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VIV Flashcards

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1
Q

What is the presentation of a patient with HSV keratitis? (Signs/Symptoms)

A

Two types of HSV:
HSV-1: Upper body infection (lips/face/eyes)
Primary infection: conjunctivitis, general facial infection
Recurrent infection: epithelial/disciform(endothelial)/stromal keratitis (dendritic/circular/general scaring) or anterior chamber uveitis
Tearing, foreign body sensation, photophobia, conjunctival hyperemia, blurred vision, eyelid vesicles, corneal desensitization, IOP increase
Epithelial: Epithelial scar seen via fluroescein/lissamine green, painless
Disciform: often after epithelial keratitis history, painful, reversible vision loss
Stromal: necrosis of stroma, pain, irreversible vision loss
Anterior chamber uveitis: Iris inflammation, patchy color loss/atrophy, results in glaucoma/cataracts
HSV-2: genital

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2
Q

Clinical tests of HSV

A

Slit-lamp: Lid vessicles, corneal infiltrates, scarring (fluorescein/lissamine green)
Q-tip test corneal sensation
VA + pinhole (pinhole will increase VA when refractive error is cause of VA loss)
Viral culture of lesion when appearance is not conclusive

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3
Q

Endothelial scarring in HSV infection presentation with staining

A

Dendritic ulcer: fluroescein stains dendrites, lissamine green stains bulbs. Can have IOP increase (trabeculitis)
Geographic ulcer: enlarged jaggered scar due to rampant replication (immunocompromised), fluorescein stains central, lissamine green stains edges.
Metaherpetic ulcer: smooth scar similar shape to dendritic/geographic due to inability to heal, fluorescein stains stroma at edges of scar, lissamine green stains migrating cells over whole ulcer.
Neurotrophic keratitis: breakdown of healthy epithelial cells due to nerve damage or immunocompromisation leads to many opaque ulcerations throughout epithelium

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4
Q

How do you manage HSV and why?

A

Often self resolving, treatment minimizes scarring
Topical ganciclovir 0.15% every 3 hours while awake, reduction of treatment after 2 weeks
Oral acyclovir 400mg 3 per day (if topical is ineffective), consistent use prevents recurrences (ophthal refferal)
Corticosteroids in addition if infection is great/stromal/uveitis (ophthal refferal)
Acetaminophen reduces photophobia
Avoid trigger factors: CLs, UV, stress
Metaherpetic/neutrophic ulcers require lubricants and ophthal treatment

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5
Q

How do you explain to someone that they have a ‘Herpes-simplex’ Infection in the eye

A

Of two HSV strands, you have HSV-1
Travels via trigeminal nerve, which branches throughout the face
Usually initial infection occurs in childhood

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6
Q

How do you explain to someone that they have a ‘Herpes-Zoster’ Infection in the eye

A

Chickenpox reactivation via trigeminal branches

Caused by varicella-zoster virus

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7
Q

What is the presentation of a patient with Herpes zoster ophthalmicus? (Signs/Symptoms)

A

Scabbing (vessicle crusting) on nose and forehead
Fever, headache
Blurred vision
IOP increase

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8
Q

What is the ocular presentation of a patient with HZO? (Signs/Symptoms)

A

Eyelid vessicles/inflammation, conjunctivitis leading to follicles/hyperemia, scleritis/episcleritis, keratitis, uveitis, retinitis/choroiditis, optic neuritis.
photophobia, blurred vision, tearing, desensitization
Epithelial keratitis: Psudodendrites lesions (smaller without terminal bulbs)
Stromal keratitis: granular infiltrates under epithelial dendrites, late-stage; corneal swelling, infiltrates throughout stroma
Keratouveitis: iris atrophy, IOP increase (trabeculitis), corneal swelling/endothelium damage

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9
Q

Risk factors for herpes outbreak/reoccurrence

A 
Stress
Hormone changes (menstruation)
Immune change (infection)
UV
CLs
Allergies
Trauma
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10
Q

How do you manage HZO and why?

