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PART ONE REVISION. > PATHOLOGY - Diseases > Flashcards

PATHOLOGY - Diseases Flashcards

1
Q

Which virus is the most common cause of conjunctivitis? Which subtype?

A

Adenovirus (DNA) –> mostly belong to subgroup D (A-F classification) –> usually type 8, 19 and 37 –> type 8 is classic cause of EKC

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2
Q

Where are psammoma bodies found?

A

In meningiomas

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3
Q

What is the difference between type 1 HIV and type 2 HIV?

A

Type 1 - urban centre areas, homosexuals and IVDUs
Type 2 - Africa, heterosexually transmitted

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4
Q

What are the different serotypes of chlamydia ? what are they responsible for?

A

A B C - trachoma
D E F G H I J K - genital chlamydia and adult inclusion conjunctivitis

L1 - L3 : lymphogranuloma venereum

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5
Q

Which cell type is responsible for inflammatory corneal damage?

A

polymorphonuclear leukocyte (PMN)s release hydrolytic enzymes that denature protein and cause tissue necrosis

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6
Q

What is the pathogenesis of Sjogren’s syndrome? (3) Which antibody is associated with Sjogren’s?

A
  1. Lymphocytic and T-cell infiltration affecting conjunctival, oral and lacrimal acinar glands
  2. Loss of conjunctival goblet cells and squamous metaplasia and keratinisation in conjunctival epithelium
  3. Impaired secretion of saliva and tears (aqueous component of tear film) - dry eyes/mouth

Antibody: Anti-Rho and Anti-La

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7
Q

What is the immunological pathophysiology behind of rheumatic eye disease?

A

T-cell and immune complex mediated vasculitis

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8
Q

What are the ocular features of rheumatic eye disease? (5)

A
  1. Peripheral corneal ulceration
  2. Corneal melt (MMP release)
  3. Macula oedema
  4. nectrotising scleritis
  5. posterior nodular scleritis
  6. scleromalacia perforans
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9
Q

What is the triad in Behcet’s disease?

A
  1. Oral aphthous ulcers (98%)
  2. Genitcal ulcers (80%)
  3. Ocular disease (70)% - panuveitis with hypopyon
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10
Q

What is the HLA-associated of Behcet’s? What age is most common? What race does it affect predominantly?

A
  1. HLA-B51
  2. 20s-40s
  3. East Asia and Mediterraneans
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11
Q

What is the ocular manifestations of Behcet’s disease?

A

Sudden onset aggresive panuveitis with hypopyon.

  1. Non-granulomatous, necrotising vasculitis with posterior segment complications; BRVO, CMO, vitritis and neovascularisation
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12
Q

What are large vessel disease vasculitis?
What are medium vessel disease vasculitis?
What are small vessel disease vasculitis?

A

LARGE: GCA, Takayasu
MEDIUM: Polyarteritis nodosa, Kawasaki
SMALL: Wegener’s, Churg-Strauss, Henoch Schonlein Purpura

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13
Q

What is sympathetic ophthalmia?

A

Bilateral granulomatous inflammation of the uvea (panuveitis) following injury to one eye, typically involving uveal incarceration in the sclera.

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14
Q

What is the pathophysiology / ocular manifestations of sympathetic ophthalmia

A
  1. Sensitation of ocular antigens leads to uveitis by MHC Class II CD4 T cells
  2. Uveal thickening by macrophage infiltration
  3. Small granulomas (epithelioid giant cells) between Bruch’s and RPE - Dalen Fuch’s nodules (small discrete yellowish infiltrates)
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15
Q

What is the immunological pathophysiology of giant cell arteritis?

A
  1. Local dendritic cells recruit CD4 T cells causing activated macrophages, giant cells, smooth muscle cells recruitment for vascular remodelling
  2. Inflammatory infiltrate includes (1) macrophages (2) multinucleated giant cells (located near fragmented elastic lamina) (3) lymphocytes (4) plasma cells
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16
Q

What vessels are affected in GCA?

A

Fibrin thrombus obstructs vessel lumen

Central retinal artery, ophthalmic artery and cerebral arteries. Arterioles are not affected as they do not possess an elastic layer

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17
Q

What is the cause of granulomatosis with polyangiitis (Wegener’s)? What antibodies are associated with this

A

Granulomatosis inflammation and necrosis

Antibodies: c-ANCA (anti-neutrophil, anti-cytoplasmic antibody)

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18
Q

What is the viral aetiology/pathogens commonly associated with ARN? (4) What is the immune status of the patient generally?

A
  1. VZV
  2. HSV
  3. CMV
  4. EBV

Usually immunocompetent patients

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19
Q

What are the clinical phases in ARN?

