8.3 Pathology of brain Flashcards

1
Q

one of the compensatory mechanisms to maintain normal ICP is to reduce blood volume. Is this blood venous or arterial?

A

venous

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2
Q

why is an extradural haemorrhage usually lucid then sudden?

A

takes time for periosteal dura to split from periosteum of skull, but once split then arterial blood fills the space quickly

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3
Q

risk factors for berry aneurysm/SAH

A

Ehlers danlos
other connective tissue disorders
polycystic kidney disease

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4
Q

2 types of cerebral infarcts (ishaemic)

A

thrombotic occlusion
embolic occlusion

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5
Q

why would obstruction of deep penetrating arteries cause significant ant damage? examples of these

A

no collateral supply

-basal ganglia
-thalamus
-deep white matter

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6
Q

where might you get a wedge shaped necrosis in ischaemic stroke?

A

watered areas (distal artery territories) e.g MCA/ACA border. after a hypotensive episode

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7
Q

common sites of thrombotic stroke

A

carotid bifurcation, MCA origin, basilar artery

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8
Q

common sites of spontaneous intracerebral haemorrhage

A

basal ganglia, pons, cerebellum, thalamus

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9
Q

pathophysiology of cerebral amyloid angiopathy

A

lobar haemorrhages of cerebral cortices, amyloid deposition in walls of small/medium meningeal and cortical vessels, weakness wall

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10
Q

arteriovenous malformations

A

subarachnoid vessels to brain or vessels in brain

tangled vascular channels

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11
Q

cavernous malformations

A

loos vascular channels, distended, thin walled in cerebellum and pons

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12
Q

symptoms of CNS tumours

A

seizures
headaches
focal neurological deficit
raised ICP
N+V

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13
Q

identify some primary CNS tumours

A

gliomas
-astrocytic
-oligdendroglioma

parenchymal
-lymhoma
-germ cell

-meningioma

neuronal
-ganglion cell tumour
-neuroblastoma

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14
Q

investigations for meningitis

A

CT
LP

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15
Q

why is glucose decreased in meningitis LP?

A

requirements of infection

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16
Q

how do normal prion proteins become pathological?

A

normally rich in alpha helices

sporadic mutation/ingested

now beta pleated sheets, resistant to proteolysis

propagates other to beta too

17
Q

creutzfeld Jacob disease features

A

mostly sporadic

rapidly progressive dementing illness, changes in memory, cerebellar ataxia, brain may look normal

18
Q

variant creutzfeld Jacob disease features

A

slower progression, younger people, starts with behavioural issues, exposure to prion disease in cattle

19
Q

molecular pathologies in Alzheimer’s

A

amyloid plaques (alpha beta)

neurofibrillary tangles (hyperphosphorylated tau proteins)

20
Q

huntingtons disease

A

-autosomal domiannt
-CAG trinucleotide repeat expansion
-hyperkinesia