A

Epithelial keratitis: oral acyclovia 800md 5/day + preservative free lubricant (epithelial health/comfort)
Stromal keratitis/keratouveitis: corticosteroid in addition (ophthal refferal)

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11
Q

History questions when suspect Herpes infection:

A 
Unilateral/bilateral
Constant/intermittent?
Painful? What kind of pain?
Vision affected?
Discharge and type?
Light sensitivity?
Previous episodes?
Risk factors? Stress/UV/CLs/allergies/trauma
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12
Q

Barriers to corneal wound healing:

A

Sensory nerve damage (CNV palsy) decreases substance P growth factor (initiates healing)
Basement membrane abnormality, poor framework for epithelium to attach through
Tear film abnormality decreases protection to cornea

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13
Q

Phases of corneal epithelium wound healing:

A

Phases of corneal epithelium wound healing:
Latent phase: apoptosis of damaged cells, loss of gap junctions
Migration phase: surrounding cells migrate
Proliferation phase: density restored
Attachment phase: anchor complexes to basement membrane and bowman’s membrane (1 month)

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14
Q

Presenting complaints of AMD.

A 
Poor reading, facial recognition
Central vision loss (grey/cloudy/black)
Wavy
Red cobblestones (if RPE dislodged)
Poor light adaptation
Colour loss
Can by asymptomatic
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15
Q

History questions for AMD

A

When do you notice it, what are you doing?
Unilateral or bilateral?
Is it getting worse?
Risk factors: Family history/smoker/hypertension/cholesterol levels/ blood pressure/cataract surgery
LEE

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16
Q

What clinical tests would you use to assess a patient with AMD?

A

VA + pinhole (decreased pinhole VA with AMD)
Amsler chart (relative/absolute, scotoma/metamorphopsia)
Indirect fundus assessment
OCT (abnormaly small/numerous drusen, large for cholesterol deposit)
Fundus autofluorescence/exam (assess drusen/leakage)
• Check IOP before dilation
Pelli-robinson chart
Ishihara color test

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17
Q

What other conditions could cause a painless loss of central vision in an adult??

A

Central retinal artery/vein occlusion
Toxoplasmosis reactivation/retinitis
Serous retinopathy, macular oedema, macular hole (epiretinal membrane)
Eye surgery resulting in macular oedema (cataracts)
Optic neuritis/uveitis
Choroidal melanoma
Toxicity (Vit-A deficiency)

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18
Q

Types of AMD

A

Non-exudative: Small drusen, RPE detachment/atrophy/hyperpigmentation, risk developing geographic atrophy/exudative AMD(CNV)
Exudative: choroidal neovascularization (CNV) through Bruch’s membrane, retinal fluid hemorrhage, RPE detachment/tear, scarring, all leading to photoreceptor damage in macula

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19
Q

How do you explain to a patient that they require urgent referral for a CNV?

A

Caused by AMD, myopia, VEGF excess, bruch’s defect, Choroidal neovascularisation means an abnormal growth of blood vessels from choroid into your retina
New vessels do not adhere to the BRB, leaking fluid to sensitive cells.
Death of photoreceptors will result in vision loss.
Is rapid, legal blindness can occur in as little as 6 months

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20
Q

Early/dry AMD treatment

A

No reversabe treatment

Managed via risk factor cessation (smoking, hypertension, diet(antioxidants)

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21
Q

What are the Treatment options for Exudative AMD?

A

Bevacizumab, ranibizumab, aflibercept are monoclonal antibodies which bind to VEGF-A (class for angiogenesis and vessel permeability) and inhibit its binding to VEGFR.
Photodynamic therapy: verteporfin injection and laser light destroy new vessels and attenuate them to stop new formation
Laser coagulation therapy: laser destroys new vessels, not indicated as it may damage fovea, and will not stop neovascularisation.

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22
Q

Clinical presentation of retinitis pigmentosa:

A

Nyctalopia (poor light adaptation), VF constriction, poor reading, nystagmus (present from birth), squinting in light, deep-set eyes/keratokonus (eye rubbing)
Rod-Cone dystrophy (black spots on fundus), RPE atrophy, attenuated blood vessels
ERG shows full decrease in response

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23
Q

Retinitis pigmentosa causes:

A

Genetic disorder, one of many genes faulty
Autosomal Dominant: RHO (rhodopsin), common. RPE65 (common cause of blindness in children)
Autocomal recessive: USH2A (Usherin), assiciated with deafness. EYS (epidermal growth factor) common in asia
X-linked: RPGR, variable in females

