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Ophthalmology Boards Review > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

What are the contraindications to prostaglandins?

A

• Active uveitis
• CME
• Herpetic keratitis

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2
Q

What are the risk factors for failure of trabeculectomy?

A

• Young age
• Aphakia/pseudophakia
• Disturbance of conjunctiva
• African American
• Active inflammation
• Neovascularization

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3
Q

What are the last portions of the visual field (VF) to be affected in end-stage glaucoma?

A

• Central VF
• Inferotemporal VF

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4
Q

What are the functions of M cells?

A

• Motion vision
• Large diameter “Massive”
• Sensitive to light in scotopic conditions

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5
Q

What is the function of P cells?

A

• Concentrated in macula
• Small diameter ”Petite”
• 80% of RGCs
• Responsible for color and fine detail

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6
Q

What is the most common complication after filtering surgery?

A

• Visually significant cataract (20-40%)

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7
Q

What is phacolytic glaucoma?

A

• Mature or hypermature cataract
• Increased concentration of high molecular weight lens protein
• Proteins released through MICROscopic openings in lens capsule
• Protein clogs trabecular meshwork
• Macrophages phagocytize large proteins clog trabecular meshwork
• Cytology of aqueous = lens laden macrophages
• LACK OF KERATIC PRECIPITATES
• OPEN angle
• Intact lens capsule

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8
Q

What is phacoanaphylaxis (AKA phacoantigenic glaucoma)?

A

• Capsular bag violated (i.e. trauma, surgery)
• Leads to granulomatous inflammation
• Keratic precipitates

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9
Q

What is phacomorphic glaucoma?

A

• Shallow anterior chamber
• Lens becomes large, thick → pushes iris forward and closes angle
• Treatment: cataract removal

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10
Q

What is lens particle glaucoma?

A

• MACROscopic lens pieces in anterior chamber

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11
Q

What is the differential diagnosis for shallow anterior chamber with patent PI?

A

• Aqueous misdirection, malignant glaucoma
• Choroidal effusion
• Suprachoriodal hemorrhage

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12
Q

What is the treatment of aqueous misdirection, malignant glaucoma?

A

• Medical: intensive aqueous suppressant, cycloplegics, hyperosmotics. NEVER use miotics
• Surgical (disruption of anterior vitreous face): YAG laser through patent iridotomy or pars plana vitrectomy (definitive)

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13
Q

What is the treatment for plateau iris?

A

• Laser iridoplasty
• Chronic cholinergics

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14
Q

What types of renal stones are caused by systemic carbonic anhydrase inhibitors?

A

• Calcium oxalate
• Calcium phosphate

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15
Q

What is the mechanism of action of latanoprostene bunod 0.024% (Vyzulta)?

A

• Latanoprost component reduces IOP by long term remodeling of extracellular matrices in ciliary body (via uveoscleral pathway, “nonconventional”)
• Nitric oxide component reduces IOP by “conventional” pathway via relaxation of trabecular meshwork and Schlemm’s canal

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16
Q

What is the purpose of dynamic gonio?

A

Determines whether closed angle is due to appositional versus synechial closure

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17
Q

Which gonio lenses can and cannot be used for dynamic gonio?

A

• Dynamic gonio: Zeiss, Posner, Sussman (posterior lens diameter < corneal diameter)
• Cannot do dynamic gonio: Goldmann lens (posterior lens diameter > corneal diameter)

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18
Q

The TIGR/MYOC gene mutation leads to which conditions?

A

• Mutations produce protein myocilin
• Chromosome 1
• Seen in juvenile open angle glaucoma and adult onset POAG

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19
Q

The OPTN gene mutation leads to which condition?

A

• Normal tension glaucoma

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20
Q

Which genes are associated with congenital glaucoma?

A

• GLC3A gene mutation (most common)
• CYP1B1 gene mutation (more severe form)

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21
Q

Which condition has a LOXL1 gene mutation?

A

• Pseudoexfoliation glaucoma

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22
Q

What is the pathway of pressure sensitive trabecular outflow?

