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Ocular Disease II > Glaucoma: Secondary Glaucoma > Flashcards

Glaucoma: Secondary Glaucoma Flashcards

1
Q

Secondary Open Angle

  1. 6 of them
A
  1. Pigment Dispersion
  2. Exfoliation
  3. Steroid Response
  4. Traumatic
    a. Hyphema
    b. Angle Recession
  5. Phacolytic
  6. Uveitic
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2
Q

Secondary Angle Closure (4 of them)

  1. Uveitic
  2. Neovascular
  3. Epithelial Down Growth
  4. Phacomorphic
A

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3
Q

Pigment Dispersion Syndrome: What is it?

  1. Patient Demographics/History
  2. Clinical Findings
    a. Cornea
    b. Iris
    c. Anterior Chamber
    d. Lens
    e. Gonio
  3. Pathophysiology
  4. Management
    a. Medication
    b. Surgery (LPI) (Study Shows what?)
    c. Medical
    d. ALT/SLT
    e. Trabeculectomy/Tube Shunt
    f. Follow UP?
A

BILATERAL; Pigment is RELEASED from POSTERIOR Pigment Epithelium of the IRIS and is Deposited throughout the ANTERIOR SEGMENT!

  1. Young (20-45), MYOPIC; WHITES; Male (2:1)
    a. History: Usually MYOPIA, Possible FHx; USUALLY ASYMPTOMATIC; Maybe Blurred vision w/EXCERCISE due to RELEASE of PIGMENT and INCREASED IOP
  2. a. Krukenberg Spindle (Pigment deposited on Corneal ENDOTHELIUM in a VERTICAL Distribution)
    b. Mid-Peripheral Slit-Shaped Transillumination defects, Fine Pigment Granules on the Iris Surface

c. DEEP
d. Pigment Also Accumulates on Lens (SCHEIE STRIP)
e. CONCAVE ANGLE (backward Bowing of the IRIS; Mod to DENSE Pigment in TM)

  1. Posterior Bowing of iris increases Contact b/w iris and Zonules; Mechanical rubbing of Iris and Zonules releases Pigment into the AC; IOP Increased due to Pigment Obstruction of Inter-trabecular Spaces AND CHRONIC DAMAGE to TRABECULAR CELLS
    a. 30-50% w/PDS develop Pigmentary Glaucoma
  2. a. Pilocarpine: Shift iris forward and cause Miosis (decreases contact b/w iris and Zonules) (Side Effects: Ciliary Spasm, Induced Myopia, headache, Brow Ache, Increased risk of RD)
    b. Relieves Posterior Bowing. Equalizes Pressure in AC and PC, Eliminating Contact B/W POSTERIOR IRIS and ZONULES (Study showed there’s no benefit of the LPI in PREVENTING progression from PDS to PG)
    c. Prostaglandins and Aqueous Suppressants (Beta-blockers, Alpha-agonists, CAIs)
    d. Effective in Pts uncontrolled medically, but IOP reduction is usually only temporary
    e. ONLY In SEVERE CASES when Medical and Laser Tx don’t work
    f. Every 3-6 months. Depends on Severity
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4
Q

Pseudophakic Pigmentary Glaucoma

  1. What is it?
A
  1. Pigmentary Glaucoma can occur in Pseudophakic Patients if the Haptics of the ioL rub AGAINST the POSTERIOR SURFACE of the IRIS!
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5
Q

Exfoliation Glaucoma (Pseudoexfoliation Syndrome)

  1. Type of Condition?
  2. Characteristics?
    a. What can it progress to?
A
  1. Systemic.
  2. Grey-white FLAKY MATERIAL deposited throughout the ANTERIOR SEGMENT of the EYE. MOST EASILY SEEN ON THE LENS
    a. To Exfoliation Glaucoma
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6
Q

Exfoliation Syndrome

  1. Pt
    a. Ethnicity?
    b. Over what Age?
    c. Males/Females?
  2. History?
A
  1. a. Scandinavian Descent and Navajo
    b. Over Age 50. Increases w/Age (Prevalence)
    c. Same
  2. Usually ASYMPTOMATIC; Family History
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7
Q

