Flashcards in Clinicals Deck (219):
Orbital fx eval
1. if adult
2. if child
3. indications for surgery @ 2 wks
4. signs of muscle entrapment
5. racoon eyes
?entrapment (forced ductions -> can use oculocardiac reflex to gage)
1. next day surgery
2. emergent surgery
3. fx>50%, enophthalmia >2mm, diplopia
4. n/v/bradycardia w muscle tug, pain w muscle mvmt
5. orbital hemorrhage -> decompress if compartment syndrome develops (IOP>40)
1. optic nerve signs
2. orbital signs
1. RAPD, color plates, red desat, brightness
2. proptosis, ptosis, EOM restriction
2. if glass
1. CT 1mm cuts
2. Ca will still show on CT
Signs of herniation
1. temporal uncal
2. cerebellar tonsillar
1. most likely compresses 6th nerve: ICH and clivus is hard. But CN3 is the closest anatomically.
2. downbeating nystagmus (fast/corrective phase is down)
nystagmus worsens when looking in direction of the nystagmus
types of glaucoma
1. phacomorphic: fellow eye at risk? tx?
2. phacolytic. Tx?
3. phacoanaphylactic = phacoantigenic uveitis
4. lens particle
5. angle closure: risk factors? Fellow eye at risk? Tx?
6. 2nd line laser tx meant to help with all types of glaucoma?
1. phacomorphic: big lens from cataract. No. LPI -> CEIOL +/- trabeculostomy
2. phacolytic: porous anterior capsule -> macrophages engulf leaked lens material and closes angle. Drops + diamox -> CEIOL
3. phacoanaphylactic: broken capsule
4. lens particle: iatrogenic after CEIOL
5. asians, hyperopic, mid-dilation. Yes. B/l YAG LPIrotomy +/- trab in affected eye
6. LPiridoplasty: partial thickness holes 360 degrees, meant to contract iris away from angle
mgmt of chemical burn
1. document clock hours affected
2. irrigate until pH 7-7.4 (but let proparacaine dry first as it affects pH)
3. check fornices
4. AT + abx + steroids + manage IOP & pain
5. follow daily until epi defects heal
mgmt of orbital cellulitis
causes of preseptal vs. orbital
1. IV abx
2. CT to assess surrounding structures
3. involve ENT; operate if optic nerve signs
URI / trauma / severe conjunctivits vs. sinus (usually ethmoid) disease
mgmt of subperiosteal abscess
1. IV abx
2. IV abx + OR drainage
mgmt of corneal ulcers
1. document size, depth, ?hypopion, ?cell&flare (if pain out of proportion to exam w enlarged corneal nerves and ring ulcers, think acanthemeba/pseudomonas and cx contact lens)
3. ocuflox if small & peripheral, otherwise concentrated vanc & tobra alternating q30min
4. once healing, add doxy, vitC +/- steroids
indications for PRP
1. CRVO / BRVO
postop shallow chamber + high IOP
1. malignant glaucoma.
2. aqueous displacement 2/2 posterior pressure (exact mechanism unclear)
3. vitrectomy w hyloidectomy to break hyloid interface.
1. good light rxn vs. poor light rxn
2. no dilation lag vs. yes dilation lag
3. good accomodation vs. sluggish accomodation vs. no accomodation
4. dilation w cocaine vs. no dilation w cocaine
5. reversal of anisocoria w apraclonidine
6. dilation w hydroxyamphetamine vs. no dilation
7. constriction w 0.125% pilocarpine
8. constriction w 1% pilocarpine vs. no constriction
9. EOMI rules out which condition?
1. (physiologic, Horner) vs. (Adie, trauma, pharma, 3rd nerve palsy)
2. physiologic vs. Horner
3. Adie vs. trauma vs. (3rd nerve, pharm)
4. physiologic vs. Horner
6. central Horner vs. post-ganglionic Horner
8. 3rd nerve vs. pharm
9. 3rd nerve
Mechanism & characteristics of Adie
ciliary body (where parasympathetic live) degeneration ->
1. AchR hypersensitivity
2. slow re-dilation when light is removed
3. can be asymmetric
Mechanism & uses of:
1. non-specific adrenergic agonist -> mydriatic -> reverses Horner
2. muscarinic agonist -> miotic -> 0.125% reverses Adie, 1% reverses 3rd nerve, no effect on pharm
3. inhibits reuptake of native NE -> mydriatic -> no effect on Horner
4. stimulates release of native NE: reverses central Horner, no effect on postganglionic Horner
3rd nerve palsy
1. complete palsy vs. incomplete vs. superior division vs. inferior division
2. pupil involving vs. pupil sparing
3. immediate step of mgmt if pupil-sparing
4. immediate step of mgmt if pupil-involving
5. if 2/2 ischemia, when should function return?
