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KHIO 1 VIVA > patho > Flashcards

patho Flashcards

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1
Q

Emmetropization:

A

+2D at birth > axial growth guided by blur/luminance > +1D at 2 years

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2
Q

Myopia progression

A

Retinal hyperopic defocus > signalling cascade > Axial length elongation
Steep cornea
Gene loci MYP2/3/5
Dopamine loss in retina (increase light exposure)
Near work

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3
Q

Hyperopia

A

Dysfunctional emmetropization > Short axial length (latent hyperopia)
Flat cornea
Accommodation paralysis

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4
Q

Astigmatism

A

Rubbing/lid pressure > corneal bending > 2 focal lines

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5
Q

Presbyopia

A

Increased lens/capsule thickness, weak ciliary, loss of capsule elasticity > decreased amplitude of accommodation

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6
Q

Cataract formation factors/pathophysiology:

A

Oxidative damage (radicals/mitochondrial loss > less ATP > poor ion regulation)
Defence loss (less glutathione / ascorbic acid > less radical removal / O2 level change)
Metabolic / osmotic disturbance (cell stress reduces ATP > NaK ATPase / Ca ATPase disregulation > Na / Ca influx)
Calpain activation (Ca increase > calpain overactivation > crystallin proteolysis)
Post translational modification (UV/glycation > DNA damage/change)

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7
Q

Nuclear cataract

A

UV, Diabetes (glucose > glycation), Corticosteroids
Oxidation > ^ oxidised tryptophan (protein amino acid) > Chromophore production (milliard product) > chromophore cross links with crystallin > browning

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8
Q

Cortical cataract

A

Metabolic disturbance (diabetes), lens damage
NaK ATPase dysfunction > Na influx / overhydration > crystallin aggregation

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9
Q

Posterior subcapsular cataract

A

Age/UV/Corticos. > Abnormal GF expression > Defective epithelium fiber production > defective cell migration to C1 > opacity formation
Age related PSC irreversible
Hypoglycaemia / corticosteroid induced PSC reversible

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10
Q

Types of aquired cataracts/causes:

A

Age related
Traumatic (secondary to surgery)
Secondary (uveitis/glaucoma)
Metabolic (diabetes)
UV
Toxic (corticosteroids)

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11
Q

DED definition:

A

Multifactorial disease of tears / ocular surface resulting in discomfort, visual disturbance, tear film instability, ocular surface damage. Accompanied by increased osmolarity of tear film and ocular surface inflammation

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12
Q

Aqueous deficient dry eye causes:

A

Sjrogrens syndrome
Lacrimal gland dysfunction/obstruction
Anti depressants/histamines
Reflex hyposecretion
CLs/herpes > reflex sensory block
CN7 damage > reflex motor block

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13
Q

Evaporative dry eye causes

A

Lagopthalmos/ectropion
Environment (AC/dust)
CLs
MGD
Increased bacterial lipase population > increased melting point
Blepharitis
Trachoma

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14
Q

Vicious cycle in depth

A

Loss of aqueous or evaporation > hyperosmolarity > epithelial irritation > Mitogen-activated protein kinase (MAPK) activation > inflammatory mediator release (IL-1/MMPs) > Matrix metalloproteinases damage epithelium / goblet cells > epitheliopathy (corneal epithelium loss) / tear instability > reduced TBUT > hyperosmolarity

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15
Q

Hordeolum

A

S aureus infection of zeiss/moll/meibomian
Red nodule, tender, pain on blink

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16
Q

Chalazion

A

Inflammation following obstruction of sebaceous/zeiss/meibomian glands
Defined nodule, firm, skin colour, painless

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17
Q

Dermoid

A

Benign malformation of tissue
Ill defined nodule, slow growing, skin colour, painless

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18
Q

Cyst of zeiss

A

Sebaceous gland (zeiss) obstructed
Small, round, skin colour/opaque, painless

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19
Q

Cyst of moll

A

Apocrine gland (moll) obstructed
Small, round, skin colour/translucent, painless

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20
Q

Molluscum contagiosum

A

Pox virus infection
Single/several small, round, waxy nodules

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21
Q

Xanthelasma

A

Lipid/immune (macrophage) accumulation on skin with age
Soft yellow plaque on lids nasally, bilateral

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22
Q

SC papilloma

A

Infection of human papillovirus (HPV)
Skin tag, or finger-like lesion

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23
Q

BC papilloma

A

Epithelial tumor from age (maybe UV)
Single/several brown plaques

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24
Q

Actinic/solar keratosis

A

UV > gene damage > mutation > proliferation/immunosupression
Defined skin area, brown/tan/pink/red, hyperkeratosis (scaly plaque), non-tender or stinging.