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24
Q

Management and testing for retinitis pigmentosa:

A 
Electrophysiology (Rod/Cone response)
Gene array panel
Counselling (low vision services)
VF
Sunglasses
Photography used sparringly as bright light damages PR
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25
Types of congenital stationary night blindness:
Complete or incomplete (type 1/2) Autosomal dominant/recessive/X-linked Type-1: loss of ON-bipolar cells Type-2: loss of OFF-bipolar cells
26
Clinical presentation of Congenital stationary night blindness:
Blind at night, poor VA in light, colour vision variable, nystagmus (present from birth), strabismus Electroretinogram (b-wave amplitude reduction)
27
What signs might occur with cancer or melanoma associated retinopathy?
Painless vision loss, Night blindness, VF defect, photopsia, nyctalopia, scotomas, poor contrast sensitivity, poor color vision ERG will show decreased b-wave amplitudes in MAR, and normal b-wave in CAR
28
Mutation in human bestrophin (hBEST1/VMD2)
Bestrophinopathies occur, abnormal chloride channels, yellow spots on fundus, vision loss. Leads to central RPE/retinal atrophy, choroidal neovascularisation, macula holes
29
Types of macula dystrophies:
``` Leber's congenital amaurosis (RPE65) Best (BEST1) Stargardt's (ABDA4) MIDD AR/AD cone-rod dystrophy (retinitis pigmentosa) ```
30
Explain the ocular surface defence mechanisms
Eyelids: protection/debris cleaning Tear film: antimicrobial proteins (immunoglobullin), IgA prevents adhesion to epithelium, mucin layer traps microbes, innate ocular surface immune responses (complement protein activation system coats pathogens) Corneal epithelium: tight junctions + strong membranes act as a barrier and prevent influx of fluid (oedema)
31
Risk factors for microbial keratitis:
``` CL wear (risk is greater with soft>silicone>daily>RGP), overnight CL wear, corneal hypoxia (epithelium dysfunction), epithelial damage, surgery, DED/ocular diseases, immunosuppression, lagopthalmos (corneal exposure) Commonly pseudomonus aeruginosa ```
32
Clinical signs of bacterial keratitis:
Increasing pain, central epithelial ulcer with hazy edges, hyperemia, corneal oedema, mucin discharge, lid swelling, stromal infiltrates
33
Clinical signs of fungal keratitis:
Gradual pain, feathery grey infiltrate, circular lesions, discharge MAY be present, hyperemia, photophobia
34
What clinical tests would you do to assess a bacterial keratitis?
``` VA + pinhole (expect decrease/no change in pinhole) Slit lamp (lid swelling, corneal hypoxia/epithelium damage) ```
35
How would you explain to a patient that they needed to reduce their wearing time?
Wearing CLs increases risk of infection, greater for the more time the CL is worn. CL provides space for microbes to contact the cornea, safe from normal barrier function.
36
Control of bacterial keratitis:
Broad-spectrum antibiotics: fluoroquinolone with ciprofloxacin Combination therapy: gentamicin(aminoglycoside) with cefazolin
37
CL complications:
Corneal hypoxia/neovascularisation/DED, 3-9o'clock staining (incomplete blink), epithelial lesions, allergic keratitis, CL giant papillary conjunctivitis, CL acute red eye (CLARE), microbial keratitis
38
What are the presenting complaints of a person with a retinal detachment?
Flashing lights (vitreo-retinal tractions), floaters (liquification of viterous), curtain over vision, reduced VA (if on macula), or asymptomatic
39
History questions for retinal detachment
``` When? Flashes? Floaters? Does it depend on time/action? Change in vision? Describe visual phenomenon Myopic? Surgery/trauma? ```
40
Clinical tests for retinal detachment
VA + pinhole Confrontation/VF test Fundoscopy (IOP before dilation) (check retinal tear/elevation/floaters)
41
Retinal detachment types:
Rhegmatogenous: tear, viterous liquefication, fluid inters and separated retina from RPE Serous: Break in blood retinal barrier (inflammation/infection), fluid enters sub retinal space resulting in detachment. Tractional: Retina detached due to new vessel growth from Diabetic retinopathy, retinal vein occlusion, uveitis, trauma
