Treatment of glaucoma Flashcards

1
Q

Why is it important to maintain a specific intraocular pressure?

A

Without pressure in the eye it can’t maintain its shape (like a beach ball), which is vital to maintain clear image

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2
Q

What is the constant pressure that the eye should be kept at?

A

10-21mmHg

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3
Q

What maintains the correct pressure in the eye (in a general sense)?

A

Constant production and drainage of aqueous humour

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4
Q

What is the name of the condition in which pressure in the eye is too high (usually due to problem with aqueous drainage)?

A

Glaucoma

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5
Q

What happens in glaucoma?

A

Intraocular pressure (IOP) rises, can damage the optic nerve causing visual field defects and, if unchecked, blindness

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6
Q

How is aqueous produced in the eye?

A

It is actively secreted by the ciliary processes of the ciliary body

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7
Q

What happens once fluid has been secreted by the ciliary processes of the ciliary body?

A

Fluid cirulates under the iris and through the pupil, and into the anterior chamber (see image)

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8
Q

What is the route of drainage of the majority of aqueous from the anterior chamber?

A

90% drains out through the drainage angle of the eye through the trabceular meshwork, into the canal of Schlemm, and then into the episcleral circulation (see image)

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9
Q

What is the unconventional route of drainage, through which the second highest amount of aqueous drains?

A

10% drains through the uveoscleral route: aqueous is absorbed back into the ciliary body and under the sclera, then into episcleral blood vessels and general circulation

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10
Q

What is glaucoma?

A

A family of conditions, in which there is raised IOP causing optic nerve damage and subsequent loss of vision

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11
Q

What are the two key types of glaucoma to distinguish?

A
  1. Primary open angle glaucoma
  2. Acute angle closure glaucoma
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12
Q

What are the causes of 1. primary open angle glaucoma vs. 2. acute angle closure glaucoma?

A
  1. primary open angle glaucoma has no cause identified; no change in eye other than other than raised IOP and consequent damage
  2. AACG is due to aqueous blockage due to closed angle
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13
Q

How can the closed drainage angle in acute angle closure glaucoma be identified?

A

Gonioscopy

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14
Q

How is primary open angle glaucoma often detected?

A

Often picked up incidentally during routine optician checks

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15
Q

What is the presentation of of acute angle closure glaucoma like?

A

Acute, extremely painful red eye and loss of vision

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16
Q

What refractive errors are associated with 1. POAG and 2. AACG?

A
  1. POAG may have any refractive error but more common in short-sighted patients
  2. AACG exclusively occurs in hypermetropes (long-sighted)
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17
Q

Why does acute angle closure glaucoma exclusively occur in hypermetropes?

A

Eye is shorter, so drainage angle is naturally narrower and more susceptible to becoming closed

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18
Q

What are 5 key elements of the management of acute angle closure glaucoma?

A
  1. Admission to specialist unit
  2. Pupil constriction with pilocarpine
  3. Drugs to lower IOP
  4. Peripheral iridotomy
  5. Offer analgesia ± antiemetics
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19
Q

Why is it vitally important to reduce IOP in AACG?

A

Iris is often ischaemic due to high pressure inside the eye which prevents constriction, so must reduce pressure

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20
Q

What drugs are give to reduce IOP in AACG? 3 key groups.

A
  1. Acetazolamide (Diamox): 500mg IV over 10 minutes + 250mg slow release tablet after 1 hour
  2. Topical ocular anti-hypertensives: timolol, prednisolone drops (phenylephrine if don’t have own lens)
  3. If these don’t work, systemic hyperosmotics e.g. mannitol, glycerol
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21
Q

How does peripheral iridotomy work to treat AACG?

A

Small hole in the iris is made with a YAG laser which allows aqueous to flow and avoid the route through the pupil. This prevents pupil block and prevents further attacks

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22
Q

What is the definitive treatment for acute angle closure glaucoma?

A

Peripheral iridotomy (making a hole in the iris with YAG laser)

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23
Q

What is the mainstay of treatment for primary open angle glaucoma?

A

Topical treatment i.e. eyedrops

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24
Q

What is the only change in the life of most patients with POAG?

A

Regular use of eye drops - since visual loss not initially noticed but have high IOP

25
Q

What does the arrow in the picture show?

A

Hole made in iris during peripheral iridotomy to treat AACG

26
Q

What are 3 ways to target lower IOP in POAG? Give the groups of drugs which achieve each of these

A
  1. Reduce secretion of aqueous: beta blockers, carbonic anhydrase inhibitors
  2. Increase outflow: prostaglandin analogues ( + pilocarpine)
  3. Both increase outflow and decrease production: alpha-2 agonists
27
Q

What are 2 types of topical treatments for POAG that work by reducing the secretion of aqueous?

A
  1. Beta blockers
  2. Carbonic anhydrase inhibitors
28
Q

What are 2 types of topical treatments for POAG that work by increasing the outflow of aqueous?

A
  1. Prostaglandin analogue
  2. Pilocarpine
29
Q

What is one type of topical treatment for POAG that works by both increasing outflow of aqueous and reducing its production?

