Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology > Disease entities > Flashcards

Disease entities Flashcards

(56 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

VKH - acute granulomatosis reaction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Vogt-Koyanagi syndrome

A

 Chronic severe anterior uveitis
 Alopecia
 Poliosis
 Vitiligo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Harada’s disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

sight threatening complications of thyroid eye disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

cystinosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

aging and degeneration - hyalinisation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

aging and degeneration - elastic fibre degeneration

Study These Flashcards
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

Study These Flashcards
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
aging and degeneration - macular degeneration
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
age related changes
cornea: hassal-henlewarts, peripheral excrescnes of descements ciliary epithelium hyperplasia retina: periheral micoscytoiud degeneration
27
calcification
 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
amyloid
 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
types of amyloid
1. Systemic - light chain derived OR serum AA protein derived 2. localised
30
systemic amyloid
 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
localised amyloid
 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
occular associations with amyloid
Solitary nodule in eyelid, orbit, conjunctiva Amyloid deposition in choroid and vitreous in systemic amyloidosis Amyloid deposition in cornea Characteristic of lattice dystrophy
33
pseudo-exfoliation syndrome
 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
pigment dispersion syndrome
 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
cotton wool spots
microinfarctions cause swollen axonal endings
36
hard exudate
underperfusion damages vascular endothelium leading to plasma leakage into the outer plexiform layer. These exudates are eosinophilic masses containing foamy macrophages
37
micro-aneurysms
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
flame haemorrhages
arteriole rupture with blood tracking the nerve fibre layer
39
dot haemorrhages
capillary rupture within the outer plexiform layer
40
blot haemorrhages
capillary bleeding between the photoreceptors and RPE
41
neovascularisation
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
diabetic retinopathy
 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
coat's disease
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
cataract
 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
secondary cataract
related to metabolic disturbance, radiation or trauma may disrupt lens epithelial ionic transport mechanisms causing disorganisation or lens proteins
46
conditions associated with keratoconus
retinitis pigmentosa vernal keratoconjuncitivs ROP down's syndrome and marfans
47
Cuases of leukocoria
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
Primary open angle glaucoma
 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
Genes associated with POAG
 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
secondary open angle glaucoma
angle obstruction by  Inflammatory cells  Haemorrhage  Tumour cells  Lens matter and macrophages (following degenerative rupture of the lens capsule)
51
lens associated glaucoma
o Phacolytic glaucoma: open angle, pseudohypopyon o Phacoanaphylactic: autoimmune granulomatous reaction following rupture of the capsule
52
primary angle closure glaucoma
 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
secondary closed angle glaucoma
 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
PAC suspect
occludable angle 180 degre normal IOP and disc
55
PAC
ocludable angle +/- increase in IOP or PAS normal optic nerve and no field damage
56
PACG
PAC with optic nerve damage and field loss

Pathology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions