Histopathology - Cerebral Pathology Flashcards

1
Q

What is a stroke?

A

A clinical syndrome characterised by rapidly developing focal/global neurological deficit lasting > 24 hrs (of presumed vascular origin)

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2
Q

How long does a TIA last for?

A
  • <24hrs with complete resolution of Sx
  • Most = 1-5mins
    -1/3 lead to strokes after 5 years if untreated
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3
Q

What is the most common modifiable RF for all kinds of strokes?

A

HTN

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4
Q

What is ischaemia?

A

A lack of oxygen supply to tissue

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5
Q

What is an infarction?

A

An area of tissue death due to lack of oxygen

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6
Q

What is a the most common cause of brain infarction?

A

Cerebral atherosclerosis

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7
Q

What percentage of strokes are caused by infarctions?

A

70-80%

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8
Q

What are some causes of brain infarctions?

A
  • Embolism from intra/extra-cranial plaques
  • Cerebral atherosclerosis
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9
Q

What are an important future predictor of strokes?

A

TIAs

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10
Q

What is the epidemiology and clinical presentation of a stroke?

A

Epi:
- 100,000 new strokes/yr in UK

Sx:
- Sudden onset
- FAST
- Numbness
- Loss of vision
- Dysphagia

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11
Q

What vascular territories are commonly affected in strokes?

A
  • Anterior vs posterior territory
  • Most common = MCA
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12
Q

What are the investigations and management of a stroke?

A

Ix:
- CT/MRI (infarct vs haemorrhage)
- Ix for vascular risk (BP, FBC, ESR, U+E, Glucose, Lipids, ECG, Carotid doppler)

Mx:
- Aspirin +/- dipyridamole
- Thrombolytics (IF <3hr from event)
- +/- carotid endarterectomy
- Long term: Treat HTN, Lower Lipids, Anticoag

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13
Q

What are the causes/RFs for strokes + TIAs?

A
  • Smoking
  • DM
  • HTN
  • FHx
  • Prev. TIAs
  • OCP
  • PVD
  • Increased ethanol usage
  • Hyperviscosity (e.g. sickle cell, polycythaemia)
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14
Q

What is the epidemiology and clinical features of TIAs?

A

Epi:
- 0.4/1000 /yr
- 15% of 1st strokes preceded by TIAs

Sx:
- Sx last <24hrs
- Amaurosis fugax
- Carotid bruit

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15
Q

What vascular territories are commonly affected by TIAs?

A

Any
- Characteristically embolic atherogenic debris from carotid artery travels to ophthalmic branch of internal carotid

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16
Q

What are the investigations and management for TIAs?

A

Ix:
- Carotid US
- Ix for vascular risk (BP, FBC, ESR, U+E, Glucose, Lipids, CXR, Carotid doppler)

Mx:
- Aspirin + dipyridamole
- +/- carotid endarterectomy
- Long term: Treat HTN, Lower lipids, Anticoag

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17
Q

What are some stroke syndromes when caused at the ACA (anterior cerebral artery)?

A
  • Contralateral leg paresis
  • Sensory loss
  • Cognitive defects (e.g. apathy, confusion + poor judgement)
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18
Q

What are some stroke syndromes when caused at the MCA (Middle cerebral artery)?

A

Proximal occlusion:
- Contralateral weakness + sensory loss of face + arm
- Cortical sensory loss
- ?Contralateral homonymous hemianopia/quadrantanopia
- IF Dominant (left) hemisphere: asphasia
- IF non-dominat (right) hemisphere: neglect
- Eye deviation towards side of lesion + away from weak side

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19
Q

What are some stroke syndromes when caused at the PCA (posterior cerebral artery)?

A
  • Contralateral hemianiopia/quadrantanopia
  • Midbrain findings: CN III + IV aplsy/pupillary changes, hemiparesis
  • Thalamus findings: Sensory loss, amnesia, decreased level of consciousness
  • IF Bilateral: Cortical blindness/prosopagnosia
  • Hemiballismus
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20
Q

What are some stroke syndromes when caused by lacunar infarcts?

A
  1. Pure motor hemiparessi (posterior limb of internal capsule): contralateral arm, leg + face
  2. Pure sensory loss (ventral thalamic): hemisensory loss
  3. Ataxic hemiparesis (ventral pons or internal capsule): ipsilateral ataxia + leg paresis
  4. Dysarthria-clumsy hand syndrome (ventral pons/genu of internal capsule): dysarthria, facial weakness, dysphagia, mild hand weakness + clumsiness
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21
Q

What are lacunar infarcts?

A
  • Deep hemispheric white matter
  • Involving deep penetrating arteries of MCA, circle of Willis, basilar, + vertebral arteries
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22
Q

What percentage of strokes are caused by haemorrhagic causes?

A

20%

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23
Q

What are the non-traumatic haemorrhages?