Exfoliation Syndrome

  1. Clinical Findings
    a. Lens
    b. Iris
    c. Zonules
    d. Gonio
A
  1. a. Flaky White Material in CENTRAL PUPIL ZONE and LENS PERIPHERY (Constant rubbing by iris scrapes the material from the mid-zone)
    b. Transillumination defects at PUPIL BORDER due to SPHINCTER ATROPHY. Pigment MAY DEPOSIT on TM, Iris Surface, and Corneal Endothelium
    c. Exfoliation Material Accumulated on the ZONULES
    d. Patchy Pigmentation of TM; May See Flecks of Exfoliation Material (looks LIKE DANDRUFF). Hard to see
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8
Q

Exfoliation Syndrome: Other Characteristics

  1. Uni/Bi
  2. Symmetric/Asymmetric?
  3. Associated with EARLY FORMATION of what?
  4. Exfoliation material also Deposits onto what 4 things?
  5. What happens to the Zonules?
    a. Increased risk of what?
  6. 40% of these patients develop what?
A
  1. BIlateral
  2. Asymmetric
  3. of CATARACTS
  4. Zonules, Ciliary Body, Vitreous Face, IOLs
  5. They WEAKEN and can FRAGMENT and be ABSENT in some AREAS
    a. of LENS or IOL SUBLUXATION
  6. Exfoliation Glaucoma
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9
Q

Exfoliation Syndrome: Patho

  1. Exfoliation collects in what?
    a. Also produced in what?
  2. Most commonly Accepted mechanism for IOP Elevation?
  3. PEX material may be what to the TM.
    a. What does this cause?
A
  1. in the ANGLE
    a. in TM
  2. Clogging of TM by Exfoliation material and Pigment
  3. Toxic
    a. Trabecular Endothelial Cell Dysfunction
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10
Q

Exfoliation Syndrome: Management

  1. What IOP Fluctuations are Common?
  2. Medical Tx? (drugs)
  3. ALT/SLT
  4. Trabeculectomy/Tube Shunt
  5. Increased Risks of what surgery? Why?
  6. F/U?
    a. PROGRESSION can occur much more RAPIDLY in EXFOLIATION GLAUCOMA than in what?
A
  1. LARGE DIURNAL
  2. Prostaglandins and Aq. Suppressants. Topical drugs = FIRST LINE Tx: Usually LESS EFFECTIVE than in POAG
  3. Can be VERY EFFECTIVE due to TM pigmentation, but usually only temporary
  4. Only done in SEVERE CASES. Similar results to POAG
  5. of CATARACT SURGERY; Cuz of Weakened Zonules
  6. every 3-6 months; POAG
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11
Q

Steroid Response Glaucoma

  1. Giving someone steroids has the potential to elevate IOP and cause a secondary OAG.
    a. IOP ELEVATIONS can be what?
A
  1. a. SEVERE and PROLONGED
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12
Q

Steroid Response Glaucoma

  1. Pt
    a. % of General Pop that are steroid responders?
    b. % of Pts w/POAG that are Steroid Responders?
  2. History
    a. Symptoms usually what?
A
  1. a. 5-10%
    b. 50%
  2. a. usually Asymptomatic. Steroid use a crucial aspect of history
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13
Q

Steroid Response Glaucoma

  1. How long does it take after starting steroid use for IOP to increase?
  2. What steroids can cause an ACUTE rise in IOP?
  3. Degree of Steroid response depends on what?
A
  1. 2 weeks
  2. Intravitreal and Periocular
  3. on Potency and Route of Administration
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14
Q

Steroid Response Glaucoma

  1. Clinical Findings
    a. Steroid Associated what?
    b. Ocular condition for which steroids were prescribed
    c. Gonio?
    d. Nerve?
    i. Can mimic what?
A
  1. a. Cataracts
    c. Usually nothing of note

d. Glaucomatous Optic Nerve Damage if ELEVATED IOP is high enough and PROLONGED
i. can mimic NTG if Optic Nerve is Damaged w/VF Loss, but IOP has returned to normal after discontinuation of the steroid

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15
Q

Steroid Response Glaucoma: Patho

  1. Theory
    a. What SWELL in the TM that IMPEDES Aq. OUTFLOW?

b. Corticosteroids Suppress activity of what?
c. Steroid particles have been seen in ANGLE after what?

