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MCRP: Clinical Sciences > Pathology > Flashcards

Pathology Flashcards

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
Q

What is the function of collagen III?

A

Reticular fibre, granulation tissue

26
Q

What is the function of collagen IV?

A

Basal lamina, lens, basement membrane

27
Q

What is the function of collagen V?

A

Most interstitial tissue, placental tissue

28
Q

What genetic disease is associated with mutation of collagen I ?

A

Osteogenesis imperfecta

29
Q

What genetic disease is associated with mutation of collagen III?

A

Vascular type Ehlers danlos

30
Q

What genetic disease is associated with mutation of collagen IV?

A

Alport syndrome
Goodpasteur syndrome

31
Q

What genetic disease is associated with mutation of collagen V?

A

Classical variant of Ehlers-Danlos syndrome

32
Q

What are the features of congenital rubella syndrome?

A

Sensorineural deafness
Congenital cataracts
Congenital heart disease (e.g. patent ductus arteriosus)
Glaucoma
Purpuric skin lesions
‘Salt and pepper’ chorioretinitis

33
Q

What are the features of congenital toxoplasmosis infection?

A

Cerebral calcification
Chorioretinitis
Hydrocephalus

34
Q

What are the features of congenital CMV infection?

A

Low birth weight
Purpuric skin lesions
Sensorineural deafness
Microcephaly

35
Q

What is the commonest cause of end stage renal failure in West?

A

Diabetic nephropathy

36
Q

What is the pathophysiology of diabetic neprhopathy?

A

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
Q

What are kimmesteil wilson lesions?

A

Nodulular hyaline areas develop in the glomuli - Kimmelstiel-Wilson nodules

38
Q

What are non-modifiable risk factors of diabetes?

A

Male sex
Duration of diabetes
Genetic predisporsiation

39
Q

What are the causes of DIC?

A

Infection
Malignancy
Trauma e.g. major surgery, burns, shock, dissecting aortic aneurysm
Liver disease
Obstetric complications

40
Q

What is DIC?

A

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
Q

What blood features do you see in DIC?

A

Prolonged clotting times
Thrombocytopenia
Decreased fibrinogen,
Increased fibrinogen
Degradation products

42
Q

What are the layers of epidermis?

A

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
Q

What are the stages of differentiation in haematopoiesis?

A

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
Q

How does HIV infect cells?

A
  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
Q

What are the immunological changes in HIV?

A

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
Q

What is the most common nephrolithasis?

A

Calcium oxalate

47
Q

What are the features of calcium oxalate kidney stones?

A

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
Q

What are the features of cystine kidney stones?

A

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
Q

What are the features of uric acid kidney stones?

A

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
Q

What are the features of calcium phosphate?

A

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
Q

What are the struvite kidney stones?

A

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
Q

Features of giant cell arteritis?

A

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
Q

What does troponin C bind to?

A

Calcium

54
Q

What does troponin T bind to?

A

binds to tropomyosin, forming a troponin-tropomyosin complex

55
Q

What does troponin I bind to?

A

Actin

56
Q

What are features of macrophage activation syndrome?

A

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
Q

What causes macrophage activation syndrome?

A

Interferon gamma

58
Q

What eye movement does the trochlear nerve do?

A

Inferior nasal - superior oblique

59
Q

What eye movement does abducens nerve complete?

A

lateral rectus - lateral gaze

60
Q

Pathological description of kimmisteil Wilson lesions?

A

nodular glomerulosclerosis
Hyaline atherosclerosis

61
Q

What makes it more likely that haematuria is from glomerular origin?

A

Dysmorphic red blood cells if found in urine sediment indicates a glomerular origin of hematuria

62
Q

How should a prolactinoma be treated?

A

Cabergolin

MCRP: Clinical Sciences (11 decks)

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