Pathology Flashcards

(62 cards)

1
Q

What is the most common form of brain tumour?

Which tumours spread to brain?

A

Metastasis

lung (most common)
breast
bowel
skin (namely melanoma)
kidney

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2
Q

What is the most common primary brain tumour?

A

Glioblastoma multiforme

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3
Q

What is the imaging of a glioblastoma multiforme?

A

Solid tumours with central necrosis and a rim that enhances with contrast.
Disruption of the blood-brain barrier and therefore are associated with vasogenic oedema.

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4
Q

What is the histology of glioblastoma multiform?

A

Pleomorphic tumour cells border necrotic areas

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5
Q

What is the second most common primary brain tumour?

A

Meningioma

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6
Q

What do meningioma arrise from?

A

Arachnoid cap cells of the meninges and are typically located next to the dura and cause symptoms by compression rather than invasion.

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7
Q

What is the histology of meningioma?

A

Spindle cells in concentric whorls and calcified psammoma bodies

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8
Q

What is a vestibular schwanoma?
Presentation?

A

Benign tumour
Located at cerebellopontine angle

Hearing loss, facial nerve palsy (due to compression of the nearby facial nerve) and tinnitus.

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9
Q

What genetic condition is associated with vestibular schwannoma?

A

NF2 - associated with bilateral vestibular schwannoma

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10
Q

What is the most common brain tumour in children?

A

Pilocytic astrocytoma

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11
Q

What is the histology of a pilocytic astrocytoma?

A

Rosenthal fibres (corkscrew eosinophilic bundle)

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12
Q

What are the features of a medulloblastoma?

A

Agressive paediatric tumour

arises within the infratentorial compartment

Spreads throughout the CSF

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13
Q

What is the histology of medulloblastoma?

A

Small, blue cells. Rosette pattern of cells with many mitotic figures

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14
Q

Where is a ependymoma located?

A
  • Commonly seen in the 4th ventricle
  • May cause hydrocephalus
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15
Q

What is the histology of a ependymoma?

A
  • Histology: perivascular pseudorosettes
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16
Q

What is a benign slow growing tumour in the frontal lobe?

A

Oligodendroma

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17
Q

What is the histological appearance of an oligodendroma?

A

Calcifications with ‘fried-egg’ appearance

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18
Q

What is a vascular tumour of the cerebellum?

A

Haemangioblastoma

Histology: foam cells with high vascularity

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19
Q

What is haemangioblastoma associated with?

A

von Hippel-Lindau syndrome

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20
Q

What is a pituitary adenoma and how is it classified?

A

Benign tumour of the pituitary gland

Divided into microadenomas (smaller than 1cm) or macroadenoma (larger than 1cm).

May secrete extra hormone

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21
Q

What is the most common supratentorial paediatric tumour?

A

Craniopharngyoma

solid/cystic tumour of the sellar region that is derived from the remnants of Rathke’s pouch.

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22
Q

How does a craniopharngyoma present?

A

hormonal disturbance, symptoms of hydrocephalus or bitemporal hemianopia.

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23
Q

What is the function of collagen I?

A

Bone, skin and tendon

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24
Q

What is the function of collagen II?

A

Hyaline cartilage, vitreous humour

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25
What is the function of collagen III?
Reticular fibre, granulation tissue
26
What is the function of collagen IV?
Basal lamina, lens, basement membrane
27
What is the function of collagen V?
Most interstitial tissue, placental tissue
28
What genetic disease is associated with mutation of collagen I ?
Osteogenesis imperfecta
29
What genetic disease is associated with mutation of collagen III?
Vascular type Ehlers danlos
30
What genetic disease is associated with mutation of collagen IV?
Alport syndrome Goodpasteur syndrome
31
What genetic disease is associated with mutation of collagen V?
Classical variant of Ehlers-Danlos syndrome
32
What are the features of congenital rubella syndrome?
Sensorineural deafness Congenital cataracts Congenital heart disease (e.g. patent ductus arteriosus) Glaucoma Purpuric skin lesions 'Salt and pepper' chorioretinitis
33
What are the features of congenital toxoplasmosis infection?
Cerebral calcification Chorioretinitis Hydrocephalus
34
What are the features of congenital CMV infection?
Low birth weight Purpuric skin lesions Sensorineural deafness Microcephaly
35
What is the commonest cause of end stage renal failure in West?
Diabetic nephropathy
36
What is the pathophysiology of diabetic neprhopathy?
Increased glomerular capillary pressure due to glycosylation of the basement membrane is Leads to 1. basement membrane thickening, 2. capillary obliteration, 3. mesangial widening.
37
What are kimmesteil wilson lesions?
Nodulular hyaline areas develop in the glomuli - Kimmelstiel-Wilson nodules
38
What are non-modifiable risk factors of diabetes?
Male sex Duration of diabetes Genetic predisporsiation
39
What are the causes of DIC?
Infection Malignancy Trauma e.g. major surgery, burns, shock, dissecting aortic aneurysm Liver disease Obstetric complications
40
What is DIC?
Simultaneous coagulation and haemorrhage caused by the initial formation of thrombi which consume clotting factors (factors 5,8) and platelets, ultimately leading to bleeding.
41
What blood features do you see in DIC?
Prolonged clotting times Thrombocytopenia Decreased fibrinogen, Increased fibrinogen Degradation products
42
What are the layers of epidermis?
Stratum corneum - Flat, dead, scale-like cells filled with keratin Stratum lucidum- Clear layer - present in thick skin only Stratum granulosum- Cells form links with neighbours Stratum spinosum- Squamous cells begin keratin synthesis. Thickest layer of epidermis Stratum germinativum - The basement membrane - single layer of columnar epithelial cells
43
What are the stages of differentiation in haematopoiesis?
Haematocytoblast - Multipotent stem cell for all types of blood cells Proerythroblast - Cell has become committed to its developmental pathway Basophilic erythroblast - Ribosomes start to accumulate and the nucleus begins to shrink Polychromatophilic erythroblast - Nucleus and total cell volume continue to shrink Normoblast - Cell nucleus is ejected before developing further Reticulocyte - Cells enter the circulation Erythrocyte -Fully matured cell
44
How does HIV infect cells?
1. Fusion of HIV to host cell 2. HIV RNA, integrase, transcriptase enter cell 3. Viral DNA transformed by reviser transcriptase 4. Viral DNA transported to nucleus and integrates into DNA 5. Transcription makes new viral mRNA to make viral components
45
What are the immunological changes in HIV?
Reduction in CD4 count Increase B2-microglobulin (component of MHC) Decreased IL-2 production Polyclonal B-cell activation Decrease NK cell function Reduced delayed hypersensitivity responses
46
What is the most common nephrolithasis?
Calcium oxalate
47
What are the features of calcium oxalate kidney stones?
Hypercalciuria is a major risk factor (various causes) Hyperoxaluria may also increase risk Hypocitraturia increases risk because citrate forms complexes with calcium making it more soluble Stones are radio-opaque (though less than calcium phosphate stones) Hyperuricosuria may cause uric acid stones to which calcium oxalate binds
48
What are the features of cystine kidney stones?
Inherited recessive disorder of transmembrane cystine transport leading to decreased absorption of cystine from intestine and renal tubule Multiple stones may form Relatively radiodense because they contain sulphur
49
What are the features of uric acid kidney stones?
Uric acid is a product of purine metabolism May precipitate when urinary pH low May be caused by diseases with extensive tissue breakdown e.g. malignancy More common in children with inborn errors of metabolism Radiolucent
50
What are the features of calcium phosphate?
May occur in renal tubular acidosis, high urinary pH increases supersaturation of urine with calcium and phosphate Renal tubular acidosis types 1 and 3 increase risk of stone formation (types 2 and 4 do not) Radio-opaque stones (composition similar to bone)
51
What are the struvite kidney stones?
Stones formed from magnesium, ammonium and phosphate Occur as a result of urease producing bacteria (and are thus associated with chronic infections) Under the alkaline conditions produced, the crystals can precipitate Slightly radio-opaque
52
Features of giant cell arteritis?
Age of onset older than 50 years New-onset headache or localized head pain Temporal artery tenderness to palpation or reduced pulsation ESR > 50 mm/h
53
What does troponin C bind to?
Calcium
54
What does troponin T bind to?
binds to tropomyosin, forming a troponin-tropomyosin complex
55
What does troponin I bind to?
Actin
56
What are features of macrophage activation syndrome?
Paitent with juvenile idiopathic arthritis Ferritin level is > 684 ng/ml Two of the following are present: - (platelets < 181 * 109/L, AST > 48 U/L, triglycerides > 156 mg/dl, fibrinogen < 360 mg/dl). Refractory fever and hepatosplenomegaly are typical clinical features
57
What causes macrophage activation syndrome?
Interferon gamma
58
What eye movement does the trochlear nerve do?
Inferior nasal - superior oblique
59
What eye movement does abducens nerve complete?
lateral rectus - lateral gaze
60
Pathological description of kimmisteil Wilson lesions?
nodular glomerulosclerosis Hyaline atherosclerosis
61
What makes it more likely that haematuria is from glomerular origin?
Dysmorphic red blood cells if found in urine sediment indicates a glomerular origin of hematuria
62
How should a prolactinoma be treated?
Cabergolin