A
  1. a. Glycosaminoglycans in TM
    b. Phagocytic Activity of Trabecular Endothelial Cells (Allow debris to accumulate in TM)
    c. Intravitreal Steroid Injection in Pts w/ACUTE IOP SPIKE
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16
Q

Steroid Response Glaucoma: Management

  1. Big thing to do?
  2. Medical/Laser
A
  1. STOP STEROIDS (look at risk/benefit of doing this); reduce Dose; Maybe use Weaker steroid; NSAIDS or some other immunosuppressants
  2. Glaucoma meds and Laser Trabeculoplasty can be used to lower IOP
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17
Q

Traumatic Hyphema

  1. What is a Hyphema?
    a. Due to what?
  2. What is an 8-Ball Hyphema?
A
  1. Blood in Anterior Chamber
    a. Blunt/Penetrating injury to Globe…tear in Iris or CB and thus bleeding from Major Arterial Circle
  2. TOTAL HYPHEMA: Clotted and appears BLACK in COLOR (Worse prognosis than a hyphema w/Bright red blood)
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18
Q

Traumatic Hyphema

  1. Pt
    a. Usually seen in whom?
    b. Rebleeding usually seen in whom?
  2. History
    a. …What causes it…
A
  1. a. Active Young Men (3:1)
    b. Pts w/Sickling hemoglobinopathies
  2. Blunt or penetrating Trauma
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19
Q

Traumatic Hyphema: Clinical Findings

  1. Cornea
  2. Anterior Chamber
  3. Iris
  4. Lens
  5. Gonio
    a. If it’s apparent (hyphema..)
    b. Should be performed when?
    c. Evaluate for what?
A
  1. Corneal Blood Staining; Endothelial Dysfunction
  2. Circulating RBCs or a layered Hyphema (Microhyphem = Visual only w/a Slit Lamp)
  3. Maybe Iridodialysis; Sphincter Tears; Angle Recession
  4. Traumatic Cataract
  5. a. Delay gonio until risk of rebleeding has passed
    b. 4 Wks after injury.
    c. Angle Recession: 60-90% of pts have it. DARK PIgment Clumps in TM may mean there was a previous Hyphema. PAS
20
Q

Traumatic Hyphema: Patho

  1. Blunt trauma causes compressive forces that rupture what?
  2. RBCs and Inflammatory Cells do what?
    a. usually blood will what?
  3. 8-Ball Hyphema can cause what?
A
  1. Vessels of Iris and CVB. Penetrating Trauma = DIRECT DAMAGE to BVs
  2. Clog TM and cause a RISE in IOP
    a. Clear TM in a few days, but Rebleeds can occur
  3. Pupillary Block that leads to a Secondary Angle-Closure Glaucoma
21
Q

Traumatic Hyphema:

  1. Hyphema associated Glaucoma: Risk Depends on Size

a. 13%
b. 27%
c. 52%

  1. Glaucoma more common with what?
A
  1. a. 1/2 AC is filled
    c. 52% for total Hyphema
  2. with REBLEEDS
22
Q

Traumatic Hyphema: Management

  1. Most traumatic Hyphemas are what?
  2. What should you tell the patient to do?
    a. What drugs should be AVOIDED!?
    b. Mydriatic/Cycloplegic?
    c. Topical Steroids?
    d. Medical?
    e. Surgical
A
  1. Small and transient….Don’t need Tx.
  2. LIMIT ACTIVITY; Sleep with Head Elevated;
    a. ASA and NSAIDs should be AVOIDED

b. Immobile Pupil minimizes risk of Rebleed; Cycloplegic relieves pain of associated traumatic uveitis
c. Reduce inflammation and risk of Rebleed
d. Aq. Suppressants (Avoid CAIs in pts w/SICKLE CELL!). NO Miotics
e. Evacuation of blood indicated in cases w/non-clearing Hyphema, uncontrolled IOP, or Corneal Staining