42
Signs of retinal detachment?
Retinal tear, Lattice degeneration (retinal thinning at vitreoretinal adhesions), retinal vein occlusion, neovascularisaion, macula oedema, melanoma
43
Epiretinal membrane symptoms and testing
Metamorphopsia, reduced VA, asymptomatic | VA, pinhole, OCT, fundoscopy (check IOP before)
44
Epiretinal membrane surgical management
``` Vitrectomy with epiretinal peel, trypan blue dye shows membrane and it is peeled off. Risks cataract (is done with cataracts surgery), retinal break, hemorrhage, macula hole ```
45
Surgical treatment of retinal detachment
Scleral buckling: band around eye connects NSR with RPE | Pars planar vitrectomy: removal of viterous and replacement with gas to increase internal pressure.
46
Explain how a vein/artery occlusion occurs
Artery: Emboli from larger vessel/calcific hypertension deposits. Associated with diabetes and heart surgery. Vein: hypercoagulation/blood flow stasis/ endothelial damage
47
Presentation of artery and vein occlusion
Branch AO: VF constriction, macula preserved via choroidal circulation/cilioretinal artery CRVO: blurry vision, worse when ischemia present CRAO: greatly decreased vision unless cilioretinal artery present
48
What are the signs of ocular hypertension how would you explain this to a patient?
``` Narrow A:V ratio Arteriovenous nipping Silver wiring on artery Cotton wool spots (swelling of NFL axons due to hypoxia) Flame/dot blot haemorrhages Optic disk oedema Microaneurysms Exudates ```
49
Pathophysiology of hypertension:
High BP compresses/damages veins, thrombus/turbulent flow formation, leads to vein occlusion, increase venous pressure, leakage/hypoxia, leading to neovascularisation
50
Artery/vein occlusion clinical tests:
``` VA VF Amsler Fundoscopy (IOP check) OCT ```
51
What is the mechanism of myasthenia gravis?
Antibodies target nicotinic acetylcholine postsynaptic receptors at neuromuscular junction Weakened muscle, mimics ocular motility defect/diplopia/ptosis. Frequent in women
52
Treatment of myasthenia gravis
Anticholinesterases Azathioprine Oral steroids Thymectomy (removes B cells)
53
Graves disease
Hyperthyroidism. Antibodies bind to TSH receptors, increase of T4/3, decreases TSH from ant. Pituitary. Leads to ophthalmopathy, DED, infection risk. Bulging eyes, diplopia, optic nerve compression/vision loss
54
Hashimotos thyroiditis
Hypothyroidism. No T4 secretion and iodination. T cells destroy thyroid Mostly females.
55
How can you manage a patient with thyroid eye disease?
Graves (hyperthyroidism): anti-thyroid drugs, beta blockers, thyroid removal Hashimotos: synthetic thyroxine
56
What are some other symptoms a patient with a red eye might present with
Pain Blurred vision Light sensitivity Discharge
57
What questions would you ask in history taking for red eye?
``` When? Unilateral/bilateral? Constant or intermittent? Worsening? Pain? What type? Vision affectd? Discharge? What type? Light sensitivity? History of red eye? Risk factors (CLs/allergies/trauma)? ```
58
What clinical tests can assess red eye?
VA + pinhole Slit lamp (papillae/follicles, corneal defect, anterior chamber) Pupil response IOP
59
Pathophysiology of AMD:
Lipofucin accumulates from poor photoreceptor metabolism in RPE Forms A2E which inhibits metabolism, forming drusen(cholesterol) between RPE and bruch's membrane, causing ischemia Leads to Wet AMD, neovascularisation from A2E angiogenic factors/VEGF
60
Types of conjunctivitis:
Infectious: Bacterial, adenoviral, HSV, chlamydial, fungal Non-infectious: molluscum contagiosum, keratoconjunctivitis Allergic: seasonal, giant papillary conjunctivitis
61
Signs of conjunctival inflammation
Hyperemia (vessel dilation), oedema (serous fluid leak from tight junctions), discharge, scarring, follicles (lymphocyte mass rice like), papillae (collagen from histamine reaction), membranes
62