1. abduction only vs. partial limitation in mvmt vs. (limited upgaze, ptosis) vs. (limited adduction and downgaze)
2. compressive (pcomm aneurysm - supramedial to nerve where the parasympathetic fibers are, uncal herniation) vs. ischemic (motor function located deep in nerve and vessels run on the surface)
3. CNS imaging (even if pupil sparing unless clearly ischemic - old+RFs+acute)
4. CTA in >10yo (kids can have ophthalmoplegic migraines). If neg, consider LP
5. within 3 months (but check in 1 wk to make sure pupil has not become involved and there is no aberrant regeneration)
ddx for 3rd nerve
1. b/l slowly progressive ptosis and motility limitation, no pupil involvement or diplopia
2. pain and proptosis
3. adduction deficit w horizontal nystagmus of opposite abducting eye, no ptosis
4. asymmetric vertical deviation
5. normal accomodation, eyelid retraction, upgaze paralysis, convergence retraction nystagmus, no ptosis
6. pupil not involved, has headache and jaw claudication
1. chronic progressive external ophthalmoplegia
2. idiopathic orbital inflammatory syndrome
4. skew deviation (supranuclear brainstem lesion)
6. GCA involving long posterior ciliary arteries causing muscle ischemia
1. Antibody panel > ice, rest or edrophonium
2. ESR, CRP, platelets
Thyroid eye disease
2. manifestations of disease, ranked based on severity
1. lagophthalmos, lid flare (2/2 lateral aponeuroses being thicker than medial aponeuroses), lid lag (2/2 thyroxine x-reactivity with epi receptors on Muller's), proptosis (2/2 muscle deposition in older patients and fat in younger patients), conj injection, optic nerve signs, orbital signs
2. compressive optic neuritis > orbitopathy > strabismus > DES
mgmt of dacrocystitis
1. massage and warm compresses (don't probe or irrigate)
2. PO abx (bactrim, augmentin, keflex)
3. may need surgery to eliminate obstruction but after inflammation has settled (also don't incise 2/2 risk of fistula)
nasalacrimal duct obstruction -> chronic tear stasis -> secondary infection -> can lead to orbital cellulitis
tear drainage tests
1. dye disappearance test: look for significant or asymmetric dye at 5 min.
2. Jones 1: fluorescein -> 5 min -> recover it in the nose w cotton tip
3. Jones 2: failed jones 1 -> wash away remaining fluorescein -> irrigate w saline -> some dye in the irrigation means partial obstruction, no dye means full obstruction
ddx for leukocoria
RB, Coat's disease, cataracts, ROP
Epiphora, photophobia, blepharospasm in babies
1. congenital glaucoma.
2. Nerve damage can be reversible as the globe is more stretchy in children.
3. medications + surgery
4. galactosemia, rubella, PHPV
cataract surgery in adults vs. children
restorative of VA vs. not
5 layers of the cornea
epi (surface cells, wing cells, basal cells) -> bowman’s layer -> stroma -> descemet’s membrane -> endo (single layer)
3 layers of the tear film and the cells that produce them
1. oil - meibomian, zeiss, moll
2. water - lacrimal + accessory (Kraus and Wolfring)
3. mucous - goblet cells in the conj
Dry eye and
1. contacts are supposed to expand w wetting to create holes for O2 exchange so dry eye patients shouldn't wear contacts
2. lasik severes some corneal nerves and induces dry eye, so optimize tear film prior to surgery
cornea epi cell turn over
what to do about corneal transplants in patients with compromised limbus?
must transplant limbal stem cells first or else there is nothing to repopulate the transplanted cornea
Orbital wall bones
2,2,3,4, keep the sphenoid off the floor
2 superior: frontal and sphenoid
2 lateral: zygomatic and sphenoid
3 inferior: maxillary, zygomatic, palatine
4 medial: lacrimal, sphenoid, ethmoid, maxillary
enhance vs. hyperintense
hyperintensities on T1
hyperintensities on T2
T1: dark water, bright white matter (emphasizes fat)
T2: bright water, dark white matter
T2 flair: dark water, dark white matter (suppresses FREE water = water not in a cell; edema is hyperintense)
post contrast bright (pathologies under 6wks old) vs. no contrast bright
bright on T2, dark on T2 flair
T1: fat, mucin, pigment, subacute blood
hemi desmosomes vs desmosomes in the cornea
pain and abrasion upon waking in the AM?
attach to basal lamina vs. seals between cells
recurrent erosion syndrome (hemidesmosomes damaged during initial injury so regenerated basal cells cannot attach well); similar to epithelial basement membrane disease
are corneal nerves myelinated?
No, to enable transparency
superficial limbal vascularization in contact lens wearers
if >2mm, switch to a lens w higher DK
normal cell density of endothelium
3000-3500 cells/mm2; do not use for transplant if <2500
1. yellow fibers @ 9 and 3 of fundus
2. radial yellow fibers in the 4 quadrants
1. long ciliary nerves
2. short ciliary nerves
tumors that go to the eye
GU (RCC, prostate)
avoid which drops in glaucoma?
pilocarpine (muscarinic agonist -> miotic but shifts forward iridolenticular diaphragm)
What is Schwalbe's line
border of cornea endo and trabecular endo. @ intersection of corneal wedge.
what blocks the angle in NVG?
pigmented (RPE) cells in the vitreous. Highly indicative of retinal tear.
