KHIO midsem Flashcards
(124 cards)
1
Q
Refractive error with age
A
Born with hyperopia, myopic shift by 2D
Hyperopic shift continues till 50
2
Q
Myopia presence worldwide
A
Greatest in Asia, least in Africa.
3
Q
Myopia types
A
Simple: >-6D Nocturnal: increased accommodation in dark Pseudomyopia: overaccommodation Degenerative: retina breakdown Induced: atropine/diabetes/cataracts
4
Q
Risk factors for myopia
A
Low outdoor activity (<2h) Low light levels Prolonged near tasks Urban living Parental myopia
5
Q
Fundus exam of myopia
A
Slanted optic disc
Disk atrophy (glaucoma risk)
Retinal detachment
6
Q
Myopia control
A
Laser
IOL
orthoK
atropine
7
Q
Hyperopia complications
A
Crowded ONH
Angle closure glaucoma risk
8
Q
Presbyopia mechanics
A
Ant. Pole thickens Lens thickens Ciliary muscle weakens Lens opacifies Occurs at 40 years
9
Q
Astigmatism over time
A
Eyes tend to be symmetrical
Axis has shift towards 90 over time
10
Q
Lens RI, water content
A
RI=1.39 depending on protein conc
Water=66%
Protein=33%
11
Q
How lens transparency is maintained:
A
Avascular
Less nerves/organelles
Regular organization of proteins
Crystallin aggregates do not produce scatter
12
Q
How lens loses transparency
A
Oxidation
Protein disorganization
Metabolic byproducts
13
Q
Nuclear cataract causes
A
Nuclear cataract causes Altered protein levels Abnormal proliferation Ion imbalance Protein oxidation Decreased antioxidants
14
Q
Nuclear cataract on vision
A
Myopic shift, increased RI
Decreased VE
Tritan color defect, blue light blocked by yellow fibers.
15
Q
Cortical cataract causes
A
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.
16
Q
Cortical cataract on vision
A
Loss of contrast
Astigmatism (localized RI change)
Nocturnal VA loss
17
Q
PSC pathophysiology
A
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.
18
Q
PSC on vision
A
Rapid development, vacuoles appear and disappear
VA loss
Contrast loss
19
Q
Congenital cataract types
A
Polar (Ant.Pos.)
Sutural
Cortical
Blue dot
20
Q
Congenital cataract causes
A
Lens gene mutations
Metabolic disorders
21
Q
Cataract history risk factor questions
A
Age, diabetes, disease
Smoking, alcohol, radiation, nutrition
Corticosteroids, alpha-antagonists
Refractive history
22
Q
Clinical tests for cataracts
A
VA, pinhole, tritan testing, contrast (pelli-robson W/glare), slit lamp (LOCS III grade)
23
Q
LOCS III grading
A
Lens opacities classification system
Image of lens, determined via opalescence or cortical/posterior from 1-5 scale
24
Q
Cataract management
A
Surgery IOL implant: (intra/extra capsular)
Extra: lens capsule retained for internal barrier.
Phacoemulsification: lens removed by ultrasound
25
Phacoemulsification
Cornea/sclera/capsule incision through ant. Chamber
| Probe emulsifies and disposed with suction pump
26
Types of IOLs
```
Flexible: easy surgery
Rigid: PMMA
Aspheric
Toric
Accommodating
Multifocal
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27
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
28
Dry eye disease risk factors:
Lipid: Meibomian
Aqueous: lacrimal
Mucous: goblet
29
Content of tear film layers
Lipid :cholesterol, phospholipids
Aqueous: water, ions, lysozyme (antimicrobial)
Mucin: MUC1,3,16 membrane bound proteins to glycocalyx
30
Lacrimal gland stimulation:
From CNVII, through pons, medulla, down spinal cord, leaves spinal cord as preganglionic sympathetic nerve to superior cervical ganglion in chest, reaches lacrimal gland as postganglionic sympathetic nerve
31
Meibomian oil function
Stability, reduce evaporation, barrier, smooth surface, anti-microbial, seal lids during long closure.
