ocular diease Flashcards
most common CN palsy
Why?
CN6
- usually due to micveovascular infact
Complete CN3 palsy is characterized by:
complete external opthalmoplegia - all of the muscles that CN3 controls are dead
Adie’s
- 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
what is used to diagnose a pupil involved CN3 palsy
1% pilo will cause constriction
Cause of post ganglionic horners
-Cavernous sinus issues (sympathetics travel on the ICA in the Cav sinus)
- CA Dissection
- Internal Carotid Artery Aneurysm
what does internal ophthalmoplegia mean
paralysis of the pupil
Abnormal pupil is large:
- what are in the differentials?
- Adies
- CN3 palsy
- Iris Sphincter trauma
- pharm dilation
causes of APD?
what would never cause an APD?
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)
optic nerve colobomas are located
Inferior nasal
early signs of Leber’s Optic neuropathy
optic disc hyperemia that progresses to optic disc pallor in late stages.
Most common type of functional pituitary tumor
macroadenoma PROLACTIN SECRETING tumor
(amenorrhea, galactorrhea, infertility)
PIGS ON ACID (acid cells)
Retrograde degneration example
How does it affect the ON
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
why is CN6 affected in IIH
CN6 travels along the Pretrous ridge of the temporal bone. Can be compressed when ICP is high
is an MRI or a lumbar puncture done first?
MRI - make sure there are no space occupying lesions
What is the only way to diagnose papilledema
spinal tap
What is the acuity in the third decade of StARgardts patient
Usually around 20/200 in the pts 30s and doesn’t get worse after that.
Rapid vision loss and color vision abnormalities
StARgarts
Fish tail flecks
RPE mottling
Beaten Bronze - bullseye
Salt and pepper
Most common macular dystrophy, inheritance
Stargardt’s
AR inheritance
stARgardt’s = AR
In early stages of RP, what test is abnormal
Scotopic ERG
RP triad
Can you name 4 other things seen ?
Waxy ON (pallor)
Bone Spicules
Artery Attentuation
PSC
Optic disc Drusen
Macular changes
Keratoconnus
Symptoms for RP, vision by 30?
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
Ushers syndrome inheritance
RP + Hearing loss
AR
Average age of diagnosis for RP
9-19yo
Albinism may be associated with severe systemic conditions including :
Hermansky Pudluk
Chediak Higashi
Severity of vision loss in albinism is due to:
Degree of iris/ fundus hypopigmentation and foveal hypoplasia
Albinism is caused by a decrease in melanin or melanocytes
albinism = decrease in MELANIN
Normal recovery for a macular photostress test
<60 seconds
Macular holes:
Stage 1
Stage 2
Stage 3
Stage 4
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
Cause of macular hole
Sex that gets macular holes more common
Macular hole results from posterior vitreous traction on the macula.
MC in female and most common cause is aging
Are males are females more likely to get ERMs.
What causes ERMS?
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
Signs seen in pathological myopia
- 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
Hallmark for pathological myopia
Posterior staphaloma = posterior bulging of a weak sclera
Refractive error associated with myopic degeneration/pathological myopia ?
What is the axial length associated?
> -6.00
26.5mm - measured with A scan
Triad for histo
Is the vitreous clear?
Punched out spots
Peripapillary atrophy
CNVM Maculopathy (CHBALA)
VITREOUS IS ALWAYS CLEAR IN HISTOPLASMOSIS
Is histo a retinitis or a choroiditis
Histoplasmosis is a choroiditis
What is the FA sign seen in CSCR
10% - smoke stack
90% PED
CSCR
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
Classic vs Occult CNVM
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
Causes of CNVM
CHBALA
Choroidal rupture
Histo
Best
Angioid streaks
Laquer cracks
Amd
can PEDs occur in dry ARMD?
Yes - called drusenoid PED
due to build up of conclude that soft Drusen on Bruchs membrane
4 outcomes from CNVM in wet ARMD
- Subretinal heme
- Sub RPE heme
- Sub retinal detachment - AKA Serous retinal detachment (plasma)
- RPE detachment - AKA: PED - (plasma)
PLASMA = Detachment
BLOOD = HEMORRHAGE
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
- Multiple soft Drusen
- Focal hyperpigmentation
- Smoking
- HTN
What is dry AMD characterized by ?
