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OPTO3003 > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

The emmetropisation mechanism:

A

Hyperopic defocus decreases amplitude of response from retinal cells
Altered signal communication through RPE and choroid to sclera
Gene expression in scleral fibroblast altered
Scleral ECM remodelled, increasing scleral creep rate
Axial elongation > decreased hyperopic defocus

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2
Q

Theories for myopia development:

A

Dopamine theory: Decreased sun > poor activation of dopamine receptors in sclera > myopic development
Hyperopic defocus theory: peripheral hyperopic defocus (accom lag from near work) > axial elongation to resolve peripheral blur > foveal blur

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3
Q

Hyperopia pathophysiology:

A

Product of poor emmetropisation (commonly 0.5D)
Genetic factors/environment > dysfunction of signalling loop

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4
Q

Consequences of uncorrected hyperopia:

A

Anisometropia (different refractive error) > poor development of visual pathway > amblyopia
Excess accommodation > over convergence (near triad) > esophoria greater at near > strabismus / diplopia > amblyopia

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5
Q

Accommodation process in latent hyperopia:

A

Blur signal received by visual cortex > bilateral Edinger Westphal nuclei (CN3 oculomotor) in midbrain > preganglionic parasympathetic fibres move with CN3 to ciliary ganglion to synapse to postganglionic neurons > neurons travel with CNV1 ciliary nerves to ciliary muscle and pupillary sphincter muscle > activation of muscarinic receptors by Ach > contraction of ciliary muscle and sphincter muscle

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6
Q

Helmholtz theory of accommodation (what ciliary contraction does)

A

Contraction > forward movement of muscle, slacking zonules attached to lens > lens bulges naturally > increased curvature/thickness/refractive power > image focus moved forward onto retinal plane.

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7
Q

Convergence process in accommodation:

A

Blur/disparity activates supraocular motor nuclei > innervating oculomotor nuclei > axons sent to medial longitudinal fasiculus > contraction of medial rectus via CN3 > convergence while accommodating

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8
Q

Pupil constriction process in accommodation :

A

Detection of blur in visual cortex > activation of bilateral pretectal nuclei > bilateral Edinger Westphal nuclei > preganglionic parasympathetic nerves with CN3 move to ciliary ganglion > post ganglionic fibres with CNV1 to iris sphincter muscle > contraction of iris

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9
Q

Accomodation reflex mechanism:

A

Hyperopic defocus > LGN/optic radiations > visual cortex in occipital lobe >
CN3 with edinger westphal activation > ciliary ganglion > Accomodation/miosis/convergence

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10
Q

Presbyopia pathophysiology:

A

^ thickness / loss of Ant. Capsule pliability > capsule failure to mould lens
Loss of lens elasticity with constant growth (mitosis) > decreased amplitude of accommodation
Ciliary muscles undergo compensatory hypertrophy (50% stronger than at birth)

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11
Q

Mechanisms of cataract formation:

A

1: Cell proliferation/differentiation disruption (Growth factors)
2: Metabolic disturbance/osmotic regulation (Na/Ca)
3: Calpains
4: Post-translational modification (lens proteins)
5: Oxidative damage
6: Loss of defense mechanisms

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12
Q

Patho of nuclear cataracts:

A

Mechanisms 1-6
1. Na/Ca transport loss > osmotic imbalance > intracellular vacuoles/high-mol-weight aggregates
2. Calpain overactivation > disruption of crystallin structure > light scatter
3. PTM glycation of tryptophan > fluorescent chromophore > brunescence
4. Protein oxidation
5. Cortex-nucleus barrier to glutathione

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12
Q

Patho of cortical cataract:

A

Mechanisms 2/3
Dysfunctional Na/K from damage > NA/K homeostasis loss > Ca/Na influx > overhydration/ calpain activation
Crystallin proteolysis > soluble protein decrease (relative insoluble increase) > ray-like space opacify

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13
Q

Patho of PSC:

A

Mechanism 1
DM / Cort. / age > Change in GF expression (FGF) > aberrant epith. Proliferation at germinative zone
Dysfunctional cells collate with adjacent fibers forming balloon cells
Organelle retintion > Poor Na/K atpase transport > swelling > vacuoles / extracellular granular material

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13
Q

Growth factors in lens mitosis:

A

Fibroblast (FGF)
Epidermal (EGF)
Insulin-like (IGF)
Platelet-derived (PDGF)
Transforming (TGF-beta)

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14
Q

Disturbed cell proliferation in cataracts:

A

Fibroblast growth factor (FGF) stimulates proliferation/differentiation of epithelia (^FGF at equator)
Change in homeostasis of GFs / cytokine-mediated inhibition of production > opaque PSC

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15
Q

Post-translational modification (PTMs) in cataracts:

A

Additive / Subtractive / Neutral PTMs
Crystallin modifications > change in weight/conformation > thiol group exposure > oxidation > disulphide bond formation > aggregation

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15
Q

Metabolic disturbance in cataracts:

A

Altered gene expression > enzyme/GF/membrane protein dysregulation > ATP/ion transport/Ca metabolism/antioxidant dysregulation
Na/K ATPase pump loss > Na influx > water influx (^with membrane protein alteration) > swelling
Altered membrane protein > Ca influx (from ^aqueous conc.) > Ca oxylate crystals/ Ca-protein bonds/ calpain activation/ epithelia differentiation alteration

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16
Q

Calpains in cataracts:

A

Ca activated intracellular cysteine proteases
Decreased calpains > increased damaged protein levels
^Ca > excess activation > proteolysis of crystallin < precipitation of proteins < disorganization of refractive components

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17
Q

Additive PTMs in cataracts:

A

Disease: diabetes (glucose/ascorbate)/renal loss (cyanate)/aging (photo-oxidation products)/steroids (ketoimines) > methylation/acetylation/carbamylation/glycation > molecules added to lens proteins > alteration > aggregation
Polymerization > protein susceptible to photo-oxidation (UV) > modification of protein-bound tryptophan (or glycation) > presence of fluorescent chromophores > brown coloration

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18
Q

Neutral PTMs

A

Isomeration/deamidation > conformation change
Alpha-crystallin (chaperone) isomeration (time related) > loss of b/y crystallin regulation, and aggregation

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18
Q

Subtractive PTMs

A

Proteolysis/cleavage of crystallins > protein precipitate build up
Cleavage of membrane proteins (channel) > ion/glutathione transport dysregulation > vacuole formation/oxidative damage

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19
Q

Other types of cataracts:

A

Congenital (blue dot)
Trauma (Rosette)
Metabolic (myotonic dyst. > Christmas)
Disease (Uveitis > PSC)
Toxic (cort. > modified Na/K)

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19
Q

Loss of defence mechanisms in cataracts:

A

Glutathione/ascorbate (from vit.)/tocopheroles/carotenoids/antioxidant enzymes keep proteins from oxidation.
Age > nucleus-cortex glutathione barrier
Vitreous degeneration (age) / vitrectomy > ascorbate loss > nuclear cat

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19
Q

Systemic disorders in cataracts:

A

Diabetes > ^glucose > conversion to sorbitol by aldose reductase in lens > water influx > lens fiber swelling/rupture > PSC/Cortical opacity
Glycation PTM > aggregation
Sorbitol reduction > antioxidant loss > ^oxidative stress
Diabetes > snowflake cataracts

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19
Q

Vicious cycle:

A

Loss of aqueous or evaporation > hyperosmolarity > epithelial irritation > Mitogen-activated protein kinase (MAPK) & NFkB activation > inflammatory mediator release (IL-1 & TNF-1/MMPs) > Matrix metalloproteinases damage epithelium / goblet cells > epitheliopathy (corneal epithelium loss) > pain > reflex stimulation
ADDE > lack of watering > further hyperosmolarity
EDE > poor lipid layer > watering

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20
Q

Lipid layer:

A

Thin outer meibum layer from sebaceous glands in tarsal plate (Meibomian glands) secreted during blink
Prevent evapouration, acts as surfactant (spreads film)
Non-polar cholesterol, esters, phospholipids, alcohols

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20
Q

Oxidative damage in cataracts:

A

Cortex mitochondria must keep O2 conc. Low in nucleus, crystallin oxidation > high weight aggregate formation > ^RI/scatter/hardening (nuclear sclerosis)
Age* > mitochondrial function loss > ^ROS presence > ^O2/ROS in nucleus
UV filter breakdown/photosensitizer breakdown > ^ROS
Antioxidant loss > decreased O2 consumption > ^O2 exposure of proteins > ^crystallin oxidation
Age > nucleus-cortex antioxidant barrier > glutathione loss > ^nucleus generated oxidative components (H2O2)

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20
Q

Traumatic cataract:

A

Blunt (without capsule rupture) > ant./PS cataract from rapid water influx > opacity (rosette cat)
Opacity will subside if capsule is not ruptured
Heat > IR exposure > glass blowers cat

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21
Q

Aqueous layer Components:

A

Water, electrolytes, proteins, growth factors, pro-inflammatory interleukin cytokines (accumulate during sleep), Lysozyme, lactoferrin, urea, glucose, ions (Ca/Mg/Na/K), IgA

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22
Q

Mucin layer composition

A

Thinnest layer of mucus from goblet cells in conj. / plica semilunaris / glands of henle & Manz
Hydrophilic High mol. Wgt. Mucin glycoproteins (transmembrane or secretory)
Transmembrane mucins bind glycolax from corneal epith.
Secretory are soluble in aqueous forming gel

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23
Q

Lacrimation reflex:

A

Stimulation > CN5 sensation > brainstem > parasympathetic nucleus of CN7 / sympathetic of medulla > lacrimal gland / spinal cord > lacrimal gland

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23
Q

ADDE from secretion stimulation alteration:

A

Reflex hyposecretion from reflex sensory block (CLs/LASIK/herpes/diabetes) or reflex motor block (CN 7 lesion)
Blockage of para/sympathetic nerves to lacrimal gland
Decreased androgen from hormone loss (age)
Exposure to anti depressants/histamines/birth control

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24
Q

Eitology of DED symptoms:

A

Nociception from long/short ciliary of CNV1 from:
Tear breakup > exposure
Mechanical friction from lid/globe
Inflammatory mediators

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24
Q

Meibomian gland dysfunction causes:

A

Drop out (age>50)
Gland replacement (Distichiasis)
Hypersecretory glands (Seborrhea / retinoid therapy)
Gland obstruction
Glaucoma medication (pilocarpine)

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25
Q

BCC patho:

A

UV on puripotent stem cells > mutation > unregulated proliferation of abnormal basal cells

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26
Q

SCC patho:

A

UV > proliferation (^mutation) / gene alteration / immunosupression > p53 / melanocortin-1 receptor gene alteration > unregulated proliferation of squamous epith. w/o apoptosis > dermis invading tumor

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27
Q

SGC patho:

A

Idiopathic > proliferation of sebaceous gland cells > neoplasm of lipid containing cells

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27
Q

Malignant melanoma patho:

A

UV/age/genetics/freckle > Malignant tranformation of intraepidermal melanocytes > atypical melanocyte proliferation

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28
Q

Pingueculum patho:

A

UV/age > degeneration of stromal elastin/collagen

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29
Q

Dilator pupillae muscle:

A

Single layer of myopeithelium (muscle base, epith. Apex) at pupil base.
Innervated via postganglionic sympathetic fibers from sup. Cervical ganglion.
Nerves travel with long ciliary nerves of CN6
*supplied via noradrenaline

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29
Q

UV factors in pterygium formation:

A

Fibrovascular proliferation of degenerative bulbar conj. UV > several causative factors:
Endogenous photosensitiser activation > ^ROS > oxidation breaks ECM > altered collagen/elastin synthesis
^Expression of epidermal GFs > cytokine production (IL-6/8) and MMP-1
Genetic mutations (possible p53)

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30
Q

Pterygium patho following UV:

A

^pro-inflammatory cytokines (IL/TNF-a) > inflammatory influx
Epidermal GF / PDGF > cell proliferation / migration
^expression of pro-angiogenic factors (IL-6/8, VEGF, MMPs) > vascularisaion
^MMPs > ECM remodelling > Bowmans layer breakdown
Lesion invades cornea following bowmans damage

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31
Q

Sphincter pupillae muscle:

A

Circular smooth muscle at inner ring of pupil.
Innervated via post ganglionic parasympathetic fibers from ciliary ganglion.
Nerves travel with CN3 to ganglion, then with short ciliary fibers of CN6
*supplied via ACh

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32
Q

Afferent pupil pathway:

A

Retinal light input > Ganglion cell axions > optic tract > split at chiasm > split before LGN > sup. Colliculus > synapse with olivary pretectal nucleus.
Afferent (retina) / Efferent (midbrain light reflex) signals processed > ipsi/contralateral Edinger Westphal > parasympathetic path.

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32
Q

Parasympathetic pupil pathway:

A

Edinger Westphal > with CN3 (accommodative axons) > cavernous sinus > synapse at ciliary ganglion > with short ciliary via subarachnoid space > iris sphincter > bilateral / equal constriction

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33
Q

Sympathetic pupil pathway:

A

1st neuron: hypothalamus > ciliospinal Centre of bulge and Waller (C8/T2)
2nd: preganglionic fibers pass stellate ganglion (lung apex) > sup. Cervical gang. (jaw)
3rd: postganglionic fibers plexus with carotid > cavernous sinus > SO fiss. With nasociliary of CN5 > long ciliary in suprachoroidal space > dilatory > mydriasis
Also innervate mullers. facial innervation splits before sup. Cervical G.

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34
Q

Adies tonic pupil:

A

Segmental denervation of post gang. Parasym. > sphincter loss > dilation and wormlike light response
Blur in affected eye with light-near dissociation (accomodative response is healthy following aberrant regen)
Caused by viral infections, usually women

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35
Q

Myasthenia gravis:

A

Autoimmune disorder > auto antibodies against Ach receptors of striated muscle > weakness
Causes limb weakness, lack of expression, ptosis +_ diplopia worsening over the day.
Tested via 1minute upgaze, or ice pack for 2m (improves neurotransmission)

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36
Q

Aberrant regen:

A

Adies: acc. Parasym. From ciliary muscle innervate iris sphincter (2 months) > light/near dissociation > reversal of anisocoria greater in dark
CN3 palsy: accom. Parasym. Regenerate denervated pupils > miosis (anisocoria reversal). Regen can come from oculomotor fibers > miosis on different gaze

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37
Q

Follicles and papillae:

A

F: lymphocyte hyperplasia at fornix/tarsal > grey (macrophage) masses > rice grains
P: epith. Hyperplasia w/ infiltrate mast cells/eosinophils/fibroblasts > small tarsal vascular cobblestones

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37
Q

Functions of the conjunctiva:

A

Connect lids to eye (enclosed sac)
Mucin/aqueous production
Immune function (Macrophages, langerhans cells)
Mediates passive/active immunity

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37
Q

Structure of conjunctiva:

A

Epithelium: columnar W/ goblet apocrine glands and langerhan immune cells
Substantia propria: lymphoid layer (neutrophil/mast/Tcells) and fibrous layer (BV/nerves)

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38
Q

SAC/PAC patho:

A

Year long (Periennial) or seasonal allergens > type 1 immediate hypersensitivity
Allergen binds IgE on mast cells > degranulation > release of histamine (itch), prostaglandins (dilation/pain)

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39
Q

Vernal keratoconjuntivitis patho:

A

Allergen exposure usually worse in spring(vernal) > type 1 hypersensitivity
Allergen binds IgE on mast cells > degranulation > release of histamine (itch), prostaglandins (dilation/pain)
Activation of T cells > severe inflammation > diffuse papillary hypertrophy / tarantas dots

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40
Q

Atopic keratoconjuntivitis patho:

A

Allergen exposure (Px usually have many allergens) > type 1 immediate hypersensitivity with type IV delayed hypersensitivity.
IgE > degranulation > histamine/prostaglandin.
Activation/infiltration of T cells > conj. Ciatration (severe inflammation)