A

Uveal TM → corneoscleral TM → juxtacanalicular TM (most outflow resistance) → Schlemm canal → collector channels (25-30) → deep and midscleral venous plexi → episcleral veins → anterior ciliary and superior ophthalmic veins → cavernous sinus
<img></img>

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23
Q

What is the pathway of pressure insensitive trabecular outflow?

A

• Ciliary muscle → supraciliary and suprachoroidal spaces → intact sclera
• 45% of total aqueous outflow
• Increased by cycloplegia, adrenergic agents, prostaglandins
• Decreased by age, glaucoma, miotics
<img></img>

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24
Q

What is tilted disc syndrome?

A

• Situs inversus (vessels go nasally before turning temporally)
• Superotemporal or bitemporal VF defects
• Associated with myopic astigmatism and X-linked congenital stationary night blindness

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25
Q

What is the mechanism of action of pilocarpine?

A

● Contraction of longitudinal ciliary muscle where it inserts into scleral spur and TM → improves outflow
● Reduces IOP 15% to 20%
● Associated with:
○ Angle closure (forward shift of lens-iris diaphragm); myopic shift secondary to ciliary muscle contraction; headache, brow ache (ciliary muscle spasm); cataract formation; RD; breakdown of blood-aqueous barrier; iris pigment epithelial cysts; epiphora (lacrimal stimulation and punctal stenosis); ocular surface changes (drug-induced pseudopemphigoid)

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26
Q

What virus is associated with Posner Schlosmann and Fuchs iridocyclitis?

A

• Posner Schlosmann: CMV
• Fuchs: Rubella & CMV

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27
Q

What is hypotony maculopathy?

A

• Common complication in young myopes (versus choroidal detachments which are more common in older pts)
• Complication of over filtration
• Fundus findings: optic disc edema, macular folds, CME
• Hypotony maculopathy and choroidal detachments do not occur together

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28
Q

What are examples of direct gonioscopy (used in the operating room)?

A

• Koeppe
• Barkan
• Wurst
• Swan-Jacob
• Richardson

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29
Q

What are examples of indirect gonioscopy?

A

• Zeiss
• Sussman
• Posner
• Goldmann (3 mirror)

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30
Q

What is the prognosis for primary congenital glaucoma?

A

• Best if diagnosed between 3 months to 12 months of age
• Worse when diagnosed within 1 month of life or >12 months of age
• >50% of patients with newborn PCG develop legal blindness
• Worse prognosis if corneal diameter >14 mm at diagnosis

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31
Q

What medications lower IOP and what is their mechanism of action?

A

• Topical beta blockers: reduce aqueous production, inhibit cAMP production
• Topical alpha agonists: reduce cAMP production by binding alpha 2 receptors. With long term use also increases uveoscleral outflow
• Topical CAI: reduce aqueous production by inhibiting carbonic anhydrase
• Topical pilocarpine, echothiophate, parasympathomimetics: increase outflow through TM by contraction of longitudinal ciliary muscle fibers
• Topical prostaglandins analogs: increase uveoscleral outflow, activates MMP which remodels tissues along this pathway

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32
Q

What are the side effects of IOP-lowering medications?

A

• Topical prostaglandins: conjunctival hyperemia, hypertrichosis, increased pigmentation of iris and periocular skin, CME, anterior uveitis, reactivation of herpes simplex virus keratitis. Rarely, flu-like symptoms and joint/muscle pains
• Topical CAI: bitter taste, corneal edema secondary to effecting corneal endothelium pump
• Topical beta blocker: decreased exercise tolerance. Use with caution in asthma and COPD
• Topical alpha agonists: dry mouth, follicular conjunctivitis, contraindicated in children and while breastfeeding, safest medication during pregnancy but stop after birth of baby due to causing systemic hypotension and apnea

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33
Q

What is topiramate-induced angle closure?

A

• Sulfamate-substituted monosaccharide medication
• Causes bilateral acute myopia and angle closure
• Ciliochoroidal swelling
• Anterior rotation of ciliary body
• First-line treatment: stop medication, start cycloplegia, hypotensive agents
• Refractory cases: laser iridoplasty

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34
Q

What are the focal signs of glaucomatous cups?