What is the end stage of dry AMD
Drusen, RPE abornalities, PED
Geographic atrophy - this can cause severe vision loss (defined as >6lines of vision loss)
Symptoms of wet AMD
- central scotoma
- metamorphopsia
- RAPID vision loss (not seen in dry AMD)
Is dry or wet AMD more common.
Does Dry or wet AMD make up the greatest amount of vision loss?
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.
Risk factors for ARMD
Smokers (2.5x)
Hyperopia
>75 yo
Family Hx
Light toxicity
Obesity
NOT: APHAKIA
MC primary intraocular malignancy
Choroidal melanoma
the choroid has a TON of melanin
Pneumonic for transformation into malignant melanomas
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
What percent of choroidal nevus progress to malignant melanoma of the choroid?
10%
Bilateral multifocal CHRPE are associated with:
Gardners Syndrome
FAP –>
(Colon CANCER)
Do Colonoscopy
Differentials for leukocoria
RB
Coats’
ROP
Toxocariasis
Heritable retinoblastoma will be unilateral or bilateral
BILATERAL = HERITABLE – 50% chance of passing it on
UNILATERAL = SPORATIC
Signs/symptoms: leukocoria, strabismus, inflammation, decreased vision
Most common intraocular malignancy in children
Most common intraorbital malignancy in children
RB - intraocular - retinoblastoma
RMS - intraorbital - Rhabdomyosarcoma
Which part of the retina is most likely to have a Tractional RD in ROP
Anterior Temporal –> the temporal retinal is the last to receive vasculature in the 9th month gestation
Who gets ROP?
Out comes of ROP
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
Coats’ dz
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.
What are the most common causes of vascular sheathing and periplebitis
Sarcoidosis
Syph
Pars Planitis
Sickle Cell
Talc Retinopathy presents in what kind of patients
IV drug users
Interferon Retinopathy is seen _________ many months after the interferon is started,
3-5 months
Interferon is given with Ribavirin (tons of SE) to treat Hep C (MC way to contract: sharing needles)
Most common ocular manifestation of HIV/AIDS patients.
HIV retinopathy - signs include CWS, retinal hemes, similar to DR and early CMV retinitis
Hyperviscosity Retinopathy is most commonly caused by:
Hyperglobulinemia - condition found in these diseases:
Waldenstrom macroglobulinemia, multiple myeloma, serum positive RA, SLE, HIV
Transient monocular vision loss that last seconds and returns to normal is most commonly caused by:
Amaurosis Fugax
- caused by a carotid emboli
Age profile for OIS
-Symptoms of OIS
-Signs of OIS
-Name for OIS if only retinal signs are seen with no anterior seg neo
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
Secondary conditions that can arise from uncontrolled HTN
- macroaneurysm (includes all layers of retina)
- NAION (high association with vasculopathic dz)
- Oculomotor palsies (usually CN6)
- Worsening of DM (weak vessel walls)
Stage 1 Keith Wagener Barker
Stage 2 KWB
Stage 3 KWB
Stage 4 KWB
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
Where are the two places in the eye where autoregulation of blood vessels can occur
Retina
ON
What is essential HTN
Essential HTN accounts for 95% of all HTN cases and is defined as elevated BP without a known cause
CSME is defined as:
- Retinal thickening w/in 500 microns of the foveal center
- Retinal head exudates w/in 500 microns of the foveal center if associated with retinal thickening
- Retinal thickening of at least 1DD w/in 1DD
Most important cause of vision loss in DR
Macular edema - can occur at any stage of NPDR or PDR
High risk characteristics are defined as:
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)
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?
Mild - 5%
Moderate - 15%
Severe - 52%
Very Severe - 75%
The most important risk factor for the development of DR in a patient with Insulin dependent diabetes mellitus
Duration of the disease
What is the leading cause of new cases of blindness in the US
Diabetes
F/U for severe NPDR or PDR
2-4 months
F/U for mild to mod NPDR
6-12 months
F/U for patient with no NPDR and type 2 DM
1 yr
When should a DM type 1 patient have a diabetic retinal exam?
