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
2
Q
Where are psammoma bodies found?
A
In meningiomas
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
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
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
6
Q
What is the pathogenesis of Sjogren’s syndrome? (3) Which antibody is associated with Sjogren’s?
A
- Lymphocytic and T-cell infiltration affecting conjunctival, oral and lacrimal acinar glands
- Loss of conjunctival goblet cells and squamous metaplasia and keratinisation in conjunctival epithelium
- Impaired secretion of saliva and tears (aqueous component of tear film) - dry eyes/mouth
Antibody: Anti-Rho and Anti-La
7
Q
What is the immunological pathophysiology behind of rheumatic eye disease?
A
T-cell and immune complex mediated vasculitis
8
Q
What are the ocular features of rheumatic eye disease? (5)
A
- Peripheral corneal ulceration
- Corneal melt (MMP release)
- Macula oedema
- nectrotising scleritis
- posterior nodular scleritis
- scleromalacia perforans
9
Q
What is the triad in Behcet’s disease?
A
- Oral aphthous ulcers (98%)
- Genitcal ulcers (80%)
- Ocular disease (70)% - panuveitis with hypopyon
10
Q
What is the HLA-associated of Behcet’s? What age is most common? What race does it affect predominantly?
A
- HLA-B51
- 20s-40s
- East Asia and Mediterraneans
11
Q
What is the ocular manifestations of Behcet’s disease?
A
Sudden onset aggresive panuveitis with hypopyon.
- Non-granulomatous, necrotising vasculitis with posterior segment complications; BRVO, CMO, vitritis and neovascularisation
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
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.
14
Q
What is the pathophysiology / ocular manifestations of sympathetic ophthalmia
A
- Sensitation of ocular antigens leads to uveitis by MHC Class II CD4 T cells
- Uveal thickening by macrophage infiltration
- Small granulomas (epithelioid giant cells) between Bruch’s and RPE - Dalen Fuch’s nodules (small discrete yellowish infiltrates)
15
Q
What is the immunological pathophysiology of giant cell arteritis?
A
- Local dendritic cells recruit CD4 T cells causing activated macrophages, giant cells, smooth muscle cells recruitment for vascular remodelling
- Inflammatory infiltrate includes (1) macrophages (2) multinucleated giant cells (located near fragmented elastic lamina) (3) lymphocytes (4) plasma cells
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
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)
18
Q
What is the viral aetiology/pathogens commonly associated with ARN? (4) What is the immune status of the patient generally?
A
- VZV
- HSV
- CMV
- EBV
Usually immunocompetent patients
19
Q
What are the clinical phases in ARN?
A
- Acute phase
- Episcleritis/scleritis
- Granulomatous uveitis
- Vitritis
- Retinitis (peripheral)
- Viral inclusion bodies seen on light microscopy - Late cicatricial
- Retinal tears and detachment
- PVR
20
Q
What is the difference between progressive outer retinal necrosis and ARN? (3)
A
- Usually impacts immunocompromised patients vs immunocompetent patients in ARN
- Typically minimal intraocular inflammation, AC and vitreous involvement in ARN, not in PORN.
- Large well-defined white retinal patches which can be peripheral or central
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
22
Q
What are the HLA associations with VKH?
A
HLA-DR1 and HLA-DR4
23
Q
What are the two clinical phases phases in VKH? What is the immunological pathophysiology?
A
- Acute granulomatous phase
- chronic non-granulomatous phase
- Uveal thickening
- Lymphocyte infiltration
- Epithelioid collections
- Dalen-Fuch’s nodules (granulomas/macrophages between RPE and Bruch’s) - also seen in sympathetic ophthalmia
24
Q
What are the systemic findings in VKH? (5)
A
Dermatological - Alopecia, Vitiligo, Poliosis
Non-dermatological - sensorineural deafness, headache
25
What are the immunological manifestations of sarcoidosis (4)
Sarcoid nodules contain...
1. non-caseating epithelioid histiocytes (granulomas)
2. multinucleated giant cells (granulomas)
3. asteroid bodies
4. Schaumann bodies
26
What are the ocular manifestations of sarcoidosis (6)
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
27
What are the sight threatening complications of thyroid eye disease (2)
1. Dysthyroid optic neuropathy
2. Corneal exposure
It is tendon sparing inflammation
28
What is the immunological pathogenesis of thyroid eye disease? (5)
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 (NOT MACROPHAGES)
29
What is homocysteinuria? Dominant or recessive?
