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KHIO 1 VIVA > patho > Flashcards

patho Flashcards

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
Q

Melanocytic naevi

A

Proliferation of melanocytes from UV/genetics
Brown plaque, small if congenital / growing if aquired.

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26
Q

SC carcinoma pathophysiology and causes:

A

UV to epithelium> mutation in p53 TS > proliferation of atypical epithelium. Commonly from actinic keratoses
Second most common skin cancer, related to smoking/immunosupression

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27
Q

BC carcinoma pathophysiology can causes:

A

UV to sensitive stem cells > mutation in p53 TS > proliferation of abnormal basal cells
Most common skin cancer, related to smoking/immunosupression

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28
Q

SCC opposed to BCC identification

A

Less common, more aggressive, high metastasis risk
Often with hyperkeratosis (cutaneous horn formation)
Arises from actinic keratoses
Erythematous (red)
Ulcers and bleeds

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29
Q

BCC opposed to SCC identification

A

More common, low metastasis risk
Superficial: Red patch
Nodular: white/pink nodule
Sclerosing: white patch
Ulcerative: pearly rolled edges with vessels and central ulceration

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30
Q

Skin melanoma

A

UV/naevi/caucasian > Malignant proliferation of melanocytes
Flat > raised, varied pigment, irregular boarders, can progress rapidly and bleed

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31
Q

General differentiation for melanoma to naevus on skin

A

A: Asymmetry
B: Boarders irregular
C: Colour variation
D: Diameter >6mm
E: Evolution over time

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32
Q

Conjunctival naevus

A

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

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33
Q

Pterygium

A

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
Q

Pingueculum

A

Age/UV > hyperplasia on interpalpebral conj.
White elevation, usually nasal, does not cross over cornea

35
Q

Conjunctival intraepithelial neoplasia (CIN)

A

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
Q

Conjuntival SCC

A

OSSN, Malignant squamous epithelial cells through basement to stroma
Limbal vascular thickening of conj. May have white plaque, immobile
Metastasises to lymph

37
Q

Conjunctival melanoma

A

Rare melanocyte invasion of stroma, 60yo from PAN, otherwise nevus/de novo.
Pigmented vascular elevation anywhere on conj. Immobile
Metastasises to lymph

38
Q

PAM

A

Melanocytes near basal epitheilum.
Brown pigment, scattered through conj. (usually Caucasian)
Atypia melanocytes =50% risk malignant melanoma

39
Q

Choroidal melanoma

A

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
Q

Choroidal naevi likelihood to from malignancy

A

> 2mm depth
5 mm width (1.5 disk diameters)
Orange lipofuscin (fatty acid/lipid accumulation)
Irregular boarders
Serous RD
Hollow on OCT

41
Q

Lid dishinence (apoptotic neurosis)

A

LPS tendon less from tarsal from rubbing, CLs, age, trauma/surgery
Low lid, high crease, normal range of motion

42
Q

Tonic pupil/ Adie’s

A

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
Q

Myasthenia gravis

A

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
Q

Parasympathetic pathway for iris: q

A

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
Q

Sympathetic pathway for iris:q

A

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
Q

Bacterial conjunctivitis pathophysiology

A

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
Q

Herpes simplex keratitis life cycle

A

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
Q

Herpes Zoster life cycle

A

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
Q

Seasonal/Perennial allergic conjuntivitis pathophysiology

A

Airborne allergen > mast cell IgE binding (type 1) > degranulation > histamine/prostaglandin release > eosinophil/basophil attraction

50
Q

Vernal keratoconjuntivitis patho

A

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
Q

Atopic keratoconjuntivitis patho

A

Inflammatory disorder 20-50 years and male mainly
With atopic diseases 95% (dermatitis).
Type I/IV hypersensitivity, Reduction in MUC5AC

52
Q

Giant papillary conjuntivitis patho

A

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
Q

Contact blepharoconjunctivitis patho

A

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
Q

Mycotic keratitis

A

Attach via adhesins > proteolytic enzyme secretion allow invasion of stroma
Filamentous (Fusarium): feathery infiltrate
Yeast-like (Candida): button infiltrate
Usually from CL biofilm