32
Vicious cycle:
Hyperosmolarity -> damage -> inflammation (protease release) ->goblet/epithelial damage -> tear film instability -> reduced tear break up -> hyperosmolarity
33
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
34
Schirmer test:
tear film production measured via paper strip in closed eyes, level of liquid absorption on strip in given time shows basal (not reflex) tear production
35
Conjunctiva damage measure
Via lissamine green pooling in conjunctival holes, shows DED due to damage.
36
Step 1 in DED management
Modification of environment, diet, medication, lubricant type, hygiene
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Step 2 in DED management
Preservative free lubricant, punctual occlusion, pulsed light therapy (for MGD), topical antibiotic/steroid/corticosteroid.
38
Step 3 DED management
Oral secretagogues, serum drops, bandage/scleral contacts
39
Step 4 DED management
Long term corticosteroids, surgical punctual occlusion, salivary gland transplant
40
Ocular neoplasia
Cell proliferation due to tumor, resultant from growth regulation gene disorder
Oncogenes for growth factor
Tumor suppressor genes for tumor repression
41
Triggers for neoplasia
Virus (Retrovirus, HIV/HPV)
Immune failure
Carcinogens
UV exposure
42
Non-malignant lid lesions:
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Chalazion
Hordeolum
Papilloma
Birthmark
Keratosis
Xanthelesma
Mossuscum contagiosum
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43
Chalazion
Meibomian blockage, likely from blepharitis.
Inflammatory bump on lid
Painless, autoresolving
44
Hordeolum:
Meibomian (large)/moll (small) Inflection, likely Staph normally present in eye
Tender red bump on lid, self resolving
45
Lid papilloma
Wart, possibly by HPV
| Basal: brown mark, possibly UV related
46
Actinic keratosis
Scaly plaque from UV
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Xanthelasma
Soft yellow plaque
| Bilateral, benign
48
Molluscum contagiosum
White bump from viral infection
| Self resolving
49
Malignant lid lesions
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Squamous cell carcinoma
Basal cell carcinoma
Sebaceous gland carcinoma
Melanoma
Merkel cell carcinoma
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50
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
51
Basal cell carcinoma pathophysiology
UV on stem cells leads to immunosuppression from cytokines
52
SCC vs BCC
SCC less common 1:10, more aggressive
| SCC risk of metastasis
53
Carcinoma treatment
Surgical: layered excision, each layer checked until no carcinoma
Chemotherapy
Enucleation
54
Conjunctival naevus
Common lesion, less likely malignant, is benign
| Mobile
55
Conjunctival papilloma
HPV related, dendritic growth
56
Dermoid
Collagen, yellow lump at limbus
| Is benign, can be irritating
57
Complexion associated melanosis
CAM, dark skin related to dark spots on conjunctiva via melanin excess.
58
Pterygium
Mass on limbus from UV
59
Iris nevi
Freckles from melanocyte elevation
| Requires documentation in case of malignancy
60
Primary acquired melanosis
PAM, brown pigment on sclera
61
Conjunctival melanoma
Black vascular pigment, mostly non-mobile, malignant
62
Ocular surface squamous neoplasia
OSSN similar to conjunctival melanoma with less malignancy
| Avascular, resembles pterygium
63
Congenital hypertrophy of the retinal pigment epithelium
CHRPE, dark spots on choroid (shown in fundus)
| May depigment over time
64
Choroidal nevi transformation to melanoma signs
Increased thickness/size.
Flashes/floaters/blur
Drusen
65
Choroidal melanoma risk factors
Age, male, genetics
66
Uveal melanoma treatment
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Brachytherapy (radioactive plaque)
Proton beam (radiation beam)
Stereotactic radiotherapy (multi directional beam)
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67
Afferent pupil pathway
Ganglion axon seperates from optic tract before LGN, to sup. Colliculus.
