.2%/Dipivefrine hydrochloride 0.1%

Question 37

what are the local adverse effects of topical sympathomimetics?

Answer 37

– Hyperaemia, burning, and stinging of the eyes.
– Dry mouth and abnormal taste in the mouth,
(associated with drainage of the drug into the
nasopharynx)

Question 38

what are the common drug interactions associated with topical sympathomimetics?

Answer 38

Central nervous system (CNS) depressants
* Monitor closely with alcohol, barbiturates,
opiates, sedatives, or anaesthetics.
– CNS depressants could potentiate the effects of
topical sympathomimetics.

Question 39

how do carbonic anhydrase inhibitors work?

Answer 39

• Reduce IOP by reducing the secretion of
  aqueous humour.

Question 40

give an example of a topical and oral carbonic anhydrase inhibitors

Answer 40

 Topical – Brinzolamide/Dorzolamide.
 Oral - Acetazolamide

Question 41

what are the local and systemic effects associated with carbonic anhydrase inhibitors?

Answer 41

• Local adverse effects:
  – Blepharitis/Eye irritation, pain, dryness/blurred
  vision.
• Systemic adverse effects – uncommon with topical
  preps