KHIO 1 Flashcards
Causes of floaters and flashes and when they might occur separately:
- Both
○ PVD
○ Retinal tear
○ RRD
○ Vit. Haem (assoc. Fibrovascular contraction) - Floaters
○ Late PVD
○ Asteroid hyalosis (Ca-Lipid deposit)
○ Uveitis/Vitritis
○ Intraocular tumours - Flashes
○ Early PVD
○ Optic neuritis
○ TRD
DDX flashes:
PVD
Retinal tear
RRD, TRD
Vit. Haem
* Migraine
* Stroke
Patho of myopia:
Dopamine theory: Low outdoor / Increased near work > Low light exposure > decreased dopamine release > increased scleral growth (uninhibited)
Hyperopic defocus: Accommodative lag / Urbanization > Altered signals from retina through to sclera > signalling cascade > axial elongation
Genetic inheritance of myopia:
7%, 25%, 50%
PAX6, GJD2 genes
MYP1/2/3 Loci
Syndromic genes:
- COL2A1 (sticklers)
- FBN1 (Marfans)
IOP changes with time:
Peak in morning due to head position
Types of glaucoma and risk factors:
POAG (common):
* African, FOH
* Myopia, DM
PACG: gradual anatomical closure
* Asian, FOH
* Hyperopia
* Shallow AC
Secondary ACG: Blockage unrelated to anatomy
* Neovasc.
* Traumatic
* Uveitic
* Phacomorphic
* Pupillary block
○ PDX
Secondary OAG:
* Pigmentary: PDS
○ Myopia, males
Steroid induced
Surgical management for glaucoma:
Trabeculectomy: OAG
* Drainage through bleb
Tube shunt:
* Baerveldt implant
SLT: Irritate TM
Laser iridotomy: ACG
Cyclodestruction: removal of CB
Vogt’s limbal girdle:
Benign white opacity at limbus (chalky)
Age/UV/Oxidative stress > collagen degeneration > Ca deposits
* Usually has interval of Vogt
Arcus senilis:
Benign white opacity at limbus
Age/hyperlipidemia > decreased lipid metabolism > aggregation at bowmans layer
* Clear interval of vogt
<50yo needs assesment for hyperlipidema/Cardiovascular evaluation
Peripheral retinal degenerations
Lattice degeneration: Myopia > NS retinal atrophy > thinning
○ Monitored > Laser for high risk
Senile Retinoschisis: Age>50 > peripheral separation of NFL from NSR > cystic cavities
○ Monitor > VF for peripheral defect > Laser/Cryo
X-linked Retinoschisis: RS1 gene > dysfunctional retinoschisin protein > poor retinal structure > separation of all layers of retina > central vision loss
○ Genetic counselling
Pavingstone degeneration: Benign Progressive degeneration of outer retinal layers > adhesion of remaining layers to bruchs
Monitored
Management of retinal holes:
- Observation: small, asymptomatic, low risk (no traction)
- Laser photocoagulation: Vit. Traction, Tears, High risk
○ Argon 488nm blue / 514nm green > Melanin/Haem > chorioretinal adhesions - Cryotherapy: Media opacity
- Pars-Planar Vitrectomy: When laser ineffective
○ Gas retinopexy - Scleral buckle: for developing RRD
In conjunction with laser
Retinal holes:
Full thickness loss of retina
- Operculated hole: PVD > mechanical separation
○ May have operculum
○ Risk RRD
- Focal/Simple hole: Hole where vit. May still be attached
○ RRD if Vit. Is attached
- Horseshoe tear: PVD > Retinal flap
○ High risk RRD; requires Laser
- Atrophic hole: Retinal degeneration (lattice) > hole
○ Asymptomatic
Risk RRD
Signs of retinal detachments:
RRD:
○ Schafer’s
○ Lattice degenerations
○ Dark vessels, corrugated
○ Fl/Fl, Curtain VF defect
TRD:
○ Diabetic, Retinal NMV
○ CWS, microaneurysms, exudates
○ Concave, no breaks
○ Gradual painless loss of vision
Exudative:
Chorioretinitis, Tumour
Stroke types:
Ischemic (90%): Obstruction of BV’s in brain
○ Thrombosis: Blood clot formed in brain
○ Embolism: Plaque debris travels to brain
Haemorrhagic: BV rupture