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41
Q

Giant papillary conjuntivitis patho:

A

Allergic or mechanical w/atopy (primary) or CLs (secondary)
Type 1 immediate HS reaction from allergens (primary) or antigen deposits on CLs (secondary)
Repeat exposure w/conj. Trauma > type IV basophil HS reaction

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41
Q

CL associated keratitis patho:

A

CLARE/CLPU > inflammation > epithelial break > vulnerable to microbial keratitis
Most commonly P.aeruginosa

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42
Q

Ocular defences:

A

Lids: physical/flushing
Tear film: IgG/A, lactoferrin, lysozyme
Cornea epith.: immunoglobins (IgG/A) defer microbe adhesion
Mucin: trap microbes
Innate immune: complement protein system
Tight junctions: prevent passage

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42
Q

Acanthamoeba patho:

A

Corneal epith. irritation > mannose glycoprotein upregulation > Acan. trophozoites adhere via acanthapodia > protease MIP133 release > epith. Cytolysis > stromal invasion / degregation
Immune neutro/macro. Influx > immune proteases > ring infiltrates
Acan. Cluster nerves > immune/anti-microbial response > form dormant cysts

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43
Q

Antigen-antibody immune response:

A

Pathogen recognition > neutrophil/machrophage influx > bacterium phagocytosis > stromal infiltrate
Bacterial proteases degrade stroma > stromal loss/scarring > corneal perforation

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43
Q

Fungal keratitis patho:

A

Adhesion following epith. Dysfunction > proteolytic enzyme release > epith. Necrosis > stromal collagen dissolution
^size > poor neutophil phagocytosis
Usually present with bacterial co-infection

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44
Q

HZO keratitis process:

A

Varicella zoster initial infection (chickenpox) > rash, flu, pneumonia
VZV moves to dorsal root and cranial nerve ganglia (retrograde transport)
Reactivation > shingles(skin) / HZO(CNV1)

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44
Q

GPC patho (CLs):

A

Allergic response type 1/4 of tarsal conj. To environment antigens adhering to mucus / proteins coating CLs
And/Or
Mechanical trauma of conj. On CKs > activation of mast cells / eosinophils / basophils > cytokine/GF recruitment > fibroblast stimulation > upregulation of collagen/ECM production > papillae formation

44
Q

Microbial keratitis from CLs patho:

A

CL overwear/^Dk/t > epith. microtrauma > CL colonised microbe (P.aeruginosa/acanthamoeba) invasion
Protective glycolax breach > microbe migration > toxin release > antigen-antibody response

44
Q

CL hypoxia patho:

A

Dt/k less than 87(overnight) or 24(daily) > Poor O2 diffusion > hypoxia > anaerobic metabolism > ATP decrease / lactic acid increase > pH decrease / ion pump loss > oedema / immune loss

45
Q

CL neovascularisation patho:

A

Extended wear/sleeping in low Dk/t CLs > poor O2 diffusion > corneal hypoxia > anaerobic metabolism > ATP loss/LA increase > ion pump loss/pH decrease > immune response > growth of conj. Vessels into cornea

45
Q

CL associated dry eye patho:

A

CL causes pre-corneal tear film instability > PCTF disruptions > tear thinning/TBUT loss > mucin increase > tear osmolarity
Poor CL hydration > CL drawing moisture from tears > dehydration

45
Q

Tight lens syndrome patho:

A

Desiccation/steepening of soft CLs during night wear > tightening of lens > loss of lens motion > ocular surface disruption

45
Q

3/9’ staining patho:

A

Mechanical trauma of RGP on limbal conj.
Abnormal bling > altered distribution of tears > desiccation > limbal staining

45
Q

Toxic/allergic conjuntivitis from CLs patho:

A

Poor neutralisation of hydrogen peroxide cleaning agent > chemical toxicity
CL solution preservative absorbtion > chronic solution toxicity
Allergic response to solution preservatives > type 1 immediate / type 4 delayed hypersensitivity reaction

45
Q

HSK reactivation manifestations:

A
  1. Epithelial: dendritic, geographic, metaherpetic ulcer, neurotrophic keratitis
    1. Stromal: stromal necrosis, immune stromal keratitis
    2. Endothelial: disciform/diffuse endothelitis
      AC: Keratouvitis / trabeculitis
46
Q

Contact lens associated acute red eye (CLARE) patho:

A

Gram- bacteria colonisation of CL (P.aeruginosa) > Exotoxin release > antigen-antibody immune response > inflammatory cascade > immune influx (infiltrates) / vessel dilation > sterile corneal inflammation

46
Q

HSK dendritic ulcer:

A

Reactivation > anterograde migration via CNV1 > active viral replication in corneal epithelium
Swollen opaque epith. Cells > punctate keratitis > Desquamation of central cells
Dendritic progression via virus laden terminal bulbs

46
Q

Culture negative peripheral ulcer / contact lens related peripheral ulcer patho:

A

Gram+ bacteria colonisation of CL (S.aureus) > toxin release > antigen-antibody immune response > inflammatory cascade > neurophil/macrophage migration from limbal vessels > sterile inflammation w/epithelial defect / stromal infiltrate

46
Q

Necrotising stromal HSK patho:

A

Live virus in stroma < immune-mediated response > neurtophil/macro. Influx > phagocytosis / proteolytic enzyme release > stromal loss
Dense infiltrates, oedema, necrosis/melting/thinning

47
Q

Geographic / Metaherpetic ulcer patho:

A

G: immunocomp./steroids > extensive viral replication
M: poor epithelial healing of G > damaged epith. Migration
M has no live virus

47
Q

Neurotrophic keratitis patho:

A

Viral migration/inflammation > Nerve damage > neural derived GF loss > devitalised epith. > spontaneous epith. Breakdown
Also caused by antiviral toxicity, immunocomp., HZO, LASIK, diabetic neuropathy
Not related to live virus

47
Q

Immune Stromal HSK patho:

A

Antibody cascade against inactive viral antigens
Nummular infiltrates, oedema, diffuse/focal opacity
Leads to stromal thinning, scarring, opacification, ghost vessels

48
Q

HSK keratouvitis patho:

A

Immune-mediated inflammation from viral particals remining in cornea > Ant. Uveitis w/wo active corneal disease
Flare/collection in trabecular mesh > trabeculitis / aqueous drainage loss > ^IOP
Iris inflammation > synechiae > patchy sectoral iris atrophy
Secondary glaucoma/cataracts

48
Q

Herpes zoster epithelial keratitis:

A

epith. Damage via invasion/replication/cell lysis
Initial punctate epith. Keratitis (several lesions of live virus)
Forms pseudo-dendrites (5d)
Requires 800mg acyclovir 1w

48
Q

Endothelial HSK patho:

A

Inactive viral antigens in endo. Post initial manifestation
Keratic precipitates, stromal oedema, ant. Chamber reaction/flare
Stromal white wessely ring > light haloes
Associated trabeculitis > ^IOP

48
Q

Nummular stromal keratitis from HZO:

A

Antigen-antibody response > stromal neutrophil/macrophages
Several granular infiltrates, usually under epith. Ulcers
Requires FML qid w/ acyclovir 3%

49
Q

HZO keratouveitis:

A

T-cell mediated response in uvea
Causes blur (spasm)
Ant. Chamber flare/cells, iris synechaie, corneal oedema, trabeculitis (or blockage from white BC), iris atrophy
Requires pred-forte 1% per 2h, w/homatropine 2% (reduce spasm pain)

49
Q

Herpes zoster disciform stromal keratitis:

A

Late stage (1mo) from type 1 and 4 hypersensitivity > upregulated immune response
Inflammation of stroma (full depth), immune ring
Limbal vascular keratitis > ^IOP
Requires pred-forte 1% per 2h (opthal)

50
Q

Post-herpetic neuralga

A

50% by 70y
Inflammation/damage of sensory nerves from viral reactivation > dysfunction of unmylenated nociceptors
Light hypersensitivity via mechanical nociceptor stimulation > severe pain (allodynia)
Sporadic pain w/o stimulation

51
Q

Phases of epithelial wound healing:

A

Latent
Migration
Proliferation
Attachment

51
Q

Barriers to corneal wound healing:

A

Nerve loss (DM/HSK) > substance-P/neurotrophic-GF loss
Basement membrane dysfunction (DM) > poor framework
Limbal loss (steven-johnson) > low epith. Production
Ocular surface inflammation (DED) > MMP-9 upregulation > epith. Damage
Lid abnormality > exposure > desiccation
Also hormone imbalance/CLs/malnutrition

52
Q

Epithelial wound healing latent phase:

A

^metabolic activity
Damaged apoptosis
Gap junction loss, desmosome remodelling, hemidesmosome disconnection
Fibronectin matrix forms in lesion to aid migration

53
Q

Epithelial wound healing migration phase:

A

Surrounding cells migrate via filapodia > monolayer
Multilayer migration follows w/ ^glycoprotein synthesis
Migration rate of 0.05mm/h

54
Q

Epithelial wound healing proliferation phase:

A

Proliferation/differentiation > density/structure restoration
Limbal cells produce amplifying cells forming basal layer
Gap/tight junctions reformed

54
Q

Epithelial wound healing attachment phase:

A

Hemidesmosome reattachment
If lesion passes stroma, complex reformation take 1-3mo w/risk of corneal erosions

54
Q

Stromal wound healing:

A

Basement membrane disruption > cytokine influx (IL-1 / TGF-b) > IL-1 activation of kerocytes > differentiation to fibroblasts > migrate to lesion edge
Transforming GF-b activation of fibroblasts > diff. To myofibroblasts containing a-SMA > wound closure
Fibroblasts secrete new collagen/ECM > opacity > ECM organisation via specific apoptosis
Takes 3-4 years to remodel

54
Q

Complications in stromal wound healing:

A

Myofibroblasts apoptosis / fibroblast inactivation > transparent scar
Myofibroblasts can remain > excess ECM > hypercellular scar > refractive changes (a-SMA stress)

54
Q

Sjogrens syndrome:

A

Genetic/environment > autoantibody (anti-Ro/SSA, anti-La/SSB) production > Immune-mediated destruction of targeted exocrine glands > ADDE/Xerostomia (dry mouth)/peripheral neuropathy/joint pain
Associated with RA/Lupus (secondary)

55
Q

Endothelial wound healing:

A

Initial loss of endo. Barrier / pump > water influx to stroma > opacity
Cell migration across lesion > polymegethism (^size) / pleomorphism (shape) > barrier restoration
Response after 6h, progresses at 1mm/day (usual 1w to heal)

