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Pathology > Disease entities > Flashcards

Disease entities Flashcards

1
Q

anaemia pre-op

A

Microcytic anaemia
Iron deficiency anaemia
Thalassaemia
Normocytic anaemia
Anaemia of chronic disease
Macrocytic anaemia
B12 deficiency
Folate deficiency
Alcohol
Hypothyroidism
Sideroblastic anaemia
Condition where iron is available but red
blood cells are unable to incorporate it into
haemoglobin

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2
Q

Sjorgen’s syndrome

A

 Affects the lacrimal gland and accessory lacrimal apparatus (glands of Wolfring
and Krause) and salivary glands
 Lymphocytic infiltrate affecting conjunctival, oral and lacrimal acinar glands and
loss of conjunctival goblet cells
 Impaired secretion of saliva and tears: dry mouth and eyes
 anti-Rho and anti-La antibodies
 Associated with other connective tissue diseases such as RA

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3
Q

rheumatoid eye disease

A

 T-cell and immune complex mediated vasculitis
 Features
 Necrotizing scleritis and scleromalacia perforans
 Peripheral corneal ulceration
 Corneal melt (due to MMP release)
 Macular oedema
 Posterior nodular scleritis (may mimic melanoma)

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4
Q

bechet’s disease

A

 Systemic vasculitis
 HLA-B51
 Prevalent in east Asia and the Mediterranean
 Onset in the second to fourth decades
Triad
 Oral aphthous ulcers (98-99% of patients)
 Genital ulcers (80-87%)
 Ocular disease (70%): panuveitis with hypopyon most commonly
An aggressive, sudden onset panuveitis
 Non-granulomatous, necrotizing, obliterative vasculitis which can cause
posterior segment complications: BRVO, CMO, vitritis, neovascularisation

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5
Q

sympathetic ophthalmia

A

 Bilateral granulomatous inflammation of the uvea (panuveitis) following injury to
one eye typically involving uveal incarceration in the sclera
 Sensitisation of ocular antigens leads to uveitis mediated by MHC-class II CD4 T
cells
 Uvea is thickened by infiltrate of macrophages
 Small granulomas accumulate in the RPE: Dalen-Fuchs nodules (small discrete
yellowish infiltrates in the RPE)

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6
Q

giant cell arteritis

A

Affects cerebral arteries, ophthalmic arteris, posterior ciliary arteries and central retinal arteries
Local dendritic cells recruit and activate CD4 T cells
 These direct the activity of activated macrophages, giant cells, smooth muscle cells
(vascular remodelling)
 Inflammatory infiltrate
 Macrophages and multinucleated giant cells
 Lymphocytes
 Plasma cells
 Giant cells are typically near the fragmented internal elastic lamina
 Fibrin thrombus obstructs vessel lumen
 NB: retinal arterioles are NOT affected as they do not possess an elastic
layer. The CRA, ophthalmic artery and cerebral arteries may be affected
 No antibodies have been detected in GCA

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7
Q

granulomatosis with polyangitis (wegener’s)

A

 Granulomatous inflammation and necrosis
 Ocular manifestations: scleritis, corneoscleral ulceration and orbital mass
 c-ANCA (antineutrophil, anticytoplasmic antibody) positive in >90% of patients
with generalised Wegener’s

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8
Q

acute retinal necrosis

A

 Viral aetiology: most commonly VZV, but also HSV. Rarely CMV and EBV
perhaps
 Immunocompetent patients (compare to CMV retinitis which typically affects the
immunocompromised)
 Clinical phases
 Acute herpetic
o Granulomatous uveitis
o episcleritis/scleritis
o Vitritis (often severe)
o Retinitis (typically peripheral, compared to the posterior pole retinitis seen
in CMV). Viral inclusion bodies can be seen on light microscopy
 Late cicatricial
o Retinal tears and detachment
o PVR
 Treatment: aciclovir or valaciclovir