When should a DM type 2 patient have a diabetic retinal exam
Type 1: 3-5 yrs of diagnosis
Type2: @ the time of diagnosis
Are BRAO or CRAO more commonly caused by Hollenhorst Plaques
BRAO
CRAO: calcific emboli from heart is more common
Is anterior seg neo more common following vein or artery Occlusions
VEIN = Anterior seg neo
What should be in the DDX of BRAO
Myelinated nerve fibers
CWS
What does the retina look like 3 weeks post CRAO
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
Other than emboli, what can cause a CRAO
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.
What commonly causes CRAO and BRAO.
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)
What should be evaluated when a BRVO does not occur at a AV crossing
Systemic Vasculitis
- remember that arteries and veins share the common adventitia
What is the retinal location that is most common for BRVO
Superior/ST is the MC location for BRVO
This is also the location for retinal detachments =)
What is the most common retinal vascular occlusive disease
BRVO is by far the most common retinal vascular occlusive disease
Where do collaterals form in CRVOs
On the disc
Definition of ischemic CRVO
Non ischemic CRVO
#1 cause of Vision loss in both types
Ischemic = >10 DD
Non ischemic <10
Macular disease is the number one cause of VL in both
Complications of CRVO
90 day glc
Vit heme
Pre Retinal heme
Tractional RD
Macular Disease (ischemia, edema, macular hemes)
What are the big 3 complications in ANY of the DRVOS diseases
Pre Retinal Heme
Vit Heme
Tractional RD
NVG (only in DM and Vein Occlusions)
Also: Macular Disease
What should be considered in CRVOs and BRVOs in young patients
Oral contraceptives
Protein C/S Def
Antithrombin 3 def
Factor 12 def
AIDS
Collagen vascular dz
What other ocular condition is highly associated with CRVO
POAG is commonly associated with CRVOs up to 40-60% of patients have POAG — WATCH THE OTHER EYE IN YEARS TO COME
Cause of vein occlusion
Cause of artery occlusion
Vein - thrombi
Artery - emboli from carotid or heart
1 risk factor for CRVO BRVO CRAO BRAO
HTN
Number one cause of vascular related vision loss
Diabetes
What is the most common cause of spontaneous vitreous heme
Diabetes
What is the difference between a pre-retinal heme and a vitreous heme. What must occur for a vitreous heme to happen?
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
Why is pre-retinal neo leaky
Lack of endothelial tight junctions
Cause of pre-retinal neo
DRVOS
DM
ROP
Vein Occlusions
OIS
Sickle Cell
WHAT ARE THE K’S?
Mild Keratoconnus
Moderate
Severe
48D - mild
48-54 - moderate
>54 = severe
What are late signs seen in Keratoconnus
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
Early signs seen in Keratoconnus
- Fletcher’s ring
- scissoring reflex w/ ret
- irregular mires on Keratometry
- INFERIOR STEEPING with topography
Which corneal ectasia can cause Hydrops
All of them can end in Hydrops
- Keratoconnus
- PMD
- Keratoglobus
Location of choroid all rupture . Long term risk?
Temporal to nerve in a C shape curved to the nerve – associated with CNVM in 10 %
Acute chest compressing trauma:
Purtchers retinopathy = diffuse retinal Hemes, exudate so, and cotton wool spots
Appearance of a peripheral iris hole: what are you looking at ?
Iridodialysis - location: b/t iris root and CB
CAREFULLY MONITOR FOR ANGLE RECESSION GLC
What location of the retina is damaged in Commotio Retinae
OS of PR and RPE
- consequence of trauma
- discoloration of the retina
- resolves in 23-48 hours
- called Berlins Edema in the Macula
In which direction will the gaze be limited in a patient with a maxillary bone fracture
They will not be able look up - IR is trapped and will not relax allowing the SR to contract
What nerve is responsible for hypoesthia of the upper cheek after a orbital blow out fracture
Infraorbital - branch of V2
What bone and specific location on bone is most commonly to be fractured in a orbital fracture
POSTERIOR MEDIAL Maxillary bone
What is the indicator of ischemia after a chemical burn
Vessel blanching
stage 3: when you loose iris details
stage 4: opaque pupil >1/3rd vessel blanching
What percent of acute symptomatic PVD will lead to a retinal break?
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)
What can vitreous traction cause?