55
Q

General process of autoimmune reaction:

A

Genetic predisposition + environmental factors > antigen presentation of self-antigen + faliure of self tolerance > generation of autoantibodies and self-reactive T cells > inflammation and destruction of self tissues

56
Q

Environmental triggers for autoimmunity:

A

Disruption to normal immune regulation > creation/activation of auto reaction
Infections, chemicals/toxins, hormone changes, physical/psych. Stress, compounded with genetic predisposition

56
Q

Adaptive immune process in autoimmune:

A

Antigen presenting cells (dendritic/macro.) endocytose FB > process into peptide antigens > presented to naive CD4+ T cell via MHC on APC surface > Differentiate to T helper cell (Th1/2) > mediate inflammation via cytokines

57
Q

T cells in autoimmune:

A

Th1: cell mediated with TFN and IFN-gamma
Th2: antibody mediated with interleukins

58
Q

Autoantibodies in autoimmune:

A

Self reactive B cells > antibodies against self-antigens > Immune complex deposited in tissue > immune reaction
Common autoantibodies: rhematoid factor (RA), anti-nuclear antibodies in lupus

58
Q

Activation of autoimmune response:

A

Molecular mimicry/self-presenting dendritic cell autoantigen exposure > autoimmune response > inflammatory cascades > cytokine release/macrophage recruitment > tissue damage
Sjogrens syndrome:
Genetic/environment > autoantibody (anti-Ro/SSA, anti-La/SSB) production > Immune-mediated destruction of targeted exocrine glands > ADDE/Xerostomia (dry mouth)/peripheral neuropathy/joint pain
Associated with RA/Lupus (secondary)

59
Q

Giant cell arteritis patho:

A

Systemic vasculitis, usually >50yo women
Autoimmune against adventitial layer of large BV walls > thickening > narrowing of lumen > artery occlusion > infiltration of mononuclear cells in wall > giant cell formation

59
Q

Myathenia gravis:

A

Auto-antibodies block AChR of striated muscle > immune mediated destruction > poor Ach uptake > fatigue

59
Q

Multiple sclerosis patho:

A

Autoimmune against myelin > inflammation/demylination/secondary axonal damage > disrupted conduction
Affects ON, brain, spinal cord

60
Q

Macula hole patho:

A

PVD > persistent vitreofoveal attachment > Ant/Pos traction
OR
Fluid motion in vit. > tangential traction on vitreo-retinal interface
Traction at fovea > pulls muller cell cone from foveal PRs > cystic lesion > dehiscence of cystic cavity > centrifugal displacement of photoreceptors

60
Q

ERM types:

A

Idiopathic: most common, u/>50y, 10% bilateral, 90% w/PVD
Secondary: u/retinal detachment Sx, then disease, trauma, vit. Inflammation, BRB loss

61
Q

T1DM patho:

A

Autoimmune against pancreatic beta cells > insulin loss > systemic hyperglycaemia > vascular damage

61
Q

Graves’ disease patho:

A

Unknown trigger > production of IgG antibodies against thyroid stimulating hormone receptor
Activation of TSHRs > ^thyroid hormone production > hyperthyroidism
Thyroid ophthalmopathy occurs seccondary to Graves’

61
Q

Lamellar macula hole patho:

A

An aborted macula hole
Inner retinal layers lost from foveal PVD but outer photoreceptor layers retained
Continued progression unlikely as vitreofoveolar separation has completed

62
Q

Macula pseudo hole patho:

A

Similar to full-thickness holes
No loss of retinal tissue, with normal foveal thickness
Formed by perifoveal retinal distortion secondary to epiretinal membrane or vitreomacular traction

62
Q

Muller cell cone:

A

Central glial component at fovea, maintains orient and placement of retinal foveal components.

62
Q

CSR description:

A

Central Serous CHORIORETINOPATHY
Accumulation of fluid under retina and/or RPE, causing localised detachment of neurosensory retina and/or RPE

62
Q

HT discription:

A

Hypertension is elevated BP
Stage 1: >140/90 mmHg
2: > 160/100
3: > 180/110
Malignant HT (1%): >200/140
BP = cardaic output*peripheral resistance

62
Q

CSR patho:

A

*idiopathic
Abnormality in choroid/RPE > choroid BV dysfunction > fluid leakage/build-up under RPE > RPE function disruption > local external BRB loss > pooling under retina > neurosensory detachment from RPE

63
Q

HT risks:

A

^heart rate (sympathetic fight/flight)
^blood volume (renal retention)
^BV resistance (arteriosclerosis)
Age, stress, smoking, obesity, physical inactivity

64
Q

TED patho:

A

IgG against TSHRs cross-react with similar antigens in orbit soft tissue fibroblasts/adipocytes (TSHR mRNA)
Cross-reactivity > autoreactive T cells infiltration to orbit fat/muscle (initiation) > T-cells release cytokines stimulating fibroblast proliferation and GAG production > GAG water retention/cellular infiltration > orbit fat/adipocyte/EOM swelling

64
Q

ERM patho:

A

Idiopathic: *PVD > ILM defects > triggering migration/proliferation of glial cells, and proliferation of hyalocytes remaining on ILM
Secondary: *Vit irritation(Sx) > proliferative vitreoretinopathy following liberation / proliferation of RPE and glial cells within vit cavity

65
Q

Essential HT causes:

A

^BP > Arteriosclerosis/Arteriolosclerosis > lumen size loss / ^BV resistance
^BP > Atherosclerosis > atheromatous plaque in intima layer > thrombosis

65
Q

Plaque formation in Atherosclerosis:

A

HT/DM/smoking/obesity > endo. Damage > ^vascular permeability > Leukocyte/lipid adhesion to endo > intima invasion > macro. Phagocytose lipoproteins > lipid-laden foam cells / inflammation > intima smooth muscle proliferation / ^ECM production > atheromatous plaque of leukocyte/lipid/ECM/smooth muscle

65
Q

Late stage atherosclerosis:

A

Plaque enlarges > narrow lumen / ^BV resistance > ^BP
Plaque may rupture > leakage into blood > thrombosis > ^lumen occlusion
Plaque/thrombus may separate > emboli in smaller BV downstream

66
Q

CWS:

A

Microvascular damage > NFL ischemia > NF swelling > adjacent NF compression > ^ischemia/swelling of axons
Swollen axons disrupt spacing > altered refractive composition > visible spot

66
Q

Hypertensive retinopathy stages:

A

Vasoconstrictive
Sclerotic
Exudative
Related conditions > HT choroidopathy, HT optic neuropathy

66
Q

HT sclerotic stage:

A

Chronic ^BP > media BV layer hyperplasia > intima thickening / hyaline degeneration >
^BV attenuation
^BV tortuosity (focal change in wall hardening)
^arteriolar light reflex from thickened wall (copper>silver wiring)
AV nipping (venous compression where AV share adventitial sheath)

67
Q

HT vasoconstrictive stage:

A

HT > Vasocon. Factors (angiotensin II, adrenaline, vasopressin) released > retinal BV ^vascular tone > ^arteriolar narrowing (norm 1:3 > HT 2:3 AV ratio)
Vessels with arteriosclerosis show focal narrowing from loss of elasticity/immobility of hardened wall

67
Q

HT exudative stage:

A

Late stage chronic HT > endo damage > BRB loss >
Microaneurysms (outpouching wall > tight junction strain > leak/haemorrhage)
Retinal/macula oedema/hard exudate
Retinal haemorrhages
Cotton wool spots

68
Q

Retinal haemorrhages in HT:

A

Flame: NFL, bright red, arcuate, pools between axons
More common in HT than DM (BP in NFL arterioles)
Dot/blot: OPL/NFL, small, dark red, round
Damage to pre-venular capillaries, small from intraretinal compression
Pre-retinal / sub-hyaloid: ILM-NFL / ILM-Vit. Hyaloid. Appear as D- / Boat- respectivley
Associated with damaged superficial retinal arterioles

69
Q

Hard exudates in HT:

A

Damaged endo./tight J. > plasma leak in retina > oedema
Fluid “dries” > retained lipid/debris yellow hard exudate > phagocytosed by macro.
Leakage usually self limiting > only hard exudate present on examination

69
Q

Hypertensive choroidopathy patho:

A

Rare, following severe acute ^BP, usually young adult
Choroid BV without autoregulation
HT > ^vasoconstrictive factors > ^^choroid BV constriction > BV/capillary narrowing/occlusion > RPE necrosis (pale patches under retina) > sub-retinal exudates > localised serous RD

70
Q

NAION from HT:

A

Non-arteritic anterior optic neuropathy
HT > blood flow loss in short posterior ciliary arteries > ON ischemia > ganglion cell axon swelling > oedema > loss of visual signal transmission > sudden painless VA loss / colour loss (red desaturation) / RAPD
Similar presentation to AAION (caused by autoimmune arteritis)

70
Q

C/B retinal artery occlusion from HT patho:

A

Atherosclerosis > BV plaque > seperation > emboli (contains cholesterol/CA) travel upstream > occlusion in central/branch artery

70
Q

Hypertensive optic neuropathy:

A

^BV constriction > decreased blood flow in short posterior ciliary arteries > ON ischemia > nerve fibre swelling / axoplasmic stasis
^intracranial pressure (from HT) > ON compression > axoplasmic stasis / swelling
Presents bilateral ON oedema
Late stage > ON atrophy: ganglion cell death > glial proliferation > pale OD

71
Q

C/B retinal vein occlusion in HT:

A

Virchow’s triad > clot(thrombus) in vein > blood flow blockage > ^vein pressure > ^tortuosity/thickening > vein ischemia (deoxygenated blood stasis) > leakage > “blood and thunder” blot/flame haemorrhages, exudates, oedema
Causes sudden painless loss of vision

72
Q

Virchow’s triad:

A

Endothelial injury
Stasis
Hypercoagulable stress
AV nipping > turbulent flow of venous blood > endo. Wall damage / stasis > hypercoagulability / thrombosis formation

73
Q

RPE functions:

A

Transport from choroid/Retina
Tight junctions prevent passive diffusion from choroid
Melanin absorbs light (protect)
Phago. Outer seg. (PR debris)
Produces FGF, PDGF, VEGF, PEDF

74
Q

AMD simple patho:

A

Oxidative/age related damage to PRs/RPE/Bruch’s/Choriocapiliaries
Loss of PRRPEBrMbCC complex symbiotic relationship results in macula degeneration

75
Q

AMD patho for bruchs dysfunction:

A

Progression > soft drusen (>67um) > ^size/confluent > thickening/inflammation > calcification/degeneration of elastin/collagen layers of bruchs > hydrophobic barrier to fluid/nut. > loss between outer retina/choroid