A

• Notching of rim
• Vertical elongation of cup
• Cupping to rim margin
• RNFL hemorrhage
• RNFL loss

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35
Q

What are less specific signs of glaucomatous cups?

A

• Exposed lamina cribrosa
• Nasal displacement of rim vessels
• Baring of circumlinear vessels
• Peripapillary atrophy

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36
Q

What is the classic triad of primary congenital glaucoma?

A

• Epiphora
• Photophobia
• Blepharospasm

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37
Q

What is automated static perimetry?

A

• Stimulus size constant
• Varies stimulus intensity
• Stationary stimulus at various locations

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38
Q

What is frequency doubling technology (FDT) perimetry?

A

• Low spatial frequency sinusoidal grating that undergoes rapid phase-reversal flicker
• Ability for patients to distinguish changes in contrast
• Only useful for detecting early glaucomatous loss

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39
Q

What is SWAP (short wavelength automated perimetry)?

A

• Isolates and tests the sensitivity of short-wavelength ganglion cells
• Detection of early glaucoma is higher with SWAP compared to standard automated perimetry
• VF defects predate same VF defects on standard automated perimetry
• Disadvantage = long testing time and more sensitive to media opacities
• SITA-SWAP = decrease in testing time

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40
Q

What is kinetic and tangent screen testing?

A

• Target moved into an area just until it is seen (automated or manual)

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41
Q

What are the reliability indices of visual fields?

A

• False positives(“trigger happy”): >15% is unreliable
• False negatives: does not respond when stimulus is present, indicates inattentiveness or seen in areas of damage (if high, do not throw out the test)
• Fixation loss: patient looks way from central target (“chasing lights”)

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42
Q

What is SLT and its efficacy compared to ALT?

A

• SLT: selective photothermolysis targeting pigmented cell
• Short, low-energy bursts absorbed selectively by pigmented trabecular meshwork
• Little damage to surrounding tissue
• Efficacy of SLT and ALT are equivalent

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43
Q

What is the process of aqueous production?

A

• Produced by inner non pigmented epithelial cells
• Ciliary process composed of outer pigmented and inner non-pigmented epithelial cells that face each other at their apical surface and joined by tight junctions
• Tight junctions are part of blood-brain barrier
• Inner non-pigmented epithelial cells have many mitochondria and microvilli
• Inner non-pigmented epithelial cells protrude into posterior chamber

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44
Q

What is a beta-1 selective topical beta blocker?

A

• Produced by inner non pigmented epithelial cells
• Ciliary process composed of outer pigmented and inner non-pigmented epithelial cells that face each other at their apical surface and joined by tight junctions
• Tight junctions are part of blood-brain barrier
• Inner non-pigmented epithelial cells have many mitochondria and microvilli
• Inner non-pigmented epithelial cells protrude into posterior chamber

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45
Q

What are the causes of falsely low IOP on applanation?

A

• Thin CCT
• BCL
• Corneal edema
• Corneal ectasia
• Not enough fluorescein (thin meyers)

46
Q

What are the causes of falsely high IOP on applanation?

A

• Band keratopathy
• Thick CCT
• Corneal scar
• Too much fluorescein (thick meyers)

47
Q

What is the age range for JOAG?

A

• Ages 4 to 35 years

48
Q

Which anesthetics lower IOP?

A

• Sevoflurane
• Most others

49
Q

Which anesthetics increase IOP?

A

• Ketamine
• Succinylcholine

50
Q

Which anesthetic does not have an effect on IOP?

A

• Chloral hydrate

51
Q

Which illicit drugs lower IOP?

A

• Heroin
• Marijuana
• Alcohol

52
Q

What is an ideal time to check IOP in EUA?

A

• Immediately after induction of general anesthesia and before intubation

53
Q

What are the risk factors for aphakic glaucoma?