Ocular effects of stroke:
VF defect: Based on visual pathway loss
Agnosia (recognition): Temporal lobe
Diplopia: CN3 (oculomotor), CN4(Trochlear), CN 6(Abducens)
Anisocoria and Ptosis:
○ CN3 > Mydriasis / Full ptosis
○ Horners > Miosis / Partial ptosis
CN7 > Facial Ptosis
Specific VF defects based on Visual pathway lesion:
○ Amaurosis: AAION
○ Bitemporal hemianopia: Pituitary adenoma
○ Homonymous Hemianopia: Lesion of optic tract / Radiations / Occipital
○ Sup. Quadrantanopia: Temporal lobe Myers loop
○ Inf. Quadrantanopia: Parietal lobe
Central scotoma: Occipital tip
T1DM:
AAD against pancreatic beta cells in islet’ of langerhans > insulin deficiency
○ HLA-DR3/4
Symptoms:
○ Polyuria (urination)
○ Polydipsia (thirst)
○ Polyphagia (hunger)
○ Weight loss
○ Fatigue
Management:
Life long insulin therapy
DDX Epiphora:
Reflex tearing:
○ DED
○ Blepharitis
○ Conjunctivitis
○ Trichiasis
○ Entropion
Lacrimal drainage obstruction:
○ Ectropion
Neurological:
CNV stimulation (Trigeminal neuralgia/HZO)
T2DM:
- Poor diet/physical activity > ^Fat storage > ^Lipid breakdown to glycerol/FFAs
- Chronic elevation of FFAs > insulin resistance / compensatory insulin increase > downregulation of insulin receptors > glucose uptake loss > hyperglycemia
- Chronic hyperglycimia/lipotoxicity(FFAs) > pancreatic-B cell apoptosis > insulin secretion loss
○ Decreased muscle glucose uptake
○ Increased hepatic glucogenesis
^Beta cell insulin production > beta cell failure > Insulin deficiency:
○ Glucotoxicity
Lipotoxicity (^FFAs)
Entropion types:
Involutional: Age > Laxity of lid retractors
Cicatricial: Trachoma, SJS
Spastic: ocular irritation
Congenital: birth defects
Ectropion types:
Involutional: Age > laxity
Cicatricial: Chronic inflammation, burns
Paralytic: CN7 Bells palsy
Mechanical: Lid swelling, Tumor
Congenital: birth defects
Causes of trichiasis:
Chronic blepharitis (common): Lid inflammation > lash misdirection
Trachoma: Conj. Cicatrisation
OCP: AAD > Conj. Fibrosis
SJS: Mucosal inflammation
Trauma, Idiopathic
Entropion and ectropion management:
Conservative:
○ Lubricating drops
○ Lid taping
○ BoTox
○ Moisture chamber (ectropion)
Surgical for entropion:
○ Sutures (temp > involutional)
○ Lower lid retractor reinsertion
○ Mucous membrane grafting
Surgical for ectropion:
○ Lateral tarsal strip (involutional)
Skin grafting (cicatricial
Management of Trichiasis:
Conservative:
○ Lubricating drops > ointments
○ Epilation
Temporary:
○ Electrolysis (lash destruction)
○ Cryotherapy
○ Argon laser
Surgical:
○ Lid rotation
○ Tarsotomy
Mucous membrane grafting
Trachoma presentation:
- Early stage
a. Follicular conjunctivitis (TF)
i. Mucopurulent discharge
ii. Redness, irritation
b. Papillary hypertrophy (TI)
c. Pannus- Chronic stage
a. FBS, Blur, photophobia
b. Tarsal scarring (TS)
i. Arlt’s line (sup. Tarsal)
c. Trichiasis (TT)
i. Inward turning of lid
d. Corneal opacification (CO)
Herberts pits (dark at limbus)
- Chronic stage
Conjunctival cicatrisation patho:
AAD/Infection/Injury > Innate immune response
○ Damage associated molecular pattern molecules released by cells
○ Dendritic cells recognize via Toll-like receptors
○ Recognition releases pro-inflammatory cytokines
Immune cell recruitment:
○ Neutrophil/Macrophages release cytokines
§ TNF-a, IL-1
○ T cells: CD4+ differentiate into:
§ Th1: IFN-y, TNF-a > Chronic inflammation
§ Th2: IL-4, IL-13 > Fibrosis
§ These cytokines stimulate MMP expression > Collagen dysregulation
TGF-b released by T-cells/dendritic cells/Myofibroblasts:
