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NBEO STEP 1 > ocular diease > Flashcards

ocular diease Flashcards

1
Q

most common CN palsy
Why?

A

CN6
- usually due to micveovascular infact

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2
Q

Complete CN3 palsy is characterized by:

A

complete external opthalmoplegia - all of the muscles that CN3 controls are dead

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3
Q

Adie’s

A
  • diagnose with .125% pilo - will constrict due to up regulation of receptors on iris sphincter

decreased deep tendon reflects
young female
veriform eye movements
slow constriction to near but not to light

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4
Q

what is used to diagnose a pupil involved CN3 palsy

A

1% pilo will cause constriction

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5
Q

Cause of post ganglionic horners

A

-Cavernous sinus issues (sympathetics travel on the ICA in the Cav sinus)
- CA Dissection
- Internal Carotid Artery Aneurysm

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6
Q

what does internal ophthalmoplegia mean

A

paralysis of the pupil

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7
Q

Abnormal pupil is large:
- what are in the differentials?

A
  • Adies
  • CN3 palsy
  • Iris Sphincter trauma
  • pharm dilation
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8
Q

causes of APD?

what would never cause an APD?

A

CAUSES OF APD
- dense vitreous heme
- extensive retinal damage
- optic nerve damage (only when unsymmetrical b/t eyes)

NEVER CAUSING AN APD
- cornea
-iris
- lens
- optic tract
- optic radiations
- occipital lobe
(anything posterior to chiasm)

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9
Q

optic nerve colobomas are located

A

Inferior nasal

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10
Q

early signs of Leber’s Optic neuropathy

A

optic disc hyperemia that progresses to optic disc pallor in late stages.

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11
Q

Most common type of functional pituitary tumor

A

macroadenoma PROLACTIN SECRETING tumor
(amenorrhea, galactorrhea, infertility)

PIGS ON ACID (acid cells)

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12
Q

Retrograde degneration example
How does it affect the ON

A

pituitary tumor is a cause of RETROGRADE DEGENERATION.

BOW TIE PALLOR of the ON (remember that fibers that are b/t the macula and the ON are NASAL) – this is reason for the bow tie pallor… all of those fibers cross and are compressed by the tumor

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13
Q

why is CN6 affected in IIH

A

CN6 travels along the Pretrous ridge of the temporal bone. Can be compressed when ICP is high

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14
Q

is an MRI or a lumbar puncture done first?

A

MRI - make sure there are no space occupying lesions

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15
Q

What is the only way to diagnose papilledema

A

spinal tap

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16
Q

What is the acuity in the third decade of StARgardts patient

A

Usually around 20/200 in the pts 30s and doesn’t get worse after that.

Rapid vision loss and color vision abnormalities

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17
Q

StARgarts

A

Fish tail flecks
RPE mottling
Beaten Bronze - bullseye
Salt and pepper

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18
Q

Most common macular dystrophy, inheritance

A

Stargardt’s
AR inheritance

stARgardt’s = AR

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19
Q

In early stages of RP, what test is abnormal

A

Scotopic ERG

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20
Q

RP triad
Can you name 4 other things seen ?

A

Waxy ON (pallor)
Bone Spicules
Artery Attentuation

PSC
Optic disc Drusen
Macular changes
Keratoconnus

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21
Q

Symptoms for RP, vision by 30?

A

Night blindness - the Cones and rods are both affected by rods are more affected than cones
Peripheral vision loss.

75% of RP patients at age 30 are asymptomatic

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22
Q

Ushers syndrome inheritance

A

RP + Hearing loss
AR

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23
Q

Average age of diagnosis for RP

A

9-19yo

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24
Q

Albinism may be associated with severe systemic conditions including :

A

Hermansky Pudluk
Chediak Higashi

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25
Q

Severity of vision loss in albinism is due to:

A

Degree of iris/ fundus hypopigmentation and foveal hypoplasia

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26
Q

Albinism is caused by a decrease in melanin or melanocytes

A

albinism = decrease in MELANIN

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27
Q

Normal recovery for a macular photostress test

A

<60 seconds

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28
Q

Macular holes:
Stage 1
Stage 2
Stage 3
Stage 4

A

Stage 1 - loss of foveal depression - yellow spot on fovea
Stage 2 - Round small full thickness hole with a PSEUDO-OPERCULUM – looks like the top of a can
Stage 3 - full thickness with a true operculum. Positive Watze Allen
Stage 4 - stage 3 + PVD

Positive Watze Allen is seen in stage 3 and 4 - complete break in the middle of the thin line projected within the macula

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29
Q

Cause of macular hole
Sex that gets macular holes more common

A

Macular hole results from posterior vitreous traction on the macula.