A
  • Intraparenchymal haemorrhage
  • Subarachnoid haemorrhage
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24
Q

What are some features of an intraparenchymal haemorrhage, including its most common site?

A
  • 50% due to HTN
  • Abrupt onset
  • Can cause Cahrcot-bouchard microaneurysms (likely to rupture)
  • Common site: Basal Ganglia
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25
Q

What is the most common cause of haemorrhagic strokes?

A

HTN

26
Q

What are some features of subarachnoid haemorrhages, including some buzzwords?

A
  • 85% from ruptured berry aneurysms
  • Most at internal carotid bifurcation (+ posterior communicating artery)
  • F>M, <50yrs
  • Thunderclap headache, vomiting + LoC
  • Increased risk in APKD, Ehler’s Danlos + Aortic coarctation
  • BUZZWORDS: HYPERATTENUATION AROUND CIRCLE OF WILLIS
27
Q

What are some rare non-traumatic haemorrhagic causes of stroke?

A
  • AV malformations (young people <50yrs)
  • Cavernous angiomas (recurrent low pressure bleeds)
  • Capillary telengiactasias
  • Connective tissue disorders (e.g. Ehlers-Danlos)
28
Q

What are some traumatic haemorrhages?

A
  • Extradural haemorrhge
  • Subdural haemorrhage
  • Traumatic parenchymal injury
29
Q

What are some features of an extradural haemorrhage?

A
  • Skull fracture from truama (usually at pterion)
  • Most common site = MIDDLE MENINGEAL ARTERY
  • Rapid arterial bleed, lucid interval then LoC
  • Buzzword = Lemon shape
30
Q

What are some features of a subdural haemorrhage?

A
  • Previous history of minor head trauma
  • Damaged bridging verins with slow venous bleed
  • Often elderly/alcoholic/on anticoagulation
  • A/w gradual headache, fluctuating consciousness + behavioural changes
  • Buzzword: Banana/crescent shape
31
Q

What are the different types of traumatic parenchymal injury?

A
  • Traumatic brain injury
  • Concussion
  • Contusions
  • Diffuse axonal injury
  • Skull fractures
32
Q

What is a concussion?

A

Transient LoC + paralysis, recovery in hours/days

33
Q

What is a contusion?

A

Collision between brain + skull
- Coup = where impact occurs
- Contracoup = opposite region of impact

34
Q

What are some features of a diffuse axonal injury?

A
  • Occurs at moment of injury due to shear tensile forces breaking axons apart
  • Commonest cause of coma
  • Midline strictures like Corpus Callosum, rostral brainstem + septum peelucidum affected
  • Causes vegetative state + post-traumatic dementia
35
Q

What should be looked out for when skull fractures occur (in terms of brain injury)?

A
  • Otorrhea/rhinorrhoea
  • Buzzword = STRAW-COLOURED FLUID = CSF + Battle’s sign
36
Q

What is a Battle’s sign

A

Haemorrhage on mastoid process

37
Q

What is the single largest cause of death in under 45s?

A

Traumatic brain injury

38
Q

What are some causes of raised ICP?

A
  • Oedema
  • Space occupying lesion (e.g. tumour/abscess)
39
Q

What can raised ICP lead to?

A

Brain herniation

40
Q

What are the three main types of brain herniation and their features?

A

Subfalcine:
- Hernation of singular corex beneath flax (midline fold of dura)

Transtentorial/uncal:
- Herniation of medial temporal lobe under tentorium (horizontal dura mater between parietal lobes + cerebellum)

Tonsillar herniation:
- Hernation of cerebellum through foramen magnum
- Compresses brainstem leading to cardiorespiratory arrest + death (risk if doing LP with raised ICP)

41
Q

What is oedema and its types?

A

Excess accumulation fo fluid in brain parenchyma
- Vasogenic = disruption of blood brain barrier permeability
- Cytotoxin = secondary to cellular injury (e.g. ischaemc or hypoxic)

42
Q

What is hydrocephalus?

A

An increase in CSF + enlargement fo ventricular system

43
Q

What are three types of hydrocephalus and the differences between them?

A

Communicating:
- Obstruction in outflow of CSF
- E.g. in neonates, lateral ventricles obstruct cerebral aqueduct causing build-up of CSF in lateral ventricles leading to enlarging brain + ventricles

Non-communicating:
- Reduced absorption of CSF into sinus veins
- E.g. in meningitis the meninges can become fibrous which reduces absorption

Normal pressure:
- Gait disturbances
- Urinary incontinence
- Confusion

44
Q

What is the normal flow of CSF?

A
  • Produced by choroid plexus
  • Flows through interventricular forament into 3rd ventricle
  • Flows via cerebral aqueduct into 4th ventricle
  • Goes to sub-arachnoid space
  • Goes to spinal cord + brain
  • Reabsorption via superior sagittal sinus into venous system
45
Q

Where do primary brain tumours originate?

A

CNS

46
Q

What are the two types of primary brain tumours and where do they originate/the type of tumour?