A
  1. Acute phase
    - Episcleritis/scleritis
    - Granulomatous uveitis
    - Vitritis
    - Retinitis (peripheral)
    - Viral inclusion bodies seen on light microscopy
  2. Late cicatricial
    - Retinal tears and detachment
    - PVR
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20
Q

What is the difference between progressive outer retinal necrosis and ARN? (3)

A
  1. Usually impacts immunocompromised patients vs immunocompetent patients in ARN
  2. Typically minimal intraocular inflammation, AC and vitreous
  3. Large well-defined white retinal patches which can be peripheral or central
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21
Q

What is VKH? What are the epidemiological factors in VKH?

A

Typically viral illness prodome followed by Bilateral granulomatous panuveitis.

Affects young adults (second and fifth decades), moreso females and heavily pigmented patients

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22
Q

What are the HLA associations with VKH?

A

HLA-DR1 and HLA-DR4

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23
Q

What are the two clinical phases phases in VKH? What is the immunological pathophysiology?

A
  1. Acute granulomatous phase
  2. chronic non-granulomatous phase
  3. Uveal thickening
  4. Lymphocyte infiltration
  5. Epithelioid collections
  6. Dalen-Fuch’s nodules (granulomas/macrophages between RPE and Bruch’s) - also seen in sympathetic ophthalmia
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24
Q

What are the systemic findings in VKH? (5)

A

Dermatological - Alopecia, Vitiligo, Poliosis

Non-dermatological - sensorineural deafness, headache

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25
Q

What are the immunological manifestations of sarcoidosis (4)

A

Sarcoid nodules contain…
1. non-caseating epithelioid histiocytes (granulomas)
2. multinucleated giant cells (granulomas)
3. asteroid bodies
4. Schaumann bodies

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26
Q

What are the ocular manifestations of sarcoidosis (6)

A
  1. Mutton-fat KPs
  2. Trabecular meshwork (Berlin) nodules
  3. Vitreous opacities/snowballs (string of pearls)
  4. Multifocal chorioretinal lesions
  5. Peri-phlebitis
  6. Optic disc nodules/granulomas
  7. Tented peripheral synechiae
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27
Q

What are the sight threatening complications of thyroid eye disease (2)

A
  1. Dysthyroid optic neuropathy
  2. Corneal exposure

It is tendon sparing inflammation

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28
Q

What is the immunological pathogenesis of thyroid eye disease? (5)

A
  1. TSH-receptor antibodies react with orbital fibroblast antigens which have increased IGF-1 receptors –> inflammatory activation
  2. Extraocular muscle perivascular lymphocyte infiltration, tendon sparing swelling in MRI
  3. Accumulation of GAGs in extracellular matrix
  4. Fibroblasts produce mucopolysaccharides which attract water to cause swelling
  5. Patchy infiltration of lymphocytes, monocytes, mast cells and fibroblasts
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29
Q

What is homocysteinuria? Dominant or recessive?

A

Reduced levels of cystathione beta-synthetase, affects methionine

Recessive.

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30
Q

What are the clinical features and ocular pathophysiology of homocystinuria?

A
  1. Lens dislocation - metabolic abnoramlity of zonules with thick band of PAS-positive material of the surface of ciliary processes and pars plana
  2. Thromboembolic risk
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31
Q

What are the ocular manifestations of cystinosis?

A

Abnormal transport of cystine –> birefringent crystals.

Cystine crystals in cornea, retina, choroid, RPE, retina, conjunctiva

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32
Q

What causes corneal arcus?

A

Plasma lipids leak from blood vessels and are deposited into corneal stroma

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33
Q

What causes xanthelasma? Which rare conditions is associated with this

A

Lipid containing macrophages which deposite in the dermis of the eyelid

Erdheim-Chester disease - systemic disease associated with xanthelasma and lipoid granulomas

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34
Q

What causes pinguecula and pterygium?

A

Sun exposure –> elastic fibre degeneration –> elastic material deposition in the conjunctiva –> thickening and hyalinisation of conjunctival stroma –> bulbar nodules (pinguecula) and pterygium which encroaches on the cornea

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35
Q

What are the immunological / pathophysiological manifestations of pterygium?

A
  1. Predominantly basophils and fibroblast proliferation
  2. Absent cystic spaces
  3. Stocker’s line - line of iron at advancing edge
  4. Elastotic degeneration at limbus in interpalpebral fissure
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36
Q

What is the pathophysiology behind macula degeneration? Which complement factor is affected?

A

Fibrous metaplasia of RPE cells leading to collagen deposition following choroidal neovascular leakage and haemorrhage.
Associated with complement factor H gene.