MC in female and most common cause is aging

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30
Q

Are males are females more likely to get ERMs.

What causes ERMS?

A

Females
- increases with age
- idiopathic but may also be caused by PVDs and retinal breaks
- think: GLIAL CELLS on the ILM

Most patients with ERMs have a PVD

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31
Q

Signs seen in pathological myopia

A
  • posterior staphaloma
  • oblique insertion of ON
  • fuchs spots
  • laquer cracks
  • Premature cats (NS and PSC)
  • PVD
  • Peripheral retinal degeneration so (paving stone, snail tracks)
  • Retinal detachments
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32
Q

Hallmark for pathological myopia

A

Posterior staphaloma = posterior bulging of a weak sclera

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33
Q

Refractive error associated with myopic degeneration/pathological myopia ?

What is the axial length associated?

A

> -6.00

26.5mm - measured with A scan

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34
Q

Triad for histo

Is the vitreous clear?

A

Punched out spots
Peripapillary atrophy
CNVM Maculopathy (CHBALA)

VITREOUS IS ALWAYS CLEAR IN HISTOPLASMOSIS

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35
Q

Is histo a retinitis or a choroiditis

A

Histoplasmosis is a choroiditis

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36
Q

What is the FA sign seen in CSCR

A

10% - smoke stack
90% PED

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37
Q

CSCR

A

Middle aged Man
Type A
Steroid use of any kind
Hypochondriac
HTN
Unilateral

  • also associated with pregnancy
  • caused by RPE and choroid
  • serous fluid under the macula - fluid above the RPE
    -relative scotoma
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38
Q

Classic vs Occult CNVM

A

Classic: well defined membrane that fills with dye during the early phases of FA

Occult: poor defined membrane with late appearing and less intense leakage

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39
Q

Causes of CNVM

A

CHBALA
Choroidal rupture
Histo
Best
Angioid streaks
Laquer cracks
Amd

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40
Q

can PEDs occur in dry ARMD?

A

Yes - called drusenoid PED
due to build up of conclude that soft Drusen on Bruchs membrane

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41
Q

4 outcomes from CNVM in wet ARMD

A
  1. Subretinal heme
  2. Sub RPE heme
  3. Sub retinal detachment - AKA Serous retinal detachment (plasma)
  4. RPE detachment - AKA: PED - (plasma)

PLASMA = Detachment
BLOOD = HEMORRHAGE

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42
Q

According to the macular photo coagulation study group: what are the four main risk factors that increase the risk of progression from dry to wet AMD

A
  1. Multiple soft Drusen
  2. Focal hyperpigmentation
  3. Smoking
  4. HTN
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43
Q

What is dry AMD characterized by ?
What is the end stage of dry AMD

A

Drusen, RPE abornalities, PED
Geographic atrophy - this can cause severe vision loss (defined as >6lines of vision loss)

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44
Q

Symptoms of wet AMD

A
  • central scotoma
  • metamorphopsia
  • RAPID vision loss (not seen in dry AMD)
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45
Q

Is dry or wet AMD more common.

Does Dry or wet AMD make up the greatest amount of vision loss?

A

Dry - 85-90% of AMD

Even though Dry AMD makes up 85%, 88% of legal blindness caused by AMD is caused by the WET form.

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46
Q

Risk factors for ARMD

A

Smokers (2.5x)
Hyperopia
>75 yo
Family Hx
Light toxicity
Obesity

NOT: APHAKIA

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47
Q

MC primary intraocular malignancy

A

Choroidal melanoma

the choroid has a TON of melanin

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48
Q

Pneumonic for transformation into malignant melanomas

A

TO FIND SMALL OCULAR MELANOMAS USE HELPFUL HINTS
T- thickness >2mm
F - Fluid (sub retinal)
S - symptoms - blurred vision/floaters
O - orange pigment - Lipofuscin
M - Margins are irregular (remember that CHRPE have REGULAR borders)

UH- ultrasonography can hollowness - low internal reflectivity ** WILL LOOK LIKE ONE SPIKE, A FLAT LINE, THEN ANOTHER SPIKE. THE CENTER IS HOLLOW

H - halo absence (remember CHRPE can have halos)
A nevus should also be suspicious if >4DD and close to the disc

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49
Q

What percent of choroidal nevus progress to malignant melanoma of the choroid?