Reduced levels of cystathione beta-synthetase, affects methionine
Recessive.
30
What are the clinical features and ocular pathophysiology of homocystinuria?
1. Lens dislocation - metabolic abnormality of zonules with thick band of PAS-positive material of the surface of ciliary processes and pars plana
2. Thromboembolic risk
31
What are the ocular manifestations of cystinosis?
Abnormal transport of cystine --> birefringent crystals.
Cystine crystals in cornea, retina, choroid, RPE, retina, conjunctiva
32
What causes corneal arcus?
Plasma lipids leak from blood vessels and are deposited into corneal stroma
33
What causes xanthelasma? Which rare conditions is associated with this
Lipid containing macrophages which deposite in the dermis of the eyelid
Erdheim-Chester disease - systemic disease associated with xanthelasma and lipoid granulomas
34
What causes pinguecula and pterygium?
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
35
What are the immunological / pathophysiological manifestations of pterygium?
1. Predominantly basophils and fibroblast proliferation
2. Absent cystic spaces
3. Stocker's line - line of iron at advancing edge
4. Elasttic degeneration at limbus in interpalpebral fissure
36
What is the pathophysiology behind macula degeneration? Which complement factor is affected?
Fibrous metaplasia of RPE cells leading to collagen deposition following choroidal neovascular leakage and haemorrhage.
Associated with complement factor H gene.
37
What are the nutrients found in the AREDS study to reduce progression of AMD? (7)
1. Zinc
2. beta-carotene
3. Vitamins C & E
4. B Vitamins
5. Lutein
6. Zeaxanthin
7. Omega-3
38
What are the two different types of calcification on the cornea? What is their cause
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
39
What is amyloid? What are its two stains?
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)
40
What are the ocular manifestations of amyloid? (2)
1. Drusen in AMD
2. Corneal Lattice dystrophy
41
What are the systemic associations of amyloid (6)
Which are light chain amyloids?
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.
42
What is the pathophysiology behind pseudoexfoliation syndrome?
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
43
What are the epidemiological factors of pigment dispersion syndrome? (2)
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
44
What are cotton wool spots?
Microinfarctions which cause swollen axonal endings in the retinal nerve fibre layer
45
What are hard exudates? Where does it form?
Eosinophilic masses containing foamy macrophages - formed when underperfusion damages vascular endothelium leading to plasma leakage in outer plexiform layer.
46
What are microaneurysms?
pericyte necrosis secondary to ischaemia which leads to weakening of capillary wall --> bulges or blowouts. These are gradualy filled by basement membrane deposits.
47
What are the different types of haemorrhages? Where do they occur?
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
48
What causes neovascularisation generally in the eye?
Ischaemia --> growth from venous side of capillary bed. Vasoformative factors diffuse through vitreous, PC and PC and induce rubeosis iridis and neovascular glaucoma.
49
What is the pathophysiology behind diabetic retinopathy? (5)
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
50
What is the pathophysiology of Coat's disease? What are the ocular manifestations? Is it unilateral or bilateral?
Affects males predominantly --> Abnormal arterial and venous endothelium --> leakage of lipid-rich plasma into retinal and subretinal space
UNILATERAL --> Causes exudative retinal detachment and vascular abnormalities
51
What is the pathogenesis of cataract?
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
52
What are the causes of secondary cataract?
1. Metabolic disturbance
2. Radiation
3. Trauma
These all disrupt lens epithelial ionic transport mechanisms causing disorgainsation of lens proteins
53
What is the genes involved in pathophysiology of primary open angle glaucoma? (3)
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
54
What is the pathophysiology of primary open angle glaucoma? (3)
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
55
What is the pathophysiology of primary closed angle glaucoma? (4)
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
56
What is the pathophysiology / immunological process behind secondary open angle glaucoma? (4)
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
57
What are the possible mechanisms behind secondary closed angle glaucoma? (5)
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
What are the main causes of uveitis (6)
1. Idiopathic
2. Seronegative arthropathies
3. JIA
4. Herpes
5. Sarcoidosis
6. SLE
59
What gene is usually reponsible for some epithelial and stromal corneal dystrophies ?
1. TGF-B gene in 5q31 chromosome (dominant)
This is expressed on epithelial and keratocyte membranes and regulates wound healing
60
What are the 7 different epithelial corneal dystrophies?