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37
Q

What are the nutrients found in the AREDS study to reduce progression of AMD? (7)

A
  1. Zinc
  2. beta-carotene
  3. Vitamins C & E
  4. B Vitamins
  5. Lutein
  6. Zeaxanthin
  7. Omega-3
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38
Q

What are the two different types of calcification on the cornea? What is their cause

A
  1. Metastatic calcification in hypercalcaemia –> band keratopathy which is calcium deposition in Bowman’s layer - removed in EDTA therapy
  2. Dystrophic calcification in damaged/degenerating tissues seen in phthisis bulbi
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39
Q

What is amyloid? What are its two stains?

A

Insoluble fibrillar glycoprotein deposited in blood vessels and basement membrane as extracellular eosinophilic hyaline material

  1. Congo Red - stains Apple green birefringent
  2. H&E - stains pink (eosin)
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40
Q

What are the ocular manifestations of amyloid? (2)

A
  1. Drusen in AMD
  2. Corneal Lattice dystrophy
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41
Q

What are the systemic associations of amyloid (6)

Which are light chain amyloids?

A
  1. myeloma (monoclonal plasma cell proliferation)
  2. Alzheimer’s (prealbumin)
  3. Thyroid carcinoma (polypeptide hormones)
  4. Chronic inflammation in RA (serum AA protein)
  5. Waldenstrom’s macroglobulinaemia
  6. Mediterranean fever

Light chain
1. Waldenstrom macroglobulinaemia
2. MUltiple myeloma.

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42
Q

What is the pathophysiology behind pseudoexfoliation syndrome?

A

white deposits on lens/ciliary process/ iris surface and inner TM –> sampaoeli’s line on gonioscopy

Granular eosinophilic material with elastin and fibrillin produced by abnormal basement membranes of aging epithelial cells accumulate in trabeculum, lens capsule, iris and ciliary body.

More common in females

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43
Q

What are the epidemiological factors of pigment dispersion syndrome? (2)

A
  1. Commoner in caucasians
  2. Increased risk in myopia due to concavity of mid-peripheral iris which increases contact between peripheral iris and zonules –> mechanical friction and pigment release
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44
Q

What are cotton wool spots?

A

Microinfarctions which cause swollen axonal endings in the retinal nerve fibre layer

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45
Q

What are hard exudates? Where does it form?

A

Eosinophilic masses containing foamy macrophages - formed when underperfusion damages vascular endothelium leading to plasma leakage in outer plexiform layer.

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46
Q

What are microaneurysms?

A

pericyte necrosis secondary to ischaemia which leads to weakening of capillary wall –> bulges or blowouts. These are gradualy filled by basement membrane deposits.

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47
Q

What are the different types of haemorrhages? Where do they occur?

A

Flame haemorrhage : arteriole rupture within blood tracking the nerve fibre layer

Dot haemorrhage: capillary rupture within outer plexiform layer

Blot haemorrhage: capillary bleeding between photoreceptors and RPE

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48
Q

What causes neovascularisation generally in the eye?

A

Ischaemia –> growth from venous side of capillary bed. Vasoformative factors diffuse through vitreous, PC and PC and induce rubeosis iridis and neovascular glaucoma.

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49
Q

What is the pathophysiology behind diabetic retinopathy? (5)

A
  1. Loss of pericytes (contractile cells that wrap aroudn capillaries and are embedded in BM)
  2. thickening of capillary basement membrane of ciliary processes
  3. Degeneration of capillary endothelial cells
  4. Breakdown of inner blood-retinal barrier with leakage to cause formation of exudates, microaneurysms
  5. Vacuolation of iris pigment epithelium
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50
Q

What is the pathophysiology of Coat’s disease? What are the ocular manifestations? Is it unilateral or bilateral?

A

Affects males predominantly –> Abnormal arterial and venous endothelium –> leakage of lipid-rich plasma into retinal and subretinal spac

Causes exudative retinal detachment and vascular abnormalities

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51
Q

What is the pathogenesis of cataract?

A
  1. Lens crystallins break down to albuminoids in response to aging and UV radiation
  2. Tyrosine is released and converted to adrenaline and melanin
  3. Lens pigemtnation progresses from yellow to brown then to black
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52
Q

What are the causes of secondary cataract?