A

10%

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50
Q

Bilateral multifocal CHRPE are associated with:

A

Gardners Syndrome
FAP –>
(Colon CANCER)

Do Colonoscopy

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51
Q

Differentials for leukocoria

A

RB
Coats’
ROP
Toxocariasis

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52
Q

Heritable retinoblastoma will be unilateral or bilateral

A

BILATERAL = HERITABLE – 50% chance of passing it on
UNILATERAL = SPORATIC

Signs/symptoms: leukocoria, strabismus, inflammation, decreased vision

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53
Q

Most common intraocular malignancy in children
Most common intraorbital malignancy in children

A

RB - intraocular - retinoblastoma

RMS - intraorbital - Rhabdomyosarcoma

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54
Q

Which part of the retina is most likely to have a Tractional RD in ROP

A

Anterior Temporal –> the temporal retinal is the last to receive vasculature in the 9th month gestation

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55
Q

Who gets ROP?
Out comes of ROP

A

Babies born <32 weeks (definition of premature <37weeks)

Or: birthweight <1500grams in babies who received oxygen treatment

SIGNS:
Pre-retinal Heme/Vitreous heme
Tractional RD
Neo

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56
Q

Coats’ dz

A

Unilateral, telangeictatic dilated vessels that display a lightbulb appearance. Progression can lead to marked hard exudates, exudative RD, neo glc, — results in red, painful, blind eye

  • 8yo boy with UNILATERAL hard exudates with exudative RD.
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57
Q

What are the most common causes of vascular sheathing and periplebitis

A

Sarcoidosis
Syph
Pars Planitis
Sickle Cell

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58
Q

Talc Retinopathy presents in what kind of patients

A

IV drug users

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59
Q

Interferon Retinopathy is seen _________ many months after the interferon is started,

A

3-5 months

Interferon is given with Ribavirin (tons of SE) to treat Hep C (MC way to contract: sharing needles)

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60
Q

Most common ocular manifestation of HIV/AIDS patients.

A

HIV retinopathy - signs include CWS, retinal hemes, similar to DR and early CMV retinitis

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61
Q

Hyperviscosity Retinopathy is most commonly caused by:

A

Hyperglobulinemia - condition found in these diseases:

Waldenstrom macroglobulinemia, multiple myeloma, serum positive RA, SLE, HIV

62
Q

Transient monocular vision loss that last seconds and returns to normal is most commonly caused by:

A

Amaurosis Fugax
- caused by a carotid emboli

63
Q

Age profile for OIS
-Symptoms of OIS
-Signs of OIS
-Name for OIS if only retinal signs are seen with no anterior seg neo

A

Ocular ISchemic Syndrome:
Men (2:1) - 50-80 yo

Symptoms: Gradual UNILATERAL vision loss/dull HA/Amarosis Fugax

Signs: unilateral dot blots in the mid periphery. DILATED NON TORTUOUS VEINS, NARROW ARTERIES, possible neo of the disc and anterior segment

If only seen in the retina with no anterior seg neo: venous stasis retinopathy

64
Q

Secondary conditions that can arise from uncontrolled HTN

A
  • macroaneurysm (includes all layers of retina)
  • NAION (high association with vasculopathic dz)
  • Oculomotor palsies (usually CN6)
  • Worsening of DM (weak vessel walls)
65
Q

Stage 1 Keith Wagener Barker
Stage 2 KWB
Stage 3 KWB
Stage 4 KWB

A

Stages used for HTN Retinopathy
Stage 1 - diffuse narrowing of retinal arteries

Stage 2 - Focal narrowing, nicking, wide arterial light reflex

Stage 3 - COLOR + Blood/CWS/Macular star (copper wire)

Stage 4 - Papilledema - usually seen in malignant HTN 220/120

66
Q

Where are the two places in the eye where autoregulation of blood vessels can occur

A

Retina
ON

67
Q

What is essential HTN

A

Essential HTN accounts for 95% of all HTN cases and is defined as elevated BP without a known cause

68
Q

CSME is defined as:

A
  1. Retinal thickening w/in 500 microns of the foveal center
  2. Retinal head exudates w/in 500 microns of the foveal center if associated with retinal thickening
  3. Retinal thickening of at least 1DD w/in 1DD
69
Q

Most important cause of vision loss in DR

A

Macular edema - can occur at any stage of NPDR or PDR

70
Q

High risk characteristics are defined as:

A

NVD >1/4DD w/ in 1DD
NVD any size with Vit heme
NVE elsewhere > 1/2DD with a vitreous or pre-retinal heme

(Remember that 1DD is 1500 microns or 1.5mm)

71
Q

Mild NPDR risk of progression to PDR?