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9
Q

progressive outer retinal necoriss

A

 Part of a spectrum of herpetic retinopathies continuous with ARN
 Rapidly progressive
 Immunocompromised patients
 Again, typically caused by VZV, or HSV
 Key feature: minimal intraocular inflammation
 Typically no AC reaction or vitritis
 Large, well-defined patches of white retinal opacification consistent with deep
necrosis
 Peripheral or central
 Multifocal
 Retinal vasculopathy: sheathing and occlusion
 Late staining on FFA
 Retinal detachment

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10
Q

vogt-koyangi-harada (VKH)

A

 Bilateral granulomatous panuveitis
 Young adults (second and fifth decades)
 Predominance in heavily pigmented patients
 Female predominance
 HLA-DR1 and HLA-DR4

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11
Q

VKH - acute granulomatosis reaction

A

 Uveal thickening
158
 Lymphocytic infiltrate
 Epithelioid collections
 Dalen-Fuch’s nodules: granulomas between RPE and Bruch’s

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12
Q

Vogt-Koyanagi syndrome

A

 Chronic severe anterior uveitis
 Alopecia
 Poliosis
 Vitiligo

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13
Q

Harada’s disease

A

 Harada’s disease
 Bilateral exudative uveitis
 CSF pleocytosis

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14
Q

VKH

A

 Typically a viral illness prodrome leading to an acute uveitis stage
 Serous retinal detachment
 Systemic findings
 Sensorineural deafness
 Headache
 Dermatological effects as above

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15
Q

sarcoidosis

A

 Afro-caribbean patients affected more than whites
 Sarcoid nodules: non-caseating epithelioid histiocytes, multinucleated giant cells,
asteroid bodies and Schaumann bodies
 Second to fifth decades
 Ocular involvement in 25%
 Mutton-fat KPs
 TM nodules
 Vitreous opacities (string of pearls)
 Multifocal chorioretinal lesions
 Peri-phlebitis
 Optic disc nodules
 Bilateral

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16
Q

thyroid eye disease

A

 Immune-mediated condition directed at orbital fibroblasts which have increased
insulin-like growth factor 1 receptors
 TSH receptor antibodies (TRAbs) cross react with orbital fibroblast antigens
resulting in inflammatory activation
 Anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin may also be detected
 Hashimoto’s thyroiditis has a weaker association with eye disease

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17
Q

histopathological changes with thyroid eye disease

A

Extraocular muscle enlargement
Patchy infiltration of lymphocytes, monocytes, mast cells and fibroblasts
Fibroblasts produce mucopolysaccharides which attract water causing swelling
Tendon sparing inflammation

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18
Q

sight threatening complications of thyroid eye disease

A

 Dysthyroid optic neuropathy
 Corneal exposure (keratopathy)
compressive optic neuropathy

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19
Q

homocystinuria

A

 Reduction in levels of cystathione beta-synthetase, affecting methionine (an amino
acid)
 Autosomal recessive
 Features
 Thromboembolic risk
 Lens dislocation: metabolic abnormality of the zonules with a thick band of
PAS-positive material of the surface of the ciliary processes and pars plana

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20
Q

cystinosis

A

 Abnormal membrane transport of cystine
 Ocular manifestations
 Cystine crystals in the cornea, retina, choroid, RPE, retina, conjunctiva
 Bi-refringent crystals

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21
Q

aging and degeneration - hyalinisation

A

replacement of normal cells by an acellular,
collagenous/glycoprotein matrix

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22
Q

aging and degeneration - fatty changes

A

: eg. arcus senilis. Plasma lipids leak from blood vessels and are deposited in
the corneal stroma. Xanthelasma are a feature of macrophages containing lipids
collecting in the eyelid dermis

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23
Q

aging and degeneration - elastic fibre degeneration

A

associated with sun exposure. Pinguecula and
pterygium represent elastic material deposition within the conjunctiva leading to
bulbar nodules (pinguecula) and at the limbus (pterygium) which can encroach on
the cornea

24
Q

aging and degeneration - pterygium

A

most common within the interpalpebral fissure
o Basophils predominate
o Absent cystic spaces
o Stromal elastosis
o Fibroblastic proliferation
o Stocker’s line: a line of iron at the advancing edge
o Conjunctival autografts and topical MMC can be used