A

Alpha-2 agonists

30
Q

What is the mechanism of action of beta blockers for treating raised IOP?

A

Reduce secretion of aqueous: blocks beta receptors in the ciliary body to decrease production

31
Q

What is the mechanism of action of carbonic anhydrase inhibitors for treating raised IOP?

A

Reduce secretion of aqueous: inhibit carbonic anhydrase present in the epithelium of the ciliary body; enzyme present here, vital to production of aqueous

32
Q

What is the mechanism of action of prostaglandin analogues in reducing IOP?

A

Increasing outflow of aqueous (via the uveoscleral route)

33
Q

What is the mechanism of action of alpha-2 agonists in treating raised IOP? 2 key routes

A

Both increase aqueous outflow and decrease production:

  1. constriction of ciliary blood vessels and aqueous suppression
  2. Increases uveoscleral outflow
34
Q

What is an example of a prostaglandin inhibitor used to treat raised IOP and its dosing?

A

Latanoprost: 0.005% once daily dosing

35
Q

What is the mechanism of action of latanoprost?

A

Increases uveoscleral outflow of aqueous

36
Q

What is the first line treatment for primary open angle glaucoma and why?

A

Prostaglandin inhibitors because they’re very effective (lowers IOP 28-36%)

37
Q

What are 3 side effects of prostaglandin inhibitors?

A
  1. Conjunctival hyperaemia
  2. Colour change of irides: blue → brown
  3. Hypertrichiasis: ultra long lashes (sometimes misused for cosmetic purposes)
38
Q

What is an example of a topical beta blocker used to treat POAG and the potency?

A

Timolol, 0.25% or 0.5%

39
Q

What was the previous first line treatment for POAG before prostaglandin analogues replaced it?

A

Beta blockers e.g. timolol

40
Q

What adverse event can occur with prolonged use of beta blockers in POAG?

A

Tachyphylaxis: decreasing response to drug following initial administration, due to upregulation of beta-adrenergic receptors in ciliary body, overcoming beta bloackade

41
Q

What are 6 systemic complications of beta blockers, due to systemic absorption?

A
  1. Exacerbation of asthma, COPD (careful in these patients)
  2. Bradycardia
  3. Hypotension
  4. Other arrhythmias e.g. heart block
  5. Nightmares
  6. Impotence
42
Q

What are 3 conditions that beta blockers to treat POAG should not be given in?

A
  1. COPD
  2. Bradyarrhythmia
  3. Bradycardia
43
Q

What should be done before prescribing beta blockers to treat POAG and why?

A

Take a thorough drug history; could have bradycardia due to eye drops

44
Q

What should be done if a patient on beta blockers for POAG develops bradycardia?

A

Stop beta blockers and continue other eye medications. Make appointment with ophthalmologist to adjust medications in the next few days

45
Q

What are 2 examples of alpha-2 agonists used to treat POAG?

A

Brimonidine, apraclonidine

46
Q

What is a common adverse event in response to alpha-2 agonist use for treating POAG?

A

Allergic reactions are common (can happen many months or years after starting treatment)

47
Q

How does the use of alpha-2 agonists to treat POAG compare to prostaglandins and beta blockers?

A

Alpha-2 agonists are less effective than both

48
Q

What are 2 examples of topical carbonic anhydrase inhibitors used to treat POAG?

A

Dorzolamide, brinzolamide

49
Q

Why are carbonic anhydrase inhibitors to treat POAG limited in effectiveness?

A

99% of carbonic anhydrase must be inhibited before aqueous is affected which is hard to achieve with topical administration

50
Q

What are 2 types of formulations of carbonic anhydrase inhibitors to treat POAG and which is better?

A

Topic and systemic; systeimc are more effective

51
Q

What is the only effective systemic carbonic anhydrase inhibitor to treat POAG?

A

Acetazolamide (Diamox)

52
Q

How is acetazolamide/ Diamox used to treat POAG?

A

can be used IV and orally

53
Q

What are 2 things to be careful of when prescribing carbonic anhydrase inhibitors?

A
  1. Sulfonamide allergy - can cause seirous allergic reactions so avoid if have had reactions to sulfa drug in past e.g. ceptrin
  2. Sickle cell disease/ trait
54
Q

What precludes long term use of carbonic anhydrase inhibitors in POAG?

A

Side effects

55
Q

How effective are carbonic anhydrase inhibitors in treating POAG?

A

Very effective at lowering IOP

56
Q

What are 7 examples of the systemic toxicity of carbonic anhydrase inhibitors?

A
  1. GI side effects e.g. diarrhoea
  2. Metallic taste in mouth
  3. Lethargy
  4. Loss of libido
  5. Paraesthesias - tingling in hands and feet
  6. Potassium loss
  7. Renal stones (precipitate of acetazolamide or phosphate crystals)
57
Q

Why can carbonic anhydrase inhibitors cause potassium loss?

A

Urine has increased potassium, phosphate, bicarbonate and decreased citrate and magnesium. These drugs cause you to urinate more frequently (use with caution if on other diuretics)

58
Q

Why are systemic ocular anti-hypertensives for emergency treatment only?

A

Due to systemic side effects