Moderate NPDR risk of progression to PDR?

Severe NPDR risk of progression to PDR?

Very severe NPDR risk of progression to PDR?

A

Mild - 5%
Moderate - 15%
Severe - 52%
Very Severe - 75%

72
Q

The most important risk factor for the development of DR in a patient with Insulin dependent diabetes mellitus

A

Duration of the disease

73
Q

What is the leading cause of new cases of blindness in the US

A

Diabetes

74
Q

F/U for severe NPDR or PDR

A

2-4 months

75
Q

F/U for mild to mod NPDR

A

6-12 months

76
Q

F/U for patient with no NPDR and type 2 DM

A

1 yr

77
Q

When should a DM type 1 patient have a diabetic retinal exam?
When should a DM type 2 patient have a diabetic retinal exam

A

Type 1: 3-5 yrs of diagnosis
Type2: @ the time of diagnosis

78
Q

Are BRAO or CRAO more commonly caused by Hollenhorst Plaques

A

BRAO

CRAO: calcific emboli from heart is more common

79
Q

Is anterior seg neo more common following vein or artery Occlusions

A

VEIN = Anterior seg neo

80
Q

What should be in the DDX of BRAO

A

Myelinated nerve fibers
CWS

81
Q

What does the retina look like 3 weeks post CRAO

A

Normal - The superficial whitening seen acutely in the inner layers resolved, vision does not improve.

ACUTE SIGNS
- narrow arteries - think: there is no blood coming from CRA… the branches are empty
- cherry red spot - can see down to the choroid
- ON pallor seen later on due to ortho grade degeneration of GC axons (ortho = towards brain)
- APD

ERG: The A wave will be NORMAL bc PR are supplied by the choroid. The B wave will be gone due to deal of the INL which is supplied by the CRA and the location of the Muller and Bipolar Cell Bodiea

82
Q

Other than emboli, what can cause a CRAO

A

GCA, Acute elevation in IOP, IV drug use, collagen vascular dz, sickle cell

the worst thing than can occur due to an acute angle closure is CRAO.

83
Q

What commonly causes CRAO and BRAO.

A

MC cause: Atherosclerosis
Emboli from the heart and from the carotid
Heart = larger = more likely to occlude the CRA
Carotid = smaller cholesterol plaques (Hollenhorst)

Patients with retinal emboli should be evaluated for underlying carotid artery and cardiac disease
Carotid Doppler and EKG/Echo (for heart)

84
Q

What should be evaluated when a BRVO does not occur at a AV crossing

A

Systemic Vasculitis
- remember that arteries and veins share the common adventitia

85
Q

What is the retinal location that is most common for BRVO

A

Superior/ST is the MC location for BRVO

This is also the location for retinal detachments =)

86
Q

What is the most common retinal vascular occlusive disease

A

BRVO is by far the most common retinal vascular occlusive disease

87
Q

Where do collaterals form in CRVOs

A

On the disc

88
Q

Definition of ischemic CRVO
Non ischemic CRVO
#1 cause of Vision loss in both types

A

Ischemic = >10 DD
Non ischemic <10

Macular disease is the number one cause of VL in both

89
Q

Complications of CRVO

A

90 day glc
Vit heme
Pre Retinal heme
Tractional RD
Macular Disease (ischemia, edema, macular hemes)

90
Q

What are the big 3 complications in ANY of the DRVOS diseases

A

Pre Retinal Heme
Vit Heme
Tractional RD

NVG (only in DM and Vein Occlusions)
Also: Macular Disease

91
Q

What should be considered in CRVOs and BRVOs in young patients

A

Oral contraceptives
Protein C/S Def
Antithrombin 3 def
Factor 12 def
AIDS
Collagen vascular dz

92
Q

What other ocular condition is highly associated with CRVO

A

POAG is commonly associated with CRVOs up to 40-60% of patients have POAG — WATCH THE OTHER EYE IN YEARS TO COME

93
Q

Cause of vein occlusion
Cause of artery occlusion

A

Vein - thrombi
Artery - emboli from carotid or heart

94
Q

1 risk factor for CRVO BRVO CRAO BRAO

A

HTN

95
Q

Number one cause of vascular related vision loss

A

Diabetes

96
Q

What is the most common cause of spontaneous vitreous heme

A

Diabetes

97
Q

What is the difference between a pre-retinal heme and a vitreous heme. What must occur for a vitreous heme to happen?