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25
Melanocytic naevi
Proliferation of melanocytes from UV/genetics Brown plaque, small if congenital / growing if aquired.
26
SC carcinoma pathophysiology and causes:
UV to epithelium> mutation in p53 TS > proliferation of atypical epithelium. Commonly from actinic keratoses Second most common skin cancer, related to smoking/immunosupression
27
BC carcinoma pathophysiology can causes:
UV to sensitive stem cells > mutation in p53 TS > proliferation of abnormal basal cells Most common skin cancer, related to smoking/immunosupression
28
SCC opposed to BCC identification
Less common, more aggressive, high metastasis risk Often with hyperkeratosis (cutaneous horn formation) Arises from actinic keratoses Erythematous (red) Ulcers and bleeds
29
BCC opposed to SCC identification
More common, low metastasis risk Superficial: Red patch Nodular: white/pink nodule Sclerosing: white patch Ulcerative: pearly rolled edges with vessels and central ulceration
30
Skin melanoma
UV/naevi/caucasian > Malignant proliferation of melanocytes Flat > raised, varied pigment, irregular boarders, can progress rapidly and bleed
31
General differentiation for melanoma to naevus on skin
A: Asymmetry B: Boarders irregular C: Colour variation D: Diameter >6mm E: Evolution over time
32
Conjunctival naevus
UV/genetics > Melanocyte cluster in basal epithelium (10-20yo) > migrate to stromal mass (20-30yo) Small elevation lesion, variable pigment, interpalpebral limbus, usually mobile (unsuspicious) <1% progression to malignant melanoma
33
Pterygium
UV > oxidative stress > altered cellular synthesis / GF expression > proliferation Wedge fibrovascular growth of bulbar conj. At 3/9 o'clock, forms over limbus to cornea
34
Pingueculum
Age/UV > hyperplasia on interpalpebral conj. White elevation, usually nasal, does not cross over cornea
35
Conjunctival intraepithelial neoplasia (CIN)
OSSN, UV > p53 mutation > proliferation of dysplasic squamous epithelia, has not invaded stroma Limbal vascular thickening of conj. May have white plaque, wont metastasise until SCC formation
36
Conjuntival SCC
OSSN, Malignant squamous epithelial cells through basement to stroma Limbal vascular thickening of conj. May have white plaque, immobile Metastasises to lymph
37
Conjunctival melanoma
Rare melanocyte invasion of stroma, 60yo from PAN, otherwise nevus/de novo. Pigmented vascular elevation anywhere on conj. Immobile Metastasises to lymph
38
PAM
Melanocytes near basal epitheilum. Brown pigment, scattered through conj. (usually Caucasian) Atypia melanocytes =50% risk malignant melanoma
39
Choroidal melanoma
Usually from separate tumour metastasis (Female breast cancer, or male lung cancer) Otherwise malignant melanoma (from nevi 5%) 50% further metastasis (1/2 die in 8 months) 60% metastasise to liver (then lung 25%/bone/brain)
40
Choroidal naevi likelihood to from malignancy
>2mm depth >5 mm width (1.5 disk diameters) Orange lipofuscin (fatty acid/lipid accumulation) Irregular boarders Serous RD Hollow on OCT
41
Lid dishinence (apoptotic neurosis)
LPS tendon less from tarsal from rubbing, CLs, age, trauma/surgery Low lid, high crease, normal range of motion
42
Tonic pupil/ Adie's
Post ganglionic parasympathetic denervation, Poor light constriction, good convergence constriction Worm like redilation/constriction from partial denervation Initially dilated pupil, long term mitotic pupil (abberant nerve regeneration)
43
Myasthenia gravis
Autoimmune against acetylcholine receptors of striated muscle. Loss of Ach uptake and damage leads to weakness of lid muscle. Fatigue, facial weakness, ptosis (LPS weak)/diplopia. Cognan's lid twitch (upper lid overshoot on upgaze) Curtaining/enhanced ptosis (contralateral drooping/elevation)
44
Parasympathetic pathway for iris: q
Afferent: Optic nerve > split at chiasm > optic track > split before LGN > sup. Colliculus > pretectal nuclei (processed) > both edinger-westphal nuclei. Efferent: Edinger-westphal nuclei > CN 3 > ciliary ganglion > with short ciliary nerves > iris sphincter
45
Sympathetic pathway for iris:q