Treatment of different types of conjunctivitis
Acute bacterial: antibiotics Herpes simplex: often self-resolving, use supportive treatment (eye drops) Chlamydial: no treatment, use supportive Seasonal: antihistamine drops Vernal/atopic keratoconjunctivitis (allergic): antihistamine drops, avoid allergens Giant papillary: cease CLs
63
Adenoviral conjunctivitis symptoms:
Fever, water discharge, Hyperemia, discomfort, oedema, lymph node swelling, pseudo membrane
64
Herpes simplex conjunctivitis:
Watery discharge, irritation, haemorrhages, HSV vesicles on lids, corneal dendritic ulcer (green lightning)
65
Chlamydial conjunctivitis:
Unilateral, watery discharge, large follicles in fornix/palpebrae, papillary hypertrophy, tender/swollen lymph nodes.
66
Seasonal conjunctivitis:
Allergens bind to IgE on mast cells, degranulation releases histamine (itching) and prosglandins (dilation/pain), oedema, mucoid discharge.
67
Allergic conjunctivitis
Bilateral, white limbus papillae, large papillary hypertrophy leading to shield ulcer Allergens bind to IgE on mast cells, degranulation releases histamine (itching) and prosglandins (dilation/pain), oedema, mucoid discharge.
68
Giant papillary conjunctivitis:
CLs/allergic hypersensitivity, papillae on tarsal conjunctiva.
69
How do you manage giant papillary conjunctivitis associated with contact lens wear?
Cease CLs until resolution, consider changing CL regime/type
70
Afferent pupil pathway
RGC layer forms afferent pupillary fibers, travel through optic tract to sup. Colliculus, then midbrain, then to Edinger-Westphal nuclei bilaterally (both sides). Then as parasympathetic pathway: Efferent fibers travel on oculomotor nerve to ciliary ganglion, then short ciliary nerves, to iris sphincter muscles for constriction
71
Sympathetic pupil pathway
1st order neuron descend from hypothalamus to ciliospinal center. Preganglionic sympathetic fibers exit spinal cord, travel pass lungs as 2nd order neurons to superior cervical ganglion near jaw. 3rd order postganglionic sympathetic fibers follow internal carotid artery, enter orbit via cavernous sinus then SO fissure with CNV. Run with long ciliary nerves to pupil dilator muscle for myadriasis.
72
Name some conditions that might present with anisocoria
CNIII palsy, Acute angle closure glaucoma, horner's syndrome, physiological dysfunction (edinger-westphal), adie's tonic pupil
73
How do you assess the afferent pupil pathway?
Swinging pupil test: RAPD grading = 1: weak constriction and great radiation 2: no motion, then great dilation 3: immediate dilation 4: dilation with no constriction after 6s
74
Horners syndrome
``` Congenital or acquired. Disruption in sympathetic innervation. Results in miosis (dilation lag in dark) Partial ptosis (muller loss) Anhydrosis (sweating) Loss of accommodation (ciliary innervation loss) Red eye (conjunctival vessel dilation) Blue eyes in young kids ```
75
Horners syndrome causes
1st order neuron lesion (brainstem/spine), or diabetic 2nd order neuron lesion (carotid aneurysm, neck lesion, trauma) 3rd order neuron lesion (internal carotid disection, cavernous sinus mass)
76
CN III palsy and anisocoria
``` Parasympathetic fibers move with CNIII, loss of blood flow or damage will interrupt miosis, leading to mydriasis of affected eye. Can be pupil sparing when related to diabetes/hypertension Full ptosis (LPS loss) Down and out diplopia (medial/sup./inf. Muscle loss) ```
77
Adie's tonic pupil
Dilated pupil from parasympathetic fiber denervation. Janky dilation in light exposure Poor near vision Poor direct and consensual response
78
Anisocoria assessment. (difference in light and dark)
If same in dark and light, is physiological If greater in dark, may be physiological, dilator issue, horners (sympathetic issue) If greater in light, is issue with sphincter, or parasympathetic to larger pupil (CN III palsy, adies tonic
79
Anisocoria greater in light how to differentiate