A

Is the posterior hyaloid intact?
Yes > Pre-retinal heme
No > Vitreous heme

If the posterior hyaloid has peeled off of the ILM (complete PVD) => vitreous heme

98
Q

Why is pre-retinal neo leaky

A

Lack of endothelial tight junctions

99
Q

Cause of pre-retinal neo

A

DRVOS
DM
ROP
Vein Occlusions
OIS
Sickle Cell

100
Q

WHAT ARE THE K’S?
Mild Keratoconnus
Moderate
Severe

A

48D - mild
48-54 - moderate
>54 = severe

101
Q

What are late signs seen in Keratoconnus

A

Vogt’s - vertical lines in the stroma
Munsons sign - lower lid protrusion on downgaze
Rizzuti’s sign - conical reflection of light seen nasally when light is shined from temporal side

102
Q

Early signs seen in Keratoconnus

A
  • Fletcher’s ring
  • scissoring reflex w/ ret
  • irregular mires on Keratometry
  • INFERIOR STEEPING with topography
103
Q

Which corneal ectasia can cause Hydrops

A

All of them can end in Hydrops
- Keratoconnus
- PMD
- Keratoglobus

104
Q

Location of choroid all rupture . Long term risk?

A

Temporal to nerve in a C shape curved to the nerve – associated with CNVM in 10 %

105
Q

Acute chest compressing trauma:

A

Purtchers retinopathy = diffuse retinal Hemes, exudate so, and cotton wool spots

106
Q

Appearance of a peripheral iris hole: what are you looking at ?

A

Iridodialysis - location: b/t iris root and CB
CAREFULLY MONITOR FOR ANGLE RECESSION GLC

107
Q

What location of the retina is damaged in Commotio Retinae

A

OS of PR and RPE
- consequence of trauma
- discoloration of the retina
- resolves in 23-48 hours
- called Berlins Edema in the Macula

108
Q

In which direction will the gaze be limited in a patient with a maxillary bone fracture

A

They will not be able look up - IR is trapped and will not relax allowing the SR to contract

109
Q

What nerve is responsible for hypoesthia of the upper cheek after a orbital blow out fracture

A

Infraorbital - branch of V2

110
Q

What bone and specific location on bone is most commonly to be fractured in a orbital fracture

A

POSTERIOR MEDIAL Maxillary bone

111
Q

What is the indicator of ischemia after a chemical burn

A

Vessel blanching

stage 3: when you loose iris details
stage 4: opaque pupil >1/3rd vessel blanching

112
Q

What percent of acute symptomatic PVD will lead to a retinal break?

A

10-15% of acute symptomatic PVD have a retinal break

  • increases to 70% if a vit heme is present
  • RPE will be released into the vit (Shaffer sign)
113
Q

What can vitreous traction cause?

A
  1. ERM
  2. Vitro macular traction – distortion of the normal macular indentation
  3. Macular hole - (+) Watze Allen when Stage 3 Mac hole (#1 risk factor of macular hole is AGE, not PVD)
  4. Weis ring/PVD
  5. Retinal Break (look for Shaffer sign - RPE cells in vitreous)
  6. Retinal heme/Vitreous heme
114
Q

Prevalence of PVD
What sex is it more common in
Other risk factors
What layers are separating in a PVD
Symptoms of a PVD
Signs of a PVD

A

50% at age 50, 65% at age 65 etc
FEMALES
- anything that causes a disruption in the vitreous - high myope, DM, intraocular inflammation, vit heme, trauma
- posterior hyaloid separates from retina (ILM)
- symptoms: acute onset of floaters, photopsias
- signs: Wies ring

115
Q

Synchysis Scintillans

A

buzz: cholesterol in vitreous

Unilateral, golden brown, refractive cholesterol Chrystals in the vitreous cavity

116
Q

Asteroid hylosis

A

Unilateral calcium phosphate deposits floating in vitreous - asymptomatic

117
Q

What color is the red free filter? When should you use it? What will happen to a choroidal Nevi w/ the red free filter

A

Red free - green in color

-Use it to look at NFL, choroidal lesions, and small retinal Hermes

  • choroidal nevi will DISAPPEAR with red free filter
118
Q

Which way should you move your lens and yourself if you see a rental heme to the right of you +20 condensing lens

A

You want to rock toward the direction you want to look as well as move the lens on that direction

119
Q

Image formed by BIO is:

A

Real
Inverted
Flipped laterally
Magnified
Located between the doctor and the condensing lens

120
Q

Image formed by a 78 or 90 is:

A

Real
Inverted
Flipped laterally
Magnified

The higher powered lens = decreased mag = increased FOV

121
Q

Images formed by three mirror are:

A

Inverted anterior to posterior but not laterally

122
Q

how does the ocular hypertension treatment trial grade ocular hypertension?