23
Q

Angle Recession Glaucoma

  1. Refers to what?
A
  1. Tear in CB muscle layers due to BLUNT or PENETRATING TRAUMA…Glaucoma can come months to years after injury
    * Risk depends on extend of CB/TM damage
24
Q

Angle Recession Glaucoma

  1. Pt
    a. usually whom?
    b. % that develop Angle Recession Glaucoma?
  2. History
    a. hmm…
A
  1. a. Young Men
    b. 4-9% of pts w/Angle recession develop glaucoma
  2. a. blunt/penetrating trauma; Most common: Ball sports, Assault, car accident, Toy guns, slingshots
25
Q

Angle Recession Glaucoma: Clinical Findings

  1. Cornea
  2. Iris
  3. Lens
  4. Common cause of WHAT?
  5. Gonio:
    a. We see an IRREGULAR WIDENING of what?
    b. Pigment?
    c. Performed on whom?
A
  1. Scarring
  2. Sphincter Tears, Iridodialysis
  3. Traumatic Cataract, Dislocated Lens
  4. Asymmetric IOP
  5. a.. of the CB band
    b. Mild to Moderate
    c. ALL Pts w/a History of BLUNT or Penetrating Injury (look for angle recession and determine Frequency of Follow Up)
26
Q

Angle Recession Glaucoma: Patho

  1. Blunt Trauma
  2. Angle recession is an Indicator of what?
    a. Is it the cause of Glaucoma?
  3. Trauma to TM stimulates what?
A
  1. Posterior Force…causes Tear b/w Longitudinal and Circular Muscles of the CB!
  2. Previous Ocular Trauma
    a. NOT CAUSE of GLAUCOMA
  3. Proliferative and Degenerative changes in the TM that leads to Obstruction of Aq. Outflow
27
Q

Angle Recession Glaucoma: Management

  1. How long do we follow these patients w/Angle Recession?
  2. Medical?
  3. ALT/SLT?
  4. Surgical?
A
  1. INDEFINITELY
  2. Aqueous Suppressants, Prostaglandin Analogs (After inflammation has resolved)
  3. Not very effective
  4. Advanced cases. But lower Success rate than in POAG
28
Q

Phacolytic (Lens Protein) Glaucoma

  1. What is it?
A
  1. 2ndary Glaucoma caused by LEAKAGE of LENS PROTEINS (from Mature cataract) into AC
29
Q

Phacolytic (Lens Protein) Glaucoma

  1. Pt
    a. Age?
    b. Where in the world?
  2. History
    a. Gradually diminish Vision from what?
    b. ACUTE ONSET of a what?
A
  1. a. Elderly
    b. Developing Countries
  2. a. from Mature Cataract
    b. PAINFUL, red eye from inflammation and elevated IOP
30
Q

Phacolytic (Lens Protein) Glaucoma: Clinical Findings

  1. Cornea
  2. Conj
  3. Anterior Chamber
  4. Lens
  5. Gonio
A
  1. Maybe Edematous due to increased IOP
  2. Injection
  3. Intense FLARE from Soluble Proteins and cell response mainly of macrophages
  4. Mature cataract visible. Sometimes white patches of macrophages observed on the lens
  5. Open Angles
31
Q

Phacolytic (Lens Protein) Glaucoma: Patho

  1. As Lens matures, what happens to the Lens Capsule?
A
  1. Very small microscopic defects can develop, allowing release of High MW proteins…which leak out from a MATURE CATARACT in this case into the AC and OBSTRUCT TM, leading to ELEVATION in IOP!
32
Q

Phacolytic (Lens Protein) Glaucoma: Management

  1. DEFINITIVE TREATMENT?
  2. Medical?
  3. Prognosis?
A
  1. CATARACT EXTRACTION
  2. Aq. Suppressants and Hyperosmotics administered to lower IOP in prep for CATARACT SURGERY.