CN III, adies, sphincter trauma, pharmacological Slit-lamp shows janky motion (adies), and trauma Adies suspect, 0.1 pilocarpine used. Up-regulation of Ach receptors will result in constriction 1% is used if failure to constrict occurs, constriction means CNIII palsy, failure means pharmacologic
80
Clinical testing for anisocoria
VA IOP (high in acute angle glaucoma/ may be low in horners from decreased aqueous production) Motility (CNIII) Ptosis assessment (full ptosis CNIII/ partial ptosis in horners) Slit lamp (worm motion Adie's/iris injury/angle closure)
81
Types and causes of ptosis:
Myogenic ptosis: Muscle disfunction, myasthenia gravis, ophthalmoplegia Neurogenic ptosis: Innervation disfunction, CN III palsy, horners, marcus Gunn jaw-winking syndrome Aponeurotic ptosis: LPS stretching, change in lid crease Mechanical: Skin growth
82
Clinical testing with ptosis:
VA Motility (CNIII palsy) Pupil assessment (horner's/palsy) Slit lamp (mechanical or aponeurotic)
83
What are some benign skin lesions you may encounter in practice?
Chalazion: Meibomian blockage, Painless, autoresolving Hordeolum: Meibomian (large)/moll (small) Inflection Tender red bump on lid, self resolving Lid papilloma: Wart Actinic keratosis: Scaly plaque from UV Xanthelasma: Soft yellow plaque, Bilateral, benign Molluscum contagiosum: White bump from viral infection, Self resolving
84
Squamous cell carcinoma pathophysiology
UV leads to cell proliferation and immunosuppressive cytokine release, resulting in mutation, leading to proliferation of atypical epithelial cells and tumor
85
Basal cell carcinoma pathophysiology
UV on stem cells leads to immunosuppression from cytokines
86
How might you differentiate a basal cell from a squamous cell carcinoma?
``` SCC less common, higher risk of metastasis. Can arise from actinic keratoses, can form ulcer and bleed BCC: Superficial: red patch Nodular: pink papule Sclerosing: white scar Ulcerative: ulcer, irregular vessels ```
87
Treatment for ocular neoplasm:
Surgical: layered excision Chemotherapy Cryotherapy: liquid nitrogen Enucleation
88
Non malignant Lesions of the ocular surface:
Naevus: Darkening patch, less likely malignant, Mobile Papilloma: Human papilloma virus, dendritic growth from fornix Dermoid: Collagen, yellow lump at limbus Complexion-associated melanosis: dark spots on conjunctiva via melanin excess. Pterygium: Mass on limbus from UV
89
Malignant lesions of the ocular surface:
Primary aquired melanosis: cloudy brown pigment on sclera Conjunctival melanoma: black, vascular, non-mobile Ocular surface squamous neoplasia: Vascular pterygium from UV
90
Symptoms of choroidal melanoma:
Blurred vision Visible tumor Mostly asymptomatic
91
What are the likely presenting complaints for a person with dry eye?
``` Dryness Gritty Burning Forieign body sensation Watering Vision loss Photophobia Pain ```
92
Risk factors for dry eye:
``` Age Female Lid dysfunction (sjogrens) Pterygium CLs Environmental Smoking ```
93
Composition and origin of layers to the tear film
Lipid: Meibomian Aqueous: lacrimal Mucous: goblet
94
Content of tear film layers
Lipid :cholesterol, phospholipids Aqueous: water, ions, lysozyme (antimicrobial) Mucin: MUC1,3,16 membrane bound proteins to glycocalyx
95
ADDE vs EDE
Aqueous deficient dry eye: Sjogren's. or age/lacrimal dysfunction, conjunctival scar, Vitamin A deficiency, neurological Evaporative: MGD, lagopthalmos (lid dysfunction), environmental, contacts
96
Vicious cycle:
Hyperosmolarity -> damage -> inflammation (protease release) ->goblet/epithelial damage -> tear film instability -> reduced tear break up -> hyperosmolarity
97
Diagnosis of DED:
Schirmer's (<10mm/ 1min) TBUT (<10s) Lissamine green staining (epithelial damage, dotting on cornea) Tear osmolarity They can fill out the dry eye questionaire
98
How would you manage Dry Eye Disease?
Step 1 in DED management: Modification of environment, diet, medication, lubricant type, hygiene Step 2 in DED management:Preservative free lubricant, punctual occlusion, pulsed light therapy (for MGD), topical antibiotic/steroid/corticosteroid. Step 3 DED management:Oral secretagogues, serum drops, bandage/scleral contacts Step 4 DED management:Long term corticosteroids, surgical punctual occlusion, salivary gland transplant