A

● Cataract surgery in the first year of life
● Glaucoma develops in 15-50% of children who undergo surgery for congenital cataracts
● Small corneal diameters
● Post-op complications
● Aphakic patients are always at risk for developing glaucoma
○ Usually aphakic glaucoma develops within 3 years after cataract surgery

54
Q

What are the relative contraindications to trabeculectomy?

A

• Prior conjunctival surgery
• Active anterior segment neovascularization
• Active uveitis or scleritis
• Younger age
• African American

55
Q

What are the findings in Axenfeld-Rieger syndrome?

A

• Corectopia
• Polycoria
• Posterior embryotoxon
• Iris strands to Schwalbe line
• Iris hypoplasia
• Maldeveloped anterior chamber angle
• Craniofacial dysmorphism (maxillary hypoplasia, telecanthus, hypertelorism)
• Dental abnormalities (microdontia/oligodontia/hypodontia)
• Redundant umbilical skin
• Hypospadias
• Growth retardation
• Cardiac valve abnormalities
• Pituitary abnormalities

56
Q

What is the aqueous humor formation rate?

A

• 2 to 3 μL/min during waking hours
• During sleep, 50% reduction in rate
• Total aqueous volume: 250 μL
• Turnover 1% per minute

57
Q

What are the racial differences in risks in POAG?

A

• POAG prevalence 3-4 times higher in African descent and Hispanic ethnicity
• Blindness 4 times more common in Black patients; up to 15 times higher risk in older than 45 years
• More likely to be diagnosed at younger age and more advanced stage in Black patients

58
Q

What is the Goldmann equation?

A

● Po = (F-U)/C + Pv
○ Po = IOP in mmHg
○ F = rate of aqueous formation
○ U = rate of aqueous drainage through pressure-insensitive uveoscleral pathway in μL/min → cannot be directly measured
○ C = facility of outflow through pressure-sensitive trabecular pathway in μL/min/mmHg
○ Pv = episcleral venous pressure in mmHg, normally 6-9 mmHg

59
Q

What is the Imbert-Fick principle?

A

• Used for Goldmann tonometer and Perkins tonometer
• Assumes CCT = 520 μm
• 3.06 mm tip diameter

60
Q

What are the causes of increased episcleral venous pressure?

A

• Sturge Weber
• Carotid-cavernous fistula
• Cavernous sinus thrombosis
• TED

61
Q

What are the contraindications and adverse effects of hyperosmotic agents?

A

• Contraindication: renal failure
• Adverse effects: headache, mental confusion, backache, acute CHF, myocardial infarct, subarachnoid/subdural hemorrhage

62
Q

What anatomical changes are found in angle recession?

A

• Tear between longitudinal and circular muscle fibers of ciliary body

63
Q

What anatomical changes are found in cyclodialysis?

A

• Separation of ciliary body from scleral spur
• Causes hypotony

64
Q

What anatomical changes are found in iridodialysis?

A

• Disinsertion of iris root from ciliary body

65
Q

What are the trabecular meshwork tear findings on gonio?

A

• Small trabecular cleft on gonio

66
Q

What are the risks for suprachoroidal hemorrhage after trabeculectomy?

A

• High myopia
• Aphakia
• Pseudophakia
• Hypotony
• Prior vitrectomy
• Advanced age
• Systemic hypertension
• Anticoagulant therapy
• History of suprachoroidal hemorrhage in fellow eye
• Large magnitude of IOP reduction from pre-op to post-op

67
Q

Which glaucoma medication is category B in pregnancy?

A

• Brimonidine

68
Q

Which glaucoma medications are category C in pregnancy?

A

• Prostaglandins (PGF 2a) → affects uterine smooth muscle and induces contraction/labor
• Carbonic anhydrase inhibitors
• Beta blockers

69
Q

What are the preservative free (BAK free) glaucoma drops?

A

• Tafluprost
• Cosopt -PF
• Timolol -PF
• Travatan Z
• Alphagan P

70
Q

What are the optic nerve lengths in various locations?