When do you get RAPD w RD?
when >10% detached; no RAPD w tears
types of retinal tears (break)
most common regions?
1. most common, still has traction
2. button, no traction.
3. break @ ora serrata, most commonly caused by blunt trauma that squishes eye sideways
4. >3 clock hrs
superior and temporal
PRP or cryo
types of types of retinal detachments (fluid under retina)
mac on vs. off
1. 2/2 tear
2. 2/2 fibrosis (e.g. diabetic), no tear
3. 2/2 subretinal fluid from inflammation / infectious (RPE cannot pump all the fluid out)
clinical dx: 20/100. OR next day vs. OR within 1wk.
location of ora serrata
5-6mm behind the limbus (thus inject @ 4mm)
where the vitreous had attached to the nerve before detachment
area os retinal thinning, usually found in high myopes
2. region that can be preserved in CRAO and why
2. horizontal strip from the nerve, supplied by cilioretinal artery, which has a different source
3. GCA, cardiac (echo, CTA for ?dissection), hypercoag
4. not much. Can try ocular massage, YAG to extrude emboli, AC tap to drop IOP and move emobli (tPA mobidity is too high)
opacities behind the anterior lens capsule
mid-dilated fixed pupil, corneal edema, elevated IOP + NVI
2. AC tap, avastin, PRP
dislocated vs. subluxed lens
1. subluxed upward -> dx?
2. pseudoexfoliation = ?
entirely detached vs. partially attached
2. weak zonules
3. pilocarpine, BB, carbonic anhydrase inhibitor, lens extraction
1. when to evacuate
2. risk of re-bleed?
1. high IOP, corneal blood stains (which can persist up to 1yr), non self resolving
2. within 1 wk
3. atropine to prevent clot dislodgement, protective shield, restrict activity
3. open vs. ruptured globe
4. most likely sites of rupture
1. Siedel+, peaked iris, 360 hemorrhagic chemosis, flat AC
2. Siedel. CT for ?IOFB (MRI if wood). Don't check for pressure.
3. penetrating vs. blunt trauma
4. behind muscle insertions, where sclera is thinnest
5. fox shield, NPO, IV levaquin 750 q24, tetanus, preop labs (BMP, CBC, PT/PTT, UA, EKG, CXR, hCG)
signs of IOFB
entry wound, iris dialysis, transillumination defect
posterior hyaloid membrane
internal limiting membrane
retinal nerve fiber layer
ganglion cell layer
inner plexiform layer
inner nuclear layer
outer plexiform layer
outer nuclear layer
external limiting membrane
photoreceptors (inner -> junction -> outer)
trauma severe enough to cause vit heme likely also involves which 2 structures
iritis and retinal defect
3 rings of obicularis
pre-tarsal, preseptal, orbital
insertion of orbicularis onto tarsus
enophthalmos vs. hypoglobus
sinking in vs. sinking down
pupil that's displaced (not round and center)
contraindications to canthotomy-cantholysis
1. IV fluoro, PO + topical azithro
types of eye pain
1. FB sensation
3. dull ache
1. FB, keratitis, dry eye
2. lid, conjunctiva
3. scleritis, uveitis, acute glaucoma
4. irtis, keratitis
5. allergy, blepharitis, dry eye
patterns of injection
3. circumcorneal / ciliary flush
1. acute, watery, follicular conjunctiva, h/o URI
2. acute, purulent
3. chronic, mucopurulent, follicular conjunctiva
4. stringy discharge, chemosis
1. viral -> no tx unless severe, then steroids
keratitis = inflammation of cornea
1. acute, h/o trauma
2. gradual, h/o organic trauma
3. h/o recurrence, no infiltrate
2. fungal -> NO STEROIDS
corneal abrasion vs. defect
line vs epi ripped away
miosis with iridocyclictis?
prominent vagal sx (e.g. n/v) in glaucoma patient
acute angle closure
maxitrol should be used for how long?
<2wks as it can elevate IOP
1. increased PF vs. unable to look down
2. increased MCD
3. absent bells
4. vs. pseudoptosis
all forms have decreased PF & MRD1, increased MFD, no lagophthalmos.
1. static = congenital myogenic vs. progressive myogenic (CPEO, kearns-sayer)
2. mechanical (mass, symblepharon) or aponeurotic
3. progressive myogenic or neurogenic (3rd nerve palsy)
4. (dermatochalasis, enophthalmos) - all measurements nml
ptosis repair approaches:
1. LF >10mm
2. LF 4-10mm
3. LF 0-4
1. phenylephrine test for MMR vs ELR
3. frontalis sling
manifestation of AML: solid collection of leukemic cells outside the bone marrow
4 categories of tearing
1. primary hypersecretion
2. secondary (conjunctivitis, allergy, dry eye)
3. lid malposition
retinal lesions: what are they and where are they located?