A
  1. Metabolic disturbance
  2. Radiation
  3. Trauma

These all disrupt lens epithelial ionic transport mechanisms causing disorgainsation of lens proteins

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53
Q

What is the genes involved in pathophysiology of primary open angle glaucoma? (3)

A
  1. Myocilin gene (MYOC) on chromosome 1 encodes myocilin involved in trabecular meshwork contractility
  2. Optineurin gene on chromosome 10 involved in exocytosis
  3. ELAM-1 (endothelial leukocyte adhesion molecule) is present which indicates stress response in trabecular meshwork
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54
Q

What is the pathophysiology of primary open angle glaucoma? (3)

A
  1. Increased IOP –> pressure induced ischaemia due to occlusive disease of posterior ciliaries and direct mechanical pressure preventing axoplasmic flow through lamina cribrosa
  2. Prelaminar optic nerve becomes atrophic (macula and papillomacular bundle are spared)
  3. The cup enlarges vertically more than horizontally
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55
Q

What is the pathophysiology of primary closed angle glaucoma? (4)

A
  1. Lens thickening leads to displacement of pupillary part of iris by anterior lens surface
  2. Leads to shallowing of AC and pressure build up behind iris
  3. Iris bombe –> peripheral iris pushing towards TM
  4. Acute pressure increased leads to blocked axoplasmic flow
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56
Q

What is the pathophysiology / immunological process behind secondary open angle glaucoma? (4)

A
  1. Inflammatory cells
  2. Tumour cells
  3. Haemorrhages
  4. Lens matter and macrophages following degenerative rupture of the lens capsule
    - Phacolytic glaucoma - open angle, pseudohypopyon
    - Phacoanalphylactic (phaco-antigenic): autoimmune granulomatous reaction following rupture of the capsule
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57
Q

What are the possible mechanisms behind secondary closed angle glaucoma? (5)

A
  1. Anterior lens displacement by tumour
  2. Anterior and posterior synechiae in uveitis
  3. Rubeotic glaucoma - fibrovascular proliferation in angle due to retinal ischaemia
  4. Malformation of the angle in congenital glaucoma
  5. phacomorphic glaucoma - lens-induced due to mature cataract formation leads to pupillary block
58
Q

What are the main causes of uveitis (6)

A
  1. Idiopathic
  2. Seronegative arthropathies
  3. JIA
  4. Herpes
  5. Sarcoidosis
  6. SLE
59
Q

What gene is usually reponsible for some epithelial and stromal corneal dystrophies ?

A
  1. TGF-B gene in 5q31 chromosome (dominant)
    This is expressed on epithelial and keratocyte membranes and regulates wound healing
60
Q

What are the 7 different epithelial corneal dystrophies?

A
  1. Cogan’s microcystic dystrophy
  2. Cogan’s map-dot fingerprint dystrophy
  3. Meesman’s dystrophy
  4. Labrador keratopathy
  5. Lisch epithelial dystrophy
  6. Gelatinous drop like dystrophy
  7. Epithelial recurrent erosion dystrophy
61
Q

What are the two different Bowman’s layer dystrophies?

A
  1. Reis’Buckler’s dystrophy
  2. Thiel-Behnke dystrophy
62
Q

What are the six main stromal corneal dystrophies?

A
  1. Lattice dystrophy (most common)
  2. Granular dystrophy
  3. Combined granular-lattice dystrophy (Avenilo)
  4. Macular dystrophy
  5. Central cloudy dystrophy of Francois
  6. Central crystalline dystrophy of Schnyder
63
Q

What are the main endothelial dystrophies of the cornea?

A
  1. Iridocorneal endothelial dystrophy
  2. Posterior polymorphous dystrophy
  3. Congenital heriditary endothelial dystrophy
  4. Fuch’s endothelial dystrophy
64
Q

What is the pathophysiology of labrador keratopathy?

A

Epithelial dystrophy.
Golden-yellow keratinoid protein particles beneath epithelium, superficial stroma and Bowman’s layer. Associated with chronic sun exposure.

65
Q

What is the difference between Meesman’s dystrophy and Cogan’s map-dot fingerprint dystrophy?

A

Both epithelial dystrophies

Meesman’s: thickened epithelium and basement membane with electron dense accumulation and microcysts seen in epithelial cells. Discrete, tiny, epithelial vesicles all over cornea, extending to the limbus but more concentrated in the palpebral fissure

Cogan’s map-dot: thickened epithelial basement membrane with fibrillar material between epithelium and Bowman’s layer

66
Q

What’s the difference between Reiss-Buckler’s and Thiel Behnke dystrophy?

A

Both Bowman layer dystrophy.

Reis Buckler’s: Fibrous nodules in reticular like pattern seen in Bowman’s layer. Stains BLUE with Masson Trichrome

Thiel-Benke dystrophy: very similar to Reiss. Subepithelial opacities in a honeycomb pattern, mainly involving the central cornea

67
Q

What genes are implicated in Meesman’s dystrophy?

A

KRT3 (type 1) and KRT12 (type 2)

68
Q

What are the different types of lattice dystrophy? What does it stain?

A

Fine criss-crossing lines in stroma of amyloid deposits. Most common corneal dystrophy.
Type 1: localised to cornea, sparing limbus
Type 2: systemic amyloid deposition, sparing central cornea

Stains conga red, crystal violet and thioflavin T stain.