55
Q

Acanthamoeba keratitis:

A

Rare protist corneal infection
Present in air, soil, fresh/tap water, hospital equipment, chlorinated pools
80% from CL wear (night/extended/submerged)

56
Q

Acanthamoeba keratitis patho

A

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
Q

Contact lens hypoxia patho

A

Decreased O2 flow > anaerobic metabolism > less ATP / lactic acid increase > dysfunction of endothelial pump / low pH > water influx > oedema/neovascularisation/weakened immune

58
Q

Contact lens induced red eye: infective

A

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
Q

Contact lens induced corneal ulcer

A

Colonisation of gram positive bacteria (streptococci) on CLs > exotoxin release > antigen-antibody immune response > macrophage/neutrophil influx to cornea

60
Q

Contact lens microbial keratitis increased risks

A

Epithelial stress from hypoxia or poor tear film/ocular surface
Corneal micro-trauma
Microbe colonisation of CLs from poor hygiene

61
Q

Bacterial keratitis patho:

A

Weakened corneal defense > stromal invasion/proliferation > leukocytic enzyme degrade stromal collage > immune influx form infiltrate
Commonly S. Aureus > Trauma
Or Pseudomonas aeruginosa > CLs

62
Q

Bacterial keratitis risk factors:

A

CLs
Surgery/truma
Ocular surface disease (DED)
Infection (viral)
Lid closure dysfunction
Immunosupression (malnutrition)

63
Q

Thyroid eye disease:

A

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
Q

Graves disease

A

Autoimmune IgG antibody production targeting thyroid stimulating hormone receptor (TSHR)
TSHR activation > increased thyroxine (T4) > hyperthyroidism
Causes weight loss, sweating, heat intolerance, fatigue

65
Q

TED manifestations:

A

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
Q

Multiple sclerosis risks:

A

Genetics (HLA-DR2), Epstein-Barr reactivation, smoking, low Vit D

67
Q

Multiple sclerosis patho

A

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
Q

MS presentation:

A

RAPD
Optic neuritis
Nystagmus

69
Q

Retinal vein occlusion risks

A

Hypertension (5x likely)
Diabetes
Stroke
Smoking

70
Q

Central retinal artery occlusion clinical presentation:

A

Sudden painless unilateral loss of vision
Whitening of retina with red macula (cherry red spot)
Plaque breakoff from large artery (carotid)

71
Q

AMD description:

A

Progressive, irreversible loss of central vision
Drusen, retinal/RPE atrophy, choroidal neovascularisation

72
Q

Causes of AMD

A

Stress from age
Oxidative damage (from light exposure)
Carcinogenic damage (smoking)
Blood dysregulation (fat/cholesterol)
Lack of antioxidant intake

73
Q

Drusen sizes

A

Small > 63um
Intermediate > 125um
Large < 125um

74
Q

Dry AMD pathophysiology:

A

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
Q

Wet AMD pathophysiology:

A

RPE ischemia / inflammatory influx > Complement factor activation > PRE secretion of VEGF > Choroidal neovascularisation (CNV)

76
Q

Lipofuscin pathophysiology:

A

Hypertension/carotid plaque/oxidative damage > Atherosclerosis (accumulation of cholesterol plaque) > altered choroidal circulation > incomplete digestion of outer photoreceptor shedding > accumulation in RPE

77
Q

Diabetic retinopathy pathophysiology:

A

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
Q

Epiretinal membrane pathophysiology:

A

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
Q

Retinitis pigmentosa definition:

A

Group of inherited disorders with progressive degeneration of rod and cone PRs
Leads to gradual loss of global vision

80
Q

RP patho

A

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
Q

Retinal remodelling in RP:

A

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
Q

RP genes

A

Autosomal dominant (mild) > usually RHO
X-linked (severe) > usually RPGR
Autosomal recessive (moderate) > Usually EYS

KHIO 1 VIVA (5 decks)

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