Glaucoma: Intro Flashcards
What is Glaucoma?
Optic neuropathy: Progressive loss of Ganglion cell axons that results in visual field damage and related to IOP
Glaucoma: Difference b/w Primary and Secondary?
- Primary: Not related to an underlying condition
2. Secondary: comes form some other Ocular or Systemic disease, trauma, or certain drug use.
Open Angle vs. Angle Closure
- Open Angle: Anatomically open angle
2. Angle Closure: Complete or PARTIAL obstruction of the angle
Ocular Hypertension vs. Normotensive Glaucoma
- Ocular Hypertension?
- Normotensive Glaucoma (NTG)
- Increased IOP w/ABSENCE of Glaucomatous damage
2. IOP w/in “Normal” range w/Glaucomatous damage
Glaucoma vs. Glaucoma Suspect
- Who is a Glaucoma Suspect?
- Pt that is monitored closely cuz of findings that suggest glaucoma w/the absence of Glaucomatous damage
- Why do we care about Glaucoma so much?
- 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)
Risk Factors:
- Age: Rate of Blindness from POAG does what with age?
- Race: More likely in whom?
a. Leading cause of BLINDNESS in what race? - Family History: More likely if who in your family has it?
- Genetics: Possible cause?
- 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? - Corneal Thickness: Who is at risk?
a. What is considered the “STANDARD OF CARE” for all glaucoma suspects and patients? - What Systemic diseases are associated with glaucoma?
- INCREASES with AGE
- AA’s
a. AA’s - Siblings > Parents
- More than 30 mutations of the MYOCILIN (MYOC/TIGR) gene have been associated with POAG
- Very strong, direct relationship w/prevalence and long-term risk.
a. more than 21 mmHg compared to those
Glaucoma and Blood Pressure
- Risk of development of NTG and POAG with what?
a. Pay particular Attention to SYSTEMIC BETA-BLOCKERS: Why?
- Low systemic BP, includes NOCTURNAL HYPOTENSION
a. If IOP is at Peak when BP is lowest, risk for development/progression of glaucoma.
2 Theories behind Pathophysiology of Glaucoma: What are they?
Mechanical Theory and Ischemic Theory
Glaucoma: Patho: Mechanical Theory (Neurotrophin Deprivation)
- What is it?
a. Cause?
b. What does this IMPEDE?
- 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
Glaucoma: Patho: Ischemic Theory (Glutamate Toxicity)
- Development of what?
a. Results in what
b. In Glaucoma, there may be faulty what?
c. Local Ischemia may affect what 2 things?
- 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)
- Essentially: Blindness is due to what?
- Compromise of Ganglion cell Axons at level of Lamina Cribrosa that leads to Apoptosis
Patho: Neurotrophin Deprivation
- Disruption of Axonal Transport compromises Ganglion cells and Stimulates Apoptosis at NORMAL IOP: What does it do at Elevated IOPs?
- Increases the response
Patho: Glutamate
- Low Levels = ?
- High levels = ?
- 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?
- Excitatory NT in Retinal Ganglion Cells
- Neurotoxin to Retinal Ganglion Cells
- 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