Retinal illumination and current pupil reflex integrate, axons sent to ipsilateral and bilateral edinger wetphal nuclei.
68
Parasympathetic pupil pathway
R/L edinger-westphal nuclei send preganglionic fibers to R/L CNIII, move through subarachnoid space, cavernous sinus, to ciliary ganglion.
Post ganglionic neurons travel with short ciliary nerves to iris sphincter resulting in miosis.
69
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.
70
PERRLA examination
Direct response
Consensual response
Near response
71
Anisocoria causes
Different pupil size, due to efferent defect.
| Physiological, Horner's, adies tonic pupil, CN III palsy, pharmacological, pupil damage, Acute angle glaucoma
72
Physiological anisocoria
Larger anisocoria in dim light, due to edinger-westphal inhibition being different for L/R
73
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
```
74
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)
75
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)
```
76
Adie's tonic pupil
Dilated pupil from parasympathetic fiber denervation.
Janky dilation in light exposure
Poor near vision
Poor direct and consensual response
77
Pharmacologic anisocoria
Cycloplegics block muscarinic receptors (mydriasis)
Pilocarpine, muscarinic agonist (parasympathetic leads to miosis)
Alpha antagonists block alpha receptors (impair mydriasis)
Alpha agonists for glaucoma (small mydrasis from alpha-2-receptor activation)
78
Angle closure glaucoma on anisocoria
Increased pressure behind iris leads to forward bowing. Iris ischemia can reduce sphincter muscle
79
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)
80
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
81
Anisocoria greater in dark how to differentiate
Pharmacological, Horner's, aberrant regeneration of adies / CN III
Apraclonidine (a2 agonist) 0.5% will dilate pupil with Horner's
Hydroxyamphetamine releases noradrenaline, 1% will dilate normally, no dilation id postganglionic lesion present
82
Ptosis
Low position of upper eyelid
| Congenital, acquired, aponeurotic, neurogenic, myogenic, mechanical
83
Myogenic ptosis
Muscle disfunction, myasthenia gravis, ophthalmoplegia
84
Neurogenic ptosis
Innervation disfunction, CN III palsy, horners, marcus Gunn jaw-winking syndrome
85
Simple congenital myopathic ptosis
LPS issue, lid is higher in downgaze, lower in upgaze
86
Blepharomiosis syndrome
Congenital myogenic, results in smaller palpebral fissure
87
Marcus-gunn jaw winking
Neurogenic anastomosis of CN V and CN III (LPS and facial)
| Ptosis in resting state, and winking with face motion
88
CN III palsy in ptosis
Neurogenic disruption to LPS and IOMs (inf. Medial, oblique).
Down and out position with full ptosis.
Life-threatening, related to stroke/aneurysm
89
Horners syndrome and ptosis
Disruption of sympathetic innervation, leads to partial ptosis (mullers), miosis (dilator), anydrosis
90
Myasthenia gravis
Autoimmune disease, antibodies target Ach receptors or striated muscle.
Loss of Ach uptake and damage leads to weakness of lid muscle.
Also limb weakness, facial drooping, diplopia
91
External ophthalmoplegia and ptosis
Mitochondrial dysfunction results in ATP loss and weakness of muscle.
Bilateral ptosis, poor motility
92
Aponeurotic ptosis
LPS stretching and loss of function
Change in lid crease which remains during downgaze
Small ptosis
93
Pseudoptosis
Microphtalmos (artificial eye wrong size)
Contralateral lid retraction/proptosis
CN VII palsy / brow overgrowth
Dermatochalasis (eyelid skin increase
94
Measuring ptosis
Margin-reflex: upper lid to corneal reflex
Palpebral fissure Hight: between lid margins
Levator function: thumb on brow, look up
Upper lid crease: margin and sup. Lid crease in down gaze
95
Causes of red eye
Contact lens
Corneal defect
Ant. Chamber disease
Eye wall inflammation
96
Conjunctiva function
Mucin/aqueous production (goblet/accessory), immune function (macrophage)
Bulbar (on sclera): goblet cells for mucin
Fornix: joins palpebral and bulbar
Palpebral: from tarsal plate to fornix
97
Conjunctiva anatomy
Epithelium: layers of columnar cells with goblet cells and Langerhans cells (immune).