○ Signals fibroblast proliferation/differentiation > myofibroblasts > ^ECM proteins (collagen/fibronectin)
TGF-b dysregulates MMP activity > permanent scarring
DDX conjuctival cicatrisation:
AAD/Inflammatory: Usually Chronic Bilateral
○ OCP: Conj. Fibrosis > Symblepharon
○ SJS/TEN: Severe mucocutaneous reaction
○ RA/Sjogrens: Chronic inflammation
Infectious: Initially unilateral
○ Trachoma: Leading cause of blindness
○ HSV/HZO: Recurrent infections
○ Chronic bacterial: Progressive conjunctival fibrosis
Traumatic:
○ Iatrogenic: BAK toxicity, Ocular Sx
Chemical
Typical progression of myopia age range:
- 0: +2D hyperopic
- 6-8: Onset myopia
○ Near work > Hyperopic defocus - 6-16: Progression
○ 0.5-1D per year - 18-25: Stabilisation
○ Higher myopia ^age of stabilisation
45: Presbyopia > hyperopic shift
Ocular effects of hypertension:
Hypertensive retinopathy:
○ Vasoconstrictive: Angiotensin 2, adrenaline, vasopressin release ○ ^Vascular tone > Arteriolar narrowing
○ Sclerotic: Chronic ^BP > Vessel media hyperplasia and intima thickening
○ AV nicking ○ Tortuosity ○ Copper wiring
○ Exudative: Endothelial damage > BRB loss
○ Haemorrhages § Flame (common): NFL § Dot/Blot: outer plexiform > Inner nuclear ○ Microaneurysms ○ Hard exudates (macula star) ○ CWS
○ Malignant:
○ Papilledema ○ Siegrist streaks and Elshing spots (choroidal infarcts)
Hypertensive optic neuropathy:
○ Papilledema ○ Optic nerve ischemia (NAION)
Hypertensive choroidopathy: Following acute hypertension
○ Elschnig spots: choroidal infarction > yellow spots Siegrist streaks: Choroidal artery hyperpigmentation
DDX benign lid lumps:
Benign inflammatory:
○ Chalazion: Meibomian blockage (painless) ○ Hordeolum (Stye): acute infection (painful) ○ Internal: Zeiss, Moll ○ External: Meibomian
Infectious:
○ Molluscum cotagiosum: DNA poxvirus (umbilated papules) ○ Verruca vulgaris (wart): HPV (Papules)
Cystic:
○ Zeiss/Moll: Sebacous/Sweat gland obstruction ○ Epidermal inclusion: epidermis inclusion into dermis
Non-malignant:
○ Squamous cell papilloma: HPV assoc. Epithelial neoplasia ○ Pedunculated (skin-tag), or Sessile (flat) ○ Finger like projections ○ Basal cell papilloma: Seborrheic keratosis ○ UV assoc. ○ Brown plaques Actinic keratosis: UV assoc scaly plaque
BCC signs and management:
Superficial: well-defined red patch
○ Asymptomatic / itchy
Nodular BCC: Pearly nodules
○ May ulcerate > bleed
○ DDX SCC
Morphoeic: white patch
DDX Malignant lid lumps:
BCC: Common skin cancer
UVB > Pluripotent stem-cell (vulnerable) > ○ Sonic Hedgehog path: ○ Patched-1 binds Shh protein > Release of SMO protein > gene activation for proliferation ○ PTCH1 mutation > unregulated proliferation ○ P53 TS mutation > Unregulated growth
SCC: Arise from actinic keratosis
UV (290-320nm) > DNA mutation 1. Actinic keratosis 2. Bowmen's disease: full thickness epidermal dysplaia 3. Invasive SCC: Tumor invades basement membrane 4. Metastatic: spreads from lymphatics Usually to lungs
DDX peripheral corneal lesions:
Degenerative/Metabolic:
○ Arcus senilis: Age/Hyperlipidemia > Lipid deposition ○ Lipid keratopathy: Inflammation > yellow deposits ○ Salmann's nodular: Chronic keratitis > blue nodules
Inflammatory:
○ Marginal keratitis: Chronic staph blepharitis > infiltrates ○ Terriens: Age > Thinning > lipid deposits ○ Moorens: Painful ulceration
Infectious:
○ Bacterial: Wet ulceration ○ Viral: Dendritic/Geographic ○ Fungal: feathery/satellite ○ Acan.: Ring-shaped
Immunologic:
○ Superior limbic keratoconj.: TED/CLs > limbal nodules VKC: Large ulcers
SCC signs and management:
- Tender red papule
- Ulceration/hyperkeratosis
- Bleeding/expansion
Requires biopsy > excision +/- Moh’s
Pituitary anatomy:
Located below hypothalamus and optic chiasm in sella turcica
Anterior pituitary:
○ Growth hormone ○ Hyper: Gigantism/Acromegaly ○ Hypo: Lethargy ○ Thyroid Stimulating Hormone ○ Hyper: ^Metabolism / Weight loss ○ Hypo: weight gain ○ Prolactin: infertility ○ LH/FSH: Gonadotropins ○ Hypogonadism ○ Adrenocorticotropic hormone: ○ Hyper: cushings disease (HT/DM) ○ Hypo: Cold intolerance
Posterior pituitary
○ ADH: Vasopressin ○ Renal water reabsorption ○ Vasoconstriction Oxytocin
Different types of VFT:
10-2: 68 points over 10’
○ Plaquenil tox
24-2: 54 points over 24’
○ Glaucoma
30-2: 76 points over 30’
○ Stroke
Estermann: 100 points over 120’
Ocular risks of high cholesterol
○ Xanthelasma
○ Corneal arcus
○ Artery/Vein occlusion
○ Cataract
Retinopathy
Pigmentary dispersion syndrome:
Common condition, leads to pigmentary glaucoma
Iris pigment liberated via zonule movement > Melanin granules in TM > ^IOP
Signs:
* Krukenberg spindles (corneal endoth. Pigment) * Iris pigment * Dark TM > Scheie stripe * Iris transillumination
Risks:
* Male, myopic
Management:
* Monitor unless IOP abnormal
* Prostaglandin analogues (glauc)
OCT glaucoma:
RNFL: <80um (usually thicker superior and inferior)
GCC: <70um
CDR: >0.5 or 0.2 asymmetry (u/ <0.5)
Aqueous Humor production and drainage:
- Regulation: Autonomic nervous system
- Sympathetic: increase production
- Parasympathetic: decrease
- Secretion by NPE of ciliary processes on pars plica
- Active:
○ Na/K ATPase pumps Na into aqueous > Osmotic gradient draws water
○ CA forms H2CO3 > bicarb in pos. Chamber > Osmotic - Ultrafiltration: Pressure differential of fenestrated ciliary capillaries and post chamber
- Diffusion: O2/CO2 (small molecules)
- Active:
- Drainage:
- Conventional: TM > Schlemms canal > Episcleral veins
Uveoscleral: Iris/CB > Sclera > blood stream
- Conventional: TM > Schlemms canal > Episcleral veins
Genetic inheritance of glaucoma:
- POAG (common): Multifactorial inheritance
- MYOC (myocillin): altered regulation of aqueous
○ Assoc juvenile - OPTN (optineurin): Assoc NTG
- CYP1B1
- TMCO1
- MYOC (myocillin): altered regulation of aqueous
- PACG: East Asians > shallow AC
- PITX2: narrow AC
- Transforming GF-a: Regulation of AC depth
- LOXL-1:
- Congenital: AR inheritance (both parents carriers)
- CYPB1
LTPB2: latent transforming GF-b
- CYPB1
VF glaucoma scotomas:
- Paracentral scotoma: early sign
- Nasal step: Defects along horizontal midline
- Arcuate: arc from BS to nasal field
- Temporal wedge: triangle loss
- Central island of vision
Clinical analysis of optic nerve for glaucoma:
Size:
* CDR > 0.5, asymmetry of > 0.2
* Vertical 1.5mm
Rim:
* ISNT
* Bayonetting
Haemorrhages: U/NTG
NFL: Red free
* Wedge defects
PPA:
* Alpha (Myopia)
Beta: chorioretinal atrophy > Glaucoma
Allergic reaction to eye drops:
- T1HS: within minutes, Redness, chemosis, itching, lid edema
- APC process allergen > present to Th2 (CD4) > Th2 cytokine release (IL-4) > B cells form specific IgE for basophils/mast cells
- Allergen binds IgE > degranulation > histamine, trypase, leukotrines, prostaglandins
- T4HS: 3 days, Erythema, itching, blistering
- T cells differentiate into sensitized T cells
- Activation of Th1 > Cytokines (IFN-y/TNF-a) > macrophage recruitment
DM complications and diagnosis:
T1: AAD against insulin forming b cells of pancreas