69
Q

Which corneal dystrophies stain with what material? What is the mneumonic?

A

MARILYN MONROE ALWAYS GETS HER MAN IN LA CITY

Macular Dystrophy
Mucopolysaccharide
Alician Blue
Granular Dystrophy
Hyaline
Masson’s Trichome
Lattice Dystrophy
Amyloid
Congo

70
Q

What are the main differences between lattice and granular dystrophies?

A

lattice: amyloid deposits
granular: hyaline deposits in bowman’s layer and stroma

Lattice: recurs in grafts
Granular: occasionally recurs in grafts

71
Q

What is the pathophysiology of macular dystrophy? What gene is implicated?

A

Only corneal dystrophy which is recessive which affects the CHST6 gene (carbohydrate sulphotransferase gene)

Smudgy snowflake areas and localised forms of mucropolyascarides with acculumation of acidic GAGs due to error in keratan sulphate metabolism

Can affect Descemet’s membrane and endothelium.

Rarely recurs in grafts.

72
Q

What is Avelino dystrophy?

A

Combined lattice-granular dystrophy. Contains amyloid and hyaline deposits

73
Q

What is the pathophysiology of granular dystrophy? What does it stain?

A

Opaque granules with small white sharply demarcated deposits resembling crumbs. Histology shows non birefringent hyaline like bodies. Limbus is typically spared.

Stains with Masson Trichrome

74
Q

What is the difference between central cloudy dystrophy of Francois and central crystalline dystrophy of Scheider?

A

Francois: bilateral polygonal symmetric uniform grey patches, similar to crocodile shagreen

Schnyder: subepithelial crystalline deposits, eventually there is diffuse corneal haze and prominent corneal arcus by the third decade. Associated with systemic hyperlipidaemia, UB1AD1 gene is implicated.

75
Q

What is the pathophysiology and clinical findings of Fuch’s? How does the clinical appearance form?

A

Affects females more than males.
Beaten metal appearance of corneal guttata.

Guttata form by descemet’s membrane becoming multi-laminar and studded with Hassal-Henle-bodies –> Descemet’s thickening which coalesce to form guttatae.

Polymegathism (larger endothelial cells) and loss of hexagonal shape is common.

Associated with POAG.

76
Q

What is the difference between congenital hereditary endothelial dystrophy and posterior polymorphous dystrophy?

A

Congenital: Can be AD or AR and linked to SLC4A11 gene. Findings include vacuolated endothelium and abnormal layer of collagen on descemet’s membrane

posterior polymorphous: AD, mutation in VSX1 homeobox gene. Characterised as vesicles arranged in a linear or grouped pattern.
This can be associated with iris abnormalities and glaucoma

77
Q

Which corneal dystrohpies are associated with glaucoma?

A
  1. Fuch’s
  2. Posterior polymorphous dystrophy
  3. Iridocorneal endothelial syndrome
78
Q

What is the pathophysiology and clinical findings of iridocorneal endothelial syndrome?

A

Unilateral. Beaten bronze endothelial appearance (similar to Fuch’s), with PAS (peripheral anterior synechaie) and polycoria (iris hole formation)

79
Q

What are the main risk factors for proliferative vitreoretinopathy?(6)

A
  1. Large/multiple breaks
  2. Re-detachment
  3. Vitreous Haemorrhage
  4. Iris Trauma
  5. Excessive cryotherapy/laser
  6. Gas or silicon oil
80
Q

What are lincoff’s rules for retinal detachment? (4)

A

2 RULES SUPERIOR, 2 RULES INFERIOR

Rule 1: Superior detachment - primary retinal break lies within 1.5 clock hours below the higher border of detachment

Rule 2: Superior detachment crossing midline (12 o clock) - breaks 1.5 clock hours either side of 12 o clock

Rule 3: Inferior detachment - break originate on side of higher border of detachment

Rule 4: Inferior rhegmatogenous detachment with bullous quality originate from superiorly located break (above horizontal meridian)

81
Q

What is the pathophysiology of mucous membrane pemphigoid? What is the diagnosis?

A

Autoimmune response against basement membrane components - linear deposition of IgG and C3 –> fibrinous scarring and symblepharon of lids and fibrin exudation

82
Q

What diseases are Langhan’s cells found? (3)

A

Horshoe ring of nuclei

  1. GCA
  2. Sarcoidosis
  3. TB
83
Q

What histological findings are seen in sarcoidosis? (3)

A
  1. Langhan’s cells
  2. Asteroid bodies
  3. Schaumann bodies
84
Q

What histological inclusion bodies are seen in CMV?

A

Owl eye inclusion bodies in cytoplasm and nucleus

Cowdry type A inclusion bodies

85
Q

What histological inclusion bodies are seen in HSV/VZV/CMV.

