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Clinical Final Exam > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

What are the strong risk factors of glaucoma?

A 
High intraocular pressure
Aging (>40y)
Family history (primary history)
Race (blacks)
Severe myopia
Optic disc appearance
Cup:disk ratio >0.5
Corneal thickness >0.5 mm
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2
Q

What does the literature set the upper limit of intraocular pressure as?
What is the general rule if there is glucomatous damage, no matter what the pressure is?

A

21 mmHg

General rule - lower the pressure

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3
Q

What is the clinical presentation of primary open angle glaucoma (POAG)?
Unilateral or bilateral?

A

Usually asymptomatic (until substantial visual field loss occurs).
Chronic progressive if not treated.
Subtle decrease in colour and contrast sensitivity.
Bilateral.

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4
Q

What is the clinical presentation of closed angle glaucoma (CAG)?
(symptomatic and non-symptomatic signs)

A 
Symptomatic acute episodes:
-eye pain
-edematous cloudy cornea
-N/V
-abdominal pain
-unresponsive iris
Non-symptomatic:
-halos around lights (from edematous cornea)
-headache
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5
Q

What is the primary defect of OAG?

A

Usually decreased drainage of aqueous humor leading to increased pressure

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6
Q

What causes CAG?

A

Ballooning of the iris (floppy) blocks drainage of aqueous humor (blockage of trabecular meshwork)

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7
Q

Which of the glaucomas is an emergency situation?

A

Closed angle glaucoma

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8
Q

What is aqueous humor produced by?

Where is it filtered?

A

Ciliary non-pigmented epithelial cells.

Filtered and secreted into posterior chamber.

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9
Q

Where is the aqueous humor drained?

A

Trabecular meshwork and canal of schlemm (80%)

Uveoscleral (20%)

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10
Q

What does constant inflow and resistance to outflow result in?

A

Intraocular pressure

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11
Q

What are 2 ways to control intraocular pressure?

A

Decrease AH production

Increase drainage

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12
Q

What can you target to decrease AH production?

A

Receptors on the ciliary body (alpha and beta)

Carbonic anhydrase

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13
Q

3 Ways to increase AH drainage

A

Trabecular meshwork & canal of schlemm
Uveoscleral outflow
Surgical intervention

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14
Q

The 2 iris muscles and their receptors and what they cause the pupil to do

A

Circular muscle: cholinergic receptor, miosis

Radial muscle: alpha adrenergic receptor, mydriasis

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15
Q

What receptors are on the trabecular meshwork?

A

Receptors for epinephrine, dopamine, prostanoids, biogenic amines

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16
Q

What type of drug is Pilocarpine?

A

Parasympathomimetic (mitotic)

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17
Q

How does Pilocarpine work?

A

Increases AH outflow by reducing resistance to outflow through trabecular meshwork & canal of Schlemm - therby reducing IOP (by 20-30%)

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18
Q

What are the topical SE of Pilocarpine?

A

Miosis - decreased night vision and visual field.
Ciliary muscle contraction - causes accommodative spasm, frontal headache, brow ache, eyelid twitching, conjunctival irritation (decreases in 2-5 weeks)
Retinal tear or detatchment

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19
Q

What are systemic SE of Pilocarpine?

At what concentration are they seen?

A 
NVD
Cramping
Urinary frequency
Bronchospasm
Heart block
GI, salivation
(think parasympathetic stuff)
Seen in concentrations 6-8%
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20
Q

What are the sympathomimetic (adrenergic) drugs for glaucoma?

A 
Dipivefrin
Epinephrine (no longer marketed)
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21
Q

How do sympathomimetic drugs work?

What is up with depivefrine?

A

Adrenalin-mediated -
act on alpha and beta receptors in ciliary body
Increased outflow through trabecular meshwork and uvescleral route. (but may actually increase AH production)
Depivefrine is a prodrug (better tolerated)

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22
Q

What are topical SE of sympathomimetics (dipivefrin)?

A 
Tearing and burning
Brow ache
Conjunctival hyperemia
Blepharoconjunctivitis
Stenosis of NLO
Blurred vision
Adrenochrome deposits (with prolonged use)
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23
Q

What are systemic SE of sympathomimetics (dipivefrin)?

