KHIO 2 Flashcards
(30 cards)
Stages of DR:
Mild NPDR
* Microaneurysms
Moderate NPDR
* Dot/Blot haem
* Hard exudates
Severe NPDR
* 4 quad haemorrhages
* 2 quad venous bleeding
* 1 quad intraretinal microvascular abnormalities
PDR
* Neovascularisation
High-Risk PDR
* NVD > 1/3 of disc
* NVE with vit-haem
Advanced PDR
* Vit-haem
* TRD
* Rubeosis iridis (iris neovasc)
* Neovasc. Glaucoma
DME
Clinically significant macular edema
DDX corneal ectasias
Keratoconus (most common)
* Central thinning
Pellucid marginal degeneration
* Inferior thinning “crab claw”
Keratoglobus
* Generalized thinning
Terriens marginal degeneration
* Peripheral thinning w/lipid deposition
Hydrops
Decemets rupture > acute edema
Types of colour vision defects:
Congenital defects: X-linked
* Dichromacy: loss of cone type
○ Protanopia: L-cone (red)
○ Deutanopia: M-cone (green)
○ Tritanopia: S-cone (blue)
* Anomalous trichromacy: altered cone
○ Protanomaly
○ Deutanomaly (most common)
§ Red-green confusion
○ Tritanomaly
§ Blue-yellow confusion
Acquired CVD:
* RG
○ Optic neuritis
○ Galucoma
* BY
○ AMD
○ DR
○ RP
○ Cataracts
CSCR
Management of keratoconus:
- Conservative
a. RGP lenses (early-stage)
b. Scleral lenses (late stage)- Corneal-cross linking
a. Riboflavin + UVA light > strengthened cornea - Intrastromal corneal ring segments
a. PMMA implants for CL intolerance - Photorefractive keratectomy (PRK)
a. Abalation of irregular surfact
b. For stable cases - Corneal transplant
a. DALK > preserves endothelium
PK > Full thickness
- Corneal-cross linking
Keratoconus patho and diagnosis:
Altered genes HGF, VSX1, IL1B, LOX > biomechanical weakness
Risks: Eye rubbing, Floppy lid syndrome, Trisomy 21, Atopy
* Thinning of stromal matrix
* Disruption of bowman’s layer
* Irregular collagen arrangement
Bilateral assymetrical progression:
* Visual distortion
* Fleischer ring (iron deposit)
* Vogt’s striae (stromal stress lines)
* Munson’s sign (Lower lid protrusion on downgaze)
Diagnosis:
* Corneal topography
○ Irregular astigmatism
○ Asymmetric bow-tie pattern
* Pachymetry
○ CCT < 500um
* Keratometry
○ High K values (>47.2D)
Can progress to corneal hydrops
Break in decemets > influx of aqueous > corneal edema
Patho of corneal graft rejection:
Host immune response to doner antigens (GLA/MHC-1/2)
* APCs present antigens to T-helper (CD4+)
* CD4+ activate > differentiate to Th1 > Cytokine release (INF-y, IL-2)
* Macrophages/CD8+ cells attack donor cells
Epithelial rejection: most common
* Epitheliopathy, punctate staining
Stromal: T-cell mediated
* Infiltrates, hazy
Endothelial: CD4+
* Stromal edema, decemets folds, khodadoust line (inferior KPs)
Management:
* Topical prednisolone acetate 1% QID
Systemic Cyclosporin
Management of corneal hydrops;
Hypertonic saline 5% QID and Hypertonic ointment
Cyclopentolate 1% BID
Prednisolone acetate 1% QID
Chloramphenicol 0.5% QID
BCL
Fuchs endothelial dystrophy:
Progressive bilateral inherited endothelial degeneration
* Loss of endothelial cells > Guttae formation on decemets
* Loss of endothelial pump > stromal edema
* Chronic edema > bullae formation
Requires hypertonic saline 5% for edema > BCL > Endothelial keratoplasty
Causes of RAPD:
Optic neuritis: MS
Ischemic optic neuropathy: AION
ON compression: Glaucoma
ON atrophy
CRAO/CRVO
RD
Corneal guttae:
Endothelial stress > basement membrane material depositions on decements
Monitor for progression
Bullous keratopathy:
Epithelial bullae formation following endothelial faliure
* Decompensated Fuch’s dystrophy
* Iatrogenic
* Glaucoma
Requires hypertonic saline 5% > endothelial transplant (DMEK)
Cataracts Sx with comobid diseases:
Glaucoma: Sx may improve IOP
DR: Sx may risk DME requires monitoring and prophylactic Anti-VEGF
AMD: May have small vision increase
Fuch’s: Consider combined keratoplasty
Uveitis: ensure inflammation is controlled for 3mo
CRVO/BRVO:
- Venous obstruction at arteriovenous crossings
○ Endothelial damage, Turbulance, stasis > thrombus formation- Venous congestation
○ Blood pooling > capillary leakage
○ Hemorrhages, edema, exudates - Capillary non-perfusion
○ Hypoxia > VEGF > NV - Macula edema
Risk factors: - HT, DM, HL, Glaucoma, Smoking
Management: - Anti-VEGF and dexamethasone implant for macula edema
- PRP for NV
Control of risk factors
- Venous congestation
CRAO/BRAO patho:
- Acute arterial occlusion:
○ Emboli / Thrombus / Inflammatory arteritic- Ischemia of retina
○ Ex. Cilioretinal artery - Retinal cell death
○ Whitening with cherry red spot - Permenant vision loss within 2 hours
Risk factors: - Coronary disease, GCA, smoking, HT, DM
Management: - Ocular massage
- Anterior chamber paracentesis (lowers IOP)
- IOP lowering agents (acetazolamide)
Hyperbaric oxygen
- Ischemia of retina
Cataract surgery complications:
PCO: Progressive blur
* Nd:YAG laser capsulotomy
Endophthalmitis: <1 week
* Pain, redness, hypopyon
* Vancomycin
CME: metamorphopsia
* Topical NSAIDs + Cortico.