A

Cowdry type A inclusion bodies

86
Q

What histological cells are seen in optic nerve sheath meningioma?

What histological cells are seen in Neurilemmoma (Schwann cell tumour)

A
  1. Meningioma : psammoma bodies, meningothelial cells
  2. Neurilemmoma - verocay bodies
87
Q

What inclusion bodies are seen in cotton wool spots?

A

Cytoid bodies

88
Q

What is a Touton’s cell? What conditions are they seen in ?

A

Proliferation of non-Langhan’s histiocytes - ring of nuclei which enclose central eosinophilic cytoplasm from peripheral clear cytoplasm, formed by fusion of epithelioid cells

Seen in juvenile xanthogranuloma - recurrent hyphaemas and yellow-orange skin papules

89
Q

What are the genes involved in Best disease (vitelliform dystrophy)?

A
  1. BEST1 - bestrophin - a protein channel for chloride movement in RPE
  2. PRPH2 - peripherin 2 - regulates normal photoreceptor function
  3. VMD2 gene

Autosomal dominant

90
Q

What are the clinical findings and symptoms of Best disease (Vitelliform dystrophy). What is the diagnosis?

A

Loss of central acuity

Disc of yellow tissue seen in the macula (egg yolk lesion with satellite lesions) - lipofuscin accumulation in the RPEE/choroid and photoreceptor atrophy

Diagnosis confirmed by electro-oculargram showing reduced Arden ratio (<1.5)

91
Q

What are the early and advanced pathophysiological signs of Stargardt’s disease?

A

Early: lipofuscin and melanin accumulation changes in RPE

Advanced: loss of outer retinal layer and RPE as gliotic retina fuses with Bruch’s membrane

Macular atrophy with small yellow flecks

92
Q

What gene mutation is involved in Stargardt’s disease?

A

ABCA4 transporter (STGD1 gene) - located on chromosome 1 (1q21) - responsible of transport of toxins from photoreceptors

93
Q

What is the pathophysiology in Retinitis pigmentosa?

A

There is an abnormall accumulation of lipofuscin between rod and cone disc spaces

Outer nuclear layer (photoreceptor cell bodies) is lost in the periphery and is replaced by Muller cells. These muller cells fuse with RPE, which react by migrating into inner retina and proliferating, giving classic bone spicule appearance and waxy optic disc pallor.

leads to retinal atrophy, opacification and hyalinisation, and attenuation/narrowing of vessels.

94
Q

What are the ocular symptoms / features of sarcoidosis?

A
  1. uveitis (intermediate most common)
  2. Cicatriacal conjunctivitis
  3. Conjunctival nodules
  4. Dry eyes
  5. Dacroadenitis
  6. Orbital granuloma
  7. Peripheral ulcerative keratitis
  8. Interstitial keratitis
95
Q

What are the most cranial nerve neuropathies in sarcoidosis?

A

Cranial nerve 2 and 7

96
Q

What are the specific lab / blood findings for sarcoidosis? (5)

A
  1. High ACE
  2. High Liver enzymes
  3. High lysozymes
  4. CXR - biltaeral hilar adenopathy
  5. -ve tuberculin
97
Q

Serum AA protein derivative amyloid is implicated with which disease?

A

Rheumatoid arthritis

98
Q

What are the structural causes of CRAO/BRAO? (3)

A
  1. Carotid dissection
  2. Optic disc drusen
  3. Migraine
99
Q

What are the main inflammatory and infective causes of CRAO/BRAO?

A

Inflammatory
1. SLE
2. Polyarteritis nodosa
3. GPA (Wegener’s)
4. Susan syndrome

Infective
1. Lyme
2. TB

100
Q

What are the main embolic / coagulopathic causes of retinal artery occlusions?

A

Embolic: Aorta, carotid ophthalmic
Coagulopathic: Anti-phospholipid, anti-cardiolipin, high homocysteine, oral contraceptive pill

101
Q

Whats the difference between type 1 and type 2 macular telangiectasia?

What is type 3?

A

Type 1: unilateral paravofoveal telangiectasia which is affects young males, does not have loss of central red pigment

Type 2: bilteral parafoveal telangiectasia (most common) which causes reduced reflex, retinal crystalline deposits, foveal atrophy. Occurs due to muller cell defect and linked with high cholesterol

Type 3: Bilateral parafoveal telangiectasia - vasocclusive in nature.

102
Q

What are the main causes of white dot syndromes? (3)

A

Infection: Syphilis, TB
Inflammatory: Sarcoid
Masquerade: Lymphoma

Risk factor: myopia

103
Q

What are the differences between type 1, type 2, type 3 and type 4 CNVs in AMD?