1st neuron: hypothalamus > spinal cord > ciliospinal centre of bulge and waller 2nd neuron: ciliospinal > stellate ganglion (lung apex) > superior cervical ganglion (jaw) 3rd neuron: superior cervical g. > internal carotid > cavernous sinus > SO fiss. > CN 5 V1 (nasociliary div. Of ophthalmic) > long ciliary nerves > iris dilator Also innervate mullers / facial
46
Bacterial conjunctivitis pathophysiology
Acute: S. Aureus/ S. Pneumoniae/ Haemophilus influenzae Hyperacute: Neisseria gonorrhea (uncommonly related to acute bacteria) Chronic: blepharitis > build-up of microbial load (S. Aureus) > longer than 3 weeks
47
Herpes simplex keratitis life cycle
Primary infection via contact with secretions (cold sores) Replication causes primary manifestation (skin vesicles/follicular conjunctivitis) Enters sensory nerve endings, travels to trigeminal ganglion. Reactivation > infection of high sensory tissue via opthalmic branch
48
Herpes Zoster life cycle
Chickenpox/shingles Primary infection > nerve invasion > primary manifestation (fever, rash, pneumonia) VZV travels to cranial nerve sensory ganglia Reactivation > viral transport to skin (prodromal malaise) > severals days until arrival > vesicular rash HZO occurs when reactivated virus travels ophthalmic branch of trigeminal (CNV1)
49
Seasonal/Perennial allergic conjuntivitis pathophysiology
Airborne allergen > mast cell IgE binding (type 1) > degranulation > histamine/prostaglandin release > eosinophil/basophil attraction
50
Vernal keratoconjuntivitis patho
Type I/IV hypersensitivity reaction, related to atopy (exzema) Antigenic stimulation > lymphocyte activation (T-helper 2) with eosinophil infiltrate Goblet cell increase > MUC5AC increase > abundant mucous
51
Atopic keratoconjuntivitis patho
Inflammatory disorder 20-50 years and male mainly With atopic diseases 95% (dermatitis). Type I/IV hypersensitivity, Reduction in MUC5AC
52
Giant papillary conjuntivitis patho
Mechanical damage to conj. Epithelium > Th2 lymphocyte resonse Allergic component from CL/prosthetic deposits Protein deposits serving as haptens (partial allergens) > type IV delayed hypersentitivity
53
Contact blepharoconjunctivitis patho
Type IV hypersensitivity Partial antigen (hapten) binds proteins forming antigen > langerhans cells (type 2 MHC) present antigen to T helper 1 in lymph > T cells sensitize (week-months) > T cell present to ocular surface > cytokine/inflammatory cell accumulation Unlike SAC/PAC, reaction to agent takes 2-3 days instead of 2-3 hours
54
Mycotic keratitis
Attach via adhesins > proteolytic enzyme secretion allow invasion of stroma Filamentous (Fusarium): feathery infiltrate Yeast-like (Candida): button infiltrate Usually from CL biofilm
55
Acanthamoeba keratitis:
Rare protist corneal infection Present in air, soil, fresh/tap water, hospital equipment, chlorinated pools 80% from CL wear (night/extended/submerged)
56
Acanthamoeba keratitis patho
Attach to epithelial glycoproteins upregulated from damage Pass membrane via cytolytic compounds Protease release > ring infiltrate Target corneal nerves > pain Form cyst during immune response > dormant
57
Contact lens hypoxia patho
Decreased O2 flow > anaerobic metabolism > less ATP / lactic acid increase > dysfunction of endothelial pump / low pH > water influx > oedema/neovascularisation/weakened immune
58
Contact lens induced red eye: infective
Colonisation of gram negative bacteria on CLs (pseudomonas aeruginosa common) > exotoxin release > antigen-antibody immune response > inflammatory cascade > immune cell influx > conjunctival dilation Severe pain, photophobia, tearing, hyperaemia, corneal infiltrates
59
Contact lens induced corneal ulcer
Colonisation of gram positive bacteria (streptococci) on CLs > exotoxin release > antigen-antibody immune response > macrophage/neutrophil influx to cornea
60
Contact lens microbial keratitis increased risks
Epithelial stress from hypoxia or poor tear film/ocular surface Corneal micro-trauma Microbe colonisation of CLs from poor hygiene
61
Bacterial keratitis patho:
Weakened corneal defense > stromal invasion/proliferation > leukocytic enzyme degrade stromal collage > immune influx form infiltrate Commonly S. Aureus > Trauma Or Pseudomonas aeruginosa > CLs
62
Bacterial keratitis risk factors:
CLs Surgery/truma Ocular surface disease (DED) Infection (viral) Lid closure dysfunction Immunosupression (malnutrition)
63
Thyroid eye disease:
Secondary to graves disease (25-50%) IgA antibodies react with similar antigens in orbit tissue > infiltration of T-cells > orbit fibroblast activation > proliferation/glycosaminoglycan deposition > EOM / fat swelling (GAGs bind to water) May lead to IOP increase and ON compression Late stage (2y) > degeneration of muscles > myopathy/diplopia
64
Graves disease
Autoimmune IgG antibody production targeting thyroid stimulating hormone receptor (TSHR) TSHR activation > increased thyroxine (T4) > hyperthyroidism Causes weight loss, sweating, heat intolerance, fatigue
65
TED manifestations:
Proptosis: orbit tissue / EOM swelling > incomplete lid closure EOM dysfunction: fibroblast activity > fibrosis > dysfunction Sup. Inf. Lid retraction: inflammation and fibrosis of Sup. Levator and Inf. Rectus Optic neuropathy: compression of ON
66
Multiple sclerosis risks:
Genetics (HLA-DR2), Epstein-Barr reactivation, smoking, low Vit D
67
Multiple sclerosis patho
Auto-reactive T cells against myelin > microglia/macrophage break myelin > immune response > nerve damage Plaques are formed with remyelantion > slowed conduction/axonal loss Affects CNS, mainly optic nerve
68
MS presentation:
RAPD Optic neuritis Nystagmus
69
Retinal vein occlusion risks
Hypertension (5x likely) Diabetes Stroke Smoking
70
Central retinal artery occlusion clinical presentation:
Sudden painless unilateral loss of vision Whitening of retina with red macula (cherry red spot) Plaque breakoff from large artery (carotid)
71
AMD description:
Progressive, irreversible loss of central vision Drusen, retinal/RPE atrophy, choroidal neovascularisation
72
Causes of AMD
Stress from age Oxidative damage (from light exposure) Carcinogenic damage (smoking) Blood dysregulation (fat/cholesterol) Lack of antioxidant intake
73
Drusen sizes
Small > 63um Intermediate > 125um Large < 125um
74
Dry AMD pathophysiology:
Age > poor RPE metabolism of photoreceptor OS > Lipofuscin deposits in RPE (undegradable): > ROS production (light/O2 presence) > Antioxidant loss (age) > mitochondrial damage > Ischemia Age > Loss of ubiquitin pathway > Decreased protein degregation by ubiquitin> buildup of protein lipid/lipofuscin/complement deposit near bruch's membrane Drusen develops at macula Bruchs membrane deposit > local activation of complement > inflammatory influx > Drusen build-up > Bruch's degeneration > barrier to nutrient influx > ischemia > RPE apoptosis
75
Wet AMD pathophysiology:
RPE ischemia / inflammatory influx > Complement factor activation > PRE secretion of VEGF > Choroidal neovascularisation (CNV)
76
Lipofuscin pathophysiology:
Hypertension/carotid plaque/oxidative damage > Atherosclerosis (accumulation of cholesterol plaque) > altered choroidal circulation > incomplete digestion of outer photoreceptor shedding > accumulation in RPE
77
Diabetic retinopathy pathophysiology:
DM > Hyperglycemia > BV dilation (autoregulation)/Pericyte loss (capillary structure loss) > microaneurysm > vessel occlusion > retinal ischemia > Hypoxia-inducible factor 1 activation > VEGF increase > neovascularization > BRB loss > vit hemorrhage / macula oedema
78
Epiretinal membrane pathophysiology:
Ageing vitreous > liquification > Posterior vitreous detachment (PVD) > dehiscence in internal limiting membrane > microglial cell migration to preretinal surface > microglial interaction with hyalocytes/laminocytes > differentiation to epiretinal membrane
79
Retinitis pigmentosa definition:
Group of inherited disorders with progressive degeneration of rod and cone PRs Leads to gradual loss of global vision
80
RP patho
Mutations altering rhodopsin / RPE molecules > associated protein defects for PR structure/phototransduction/visual cycle/transport Dysfunction > poor phototransduction > cell initiated PC apoptosis > nyctalopia / VF constriction RPE dysruption > retinal remodeling
81
Retinal remodelling in RP:
RPE stress > Hyperplasia / migration to inner retina > bony spicules Glial cell migration / proliferation > disc pallor (whitening) PR loss > less O2 demand > vessel attenuation BRB loss > fluid leakage > macula oedema
82
RP genes
Autosomal dominant (mild) > usually RHO X-linked (severe) > usually RPGR Autosomal recessive (moderate) > Usually EYS

KHIO 1 VIVA (5 decks)

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