1. Cogan's microcystic/ map-dot fingerprint dystrophy - microcysts and fingerprints in whorl like pattern.
2. Meesman's dystrophy - mutation in KRT3 gene, tiny epithelial cysts.
3. Labrador keratopathy - crystalline deposits with clear vacuoles on epithelium.
4. Lisch epithelial dystrophy - X -linked whorl like epithelial lesions of clear vacuoles
5. Gelatinous drop like dystrophy - TACSTD2 gene - gelatinous deposits resembling mulberries
6. Epithelial recurrent erosion dystrophy - defect adhesions of epithelial cells to basement membrane.
*Corneal Maps Love Guiding Eyes*
61
What are the two different Bowman's layer dystrophies?
1. Reis'Buckler's dystrophy
2. Thiel-Behnke dystrophy
62
What are the six main stromal corneal dystrophies?
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
What are the main endothelial dystrophies of the cornea?
1. Iridocorneal endothelial dystrophy
2. Posterior polymorphous dystrophy
3. Congenital heriditary endothelial dystrophy
4. Fuch's endothelial dystrophy
64
What is the pathophysiology of labrador keratopathy?
Epithelial dystrophy.
Golden-yellow keratinoid protein particles beneath epithelium, superficial stroma and Bowman's layer. Associated with chronic sun exposure.
65
What is the difference between Meesman's dystrophy and Cogan's map-dot fingerprint dystrophy?
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
What's the difference between Reiss-Buckler's and Thiel Behnke dystrophy?
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
What genes are implicated in Meesman's dystrophy?
KRT3 (type 1) and KRT12 (type 2)
68
What are the different types of lattice dystrophy? What does it stain?
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
Which corneal dystrophies stain with what material? What is the mneumonic?
*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
What are the main differences between lattice and granular dystrophies?
lattice: amyloid deposits
granular: hyaline deposits in bowman's layer and stroma
Lattice: recurs in grafts
Granular: occasionally recurs in grafts
71
What is the pathophysiology of macular dystrophy? What gene is implicated?
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
What is Avelino dystrophy?
Combined lattice-granular dystrophy. Contains amyloid and hyaline deposits
73
What is the pathophysiology of granular dystrophy? What does it stain?
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
What is the difference between central cloudy dystrophy of Francois and central crystalline dystrophy of Scheider?
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
What is the pathophysiology and clinical findings of Fuch's? How does the clinical appearance form?
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
What is the difference between congenital hereditary endothelial dystrophy and posterior polymorphous dystrophy?
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
Which corneal dystrohpies are associated with glaucoma?
1. Fuch's
2. Posterior polymorphous dystrophy
3. Iridocorneal endothelial syndrome
78
What is the pathophysiology and clinical findings of iridocorneal endothelial syndrome?
Unilateral. Beaten bronze endothelial appearance (similar to Fuch's), with PAS (peripheral anterior synechaie) and polycoria (iris hole formation)
79
What are the main risk factors for proliferative vitreoretinopathy?(6)
1. Large/multiple breaks
2. Re-detachment
3. Vitreous Haemorrhage
4. Iris Trauma
5. Excessive cryotherapy/laser
6. Gas or silicon oil
80
What are lincoff's rules for retinal detachment? (4)
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
What is the pathophysiology of mucous membrane pemphigoid? What is the diagnosis?
Autoimmune response against basement membrane components - linear deposition of IgG and C3 --> fibrinous scarring and symblepharon of lids and fibrin exudation
82
What diseases are Langhan's cells found? (3)
Horshoe ring of nuclei
1. GCA
2. Sarcoidosis
3. TB
83
What histological findings are seen in sarcoidosis? (3)
1. Langhan's cells
2. Asteroid bodies
3. Schaumann bodies
84
What histological inclusion bodies are seen in CMV?
Owl eye inclusion bodies in cytoplasm and nucleus
Cowdry type A inclusion bodies
85
What histological inclusion bodies are seen in HSV/VZV/CMV.
Cowdry type A inclusion bodies
86
What histological cells are seen in optic nerve sheath meningioma?
What histological cells are seen in Neurilemmoma (Schwann cell tumour)
1. Meningioma : psammoma bodies, meningothelial cells
2. Neurilemmoma - verocay bodies
87
What inclusion bodies are seen in cotton wool spots?
Cytoid bodies
88
What is a Touton's cell? What conditions are they seen in ?
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
What are the genes involved in Best disease (vitelliform dystrophy)?
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
What are the clinical findings and symptoms of Best disease (Vitelliform dystrophy). What is the diagnosis?