A

Type 1: Sub-RPE (most prevalent) - occult
Type 2: Subretinal (above RPE) - classic / visible
Type 3: Intraretinal at deep capillary plexus
Type 4: Sub-RPE- PCV - affects asian population

104
Q

What are the main differentials of follicular conjunctivitis?

A
  1. Viral (EKC)
  2. Chlamydia
  3. Eyedrop allergy (iopidine)
105
Q

What are the most common symptoms /signs of thyroid eye disease?

A
  1. Conjunctival/eyelid redness
  2. Chemosis and lid swelling
  3. Lid retraction / Lid lag
  4. Proptosis
  5. Exposure keratopathy / restrictive myopathy / optic neuropathy
106
Q

What is the histopathology of a chalazion? Which drug can cause a chalazion?

A

Chronic lipogranulomatous inflammation of the meibomian glands
1. Multinucleate giant cells
2. Lipid-laden epithelioid cells
3. Lymphocytes

Associated with borteomib use (treats multiple myeloma)

107
Q

What are the 5 different subtypes of drusen? What are their characteristics?

A

Hard drusen: well-demarcated made of hyaline

Soft drusen: poorly defined, represents removal of RPE from Bruch’s membrane

Basal laminar - diffuse small drusen

Calcific drusen - refractile drusen seen near RPE atrophic areas

Reticular pseudodrusen (SDDs) - found between inner segment and outer segment junction and RPE, associated with transition to geographic AMD

108
Q

What are the main causes of Roth spots?

A

Roth spot: White centred retinal haemorrhage associated with focal ischaemia.

Haematological: anaemia, thrombocytopaenia, leukaemia

Immune mediated: PAN

Trauma: Birth trauma, NAIs

Other: AV malformations, Ocular ischaemia syndrome, fungal/bacterial infections, hypertension, diabetes, pre-eclampsia

109
Q

What is the pathophysiology of Dry AMD?

WHat are the late stage manifestations? (3)

A

Pigmentary changes occur as RPE cells migrate from Bruch’s membrane to inner retina and increased production of extracellular matrix

Geographic atrophy: confluent areas of atrophy involving photoreceptors and RPE

Neovascular AMD: Growth of abnormal blood vessels in macula region driven by hypoxia-driven VEGFA, released during oxidative stress and complement activation

VEGF-A binds to its receptor VEGFR2 promoting angiogenesis via endothelial cell proliferation pathways

Exudative neovascular AMD: new blood vessels leak, causing fluid accumulation, haemorrhages anf fibrosis

110
Q

What are the findings in pathological myopia?

A

> 6.0 dioptres
1. Progressive, abnormal elongation of the eyeball (>26.5)
2. Degenerative fundus changes
- RPE/choroidal atrophy
- lacquer cracks in Bruch’s membrane
- Subretinal haemorrhage
- CNV

111
Q

What are the causes of leukocoria?

A

CREAM PIGMENT

C - cataracts, Coats
R - retinoblastoma, ROP
E - Endophthalmitis
A - Astrocytic harmartoma
M - myelinated nerve fiber layer
P - persistent foetal vasculature
I - incontinentia pigmenti
G - Granuloma
M - melanoma
E - Exudative vitreoretinopathy (FEVR)
N - Norrie
T - Toxocariasis

112
Q

What are the age-related changes seen in the Cornea? (2)

A
  1. Hassal-Henle warts (peripheral corneal guttata)
  2. Peripheral excrescence of Descemet’s
113
Q

What are the age-related changes seen in the ciliary epithelium?

What are the age-related changes seen in pars plana?

A

Ciliary epithelium: hyperplasia
Pars plana: Teardrop cysts

114
Q

Commotio retinae shows disruption in which retinal layers?

A

Photoreceptor / RPE layers

115
Q

What are the histological cells of snowbanking?

What are contained in vitreous snowballs?

A

Snowbanking: pars plana exudation: Fibroglial cells, lymphocytes

Vitreous snowballs: Epithelioid cells, multi-nucleated giant cells

116
Q

Which cytokine is raised in intermediate uveitis (found elevated in vitreous humor)?

A

IL-6

117
Q

What are the main risk factors for corneal ulcers? (6)

A
  1. CL wearer
  2. Trauma
  3. Poor Ocular Surface
  4. Diabetes
  5. Vitamin A deficiency
  6. Immunocompromised
118
Q

What is the cause of haemorrhagic occlusive retinal vasculitis?

A

Bilatearl haemorrhagic vasculitis with diffuse ischaemia - patients who have been exposed to intraocular vancomycin during cataract surgery

T3 hypersensitivity reaction

119
Q

Which ocular manifestation is Von Hippel Lindau classically associated with?

A

Retinal capillary haemangioma

120
Q

What are the clinical features of type 1 macular telangiectasia?

What are the clinical features of type 2 macular telangiectasia?