1. hard exudates
3. cotton wool
4. cystoid macular edema
6. flame hemorrhage
1. lipids in OPL = Henle's layer
2. lipids in RPE
3. nerve fiber sheath blocks vessels underneath
5. IPL + INL + OPL
1. direct: basal tear secretion. +anesthesia. Nml is >10mm at 5min
2. Schirmer I: basal + reflex. No anesthesia. Nml is >10mm at 5min
3. Schirmer II: distinguish between fatigue block and lack of reflex. +anesthesia and nasal irritation x2min (irritation will overcome fatigue block). Nml is >15mm at 5min
normal tear breakup
crocodile tears with chewing
abberrant nerve regeneration (if Bell's palsy, then to superficial greater petrosal nerve)
Pouting of the punctum + pus + conjunctivitis
1. canniliculitis (conjunctivitis is from vessel dilation 2/2 bacterial exotoxin)
3. may need to cut out stone
species of bacteria for
2. lacrimal sac
2 valves of the lacrimal sac
1. entrance = valve of rosen-muller
2. exit = valve of hasner
mgmt of lacrimal obstructions
2. cannilicular (most common causes?)
1. probing, dilation, punctoplasty
2. intubation, reconstruction, CDCR (5-FU and taxol)
congenital lacrimal obstructions
1. structure involved?
2. unilateral or bilateral?
3. most resolve by?
1. valve of hasner
2. 2/3 unilateral, 1/3 bilateral
4. massage, shrink mucosa (afrin), irrigate, intubate, DCR
alarm signs for eyelid malignancies
3. madarosis / disruption
normal tear meniscus
signs of abnormal tears
1. >300mOsm/L or >8 difference between the 2 eyes
2. MMP, lactoferrin, lysozyme
congenital 4th nerve palsy
if right sided:
1. right hypertropia
2. worse w right head tilt
3. worse w right head turn (inducing left gaze)
mgmt of hyphema
3. atropine BID (reduces ciliary spasm, prevents lens synechiae, prevents rebleed)
4. PF QID (avoid in kids)
5. monitor IOP and ?corneal staining (indications for washout)
dx of retrobulbar?
clinical (pain, decreased VA, orbital signs, IOP > 40)
Don't CT as it takes too long
if superior lid lac, look for what other ocular damage?
AACG in renal patient -> use diamox?
yes; no need to consider renal function in acute setting
effect of CRVO on retina
path of a CN
1. at what level do you get disconjugate problems?
nucleus -> fascicle (tract of nerve within brain stem) -> nerve -> NMJ -> muscles
1. fascicle and below
1. @ edge of pupil = ? diopters
2. @ limbus = ?diopters
Papillae vs. follicles
1. follicular conjunctivitis on upper lid = ?
vascularized center vs. non-vascularized center (lymphoid tissue)
1. highly suggestive of chlamydia
Frontal eye field
3. signs of damage
1. (anterior) FEF -> motor strip -> central sulcus -> sensory strip (posterior)
2. conjugate gaze to contralateral direction
3. looks towards side of lesion (R FEF lesion -> eyes drift right)
course of CN VI
exits @ pons-medulla -> slides over clivus -> cavernous sinus -> eye
what's between the 2 thalami?
CSF in 3rd ventricle
ptosis + miosis + injection
2. reaction of pupil in dark
3. if with esodeviation
4. mechanism of injection
5. mechanism of ptosis and anhydrosis
6. if painful
7. sympathetic pathway
2. slow dilation as parasympathetic deactivate
3. localizes lesion to cavernous sinus, where the sympathetics run w CNVI
4. vasodilation by parasympathetics
5. sympathetics innervate the tarsus and sweat glands
6. dissection until proven otherwise
7. hypothalamus -> dorsal side of brain stem -> synapse @ ciliospinal center of Budge C8-T2 -> over lung apex -> under subclavian -> synapse @ superior cervical ganglion -> cavernous sinus w CN6 -> orbit with V1 -> passes ciliary body -> terminates in iris dilators
headache + b/l elevated ON and fuzzy borders + enlarged blind spot
1. presumed dx
1. brain tumor
2. check BP, same day CNS imaging (MRI >CT) -> if no tumor, then LP -> diamox (no diamox until after LP)
motility restricted vs. limited
mechanically restricted vs. muscularly limited
1. if w telangectasias
disc edema specifically 2/2 ICH
1. condition is acute as vessels haven't had time to adjust
2. venous sinus thrombosis, meningitis, hydrocephalus, tumor/pseudotumor
2. 4 types
3. why does the superior ophthalmic vein get easily involved?