T2: insulin resistance and decline in b cell function
- Microvascular complications:
- Hyperglycemia > BV/kidney/Nerve damage > Retinopathy/Nephropathy/Neuropathy
- Vision loss, renal loss, peripheral neuropathy
- Macrovascular complications:
- Atherosclerosis > Cardiovascular, Cerebrovascular disease
Diagnosed via:
- Fasting plasma glucose > 7mmol
- Oral glucose tolerance test > 11.1 mmol
- Hemoglobin A1c >6.5%
- Random plasma glucose >11.1mmol
Management of DM:
T1: Basal-Bolus (long/short) acting insulin regime
- DCCT showed T1DM insulin therapy reduced risk of microvascular complications
T2: Lifestyle, Medical control of glucose, BP, Lipids
- UKDPS showed T2DM metformin reduced complications
- AHEAD showed lifestyle improves glycemic control
- ACCORD shows Lipid control with fenofibrate
Stages and management of DR:
NPDR:
- Mild: one microaneurysm
- Observation for DME, report to GP, educate
- Moderate: haem, hard exudate, CWS
- As above, review 6mo
- Severe: Haem in 4 quadrants, Venous bleeding in 2, IRMA in 1
- Refer, FFA, endocrinology (renal assoc)
PDR:
- Early: retinal NV
- PRP (ETDRS) Anti-VEGF (DRCR.net PS)
- High-risk: NV and Vit-haem, or TRD
DME:
- Retinal thickening/Hard exudates 500um from macula
- Thickening zone of > 1DD
- Anti-VEGF (DRCR.net PT), Focal/Grid laser (non center DME), Cortico. (VEGF sensitivity)
Gonioscopy grading:
- Sheie table:
○ Wide: all structures
○ 1: CB visible
○ 2: CB obscured
○ 3: SS obscured
○ 4: TB obscured- Shaffer table:
○ 0: angle closed
○ 1: <10’
○ 2: <20’
○ 3: <35’
4: <45’
- Shaffer table:
Patho of ON damage in glaucoma:
Mechanical factors:
* ^IOP > RGC Axon compression > loss of retrograde transport > BDNF neurotrophin deficiency > RGC apoptosis
Vascular/Ischemic:
* ^IOP > hypoxia > HIF upregulation > ON ischemia
Apoptotic:
Mitochondrial oxidative stress > cellular apoptosis
SLT procedure:
532nm laser targeting pigment in TM
Stimulates macrophages to break down debris > increased aqueous drainage
○ 10-40% IOP reduction after 6mo
Contra. Heavy pigment > IOP rise
Pseudoexfoliation syndrome:
Most common cause of SOAG (Age related)
LOXL1 mutation (Risk factor, not cause) > altered elastin formation > accumulation of fibrilar material
* Three ring pattern
○ Central disc
○ Clear mid zone
○ Pupil margin ring
* Zonule weakness
* Sampaolesi line on cornea (gonio)
Management:
* Prostaglandin analogues (glauc)
* SLT
Trabeculectomy
Landmark glaucoma studies:
OHTS: Decreasing IOP > 50% lower risk of glaucoma
○ Only 4% total > Prophylactic only if high risk
EMGT: POAG treatment slows its progression
○ Early intervention critical
CIGTS: Medical and Surgery are equivalent
AGIS: IOP should be brought down to 14mmHg
CNTGS: IOP should be lowered in NTG
Management of trachoma:
SAFE (WHO)
○ Surgery for Trichiasis
○ Antibiotics
§ Azithromycin 20mg/kg once
○ Facial cleanliness
Environmental improvement
Trachoma patho:
Chlamydia trachomatis invades epithelial cells > acute inflammation
○ Neutrophils, Macrophages, Dendritic cells
○ T-cells (CD4/8) > TNF-a, INF-y, IL-1
○ B-cells synthesize antibodies
Repeat infections > Chronic inflammation and fibrosis:
○ RGF-b stimulates fibroblast activation
○ ECM production and dysregulation > scarring
Inward turning of lash > trichiasis
○ Corneal trauma
○ Risk of infection
○ Limbal stem cell def. > corneal opacity
Pannus > corneal neovasc.
CCT values and glaucoma:
Normal: 540-560um
Thin: < 540; <500 is significant risk
Thick: >560 (over-estimation of IOP)