A

Type 1
`. Dilatation of temporal macular vasculture, surrounding macula oedema and exudates. No loss of central retinal pigment

Type 2 - Muller cell defect
Reduced foveal reflex, retinal crystalline deposits, pigment hyperplasia and foveal atrophy, right angled ectaic capillaries

OCT features: inner lamellar foveal cavitations, thinned central macula retina

121
Q

What is the main pathogenesis of CRVO?

A

Usually thrombus occluding central retinal vein close to lamina cribrosa within retrolaminar portion of the optic nerve

During times of increased IOP, posterior bowing of lamina may impinge on central retinal vein

122
Q

What is the difference in occlusion site for CRVO vs ischaemic CRVO?

A

Ischaemic: occlusion of both retrolaminar central retinal artery and central retinal vein, posterior to lamina cribosa prior to collateral branching

Non-ischaemic: occlusion of cenral retinal vein at further posterior site which allows normal collateral channels to provide alternative routes of drainage

123
Q

Which conditions are associated with keratoconus? (5)

A
  1. Vernal keratoconjunctivitis
  2. Retinitis Pigmentosa
  3. Retinopathy of Prematurity
  4. Down’s Syndrome
  5. Marfan’s Syndrome
124
Q

What is the most common ocular manifestation for syphilis?

A

Anterior uveitis

125
Q

What are the histological findings in GCA? (4)

A
  1. Chronic inflammation in adventitia
  2. Infiltration of lymphocytes, plasma cells, eosinophils and macrophages
  3. Multinucleate giant cells in internal elastic lamina
  4. Skip lesions
126
Q

Where is the most common site for CRAO?

A

as it emerges from the optic nerve head

127
Q

What are trophozoites?
What are tachyzoites?
What are bradyzoites?

A

Trophozoites - infective form of acanthomoeba repliates via mitosis

Tachyzoites - rapidly infectious/growing form of toxoplasma gondii

Bradyzoites - chronic form of toxoplasma which reside in tissue cysts and persist in hosts

128
Q

What is the prevalence of anti-ACh positive in systemic myaesthenia gravis vs ocular myaesthenia?

A

Systemic: 95%
Ocular: 50%

129
Q

What is the pathophysiology of Behcet’s?

A

Non granulomatous inflammation characterised by diffuse, intense lymphocyte, plasma cell and neutrophil infiltration

130
Q

What is the pathophysiology of cystinosis?

A

Disturbance in membrane transport of cysteine –> accumulation of bi-refringent crystals in conj, cornea, choroid, RPE and retina

131
Q

A right frontal lobe lesion results in

R/L hemiparesis
R/L eye deviation
R/L gaze paresis

A

Left hemiparesis
Right eye deviation
Left gaze paresis

132
Q

Pyogenic response can occur after accumulation of what metal in tissue?

A

Copper

133
Q

What’s the main diagnosis for Behcet’s?

A

Skin pathergy test.

134
Q

What secondary glaucomas are caused by elevated episceral venous pressure? (3)

A
  1. Carotid-cavernous fisture
  2. Sturge-Weber Syndrome
  3. Obstruction of superior vena cava
135
Q

What’s the difference between Lambert Eaton Syndrome and Myaesthenia Gravis?

A

Lambert Eaton: pre-synaptic membrane - repetitive stimulation get stronger

Myaesthenia Gravis: Post-synaptic membrane - reptitive stimulation get weaker.

136
Q

What are the pathological findings of benign hypertension?

What are the pathological findings of malignant hypertension?

A

Benign:
1. Intimal proliferation and hyalisation of muscular media

Malignant
1. Fibrinoid necrosis of small arteries and arterioles

137
Q

Which risk factor is the most important for development and progression of diabetic retinopathy?

A

Duration of diabetes

138
Q

What is the difference between central retinal artery occlusion and central retinal vein occlusion in pathophysiology?

A

CRAO: Emoblus - complete occlusion and total infarction of retinal tissue and no vasoactive factors released to drive neovascularisation

CRVO: Thrombus related, vasoactive factors released –> rubeotic glaucoma (50%)

139
Q

Which growth factors are implicated in diabetic retinopathy?

A
  1. Increased VEGF
  2. Increased placental growth factor (angiogenic)
  3. Decreased PEDF (pigment epithelium growth factor) - anti-angiogenic
140
Q

Which genes are implicated in primary open angle glaucoma? Where are they located?

A

Chromosome 1: Myocilin (contractility of trabecular meshwork)
Chromosome 10: Optineurin

141
Q

Which genes are implicated in primary open angle glaucoma? Where are they located?

A

Chromosome 1: Myocilin (contractility of trabecular meshwork)
Chromosome 10: Optineurin

PART ONE REVISION. (78 decks)

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