4. low flow vs. high flow
engorged episcleral vessels + proptosis + chemosis + increased IOP (prostaglandins won't help because the pathway it promotes now has high pressures)
A: direct lead of carotid into cavernous
B: indirect branches of internal carotid into cavernous
C: indirect brances of external carotid into cavernous
D: indirect branches of both internal and external (most common)
direct connection to cavernous sinus:
inferior vortexes -> inferior ophthalmic vein -> pterygoid plexus -> juglar
superior vortexes -> superior ophthalmic vein -> cavernous sinus -> jugular
50% of low flow will self-thrombose while high flows should be surgically treated to prevent hemorrhagic/ischemic strokes
spiral of tillaux
medial 5.5 -> inferior 6.5 -> lateral 6.9 -> superior 7.7
thyroid myopathy deposition pattern
inferior -> medial -> superior -> later
effect of organophosphate poisoning on pupils
mechanism for anisocoria during migraine
serotonin receptors on the iris
what feeds the cavernous sinus posteriorly?
superior and inferior petrosal sinuses
NMO vs. MS
2. location of extra-ocular lesions
3. extent of optic nerve involvement
5. location of disease
6. if oligoclonal bands in CSF
7. if +aquaporin 4 ab
8. if very high protein in CSF
1. severe loss vs. moderate loss
2. spinal cord vs. CNS (though doesn't have to appear at the same time as optic nerve defects)
3. extensive vs. not
4. late 30s vs. late 20s
5. systemic vs. within CNS
6. 90%MS, 10% NMO
8. NMO (systemic disease needs to break down BBB to be in the CSF and the breakdown increases protein content in CSF)
9. steroids -> plasmapheresis vs. steroids -> disease modifying drugs (MS drugs can actually worsen NMO)
RAPD -> ddx?
optic nerve vs. massive retinal problem (localized retinal problem will not give a RAPD)
normal artery to vein size ratio in fundus
CRVO fundus findings
disc at risk = ?
small cup (~0.1) -> risk of nonarteritic anterior ischemic optic neuropathy (lots of nerve packed into a small space -> prone to ischemia -> edema from ischemia -> compartment syndrome)
arteritic vs. nonarteritic ischemic optic neuropathy
1. symptoms of arteritic
2. if GCA is suspected -> mgmt?
3. average ages
1. malaise (fatigue, weight loss, appetite loss, fever), headache, jaw claudication, scalp tenderness
2. check ESR, CRP, CBC; start IV solumedrol 1g x3d to protect fellow eye (50% will lose vision in fellow eye in 72hrs); temporal artery biopsy within 1 wk
3. 75 vs. 65
4. b/l vs. unilateral
RFs for NAION
amiodarone vs. NAION
3. sleep apnea (hyperventilation controls cerebral edema)
amiodarone is b/l, unlikely NAION. Metabolites deposit on nerves to cause NAION-like findings months after initiation of therapy
Amiodarone generally can recover
% of GCA patients w vision loss?
Biopsy strategy for GCA
1. very high suspicion
2. very low suspicion
3. medium suspicion
why the need to biopsy multiple sites?
1. unilateral bx -> if neg, do other side
2. unilateral bx
3. b/l bx
lesions are not contiguous; try to get ~3cm sample
temporal pallor -> ?
nonspecific finding; could be:
1. temporal quadrant is physiologically the thinnest
2. myopes have nerve tilt
3. pathology that specifically affects the temporal quadrant
neurosjogrens. Check ANA , SSa and SSb
VF loss patterns
1. nasal step
2. arcuate (complete arcuate = Bjerrum)
5. central / enlarged blindspot
1. notch by nasal VF, will develop into arcuate
2. from blind spot to temporal raphe, course above or below the macula
4. optic neuropathies that affect the papillomacular bundle, uncommon in glaucoma (think hereditary, ethambutol, vit def)
5. acute papilledema (once chronic, will turn into arcuate defect)
size of stimulus
when to use stim V?
0: 1/16 mm2
most common: III
when VA is 20/200
types of VF tests
1. quick and dirty
2. measure capillary bed in the eye
cloverfield pattern on VF indicates?
patient stopped paying attention half way through vs. functional
glaucoma = ?
optic neuropathy with characteristic ON/RNFL changes and/or corresponding changes in VF (has nothing to do with IOP)
race & ethnicity
decreased ocular perfusion pressure
thin CCT (correlates with pliable lamina cribosa, which provides less support to the ONs)
family hx (siblings only)
degrees of vision
distance between points on a HVF
distance between the arcades (macula)
1. 2 degrees
2. 6 degrees (same amount of dots as 10-2 but 3 times the degree coverage)
3. 6 degrees
18degrees = 6mm diameter = central 2 rows/columns on 30-2
what size of pupil do you start getting global depressions on HVF?