IOP spike: within hours
* Topical IOP lowering agents
RD: within months
* Vitrectomy
Corneal edema: within weeks
Hypertonic saline 5%
AAION:
CGA > Granulomatous inflammation of large/medium arteries
* Esp. Temporal, ophthalmic, posterior cilliary arteries
Lumen narrowing and Thrombosis > Ischemia of anterior ON
* Contralateral eye is at high risk
GCA symptoms:
* Scalp tenderness, Jaw claudications, headaches, malaise
Ocular symptoms:
* Pale, swollen OD
* Chaly white edema
* RAPD
Management:
* Erythrocyte sedimentation rate (ESR) > 50mm/hr
* C-reactive protein > elevated
* Platelet count > elevated
* MRI of large vessels
* Temporal artery biopsy > Granulomatous inflammation w/giant cells
Treatment:
* IV methylprednisolone 500mg/d
Oral perdnisolone 1mg/kg/day
NAION:
Hypoperfusion/occlusion of short posterior arteries > ON ischemia
* Usually with Px “Disc at risk”
○ Small, Crowded, no cupping
Risk factors:
* HT, DM, Sleep apnoea (nocturnal hypotension), smoking
Symptoms:
* Sudden painless loss of vision (u/waking up)
* Mild-Severe Vision loss
* Altitudinal VFD
* No systemic assoc.
Signs:
* Hyperemic swollen OD
* RAPD
* Contralateral disk at risk
Management:
* ESR, CRP, platelet (should be normal)
* VFT
* OCT
* Fluorescein angiography > Delayed filling in affected disc
Treatment:
* Observation > Rarely self resolves
Usually permanent with 15% risk in fellow eye
Stroke patho:
Ischemic stroke (85%)
* Obstruction of cerebral artery > ischemia
○ Thrombosis: large artery atherosclerosis
○ Embolism: debris from atrial fibrillation
○ Systemic hypoperfusion: hypotension
Hemorrhagic stroke:
* Bleed > tissue compression
○ Intracerebral (ICH): small artery rupture (HT)
Subarachnoid (SAH): aneurysm rupture
Describe hemiparesis, hemiplegia, and aphasia:
Hemiparesis: weakness of one side
Hemiplegia: paralysis of one side
Aphasia: Impaired speaking
Hypertensive retinopathy:
- Vasoconstrictive phase:
○ ^BP > autoregulatory vasospasm of retinal arterioles > Narrowing BVs- Sclerotic phase: Chronic HT
○ Thickening of arteriolar walla
○ Hyaline deposition/fibrosis
○ Copper > silver wiring
○ AV nicking - Exudative phase: Severe/Acute HT
○ Endothelial damage > BRB loss
○ Leakage > hard exudates, haem, CWS
○ Retinal edema - Malignant:
Papilldema
- Sclerotic phase: Chronic HT
Chorioretinal scarring patho:
- Initial insult
○ Infection (Toxo/CMV), Inflammation (uveitis), trauma- Acute inflammatory response:
○ Macrophage/Lymphocyte infiltrates > Cytokine/GF release
○ BRB loss > further inflammation - Tissue necrosis/repair
○ Damaged tissue necrosis
○ Surrounding tissue proliferate fibroblasts, glial cells - Scar formation
○ Fibrotic tissue replaces retina
Fibrotic contraction > RD
- Acute inflammatory response:
DDX chorioretinal scarring:
Toxo: most common
* Single/multiple scars
* Pigmented borders
* “Headlight in the fog”
Cytomegalovirus: immunocompromised
* Yellow-white lesions
* Haemorrhages
Syphilis: multifocal chorioretinitis
Tuberculosis: granulomatous
HSZ/HZO: necrotizing
* Iris atrophy
Sarcoidosis: granulomatous
* Elevated ACE
Vogt-Koyanagi-Harada: diffuse
Bilateral granulomatous uveitis
Toxoplasmosis chorioretinitis:
Intracellular protozoan infection via:
* Transplacental, postnatal injestion of oocysts
Localize in retina/chorod:
* Focal necrosis from immune damage
* Immune inflammation of retina/vitreous
* Scarring/pigmentation following infection
Parasites may reactivate if immunocompromised
Management:
* Pyrimethamine antiparasitic
○ Prevents folic acid metabolism
* Sulfadiazine
* Folinic acid
○ Prevents bone toxicity from pyri.
* Oral prednisolone
Decrease ocular inflammation
Accomodative and convergence disorders:
Accom. Insuf: reduced amplitude of accommodation
* Near point of blur less than age norm
* 18.5-(0.3 Age)
Accom. Facility: poor changing focuse near-far
* +-2D flippers
* <10-15 cycles per minute (cpm)
Accom. Excess: overaction
* Monocular esterman method (MEM) ret
* Lag > +1D
Accom Fatigue: underaction
* Minus lens to blur
* Poor reading with minus lenses
Convergence:
Convergence insuf:
* NPC > 6cm
* Exo at near
* Reduced PFV (BO prism at near)
○ Break > 15, Recovery within 6
Convergence excess:
* Eso at near
* Reduced NFV (BI at near)
Break >12, Recovery within 6