Superficial lymphoid: T cells, neutrophils, mast cells
Internal fibrous: nerves, vessels, connective tissue
98
Types of conjunctivitis:
Infectious: Bacterial, adenoviral, HSV, chlamydial, fungal
Non-infectious: molluscum contagiosum, keratoconjunctivitis
Allergic: seasonal, giant papillary conjunctivitis
99
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)
100
Acute bacterial conjunctivitis signs:
Staph/strep, yellow discharge, sticky, burning eye, papillae, hyperemia.
101
Adenovirul conjunctivitis:
Fever, water discharge, hyperemia, discomfort, oedema, lymph node swelling
102
Herpes simplex conjunctivitis:
Watery discharge, irritation, hemorrhages, HSV vesicles on lids, corneal dendritic ulcer (green lightning)
103
Chlamydial conjunctivitis:
Unilateral, watery discharge, large follicles in fornix, papillary hypertrophy, tender/swollen lymph nodes.
104
Seasonal conjunctivitis:
Allergens bind to IgE on mast cells, degranulation releases histamine (itching) and prosglandins (dilation/pain), oedema, mucoid discharge
105
Giant papillary conjunctivitis:
CLs/allergic hypersensitivity, papillae on tarsal conjunctiva.
106
Management of bacterial conjunctiva
Topical antibiotics
| No steroids', can use broad spectrum antibiotics.
107
History taking in red eye:
When? Acute/chronic? Unilateral? Increasing? Type of pain? Vision affected? Discharge? Light sensitivity? History of red eye? Risk factors?
108
Multiple sclerosis
Common demyelinating disease. Myelin phagocytosed, replaced with plaque. CNS nerve disfunction.
Causes nystagmus, optic neuritis, optic disc oedema.
109
Systemic lupus erythematosus
Antibodies against nucleic acids
110
Myasthenia gravis
Skeletal neuromuscular transmission disfunction
Weakened muscle, mimics ocular motility defect and diplopia, results in ptosis.
Frequent in women
111
Graves disease
Hyperthyroidism. Antibodies bind to TSH receptors, increase of T4/3, decreases TSH from ant. Pituitary.
Leads to ophthalmopathy, DED, infection risk
112
Hashimotos thyroiditis
Hypothyroidism. No T4 secretion and iodination. T cells destroy thyroid
Mostly females.
113
Retinal detachment types
Rhegmatogenous: tear, viterous liquefication, fluid inters and separated retina from RPE
Serous: secondary
Tractional: secondary to neovascularization
114
Serous retinal detachment:
Break in blood retinal barrier (inflammation/infection), fluid enters sub retinal space resulting in detachment.
115
Tractional vitero retinal detachment
Retina detached due to new vessel growth from
| Diabetic retinopathy, retinal vein occlusion, uveitis, trauma
116
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.
117
Lattice degeneration
Retinal tearing at points of strong vitreoretinal adhesion.
118
Rhegmatogenous RD risk factors
Myopia >-3D, trauma, Marfan's disease
119
Epiretinal membrane symptoms and testing
Metamorphopsia, reduced VA, asymptomatic
| VA, pinhole, OCT
120
Epiretinal membrane surgical management
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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.
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121
Macula hole
Traction on macula, surrounding viterous detaches resulting in bowing on OCT, cyst of hyalocytes develops, eventually a hole in macula is torn.
122
Signs of ocular hypertension
A:V ratio
123
Artery occlusion causes:
Emboli from larger vessel/calcific hypertension deposits. Associated with diabetes and hart surgery.
124
Vein occlusion
Blood changes, vessel wall degeneration, blood coagulation.
| Results in ischemia/retinal hypoxia, resulting in new vessel formation and oedema.
