Glaucoma: Intro

Question 1

What is Glaucoma?

Answer 1

Optic neuropathy: Progressive loss of Ganglion cell axons that results in visual field damage and related to IOP

Question 2

Glaucoma: Difference b/w Primary and Secondary?

Answer 2

1. Primary: Not related to an underlying condition

2. Secondary: comes form some other Ocular or Systemic disease, trauma, or certain drug use.

Question 3

Open Angle vs. Angle Closure

Answer 3

1. Open Angle: Anatomically open angle

2. Angle Closure: Complete or PARTIAL obstruction of the angle

Question 4

Ocular Hypertension vs. Normotensive Glaucoma

1. Ocular Hypertension?
2. Normotensive Glaucoma (NTG)

Answer 4

1. Increased IOP w/ABSENCE of Glaucomatous damage

2. IOP w/in “Normal” range w/Glaucomatous damage

Question 5

Glaucoma vs. Glaucoma Suspect

1. Who is a Glaucoma Suspect?

Answer 5

1. Pt that is monitored closely cuz of findings that suggest glaucoma w/the absence of Glaucomatous damage

Question 6

1. Why do we care about Glaucoma so much?

Answer 6

1. POAG is pretty much ASYMPTOMATIC and it’s about 70% of cases

and it’s the 2nd leading cause of blindness worldwide (cataracts are the first)

Question 7

Risk Factors:

1. Age: Rate of Blindness from POAG does what with age?
2. Race: More likely in whom?
   a. Leading cause of BLINDNESS in what race?
3. Family History: More likely if who in your family has it?
4. Genetics: Possible cause?
5. IOP
   a. Risk is 16x’s higher with IOP > ?
   b. Peak IOP?
   c. Which IOP: Mean, Highest, Fluctuation, or Nocturnal IOP has been consistently associated w/development of Glaucoma?
6. Corneal Thickness: Who is at risk?
   a. What is considered the “STANDARD OF CARE” for all glaucoma suspects and patients?
7. What Systemic diseases are associated with glaucoma?

Answer 7

1. INCREASES with AGE
2. AA’s
   a. AA’s
3. Siblings > Parents
4. More than 30 mutations of the MYOCILIN (MYOC/TIGR) gene have been associated with POAG
5. Very strong, direct relationship w/prevalence and long-term risk.
   a. more than 21 mmHg compared to those

Question 8

Glaucoma and Blood Pressure

1. Risk of development of NTG and POAG with what?
   a. Pay particular Attention to SYSTEMIC BETA-BLOCKERS: Why?

Answer 8

1. Low systemic BP, includes NOCTURNAL HYPOTENSION

a. If IOP is at Peak when BP is lowest, risk for development/progression of glaucoma.

Question 9

2 Theories behind Pathophysiology of Glaucoma: What are they?

Answer 9

Mechanical Theory and Ischemic Theory

Question 10

Glaucoma: Patho: Mechanical Theory (Neurotrophin Deprivation)

1. What is it?
   a. Cause?
   b. What does this IMPEDE?

Answer 10

1. Direct compression of Axonal fibers and support structures of Anterior Optic Nerve
   a. Increased IOP and/or Defects in ECM cause Compression and Distortion of the Lamina Cribrosa
   b. AXOPLASMIC FLOW of NEUROTROPHINS to retinal ganglion cells –> death of neurons

Question 11

Glaucoma: Patho: Ischemic Theory (Glutamate Toxicity)

1. Development of what?
   a. Results in what
   b. In Glaucoma, there may be faulty what?
   c. Local Ischemia may affect what 2 things?

Answer 11

1. Intraneural Ischemia
   a. Decreased Optic Nerve Perfusion

b. Autoregulatory mechanisms that leads to BF impedence
c. Axonal transport and decreased metabolic activity –> Accumulation of EXTRACELLULAR TOXINS (like Glutamate)

Question 12

1. Essentially: Blindness is due to what?

Answer 12

1. Compromise of Ganglion cell Axons at level of Lamina Cribrosa that leads to Apoptosis

Question 13

Patho: Neurotrophin Deprivation

1. Disruption of Axonal Transport compromises Ganglion cells and Stimulates Apoptosis at NORMAL IOP: What does it do at Elevated IOPs?

Answer 13

1. Increases the response

Question 14

Patho: Glutamate

1. Low Levels = ?
2. High levels = ?
3. What cells play a critical role in maintaining transport systems in the retina by keeping glutamate at what levels?
   a. What happens when the eye is hypoxic or Ischemic?

Answer 14

1. Excitatory NT in Retinal Ganglion Cells
2. Neurotoxin to Retinal Ganglion Cells
3. Mueller Cells
   a. Ganglion cell response is to produce High Levels of Glutamate which overrides Mueller Cell Control
   * Ischemia leads to Excess of Glutamate which creates a cascade of molecular events leading to Apoptosis