75
Q

AMD patho for RPE loss:

A

Nutrient loss / Drusen reabsorbtion > RPE ischemia / lipofuscin tox > ^dysfunction > apoptosis (seen as hypo/hyperpigmentation)

75
Q

AMD patho for drusen formation:

A

Age/oxidation > dysfunctional metabolism of rod OS (^at macula) > ^metabolic by-products:
Basal laminar deposit (RPE/basement): collagen (cell stress)
Basal linear deposit (inner portion of bruchs): lipid/lippofuscin/complement (soft drusen; pro-inflammatory)

76
Q

AMD patho for atrophic/non-exudative:

A

RPE loss > PR/CC dysfunction > largening chorioretinal geographic atrophy
RPE-produced trophic factor (VEGF) loss > CC atrophy > altered perfusion of choroidal vessels

77
Q

AMD patho for neovascular/exudative:

A

Choroidal BV stenosis / Drusen inflammation > CC toxicity/death > CC perfusion loss > adjacent RPE hypoxia > angiogenic compound production (VEGF) > BV growth stimulation in CC > neovascular membrane (CNV) breaking bruchs > BRB loss > serum leak > PR loss

78
Q

RP remodelling patho:

A

PR loss > RPE dysfunction >
RPE hyperplasia / inward migration (bony spicules)
Glial cell migration/proliferation (ON pallor)
PR loss > O2 consumption loss > BV attenuation
RPE degen. > BRB loss > intraretinal fluid leakage > macula edema

78
Q

Exudative AMD description/causes:

A

10% cases
PR/RPE/BrMb/CC complex insulted by stenosis of choroidal BV, pro-inflammatory response from drusen (CC toxicity)
CC loss > loss of debris exocytosis > drusen formation
Serum leak via lack of tight junctions in ne BV

78
Q

Non-exudative AMD description:

A

90% cases
Initial RPE hyperpigment, large confluent drusen
Followed drusen reabsorbtion > RPE death > hypopigment
End stage of geographic atrophy

78
Q

RP patho:

A

Mutations > altered rhodopsin/RPE/PR-structure/PTD/Visual cycle > Rod PR/RPE dysfunction
Rod apoptosis > RPE dysfunction > retinal remodelling > altered signalling to cone PRs > apoptosis > central vision loss

78
Q

Atypical RP types:

A

Diseases related-to/forms-of RP
Cone-rod dystrophy
RP sine pigmento
Retinitis puncata albescens
Sector RP
Pigmented paravenous chorioretinal atrophy

79
Q

Syndromic RP types:

A

Syndromes associated with RP forms
Bassen-kornweig syndrome
Refsum disease
Kearns-Sayre syndrome
Bardet-Beidel Syndrome
Usher syndrome

79
Q

Most common macular dystrophy:

A

Stargardt disease and fundus flavimaculatus (variations of same condition)
AD mutation in ABCA4 gene > rod OS metabolism dys. > ^RPE lipofuscin
VA 6/60
Round/pisciform yellow flecks on fundus

79
Q

Forms of macula dystrophy:

A

Stargardt disease / fundus flavimaculatus
BEST vitelliform macula dystrophy
Sorsby fundus dystrophy
X-link juvenile retinoschisis
AD drusen

80
Q

BEST vitelliform macular dystrophy patho:

A

Second most common macular dystrophy
Bestrophin gene (BEST1) AD mutation on chromosome 11q13
Altered RPE BEST ion channel > ^metabolic by-product above RPE
^by-product size > CNV / geographic atrophy

80
Q

BEST disease first 3 stages:

A

Pre-vitreliform: abnormal EOG
Vitrelliform: vitrelliform lesion (yellow drusenoid PED) at macula 6/18
Pseudohypopyon: weight of material > inferior PED development

80
Q

BESTs disease stages:

A

Pre-vitelliform stage
Vitelliform stage
Pseudohypopyon stage
Vitelliruptive stage
Atrophic stage

81
Q

Sorsby fundus dystrophy patho:

A

Rare macula dystrophy
AD mutation in TIMP3 > altered inhibition of MMP-3 > by-product buildup in RPE
Characteristic yellow drusen-like deposits along arcades

81
Q

BEST 4/5th stage:

A

Vitrelliruptive: lesion disruption (scrambled egg) 6/60
Atrophic: chorioretinal atrophy at macula > retina thinning > scarring ^6/60

81
Q

X-link juvenile retinoschisis patho:

A

RS1 gene mutation > altered retinoschisin protein secretion from PRs > poor cell-cell adhesion > NFL splitting
Characteristic spoke wheel splits in macula

82
Q

Autosomal dominant drusen:

A

EFEMP1 gene mutation > RPE matrix protein loss > drusionoid deposits
AMD by 20
Increasing drusen at macula > confluence > geographic atrophy/CNV by 50

82
Q

Lebers congenital amurosis patho:

A

Severe AR rod-cone dystrophy in kids
Mutation in RPE65, CRB1, CEP290 > altered phototransduction cycle
Characteristic Franceshetti’s oculodigital sign of eye rubbing > keratoconus/deep set eyes

82
Q

CSNB patho:

A

Congenital stationary night blindness is a group of inherited retinal dystrophies affecting PR/bipolar/phototransduction cascade
Loss of retinal signalling > vision loss / fundus changes / altered ERG

OPTO3003 (18 decks)

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