A

• Intraocular: 1 mm
• Intraorbital: 25 mm
• Intracanalicular: 10 mm
• Intracranial: 10 mm

71
Q

What are the number of axons in the optic nerve?

A

• 1.2 -1.5 million axons

72
Q

What are the risk factors for primary angle closure glaucoma?

A

• Race: Inuit (20-40 times higher than whites) or East Asian
• Small AC/short axial lengths
• >40 years
• Women > men
• Positive family history
• Hyperopes

73
Q

Which topical steroids cause IOP elevation, ranked by decreasing severity?

A

Decreasing order of effect on IOP elevation
• Difluprednate (most)
• Prednisolone
• Rimexolone
• Fluorometholone (FML)
• Loteprednol

74
Q

What are optic drusen?

A

• Abnormal axonal metabolism → mitochondrial calcification and drusen formation
• Histology: discrete basophilic zones of calcifications
<img></img>
<img></img>

75
Q

What are the different secondary glaucomas and the respective cell types involved in blocking trabecular meshwork?

A

• Hemolytic glaucoma → hemosiderin-laden macrophages
• Ghost cell glaucoma → rigid hemolyzed erythrocytes
• Uveal melanomas → pigmented epithelioid melanocytes
• Phacolytic glaucoma → eosinophilic protein-laden macrophages

76
Q

What is implicated in the excessive proliferation of tenon capsule fibroblasts?

A

• Seen with scarring of glaucoma filtration bleb
• Transforming growth factor beta and platelet-derived growth factor are implicated

77
Q

What is this finding?

A

• Haab striae
<img></img>

78
Q

What were the findings in the Ocular Hypertension Treatment Study (OHTS)?

A

● Determined the effectiveness of typical ocular hypotensive in preventing or delaying onset of glaucoma in patients with ocular HTN
● Risk factors for progression of POAG
○ Elevated IOP (for each mmHg above baseline IOP → risk of progression increased by 10%)
○ Advanced age (22% increased relative risk per decade)
○ Thin CCT (81% increase in relative risk for every 40 μm thinner CCT)
○ Large C/D ratio (for each 0.1 vertical CD ratio increase → risk of progression increased by 32%)
○ Worse pattern standard deviation on standard automated perimetry (22% increase in relative risk per 0.2 dB increase)
● Treated group: 22.5% IOP reduction; 4.4% developed optic nerve or VF damage over 5 years
● Untreated group: 4% IOP reduction; 9.5% developed optic nerve or VF damage in 5 years
● Patients with CCT > 588 had very low rates of conversation to OAG at 5 years

79
Q

What was a shared conclusion of the Collaborative Normal Tension Glaucoma study (CNTGS) and the Early Manifest Glaucoma Trial (EMGT)?

A

• Optic disc hemorrhage is a risk factor for glaucoma progression

80
Q

What were the conclusions from the Collaborative Initial Glaucoma Treatment Study (CIGTS)?

A

• Confirmed initial surgical (trab) therapy achieves better IOP than does initial medical therapy
• Results do not translate to better visual field stabilization secondary to cataracts

81
Q

What were the conclusions of the Early Manifest Glaucoma Trial (EMGT)?

A

• Examined betaxolol plus laser trabeculoplasty or observation
• Treated: 45% progressed at 6 years. Reduced IOP by 25%
• Untreated: 62% progressed at 6 years

82
Q

What are the different neuroradiologic findings in optic nerve glioma versus optic nerve meningioma?

A

• Optic nerve glioma: fusiform lesion
• Optic nerve meningioma: tram-track lesion; fusiform can also occur. Optic nerve should appear as lucency on imaging

83
Q

What is congenital glaucoma?

A

• Increased resistance to outflow through trabecular secondary to dysgenesis of neural crest cell derived angle structures
• Males > females
• Bilateral (70%)
• 2% chance of having offspring with disease
• Deep anterior chamber with high, flat anterior iris insertion
• Hypoplastic peripheral iris

84
Q

What are the findings in plateau iris?