A

Increased BP & HR
Arrhythmias, anxiety, persperation, headache, tremor (think adrenaline)
– use in caution with CV disease, cerebrovascular disease, hyperthyroid, DM
CI in closed angle

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24
Q

What are the two alpha-2 receptor agonists?

Which is more common?

A

Aproclonidine

Brimonidine (more common)

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25
Q

When is aproclonidine used?

How does it work?

A

Used post eye surgery.

Decreases peak IOP by decreasing AH production

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26
Q

How does brimonidine work?

Why is it better?

A

Decreases AH production AND increases outflow (uveoscleral)

Less SE than aproclonidine

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27
Q

Topical SE of alpha-2 receptor agonists (aproclonidine, brimonidine)

A 
Allergic type reactions: 
Itching
Eye discomfort
Lid edema
Foreign object sensation
Hyperemia
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28
Q

Systemic SE of alpha-2 receptor agonists (aproclonidine, brimonidine)

A 
Dry mouth
Dizziness, fatigue
Decreased BP
Somnolence
(caution with CV disease, renal compromise, cerebrovacular disease, or on other antihypertensives)
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29
Q

List the 4 beta blockers used for glaucoma

A

Timolol (main)
Levodunolol
Betaxolol
Cartealol

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30
Q

What drug is first line therapy because it does not cause miosis or mydriasis?

A

Beta blockers

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31
Q

What conditions are beta blockers useful for?

A

Both closed and open angle glaucoma

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32
Q

How do beta blockers decrease IOP?

By what percentage?

A

By blocking beta receptors in ciliary epithelial cells, thereby decreasing aqueous humor production
Reduce IOP by 20-30% (same as Pilocarpine)

33
Q

What conditions are beta blockers contraindicated in?

A 
Heart failure
Asthma
COPD
Diabetes
Heart block
Sinus bradycardia
34
Q

Long term use of beta blockers can result in ______ in 20-25% of patients

A

Tachyphylaxis

35
Q

What technique can you use to reduce beta blocker SE?

A

NLO technique

36
Q

Topical SE of beta blockers

A 
Stinging
Dry eyes
Blurred vision
Blepharitis
Rare: conjunctivitis, uveitis, keratitis
37
Q

Systemic SE of beta blockers

A 
Dec. HR/BP
Negative inotropy
Conduction defects
Increased lipids
Bronchospasm
Block T2DM symptoms
38
Q

What can beta blockers be used in combo with?

What shouldn’t be used with them?

A

Can be used with carbonic anhydrase inhibitors, parasympathomimetics, prostaglandins, alpha2 agonists
Don’t use with epinephrine or dipivefrin

39
Q

What are the two topical carbonic anhydrase inhibitors?

A

Dorzolamide

Brinzolamide

40
Q

How do CAIs work to reduce IOP?

By what percentage is it reduced?

A

Inhibit carbonic anhydrase II, thereby decreasing ciliary epithelial cell production of AH
Reduced ny 15-26%

41
Q

What is the dosing schedule for topical CAIs?

A

Q8-12h

42
Q

Topical SE of CAIs?

A

Burning/stinging on application
Transient blurred vision
Tearing
Rare: photophobia, lid reaction, conjunctivitis

43
Q

Systemic SE of topical CAIs?

A

Rare: sulfa allergy

44
Q

What are the oral forms of CAIs?

A

Acetazolamide

Methazolamide

45
Q

By what percentage do oral CAIs reduce IOP?

A

25-40%

46
Q

Systemic SE of oral CAIs?

A 
Acidosis
Malaise
Fatigue
Anorexia
Nausea
Depression
Decreased libido
Renal calculi
Increased uric acid
Diuresis
Blood dyscrasias
47
Q

In what patients should CAIs be used with caution?

A 
Sulfa allergy
Sickle cell disease
Respiratory acidosis
Pulmonary disorders
Electrolyte imbalance
Hepatic & renal disease
48
Q

What can you combine oral CAIs with?

A

Beta blockers
Parasympathomimetics
Prostaglandins

49
Q

What situations are oral CAIs useful for?

A

Emergencies (not for chronic use)

50
Q

List the prostaglandin analogues

A 
Latanoprost
Bimatoprost
Travoprost
Tafluprost
Unoprostone
51
Q

How do prostaglandin analogues reduce IOP?