relative position of fovea and optic nerve
optic nerve is superior -> blind spot is inferior to the meridian on HVF
size of nerves
1.5mm = 4.5 degrees -> blind spot should only fall on 1 spot of the HVF
ASB (apostilb) vs. dB
average sensitivity of fovea
1 asb = 40dB
10 asb = 30dB
100 asb = 20dB
SRF vs. PED
subretinal fluid = between neuro-retina and RPE
PED = pigment epithelial detachment = fluid under the RPE
exudates in a ring = anything focal that leaks (e.g. aneurysm)
boat shaped hemorrhage
there is a pocket of fluid inside which blood layered
1. shadow behind a pocket of blackness
2. white spots in blackness
2. WBC or RBC
causes of CNV (choroidal neovascularization)
2. myopia (stretching breaks Bruch’s membrane)
3. CSCR (central serous chorioretinopathy)
4. inflammatory processes (e.g. posterior uveitis)
5. trauma: (choroidal rupture, laser that pop’d Bruch’s)
treatment for DME
1. sequence of fill
1. choroid flush -> artery -> laminar -> AV transit (equally bright) -> late venous (veins brighter) -> -> recirculation
2. capillary drop off / non-perfusion vs. blocked by heme
stain: margin intensity grows but not size (scars, drusen, optic nerve)
pool: dye in fluid filled space
leak: margin intensity AND size grow (seen only on late phase)
autofluorescence: from RPE (but macula is dark 2/2 luteal pigments)
transmission/window defect: no growth in margin intensity or size
histology of the posterior pole
1. peripheral retina
4. retina thickest where?
1. 1 layer of retinal ganglion cells
2. multiple layers of retinal ganglion cells, higher ratio of photoreceptors, RPE with more melanosomes and volumetrically bigger
3. RNFL to INL absent, OPL very thin
4. papillomacular bundle (connection between fovea and disc)
5. pure cones
3. foveal pit
4. foveal avascular zone
what thins out retina?
where do retinal vessels end?
types of collagen
II: vitreous (vi-two-eous)
III: cornea stromal wound healing
IV: basement membrane (descemet's, not bowman's, lens capsul, Bruch's)
what stains Bruch's membrane?
1. absorbed by which layer?
4. photo disruptive
5. photo destructive
1. RPE (thus difficult in blond fundus)
2. heats proteins: PRP
3. breaks chemical bonds: LASIK
4. Mini lighting + thunder: YAG capsulotomy / iritotomy
why are high myopes more susceptible to retinal tears?
neither the retina nor the vitreous grow as the eye grows; they just get thinned out.
2. most firmly adheres to where? Other attachments?
3. vs. hyloid
2. ora (vitreous base) > optic disc, large vessels (thus hemorrhagic PVD)
3. hyloid = components of vitreous; anterior is what complicates cataract surgery
where does ciliary body insert?
indentation gonioscopy in closed angle due to synechiae?
Don't do as synechiae cannot be forced open
modified shaffer staging for gonio
1: sees schwalbe's
3. scleral spur
PAS on gonio = ?
peripheral anterior synechaie = sign of closure at some point
pathologies on gonio
1. lots of pigment + iris bowed backwards
2. lots of ciliary body + flat iris
1. pigment disperson
2. angle recession
cyclodialysis clefts = ? -> ?
ciliary body disinsertion = aqueous now has access to uveoscleral outflow -> hypotony
eviscerate vs. enucleate vs. exenterate
leave sclera (shell of globe) vs. take globe but leave extraocular muscles vs. leave nothing
iridodialysis vs. cyclodialysis
iris detachment (attaches to ciliary body) vs. ciliary body detachment (attaches to scleral spur)
b/l HSV indicates?
atopy. (NOT HIV)
artificial tears to avoid?
visine and other a1 vasoconstrictors
if suspect mucor
get MRI and call ENT
optos photos orientation
1. upside down
2. upside up
3. grab the nerve
Norms of refractive error in children
2.5yrs = 20/60,
3 yrs = 20/50,
4 yrs = 20/40,
5 yrs = 20/30
1. if respecting horizontal raphe
2. if respecting vertical raphe
1. think glaucoma
2. think neuro
do corneal ulcers cause focal scotomas?
how many degrees away from the center is the blind spot?
what does "advanced" deficits mean on a HVF?
MD < ~-15
SJS ocular signs & mgmt
fibrin exudates -> symblepharon
if servere -> corneal keratinization
amniotic membrane graft
limbal stem cell transplant
penetrating injury vs. perforating injury
no exit vs. through-through (yes exit)
corneal infiltrate vs. scar
feathery edges vs. clear edges
mgmt of corneal perf
if small (<2mm) : cyanoacrylate glue (will be pushed out naturally) or bandage lens
if large: graft
infectious scleritis mgmt?
what's cross fixation?
eyes are crossed -> left eye can see more of the right visual field -> can appear to have abduction limit
risk adduction deficit if recessing MR by > ?mm
inferior oblique overaction = ? torsion. Usually unilateral or bilater?