Steroids reduce inflammation

Cycloplegics to decrease PAIN, prevent Posterior Synechiae and stabilize Blood-Aqueous Barrier

  1. GOOD w/Cataract surgery if symptoms have been there for LESS than 1 WEEK and IOP has not been ELEVATED for an extended period
33
Q

Lens Particle Glaucoma

  1. Secondary Open Angle Glaucoma: Caused by what?
  2. Increased IOP due to what?
  3. Some Pts w/Retained lens particles in the AC don’t develop What?
  4. Management
    a. Medical
    b. Surgical Removal
A
  1. Fragmented Lens debris released during cataract surgery or injury and retained w/in the eye
  2. lens particles and inflammatory cells obstructing the TM
  3. Elevated IOP cuz Phagocytic cells in the TM can ingest the particles and clear the outflow pathways
  4. a. Aq. suppressants decrease IOP; Steroids/Cycloplegics to treat Inflammatory RxN
    (IOP usually returns to Normal once lens particles have been absorbed)

b. If IOP cant be controlled, residual lens material must be surgically removed

34
Q

Uveitic Glaucoma

  1. What is it?
  2. Prevalence increases with what?
A
  1. Intraocular inflammation in pts w/uveitis.

2. increases w/severity and chronicity of the uveitis

35
Q

Uveitic Glaucoma

  1. Pt
    a. Depends on what?
    b. % of pts that develop increased IOP?
    c. Glaucoma is more common in what types?
  2. History?
A
  1. a. Etiology of uveitis
    b. 25%
    c. in ANTERIOR or Pan UVEITIS than posterior Uveitis
  2. History of uveitis; Recurrent painful, red eyes, Photophobia
36
Q

Uveitic Glaucoma: Clinical Findings

  1. Conj
  2. Cornea
  3. AC
  4. Iris
  5. Vitreous
  6. Gonio
A
  1. Circumlimbal Injection
  2. KP (Fine or Mutton-Fat)
  3. Cells, Flare
  4. Nodules, Posterior Synechiae (Iris to Lens), PAS (Iris to TM)
  5. Cells, Snowballs
  6. PAS; Indentation can differentiate b/w PAS and Appositionally Narrow Angles
37
Q

Uveitic Glaucoma: Patho

  1. Open-Angle Mechs
    a. Obstruction of TM by what?
    b. What else w/TM?
    c. What else?
    d. Big thing to remember?
  2. Closed-Angle Mechs? (2)
A
  1. a. Inflammatory Cells
    b. Trabeculitis (swelling of Trabecular Beams)
    c. Scarring/Permanent damage to the TM and Steroid-Induced

d. EYE GETS BETTER (Aq. Production returns to NORMAL while Aq. Outflow is still reduced)
2. Posterior Synechiae (360) –> Pupil block/Iris Bombee

and PAS

38
Q

Uveitic Glaucoma: Patho

  1. Peripheral Anterior Synechiae
    a. Flare in AC makes Iris what?
    b. Iris forms adhesions to what?
    c. Iris attachments can be 1 of 2 things?
    d. PAS from Uveitis develop more frequently in eyes that already have NARROW what?
    e. More PAS Present –>
    f. ANY AMT of PAS has the potential to do what?
A
  1. a. Sticky
    b. to the TM
    c. Broad (several clock hours) or Patchy
    d. Angles
    e. –> More outflow thru the TM is blocked –> greater the likely of increased IOP
    f. to Decrease Aq. Outflow and Increase IOP
39
Q

Uveitic Glaucoma: Patho

  1. Posterior Synechiae
    a. IOP remains how? Until what?
    b. When there’s 360 Posterior Synechiae, Aq. Flow can no longer do what?
    c. Pressure in Posterior Chamber Pushes IRIS HOW?
A
  1. a. normal; 360 of Posterior Synechiae = Pupillary Block
    b. flow from the Posterior chamber to the Anterior Chamber
    c. forward into Apposition w/the Angle Structures = Iris Bombee
40
Q