A

• Anteriorly rotated ciliary process
• Anterior chamber deep central, narrow peripheral
• Gonio: narrow angle, indentation shows peripheral hump where iris is draped over anteriorly placed ciliary process

85
Q

What are the types of secondary lens-related open-angle glaucoma and their findings?

A

• Phacolytic: leakage of high molecular weight lens protein through microscopic openings in capsule of hypermature cataract; wrinkling of capsule; lack KPs or synechiae; pseudohypopyon; lens-engorged macrophages settle in inferior trabecular meshwork
• Phacoantigenic: after surgery or trauma; granulomatous inflammation; sensitized to their own lens protein; KPs; low grade vitrifies, posterior synechiae, PAS, residual lens material
• Lens particle: due to fragments of cortical lens obstructing trabecular meshwork

86
Q

What is the etiology of secondary lens-related closed angle glaucoma?

A

• Phacomorphic: enlarging, intumescent cataract grows in anterior-posterior dimension → pushes iris forward

87
Q

What are the anterior angle structures (posterior to anterior)?

A

• Iris
• Ciliary body
• Scleral spur
• Trabecular meshwork
• Schwalbe’s line

88
Q

What is the significance of the corneal optical wedge?

A

• Posterior termination of Descemet membrane and corneal endothelium

89
Q

What is the differential diagnosis for ectopia lentis?

A

• Marfans
• Weill-Marchesani
• Homocystinuria
• Hyperlysinemia
• Sulfite oxidase deficiency

90
Q

What systemic abnormalities are associated with aniridia?

A

● WAGR complex: Wilms tumor, aniridia, GU malformations, mental retardation
○ Common in sporadic aniridia (PAX6 mutation; chromosome 11p13)
● Gillespie syndrome: aniridia, cerebellar ataxia, hypotonia, mental deficiency

91
Q

What ocular anomalies are associated with aniridia?

A

• Cataract
• Corneal pannus
• Foveal hypoplasia
• Limbal stem cell deficiency
• Glaucoma
• Nystagmus
• Optic nerve coloboma
• Optic nerve hypoplasia
• Refractive errors
• Ptosis

92
Q

What fatal conditions are associated with albinism?

A

• Chediak-Higashi
• Hermansky-Pudlak

93
Q

What is Chediak-Higashi syndrome?

A

• Autosomal recessive
• Mutation in lysosomal trafficking regulator protein that renders inadequate phagocytosis
• Recurrent pyogenic infection
• Patients rarely survive past 10 years of age, die from infection

94
Q

What is Hermansky-Pudlak syndrome?

A

● Autosomal recessive
● Associated with:
○ Low platelets
○ Interstitial lung disease
○ Granulomatous colitis
● Common among Swiss or Puerto Rican descent

95
Q

What is the treatment for congenital glaucoma?

A

• Topical IOP lowering medications until surgery
• Surgery is definitive treatment
• If cornea is clear → goniotomy
• If cornea is cloudy → trabeculotomy

96
Q

What are the clinical findings in pigmentary dispersion syndrome?

A

• Krukenberg spindle: narrow or round pigment on corneal endothelium. Present in 90% of patients
• Midperipheral transillumination defects of iris → iris with concave contour, rubs against zonules → pigment release. Present in 90% of patients
• Scheie’s line or Zentmayer’s line: pigment on anterior surface along zonule and posterior surface
• Gonioscopy: open angle, trabecular meshwork densely pigments and pigment on Schwalbe’s line (Sampaolesi line)

97
Q

What are the risk factors for pigmentary dispersion syndrome?

A

• Male
• Age (usually 30’s)
• Myopia
• Concave iris and posterior iris insertion
• Flat corneas
• Family history

98
Q

What is the alcohol content of alcohol wipes?

A

• 70% isopropyl alcohol

99
Q

What is the site of presumed damage to the optic nerve in glaucoma?

A

• Lamina cribrosa

100
Q

What is Lowe syndrome?

A

• Oculocerebrorenal syndrome
• X-linked recessive; mutation of OCRL gene
• Poor visual prognosis
• Bilateral cataracts
• Glaucoma -50% of patients
• Nystagmus
• Keloids -corneal or conjunctival
• Hypotonia
• Fanconi syndrome/chronic renal failure

101
Q

What are the ocular findings in albinism?