A

greater than 24

123
Q

ISNT rule

A

nerves should have most rim tissue inferior , then superior etc

glaucoma can affect inf or superior rim

124
Q

what is PXF glaucoma associated with

A

poor pupil dilation
increased risk of lens subluxation
weak zonules - cataract surgery complications

125
Q

who gets PDG?
symptoms
signs

A

white 30-40

myopes males

blurry vision/haloes after exercise

TIDs, krukenburg spindle, TM pigment
- pigment dispersion can decrease over time as lens thickens , but TM damage permanent from pigment so IOP will stay elevated

126
Q

Bullet or thumbnail shows

A

Ora or ant chamber angle

127
Q

Square mirror shows:

A

Anterior equator to the ora
(periphery)

128
Q

Trapezoid mirror shows:

A

ON to equator

129
Q

Hruby lens
Image?
Magnification?
Stereo?

A

Erect
Magnified
Has stereo

130
Q

UGH syndrome is a very uncommon complication characterized by: and seen in what kind of IOL

A

AC-IOL rubs on the iris –> hyphema –> and uveitis –> RBC and WBC trapped in the TM = glc

131
Q

What will CME show with FANG

A

Hyerfluorescent leakage within the macula will show a petaloid pattern around the ON

132
Q

Pigmentary Dispersion Glaucoma

A

result from a temporary higher anterior chamber pressure that causes excessive bowing of the iris posteriorly, resulting in more contact between the iris and the lens zonules

asymptomatic unless exercise/ pupil dilation have blurry vision and halos

133
Q

raynaud’s phenomenon

A

decreased blood flow to fingers
- risk factor for NTG

134
Q

What layer of the retina does CME form in

A

OPL

135
Q

Pathophysiology of CME following cat sx

A

Surgical trauma => inflammation => disruption of the lens/vitreous interface => inflammatory cells (prostaglandins) have an easier time getting to the posterior pole to cause inflammation.

136
Q

peak incidence of CME post cat sx

A

6-10 weeks - most cases resolve 6 months

137
Q

most common cause of CME.

A

Cataract surgery
- called Irvine Gass Syndrome

138
Q

Elschnig Pearls

A

type of PCO that is most common in children who undergo cat extraction

139
Q

how does a PCO form

A

epithelial cells migrate (bladder cells) to and proliferate over the posterior capsule – resulting in opacification

140
Q

most common post op complication of cataract sx

A

PCO

141
Q

most common bacterial cause of post op endopthalmitis

A

Staph Epidermidis (from lids)

142
Q

What are three ocular complication of Ehler’s Danlos and Osteogenesis imperfecta

A
  1. Blue sclera
  2. Keratoconnus
  3. Megalocornea (X linked)

OI DOES NOT NOT NOT CAUSE LENS SUBLUXATION

143
Q

What systemic dz are known to cause lens subluxation

A
  1. ED
  2. Marfans
  3. Homocystinuria
  4. Weill - Marchesani (known for having a very small lens that dislocates causing pupil block)

NOT OSTEOGENISIS IMPERFECTA

144
Q

What is the most serious ocular complication in Marfans

A

RD

remember: Marfan’s patients also have heart defects

145
Q

What is most common cause of lens subluxation

A

Trauma
- also see in PXF,Marfans, ED

(not O.I.)

146
Q

What must be ruled out in toxic anterior segment syndrome? What causes it?

A

R/o: infectious endopthalmitis
caused by chemical exposure during sx, ex: preservatives, toxins

causes uveitis/immune rxn to toxins from the lens

147
Q

How many days post op cat sx is acute post op bacterial endopthalmitis seen

A

2-3 days

148
Q

Most common placement of IOL

A

Capsular bag

149
Q

Which form of ECCE breaks the cataract up into fragments with an ultrasound before the removal

A

Phacoemulsification - virtually all cat sx in America use this
uses a CLEAR CORNEAL INCISION FOR LENS REMOVAL

150
Q
A

NBEO STEP 1 (14 decks)

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