Uveitic Glaucoma: Management

  1. FIRST THING TO DO: CONTROL WHAT?
  2. Cycloplegic/Mydriatics?
  3. Medical?
  4. LPI/Surgical PI?
  5. ALT/SLT
  6. Trabeculectomy/Tube Shunt
A
  1. Inflammation w/Steroids: Prevent Structural Damage
  2. Prevent/Break Posterior Synechiae, Control Pain
  3. Aq. Suppressants may be used to reduce IOP. NO PROSTAGLANDINS! (Can worsen uveitis by increasing inflammatory mediators in the Eye). NO MIOTICS (bring iris in closer proximity to the lens, increase CB spasm, increase permeability of Blood Aq. Barrier)
  4. For Iris Bombe from Posterior Synechiae
  5. NO!
  6. More risky in Pts w/uveitis cuz eye is already inflammed
41
Q

Neovascular Glaucoma

  1. What is it?
  2. Symptoms?
    a. Early Stages?
    b. Afterwards?
  3. History? (2 types of diseases)
A
  1. 2ndary open angle or angle closure glaucoma due to new vessel growth in AC angle.
  2. a. can be asymptomatic
    b. Painful, Red eyes, Decreased vision
  3. Retinal Disease and Systemic Vascular Diseases
42
Q

Neovascular Glaucoma: Patho

  1. Caused by SEVERE what?
  2. Ischemia retinal tissue release what?
  3. Neo is accompanied by what?
    a. Open-Angle Stage?
    b. Angle-Closure Stage?
A
  1. RETINAL HYPOXIA
  2. Growth Factors (VEGF) –> cause growth of new vessels…cause retinal Neo AND can diffuse to Anterior Segment and cause iris and ANGLE NEO

Retina tries to revascularize sick tissue, but new vessels grow in the wrong place

  1. Fibrovascularization (grows over TM)
    a. At first, Angle is occluded by Fibrovascular membrane, but remains open
    b. Contracture of fibrovascular membrane will cause Closure of the Angle. (can happen QUICKLY)
43
Q

Neovascular Glaucoma: Causes

  1. BIG 3?
A
  1. DIABETIC RETINOPATHY
  2. CRVO (90 day glaucoma)
  3. Ocular Ischemic Syndrome
44
Q

Neovascular Glaucoma: Clinical Findings

  1. Cornea
  2. Iris
  3. Retina
  4. Gonio
A
  1. Can appear Hazy from Edema if the IOP is severely Elevated
  2. Fine vessels are seen at the pupillary margin and may extend across the iris (rebeosis)
  3. Underlying pathology
  4. Early Stages: Fine thin vessels seen extending across angle to TM

Later stages: Gonio: Show PAS due to contraction of the Fibrovascular Tissue and eventual total closure of the Angle

(*HYPHEMA in Pt w/o HISTORY of TRAUMA = NEO)

45
Q

Neovascular Glaucoma: Management

  1. PRP:
    a. Can PREVENT what?
A
  1. Laser Tx: Applied to Retina. Decreases Retinal O2 Demand; Allows O2 to flow from choroidal vasculature to inner layers of retina to reduce retinal hypoxia and decrease release of growth factors
    a. NVG, if performed early. by causing regression of the Anterior segment NV
46
Q

Neovascular Glaucoma Management (2)

  1. ONCE Angle is CLOSED, IOP becomes what?
  2. Medical
  3. LPI
  4. ALT/SLT
  5. Trabeculectomy/Shunt
  6. Enucleation
A
  1. VERY DIFFICULT to MANAGE and
    PROGNOSIS for VISION is POOR!
  2. Aq. Suppressants; usually don’t work in Angle-closure stage
  3. Not effective (angle is closed. Risk of Hyphema) (It’s syneched closed…not a pupillary block mechanism)
  4. Not effective. unable to see TM and risk of Hyphema
  5. only in SEVERE CASES. Outcome usually Poor
  6. Performed in case of a Blind and Painful Eye

Ocular Disease II (15 decks)

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