Dissociated Vertical Deviation = ?
alternating hyperphoria where both eyes drift up under cover (no see-saw action)
most commonly 2/2 6th nerve hypoplasia -> LR innervated by inferior division of CN3 -> contraction of both MR and LR on attempted abduction -> eyeball retraction, poor convergence
1. prevalence and disease course
2. vs. pellucid marginal degeneration vs. keratoglobus vs. posterior keratoconus
1. 1/2000, starts during puberty and progresses until 3rd or 4th decade
2. focal thinning vs. peripheral thinning vs. global thinning vs. posterior thinning
3. scissoring on retinoscopy, Munson's sign, Rizzuti's sign, Vogt's stria, fleisher ring, enlarged corneal nerves
4. no specific genes but has familial associations
3. refractive index
4. radius of curvature -> power
5. layers of epithelium
1. 11mmh x 12mmv
4. 7.8mm -> 43D
5. 4-6 layers
1. palisades of vogt = ?
2. corneal apex = ?
3. angle kappa = ?
4. corneal esthesiometry =?
5. corneal hysteresis = ?
1. where the epithelial stem cells reside
2. point of max curve, temporal to pupil
3. between optical axis (line through center of pupil & lens) and visual axis (line through center of pupil & fovea)
4. tests corneal sensation (compare between 2 sides)
5. corneal stiffness
effect on IOP of:
1. corneal edema
2. thick normal cornea
1. IOP artificially low
2. IOP artificially high
Corneal dyes stains what?
2. rose bengal
1. epi defect
2. devitalized epi
3. devitalized epi
2. kerotaconus vs. forceps during delivery
1. corneal dermoid = ?
2. cornea plana = ?
1. normal tissue in the wrong place, appears dense and white
2. congenitally flat cornea
1. megalocornea vs. megalophthalmos vs. megaloglobus vs. buthalmos
2. microcornea vs. microphthalmos vs. nanophthalmos
1. cornea >13mm vs. large anterior segment w multiple abnormalities vs. big globe but normal amount of tissue (increased risk of rupture) vs. large globe 2/2 glaucoma
2. cornea <11mm vs. small globe w multiple abnormalities vs. small but anatomically normal globe
ICE = ?
iridocorneal endothelial syndrome = spectrum disorder with 3 variants. ?herpes -> abnormal endo cloning -> reversal of light dark pattern (ICE cells have bright nuclei + bright intercellular borders)
1. Iris nevus = Cogan-Reese: multiple pigmented iris nodules, produced by congracting endothelial membrane. Middle aged F; unilateral
2. Chandler: disease confined to inner corneal surface -> corneal edema
3. Essential iris atrophy: abnormal endothelium spreads onto surface of the iris -> atrophy, corectopia and polycoria
tx w penetrating keratoplasty and endothelial keratoplasty
impression cytology findings
4. basophils and mast cells
5. plasma cells and macrophages
8. cytoplasmic inclusions
2. viral / chronic
3. allergy / parasites
4. seasonal allergies
7. tear dysfunction, mucous membrane pemphgoid, SJS
tx for neurotrophic ulcer
2. amniotic membrane graft: dissolves after 1-2 wks
3. conjunctival flap
all with abx ppx
1. what to identify and cover afterwards?
2. avoid violation of which layer?
1. muscle insertions
3. mitomycin C
tx for bullous keratopathy
bowman's layer cautery: remove epi -> cauterize corneal surface (will look like PRP scars on the cornea) -> bandage contact lens
1. when to perform?
1. pain and vision loss
2. debride epi with Tooke knife (the tool prevents violation of Bowman's) -> EDTA to chelate Ca -> remove Ca w Tooke -> micro-drill to polish bowman's layer -> amniotic membrane or BCL
Follicular conjunctivits causes
1. molluscum (if extensive, think AIDS; can self resolved but can take years)
ring ulcers -> ddx?
3. fungal and HSV (always on the ddx)
feathery infiltrate -> ddx?
avoid giving what med?
fungal -> avoid steroids
ocular abx coverage
1. vanc or cef
papilledema = ?
pathogenesis from venous sinus thrombosis?
most common site of thrombosis causing papilledema
effect on cup
disc swelling specifically due to high intracranial pressures
venous sinus thrombosis -> disrupted CSF flow -> intracranial hypertension
most commonly @ bend between transverse and sigmoid sinus
smooth dome-like elevations with hyper-reflective RNFL layer and hypoechoic areas underneath
obliterates the cup but much later
not always bilateral and often asymmetric (2/2 optic canal size asymmetry)
No RAPD(unlike optic neuropathy), 2/2 no involvement of fast axoplasmic flow, unless chronic leading to damage of RNFL
Patton's line vs. choroidal folds
circumferential folds in the retina around the nerve 2/2 disc swelling vs. horizontal folds (can slo be seen in increased pressure)
3 imaging signs of nerve swelling
2 fundus findings of true nerve swelling
1. swelling @ ON insertion
2. flattening of posterior scleral surface
3. perineural sheath cuff (bulging of the normal fluid cuff @ nerve insertion site)
1. blurry margins
2. obscured vessels
produced by choroid plexus of each ventricle -> lateral ventricle -> interventricular foramen -> 3rd ventricle -> aqueduct -> 4th ventricle -> brain & spinal cord -> drains into arachnoid granulation
empty sella = ?