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
What are the early and advanced pathophysiological signs of Stargardt's disease?
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
What gene mutation is involved in Stargardt's disease?
ABCA4 transporter (STGD1 gene) - located on chromosome 1 (1q21) - responsible of transport of toxins from photoreceptors
93
What is the pathophysiology in Retinitis pigmentosa?
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
What are the ocular symptoms / features of sarcoidosis?
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
What are the most cranial nerve neuropathies in sarcoidosis?
Cranial nerve 2 and 7
96
What are the specific lab / blood findings for sarcoidosis? (5)
1. High ACE
2. High Liver enzymes
3. High lysozymes
4. CXR - biltaeral hilar adenopathy
5. -ve tuberculin
97
Serum AA protein derivative amyloid is implicated with which disease?
Prealbumin derivative amyloid is implicated with which disease?
Polypeptide derivative amyloid is implicated in which disease?
Serum AA: Rheumatoid arthritis
Prealbumin: Alzheimer's
Polypeptide: Thyroid carcinoma
98
What are the structural causes of CRAO/BRAO? (3)
1. Carotid dissection
2. Optic disc drusen
3. Migraine
99
What are the main inflammatory and infective causes of CRAO/BRAO?
Inflammatory
1. SLE
2. Polyarteritis nodosa
3. GPA (Wegener's)
4. Susan syndrome
Infective
1. Lyme
2. TB
100
What are the main embolic / coagulopathic causes of retinal artery occlusions?
Embolic: Aorta, carotid ophthalmic
Coagulopathic: Anti-phospholipid, anti-cardiolipin, high homocysteine, oral contraceptive pill
101
Whats the difference between type 1 and type 2 macular telangiectasia?
What is type 3?
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
What are the main causes of white dot syndromes? (3)
Infection: Syphilis, TB
Inflammatory: Sarcoid
Masquerade: Lymphoma
Risk factor: myopia
103
What are the differences between type 1, type 2, type 3 and type 4 CNVs in AMD?
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
What are the main differentials of follicular conjunctivitis?
1. Viral (EKC)
2. Chlamydia
3. Eyedrop allergy (iopidine)
105
What are the most common symptoms /signs of thyroid eye disease?
1. Conjunctival/eyelid redness
2. Chemosis and lid swelling
3. Lid retraction / Lid lag
4. Proptosis
5. Exposure keratopathy / restrictive myopathy / optic neuropathy
106
What is the histopathology of a chalazion? Which drug can cause a chalazion?
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
What are the 5 different subtypes of drusen? What are their characteristics?
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
What are the main causes of Roth spots?
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
What is the pathophysiology of Dry AMD?
WHat are the late stage manifestations? (3)
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
What are the findings in pathological myopia?
>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
What are the causes of leukocoria?
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
What are the age-related changes seen in the Cornea? (2)
1. Hassal-Henle warts (peripheral corneal guttata)
2. Peripheral excrescence of Descemet's
113
What are the age-related changes seen in the ciliary epithelium?
What are the age-related changes seen in pars plana?
Ciliary epithelium: hyperplasia
Pars plana: Teardrop cysts
114
Commotio retinae shows disruption in which retinal layers?
Photoreceptor / RPE layers
115
What are the histological cells of snowbanking?
What are contained in vitreous snowballs?
Snowbanking: pars plana exudation: Fibroglial cells, lymphocytes
Vitreous snowballs: Epithelioid cells, multi-nucleated giant cells
116
Which cytokine is raised in intermediate uveitis (found elevated in vitreous humor)?
IL-6
117
What are the main risk factors for corneal ulcers? (6)
1. CL wearer
2. Trauma
3. Poor Ocular Surface
4. Diabetes
5. Vitamin A deficiency
6. Immunocompromised
118
What is the cause of haemorrhagic occlusive retinal vasculitis?
Bilatearl haemorrhagic vasculitis with diffuse ischaemia - patients who have been exposed to intraocular vancomycin during cataract surgery
T3 hypersensitivity reaction
119
Which ocular manifestation is Von Hippel Lindau classically associated with?
Retinal capillary haemangioma
120
What are the clinical features of type 1 macular telangiectasia?
What are the clinical features of type 2 macular telangiectasia?
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
What is the main pathogenesis of CRVO?
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
What is the difference in occlusion site for CRVO vs ischaemic CRVO?