A

Extra-axial:
- Cranium
- Soft tissue
- Meninges
- Nerves
- BENIGN

Intra-axial:
- Glial
- Neurones
- Neuroendocrine cells
- MALIGNANT

47
Q

What are secondary brain tumours?

A

Metastatic lesions from other parts of the body

48
Q

What are some features of secondary brain tumours?

A
  • Commonest form of adult brain tumours
  • Most common sources = lung, breast, malignant melanoma
  • Located at grey-white matter junction
  • Well demarcated, solitary or multiple with surrounding oedema
  • VERY POOR PROGNOSIS
49
Q

What are some RFs for brain tumours?

A
  • Previous tumours
  • Radiotherapy to head + neck
  • Neurofibromatosis 1+2
  • Tuberous sclerosis
  • FHx of brain cancer
50
Q

What are some signs + Sx of brain tumours?

A

Raised intracranial pressure:
- Headache
- Vomiting
- Change in mental state

Supratentorial:
- Focal neurological deficit
- Seizures
- Personality changes

Infratentorial:
- Ataxia
- Long tract signs = spasticity, hyperreflexia
- Cranial nerve palsies

51
Q

What are some neuroimaging techniques?

A
  • MRI
  • CT
  • Functional MRI
  • MR-spectroscopy
  • PET-SCAN
52
Q

What is the management of a brain tumour?

A
  • Surgical resection
  • Radiotherapy +/- chemotherapy
53
Q

What is the WHO classification of CNS tumours?

A

Tumour type: Cell of origin/lineation of differentiation:
- Astrocytes = astrocytomas
- Oligodendrocytes = oligodendrocytomas (FRIED EGG APPEARANCE)
- Ependyma = Ependyoma (VENTRICULAR TUMOUR, HYDROCEPHALUS)
- Meningothelial cells = meningioma

Tumour grade: predicted natural clinical behaviour (e.g. survival time)
- Grade 1 = benign (well differentiated)
- Grade 2 = 5yrs + survival
- Grade 3 = 1-5yrs survival
- Grade 4 = <1yr survival (poorly differentiated)

Molecular profiling
- Genetics
- Molecular markers

54
Q

What are the three different types of astrocytic brain tumours?

A
  • Pilocytic astrocytoma (G1)
  • Diffuse glioma (G2-3)
  • Glioblastoma multiforme (G4 = BAD)
55
Q

What age group does a pilocytic astrocytoma arise, what are its histological features, associated mutations and buzz words?

A

Age:
- 0-20 yrs

Histology:
- Piloid HAIRY CELLS
- Rosenthal fibres
- Slow mitotic divisions

Mutation:
- BRAF in 70%

Buzzwords:
- INDOLENT
- CHILDHOOD

56
Q

What age group does a diffuse glioma arise, what are its histological features and associated mutations?

A

Age:
- 20-40yrs

Histology:
- Low-moderate cellularity
- Low mitotic activity
- No vascular proliferation

Mutation:
- IDH A/W longer surivival + better response to chemo + radiotherapy

57
Q

What age group does a glioblastoma multiforme arise, what are its histological features, associated mutations and buzz words?

A

Age:
- 50+ yrs
- Median survival = 8mths
- MOST COMMON, AGGRESSIVE PRIMARY TUMOUR IN ADULTS

Histology:
- High cellularity
- High mitotic activity
- Microvascular proliferation
- Necrosis

Mutation:
- IDH wildtype

Buzzwords:
- AGGRESSIVE
- POOR PROGNOSIS

58
Q

What age group does a meningioma arise, what are its histological features, location and buzz words?

A

Age:
- Increased incidence with age

Histology:
- PSAMMOMA BODIES (calcifications)
- Mitotic activity determines grading

Location:
- Meninges
- Arachnoid cells

Buzzwords:
- NF2

59
Q

What age group does a medulloblastoma arise, where is it found and its buzz words?

A

Age:
- 2nd most common brain tumour in children after astrocytoma

Location:
- Cerebellum

Buzzwords:
- Squint

60
Q

Where are ependyomas found?

A
  • Posterior fossa
  • Tuberous sclerosis
61
Q

Where are craniopharyngiomas and pituitary tumours found?

A
  • Pituitary sella
62
Q

What are some familial syndromes associated with CNS tumours, and their features?

A

Von Hippel- Lindau
- Hemangioblastoma of cerebellum, brainstem + spinal cord
- Retina
- Renal cysts
- Phaeochromocytoma

Tuberous sclerosis:
- Giant cell astrocytoma
- Cortical tuber
- Supependymal nodules + calcifcations on CT

NF1:
- Optic glioma
- Neurofibroma
- Astrocytoma

NF2:
- Vestibular schwannoma
- Meningioma
- Ependymoma
- Astrocytoma

Multiple endocrine neoplasia type 1 (MEN1):
- Pituitary adenoma