A

• Foveal hypoplasia (poor vision and poor prognosis)
• Nystagmus due to poor vision from foveal hypoplasia
• Over-decussation of optic nerve fiber, 90% fiber decussates to contralateral side (normally 53%)
• Loss of stereopsis due abnormal decussation
• Transillumination defects of iris
• Strabismus
• Photophobia
• Refractive errors

102
Q

What is aniridia?

A

• Iris hypoplasia, various degrees
Genetic etiology:
• PAX6 mutation; chromosome 11p13
• Autosomal dominant (⅔) or sporadic (⅓)
• Autosomal recessive in 2% -seen with Gillespie syndrome
Management:
• Obtain renal ultrasound in sporadic aniridia to rule out WAGR

103
Q

What is neurofibromatosis type 1?

A

• Autosomal dominant
• Chromosome 17
• AKA von Recklinghausen disease
• Associated with with cafe au lait spots, iris Lisch nodules (hamartoma), neurofibromas, plexiform neurofibromas (increased risk of glaucoma; described as “bag of worms,” S shaped eyelid), optic nerve gliomas, sphenoid wing dysplasia

104
Q

What is tuberous sclerosis?

A

• Autosomal dominant
• Mutation of TSC1 (hamartin; more common for retinal lesions) and TSC2 (tuberin)
• Chromosome 9, 16
• AKA Bourneville-Pringle disease
• Triad: facial sebaceous adenomas (angiofibromas), mental deficiency, seizures (intracranial calcified astrocytic hamartomas)
• Other findings, ungual fibromas, hypomelanotic macules, Shagreen patch, multiple retinal hamartomas

105
Q

What is von Hippel-Lindau Disease?

A

• Autosomal dominant
• Chromosome 3
• Tumor suppressor gene mutation
• AKA cerebello-retinal-angiomatosis
• Associated with retinal capillary hemangioblastomas; angiomatous lesions of CNS; cerebellar hemangioblastoma; pancreatic cysts; renal cell carcinoma; pheochromocytoma

106
Q

What is ataxia telangiectasia?

A

• Autosomal recessive
• AT gene mutation → DNA damage repair
• Chromosome 11
• AKA Louis Bar syndrome
• Ocular manifestations include conjunctival telangiectasias, nystagmus, oculomotor apraxia, convergence and accommodation abnormalities, strabismus
• Increased risk of cancer and immunodeficiency

107
Q

What are the laser settings for diode cyclophotocoagulation?

A

• Power: 750 mW to 2000 mW
• Duration: 2 to 4 seconds
• Avoid 3 o’clock and 9 o’clock positions (ciliary nerves)
• 6 spots per quadrant
• Total of 18 spots (recommend 3 quadrants to avoid anterior segment necrosis)

108
Q

What medication has shown to decrease secondary hemorrhage in hyphema patients?

A

• Aminocaproic acid

109
Q

What is the medical management of traumatic hyphema?

A

• If sickle cell screen positive: beta blockers and alpha-2 agonists; avoid systemic and topical CAI’s
• If sickle cell screen negative: beta blockers, alpha-2 agonists, and CAI’s (topical and systemic)

110
Q

What are surgical indications for traumatic hyphema?

A

• If sickle cell screen positive: corneal blood staining; IOP > 25 for 24 hours; recurrent IOP spike > 30
• If sickle cell screen negative: corneal blood staining; IOP > 60 for 48 hours; IOP > 50 x 5 days; IOP > 25 for 6 days, hyphema > 50% after 8 days

111
Q

What are mechanisms of action of Mitomycin C (MMC) and 5-fluorouracil (5-FU)?

A

• Both are chemotherapeutic agents
• MMC: DNA crosslinker
• 5-FU: inhibits thymidylate synthase, ultimately inhibits DNA synthesis and repair. Cell cycle specific (G1)

Ophthalmology Boards Review (10 decks)

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