25
Q

aging and degeneration - macular degeneration

A

the scarring in disciform macular degeneration is a result of
fibrous metaplasia of RPE cells leading to collagen deposition. This follows
choroidal neovascular leakage and haemorrhage
 Associated with polymorphisms in the complement factor H gene
 The age-related eye disease study (AREDS) found that zinc, beta-carotene,
vitamins C and E reduced the progression of AMD
 Latterly, lutein, zeaxanthin, B vitamins and omega-3 were found to also reduce
progression

26
Q

age related changes

A

cornea: hassal-henlewarts, peripheral excrescnes of descements
ciliary epithelium hyperplasia
retina: periheral micoscytoiud degeneration

27
Q

calcification

A

 Metastatic calcification (occurs in hypercalcaemia)
 Band keratopathy: calcium deposited in Bowman’s layer
o Managed with ETDA (ethylenediaminetetraacetic acid) which chelates
calcium
o Epithelium should be removed to expose calcium in Bowman’s layer
 Dystrophic calcification (occurs in damaged or degenerating tissues)
 Phthisis bulbi

28
Q

amyloid

A

 Insoluble fibrillar glycoprotein deposited around blood vessels and basement
membranes as an extracellular eosinophilic hyaline material
 Stains pink (eosin) with H&E and is ‘apple’ green birefringent when examined
under polarized light with Congo red

29
Q

types of amyloid

A
  1. Systemic - light chain derived OR serum AA protein derived
  2. localised
30
Q

systemic amyloid

A

 Associated with monoclonal plasma cell proliferation eg myeloma,
Waldenstrom’s macroglobulinaemia. Light-chain derived (AL)
 Associated with chronic inflammation eg RA. acute-phase reactant derived
(serum AA protein)
 Derived from polypeptide hormones in thyroid carcinoma
 Derived from prealbumin in Alzheimer’s
 Familial Mediterranean fever

31
Q

localised amyloid

A

 Deposition in endocrine tumours
 Deposition in organs and joints of the elderly including in Alzheimers
 Component of drusen in AMD
 Deposited in the cornea in lattice dystrophy

32
Q

occular associations with amyloid

A

Solitary nodule in eyelid, orbit, conjunctiva
Amyloid deposition in choroid and vitreous in systemic amyloidosis
Amyloid deposition in cornea
Characteristic of lattice dystrophy

33
Q

pseudo-exfoliation syndrome

A

 Age-related systemic disease
 Granular eosinophilic material accumulates throughout the body
 Contains elastin and fibrillin
 Produced by abnormal basem
 ent membranes of aging epithelial cells in trabeculum, lens capsule, iris and
ciliary body
 White deposits on the lens, ciliary processes, iris surface and inner TM
 Secondary open-angle glaucoma in 60% of patients (even if IOP is normal at
presentation)
 Sampaolesi’s line on gonioscopy
 Transillumination defects due to peripupillary atrophy
 More common in females
 Cataract surgery can be challenging due to poor dilation and zonular instability

34
Q

pigment dispersion syndrome

A

 More common in whites than blacks
 Typically bilateral
 Myopia increases the risk: concavity of the mid-peripheral iris (found in myopes
and long AL eyes) increases contact between the peripheral iris and zonules
leading to mechanical friction and pigment release

35
Q

cotton wool spots

A

microinfarctions cause swollen axonal endings

36
Q

hard exudate

A

underperfusion damages vascular endothelium leading to plasma
leakage into the outer plexiform layer. These exudates are eosinophilic masses
containing foamy macrophages

37
Q

micro-aneurysms

A

pericyte necrosis secondary to ischaemia leads to weakening of
the capillary wall leading to bulges or blowouts. Gradually are filled by basement
membrane deposits and can disappear on FFA

38
Q

flame haemorrhages

A

arteriole rupture with blood tracking the nerve fibre layer

39
Q

dot haemorrhages

A

capillary rupture within the outer plexiform layer

40
Q

blot haemorrhages

A

capillary bleeding between the photoreceptors and RPE

41
Q

neovascularisation

A

grow from the venous side of the capillary bed in response to
ischaemia and leak on FFA. If the vitreous is detached they haemorrhage and form
traction bands. Vasoformative factors diffuse through the vitreous, PC and AC to
induce rubeosis iridis and neovascular glaucoma