99
What are the different types of age-related cataract?
Nuclear: Hardening, yellow opacification of nucleus, scatters and absorbs light Cortical: Opacification due to change in RI through lens cortex, progression varies Posterior subcapsular: opacification at posterior lens
100
Nuclear cataract causes
``` Altered protein levels Abnormale cell proliferation Ion transport disfunction Oxidation of lens proteins Loss of antioxidants Related to UV, age, toxins, disease (diabetes) ```
101
Nuclear cataract vision effect:
Loss of VA, contrast | Tritan colour defect (blue light blocked)
102
Cortical cataract pathophysiology
Break in epithelial cells with Na/K ATPase pump, increase Ca/Na/Cl influx results in overhydration. Crystallins aggregate, increasing insoluble proteins, resulting in opacity.
103
Cortical cataract on vision
Loss of contrast Astigmatism (localized RI change) Nocturnal VA loss
104
PSC pathophysiology
Diabetes, corticosteroids lead to epithelial proliferation at germative zone, cells fail to differentiate resulting in abnormal NaKATPase transport, leading to swelling and formation of extracellular granular material.
105
PSC on vision
Rapid development, vacuoles appear and disappear VA loss Contrast loss
106
PC with cataracts:
``` Poor/blurry dist/near vision Poor night vision Glare Reduced contrast Diplopia Colour loss ```
107
History questions for cataracts:
``` How is you reading/driving/walking in light/dark conditions Unilateral/bilateral Onset? Progressive? Allergies? Risk factors? Medications (corticosteroids) Family history? ```
108
Clinical tests for cataracts:
VA Contrast + glare Ishihara Slit lamp (IOP check)
109
Cataract management
Surgery IOL implant: (intra/extra capsular) Extra: lens capsule retained for internal barrier. Phacoemulsification: lens removed by ultrasound
110
Types of IOLs
``` Flexible: easy surgery Rigid: PMMA Aspheric Toric Accommodating Multifocal ```
111
Cataract surgery complications
Posterior capsular opacity: 2y post-op 1/2 Px epithelial cells proliferate over IOL, fixed by laser Dislocated IOL Rupture: leads to prolapse of vitreous into ant. chamber IOP increase Infection: leads to blindness
112
Refractive error with age
Born with hyperopia, myopic shift by 2D | Myopic shift until 15, hyperopic shift following
113
What are the likely presenting complaints for a person with an uncorrected refractive error?
``` Blur Dist/near Squinting Headache/eye strain Diplopia Hold books close/far May be asymptomatic ```
114
Myopia prevalence
Greatest in asia, least in africa | Mediocre in australia and america
115
Myopia types
``` Simple: >-6D Nocturnal: increased accommodation in dark Pseudomyopia: overaccommodation Degenerative: retina breakdown Induced: atropine/diabetes/cataracts ```
116
Risk factors for myopia
``` Low outdoor activity (<2h) Low light levels Prolonged near tasks Urban living Parental myopia ```
117
Fundus exam of myopia
Slanted optic disc Disk atrophy (glaucoma risk) Retinal detachment
118
Myopia control
``` Laser IOL orthoK Atropine Glasses/CLs ```
119
Hyperopia complications
Crowded ONH | Angle closure glaucoma risk
120
Presbyopia mechanics
``` Ant. Pole thickens Lens thickens Ciliary muscle weakens Lens opacifies Occurs at 40 years ```
121
Astigmatism over time
Eyes tend to be symmetrical | Axis has shift towards 90 over time
122
Macula hole
Vitreous liquification pulls on retina, leading to detachment. Strong attachment at macula leads to hole. Decreased central vision, treated with vitrectomy.
123
Horners syndrome testing:
Hydroxyamphetamine will dilate pupil when preganglionic neuron is afflicted
124
Glaucoma treatment:
Timolo/beta-blockers: reduce aqueous production in ciliary | Laser: allows flow in open-angle glaucoma

OPTO 3003 (7 decks)

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