- ERM
- Vitro macular traction – distortion of the normal macular indentation
- Macular hole - (+) Watze Allen when Stage 3 Mac hole (#1 risk factor of macular hole is AGE, not PVD)
- Weis ring/PVD
- Retinal Break (look for Shaffer sign - RPE cells in vitreous)
- Retinal heme/Vitreous heme
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
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
Synchysis Scintillans
buzz: cholesterol in vitreous
Unilateral, golden brown, refractive cholesterol Chrystals in the vitreous cavity
Asteroid hylosis
Unilateral calcium phosphate deposits floating in vitreous - asymptomatic
What color is the red free filter? When should you use it? What will happen to a choroidal Nevi w/ the red free filter
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
Which way should you move your lens and yourself if you see a rental heme to the right of you +20 condensing lens
You want to rock toward the direction you want to look as well as move the lens on that direction
Image formed by BIO is:
Real
Inverted
Flipped laterally
Magnified
Located between the doctor and the condensing lens
Image formed by a 78 or 90 is:
Real
Inverted
Flipped laterally
Magnified
The higher powered lens = decreased mag = increased FOV
Images formed by three mirror are:
Inverted anterior to posterior but not laterally
how does the ocular hypertension treatment trial grade ocular hypertension?
greater than 24
ISNT rule
nerves should have most rim tissue inferior , then superior etc
glaucoma can affect inf or superior rim
what is PXF glaucoma associated with
poor pupil dilation
increased risk of lens subluxation
weak zonules - cataract surgery complications
who gets PDG?
symptoms
signs
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
Bullet or thumbnail shows
Ora or ant chamber angle
Square mirror shows:
Anterior equator to the ora
(periphery)
Trapezoid mirror shows:
ON to equator
Hruby lens
Image?
Magnification?
Stereo?
Erect
Magnified
Has stereo
UGH syndrome is a very uncommon complication characterized by: and seen in what kind of IOL
AC-IOL rubs on the iris –> hyphema –> and uveitis –> RBC and WBC trapped in the TM = glc
What will CME show with FANG
Hyerfluorescent leakage within the macula will show a petaloid pattern around the ON
Pigmentary Dispersion Glaucoma
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
raynaud’s phenomenon
decreased blood flow to fingers
- risk factor for NTG
What layer of the retina does CME form in
OPL
Pathophysiology of CME following cat sx
Surgical trauma => inflammation => disruption of the lens/vitreous interface => inflammatory cells (prostaglandins) have an easier time getting to the posterior pole to cause inflammation.
peak incidence of CME post cat sx
6-10 weeks - most cases resolve 6 months
most common cause of CME.
Cataract surgery
- called Irvine Gass Syndrome
Elschnig Pearls
type of PCO that is most common in children who undergo cat extraction
how does a PCO form
epithelial cells migrate (bladder cells) to and proliferate over the posterior capsule – resulting in opacification
most common post op complication of cataract sx
PCO
most common bacterial cause of post op endopthalmitis
Staph Epidermidis (from lids)
What are three ocular complication of Ehler’s Danlos and Osteogenesis imperfecta
- Blue sclera
- Keratoconnus
- Megalocornea (X linked)
OI DOES NOT NOT NOT CAUSE LENS SUBLUXATION
What systemic dz are known to cause lens subluxation
- ED
- Marfans
- Homocystinuria
- Weill - Marchesani (known for having a very small lens that dislocates causing pupil block)
NOT OSTEOGENISIS IMPERFECTA
What is the most serious ocular complication in Marfans
RD
remember: Marfan’s patients also have heart defects
What is most common cause of lens subluxation
Trauma
- also see in PXF,Marfans, ED
(not O.I.)
What must be ruled out in toxic anterior segment syndrome? What causes it?
R/o: infectious endopthalmitis
caused by chemical exposure during sx, ex: preservatives, toxins
causes uveitis/immune rxn to toxins from the lens
How many days post op cat sx is acute post op bacterial endopthalmitis seen
2-3 days
Most common placement of IOL
Capsular bag
Which form of ECCE breaks the cataract up into fragments with an ultrasound before the removal
Phacoemulsification - virtually all cat sx in America use this
uses a CLEAR CORNEAL INCISION FOR LENS REMOVAL