possible cause of empty sella?
chronic pressure in the suprasella cistern -> widens the hole through which the infundibulum passes -> fluid accumulation in the sella turcica -> flattens the pituitary into a banana shape
macular dysfunction vs. ON dysfunction
1. severe VA loss
2. metamorphopsia vs. central scotoma
3. no RAPD vs. yes RAPD
4. hyperopic shift
1. macular dysfunction
2. macular dysfunction vs. ON dysfunction
3. macular dysfunction vs. ON dysfunction
4. macular dysfunction
1. disc drusen
2. myelinated NF
3. tilted disc
4. crowded disc (high hypermetropics)
tilted disc syndrome
infranasal disc tilt + hypoplasia of infranasal retina & RPE (allowing the underlying choroid to show through) -> bitemporal hemianopsia (mimics optic chiasm compression)
frontal lobe tumor (most commonly olfactory groove meningioma) -> optic nerve atrophy ipsilaterally 2/2 compression + papilledema contralaterally 2/2 altered CSF flow
ddx for transient obscuration of vision (TOV)
vessel congestion (sometimes BP can adjust to push through)
ddx for subretinal heme + PED
Anything that causes CNV
polypoidal choroidal vasculopathy
asian male in 50s-60s with sub-RPE lesions that have vasculature, which fills in late phase (polyps) on ICG
responsive to anti-VEGF?
polypoidal choroidal vasculopathy
yellow dots on fundus exam -> think what sort of processes?
inflammatory / infectious
VKH, birdshot, AMPPE (early hypo -> late hyperfluorescence)
r/o HIV, syphillus and TB before giving steroids
1. physiologic pathway
2. signs of unilateral
3. signs of bilateral
1. iFEF @ cortex -> cPPRF -> cCNVI -> cLR + (iLMF -> iCNIII -> iMR)
2. (i) slow adduction + (c) abducting nystagmus +/- (i) hyperdeviation
3. b/l adduction deficit + b/l abductin nystagmus + vertical gaze-evoked nystagmus + large XT
vertical nystagmus: b/c vertical vestibular pursuit and gaze holding pathways ascend from vestibular nuclei through MLF
large XT: 2/2 midbrain lesions near the CN3 nuclei
periventricular ovoids >3mm, suggestive of MS
Corneal disease: adenovirus
1. type of virus
2. subtype? self-limited without systemic involvement
3. subtype? flu-like symptoms
4. subtype? URI -> follicular conjunctivitis (+/- chemosis, membranes, conj hemorrhage) + PEK (+/- geographic ulcers) + preauricular adenopathy -> 7-14d later, develops multifocal subepithelial corneal infiltrates
5. viral shedding duration?
6. duration of sxs of EKC
1. dsDNA, non-envelope, icosahedron
2. follicular conjunctivitis (multiple serotypes)
3. pharyngoconjunctival fever (3, 7)
4. epidemic keratoconjunctivitis (D, 8, 19, 37)
6. months to yrs
7. supportive. If mucopurulent discharge, then think bacteria superinfection and give abx (steroids can help resolve pain and infiltrates but prolong disease course)
waste-basket terms for sub-retinal hyperreflective material on OCT
microscopic polyangitis vs. wegeners
microscopic polyangitis has microscopic granulomas and less respiratory symptoms
FA hyperfluorescence with guttering, expansile dot and smokestack
2. NO steroids and try PDT
Role of IOP in glaucoma
1. normal vs. glaucoma IOP distrubtions
2. prevalence and incidence based on IOP
3. IOP of the vast majority of glaucoma patients
4. when to treated isolated IOP elevation?
normal IOP = left skewed bell curve (with long tail of high IOPs). Mean of 16, 2 stdevs = 11 to 21.
glaucoma IOPs are barely shifted over to the right
prevalence based on IOP: steady increase until ~30, then exponential increase
incidence based on IOP: exponential increase
when IOP>50, treat for risk of venous thrombosis, not for glaucoma
mgmt strategy of glaucoma
decrease by 30% of damaging IOP; decrease by more if still progression of damage
glaucoma involves which layers?
RNFL, GCC, IPL
3 reasons for head posturing
1. nystagus null point
3. VF defect
CN3 aberrant regeneration patterns
1. lid retraction with CN3 activation
2. pupil constriction with CN3 activation
traumatic 6th and/or 7th nerve palsy -> look at what region on CNS imaging?
where the mastoid air cells turn into petrous apex as the 2 nerves travel around there