By what percentage?

A

Increase uveoscleral outflow of AH (20% is drained by this route)
Dec IOP by 25-35%

52
Q

What is the dosing regimen of prostaglandin analogues?

A

Usually once daily HS

53
Q

Topical SE of prostaglandin analogues

A

Iris pigment alteration (mixed colour becomes brown)
Increased eyelash pigment, length, thickness
Conjunctival hyperemia
Punctae corneal erosions
Uveitis
Caution with eye inflammation

54
Q

Systemic SE of prostaglandin analogues

A 
Skin reactions
URTI/cold/flu
Chest pain
GI disturbances
Muscle/joint pain
55
Q

Can you combine prostaglandins with other glaucoma agents?

A

You can combine with all other agents

56
Q

What does pilocarpipne cause in the ciliary muscle?

A

Ciliary muscle contraction, decreases AH outflow

57
Q

What does atropine cause in the ciliary muscle?

A

Ciliary muscle relaxation, increased outflow

58
Q

Name the two hyperosmotic solutions for glaucoma

A

Isosorbide (oral)

Mannitol (IV)

59
Q

When are hyperosmotic solutions used?

A

Emergency management of angle closure

May be used to decrease pressure pre-op

60
Q

When should you use hyperosmotic solutions?

A

Severe dehydration
Pulmonary edema
CHF

61
Q

What are the only 2 classes that affect the pupil?

How do they affect it?

A

Parasympathomimetics - miosis

Sympathomimetics (epinephrine/depivefrine) - mydriasis

62
Q

List the classes of agents that increase AH outflow

A

Parasympathomimetics
Sympathomimetics (epi + alpha-2 agonists)
Prostaglandin analogues

63
Q

List the agents that decrease AH production

A

Alpha-2 agonists
Beta blockers
CAIs

64
Q

What is the first line in treatment of glaucoma?

A

Beta blocker - gold standard

65
Q

What do you move to if beta blockers are contraindicated or ineffective? (2nd line)

A

Monotherapy with either:
PG analogue
Local CAIs
Alpha-2 agonist

66
Q

If monotherapy with PG analogue, CAI, or alpha-2 agonist is inneffective, what do?

A

Combo therapy:

  • Beta blocker + (PG or CAI or Miotic)
  • PG + (CAI or alpha-2 agonist)
67
Q

When are parasympathetics used?

A

Third line due to side effects

May use as miotic with PG or beta blocker

68
Q

What is the objective in the treatment of POAG?

A

Lower IOP 20-30% from baseline

decrease more if at higher risk

69
Q

List the principles of treating glaucoma

A
  1. Start in one eye - if tolerated treat both
  2. If not tolerated, switch (sometimes same drug class, different formulation)
  3. Once target IOP is reached, monitor IOP every 2-4 months.
  4. Measure visual field and optic disc once yearly (unless unstable/worsening)
  5. Ensure adherence to treatment and tolerance
  6. Separate meds by 5-10 min if using more than one agent.
70
Q

In closed angle glaucoma acute attacks, what therapy is contraindicated?
When can you use it?

A

Pilocarpine CI in papillary block (may worsen)

Can use after lowering IOP with other agents first

71
Q

In CAG acute attacks, what agent is only used short-term?

A

Hyperosmotic agents

72
Q

What 4 agents can be used in acute attacks of CAG?

A

Beta blockers
Alpha-2 agonists
Prostaglandins
CAIs

73
Q

At what pressure might the iris be eschemic and unresponsive to miotics (pilocarpine)?

A

> 60 mmHg

74
Q

What are mydriatic agents used for?

A

Eye examination

75
Q

What are cycloplegic agents used for?

A

Accurate refractions and relief from ciliary spasm during inflammation

76
Q

Name two parasympathoplegic drugs

A

Atropine (7-10d)

Tropicamide (1-6h)

77
Q

What do both parasympathoplegic drugs produce?

When are they contraindicated?

A

Produce both mydriasis and cycloplegia.

Contraindicated in glaucoma

78
Q

What is phenylephrine?

When is it used with caution?

A

A sympathomimetic mydriatic agent with little/no cycloplegia.
Used with caution in glaucoma, heart disease, HTN

Clinical Final Exam (5 decks)

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