42
Q

diabetic retinopathy

A

 Loss of pericytes (contractile cells that wrap around capillaries and are embedded
in the BM)
 Thickening of the capillary basement membrane
 Degeneration of capillary endothelial cells and breakdown of the inner bloodretinal barrier with leakage
 Exudates
 Microaneurysms
 Inner nuclear and outer plexiform layers are initially affected and then oedema
spreads to create a cystoid appearance
 Cotton wool spots: nerve fibre ischaemia
 IRMA: irregular segmental growth and dilation of vessels from the venous end of
the circulation into areas of retinal ischaemia
 Hyalinzation of vessels

43
Q

coat’s disease

A

Not hereditary
 Abnormality of arterial and venular endothelium
 Leads to massive leakage of lipid-rich plasma into the retinal and subretinal space
 Exudative retinal detachment
 Vascular anomalies
 Typically unilateral
 Male predominance

44
Q

cataract

A

 Lens crystallins break down to albuminoids in response to aging and UV radiation
 Tyrosine is released and converted to adrenaline and melanin
 Lens pigmentation progresses from yellow to brown and then to black

45
Q

secondary cataract

A

related to metabolic disturbance, radiation or trauma may
disrupt lens epithelial ionic transport mechanisms causing disorganisation or lens
proteins

46
Q

conditions associated with keratoconus

A

retinitis pigmentosa
vernal keratoconjuncitivs
ROP
down’s syndrome and marfans

47
Q

Cuases of leukocoria

A

causes of leukocoria is CREAM PIGMENT:
Cataract, Coats
Retinoblastoma, ROP
Endophthalmitis
Astrocytic hamartoma
Myelinated NFL
Persistent fetal vasculatur
Incontinentia pigmenti
Granuloma
Melanoma
FEVR (Familial EXUDATIVE vitreoretinopathy)
Norrie
Toxocariasis

48
Q

Primary open angle glaucoma

A

 Increases with age
 Increased IOP leads to pressure-induced ischaemia due to occlusive disease of
the posterior ciliaries and direct mechanical pressure preventing axoplasmic
flow through the lamina cribrosa
 The prelaminar nerve becomes atrophic but the macular and papillomacular
bundle are spared
 The cup enlarges vertically more than horizontally

49
Q

Genes associated with POAG

A

 Myocilin gene (MYOC, formerly called TIGR) on chromosome 1 encodes
myocilin involved in the TM cell contractility
 Optineurin (OPTN) gene on chromosome 10 is involved in exocytosis

50
Q

secondary open angle glaucoma

A

angle obstruction by
 Inflammatory cells
 Haemorrhage
 Tumour cells
 Lens matter and macrophages (following degenerative rupture of the lens
capsule)

51
Q

lens associated glaucoma

A

o Phacolytic glaucoma: open angle, pseudohypopyon
o Phacoanaphylactic: autoimmune granulomatous reaction following rupture
of the capsule

52
Q

primary angle closure glaucoma

A

 Also degenerative
 Lens thickening leads to displacement of the pupillary part of the iris by the
anterior lens surface
 This shallows the AC and pressure builds behind the iris
 Iris bombe involved the peripheral iris pushing towards the TM
 The acute pressure increase leads to blocked axoplasmic flow and papilloedema

53
Q

secondary closed angle glaucoma

A

 Anterior lens displacement by tumour
 Anterior and posterior synechiae in uveitis
 Rubeotic glaucoma: fibrovascular proliferation in the angle due to retinal
ischaemia
 Malformation of the angle in congenital glaucoma
 Phacomorphic

54
Q

PAC suspect

A

occludable angle 180 degre
normal IOP and disc

55
Q

PAC

A

ocludable angle +/- increase in IOP or PAS
normal optic nerve and no field damage

56
Q

PACG

A

PAC with optic nerve damage and field loss

Pathology (6 decks)

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