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
Which conditions are associated with keratoconus? (5)
1. Vernal keratoconjunctivitis
2. Retinitis Pigmentosa
3. Retinopathy of Prematurity
4. Down's Syndrome
5. Marfan's Syndrome
124
What is the most common ocular manifestation for syphilis?
Anterior uveitis
125
What are the histological findings in GCA? (4)
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
Where is the most common site for CRAO?
as it emerges from the optic nerve head
127
What are trophozoites?
What are tachyzoites?
What are bradyzoites?
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
What is the prevalence of anti-ACh positive in systemic myaesthenia gravis vs ocular myaesthenia?
Systemic: 95%
Ocular: 50%
129
What is the pathophysiology of Behcet's?
Non granulomatous inflammation characterised by diffuse, intense lymphocyte, plasma cell and neutrophil infiltration
130
What is the pathophysiology of cystinosis?
Disturbance in membrane transport of cysteine --> accumulation of bi-refringent crystals in conj, cornea, choroid, RPE and retina
131
A right frontal lobe lesion results in
R/L hemiparesis
R/L eye deviation
R/L gaze paresis
Left hemiparesis
Right eye deviation
Left gaze paresis
132
Pyogenic response can occur after accumulation of what metal in tissue?
Copper
133
What's the main diagnosis for Behcet's?
Skin pathergy test.
134
What secondary glaucomas are caused by elevated episceral venous pressure? (3)
1. Carotid-cavernous fisture
2. Sturge-Weber Syndrome
3. Obstruction of superior vena cava
135
What's the difference between Lambert Eaton Syndrome and Myaesthenia Gravis?
Lambert Eaton: pre-synaptic membrane - repetitive stimulation get stronger
Myaesthenia Gravis: Post-synaptic membrane - reptitive stimulation get weaker.
136
What are the pathological findings of benign hypertension?
What are the pathological findings of malignant hypertension?
Benign:
1. Intimal proliferation and hyalisation of muscular media
Malignant
1. Fibrinoid necrosis of small arteries and arterioles
137
Which risk factor is the most important for development and progression of diabetic retinopathy?
Duration of diabetes
138
What is the difference between central retinal artery occlusion and central retinal vein occlusion in pathophysiology?
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
Which growth factors are implicated in diabetic retinopathy?
1. Increased VEGF
2. Increased placental growth factor (angiogenic)
3. Decreased PEDF (pigment epithelium growth factor) - anti-angiogenic
140
Which genes are implicated in primary open angle glaucoma? Where are they located?
Chromosome 1: Myocilin (contractility of trabecular meshwork)
Chromosome 10: Optineurin
141
Which genes are implicated in primary open angle glaucoma? Where are they located?
Chromosome 1: Myocilin (contractility of trabecular meshwork)
Chromosome 10: Optineurin
142
What antibodies in myaesthenia are found more often in thymoma and are a marker of more severe MG?
Striational Abx
143
Which myaesthenia Abx are more specific for ocular MG? Which Abx are less specific for ocular MG?
ACh-R - 50-70% of ocular MG.
MUSK - less likely to have ocular MG.
144
What is contained within a dermoid cyst? Which condition is it associated with?
1. Contains ectodermal tissue: skin, hair, fat, sebaceous glands
2. Choristoma: normal tissue in abnormal location
3. Associated with Goldenhar's syndrome.
145
What are the ocular manifestations of Wegener's (GPA)? (3)
1. Scleritis
2. Corneascleral ulceration
3. Orbital mass.
146
What is are the symptoms and histological findings of Juvenile Xanthogranuloma?
Symptoms
1. Recurrent hyphaemas
2. Multiple yellow papules on skin
Histological finding
1. Touton cells (fusion of epithelioid cells (macrophages surroudned by foamy cytoplasm)
147
What cells are present in granulomatous / mutton fat KPs?
What cells are present in non-granulomatous KPs?
Mutton fat: macrophages
Non-granulomatous KPs : lymphocytes and polymorphonuclear leukocytes
148
Which corneal stromal dystrophy is associated with signs of systemic hyperlipidaemia such as arcus / xanthelasma?
Central crystalline dystrophy --> intrastromal accumulation of cholesterol crystals.
149
Asteroid hyalosis is associated with what systemic condition?
Diabetes.
150
Which area of retina is last to be perfused in a premature infant?
Temporal retina is last.
151
Where is the most common location for cerebral aneurysm with a third nerve palsy?
Junction of posterior communicating artery and internal carotid artery.
152
Medial hyperplasia of the retinal vasculature is seen in which condition?
Hypertensive retinopathy.
