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Nervous system > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

How do infections enter the CNS? (3 Ways)

A

direct spread e.g. middle ear, ethmoid bone
Blood-borne, sepsis or infective endocarditis
Iatrogenic -

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2
Q

what are the leptomeninges ?

A

Arachnoid

pia mater

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3
Q

what 2 features may be present in meningitis ?

A

Inflammation of leptomeninges

+/- septicaemia

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4
Q

what is a sign of meningococcal septicaemia?

what is its histological appearance ?

A

non-blanching rash

Neutrophils

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5
Q

what are caustive oragnisms in meningitis by age range :
Neonates
2-5
5-30

A

Neonates – E. coli, L. monocytogenes
• 2-5 years old – H. influenza
• 5-30 years – N. meningitidis

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6
Q

what is are features of Chronic Meningitis ?

A

Photosensitivity
Granulomas
Meningeal fibrosis
Cranial nerve entrapment

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7
Q

what are complications of meningitis ?

A 
Death due raised intracranial pressure
Cerebral infarction (stroke)
Cerebral abscess
Subdural empyema
 Epilepsy 
sepsis 
Bilateral adrenal haemorrhage
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8
Q

what is the causative organism of Chronic Meningitis ?

A

M. tuberculosis

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9
Q

what is encephalitis ?

what is it classically caused by ?

A

Inflammation of brain parenchyma not meninges -can occur as a
complication of meningitis
viral

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10
Q

what is seen histologically in encephalitis ? why?

A

intracellular viral
inclusion bodies
neuronal death

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11
Q

what affects temporal lobe in encephalitis ?

A

Herpesviruses

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12
Q

what affects spinal lobe in encephalitis ?

A

Polio

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13
Q

what affects Brainstem in encephalitis ?

A

rabies

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14
Q

where are prions found ?

A

synapses

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15
Q

how can PrP turn to PrPsc ?

A

sporadic mutation,

familial inheritance of mutated gene or following ingestion of PrPsc

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16
Q

How would ingested a PrPsc propagate itself ? why is there no immune response ?

A

PrPsc induced post translational conformational change in normal PrPs
Stable and it is recognised as self protein

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17
Q

how do prions (PrPsc) cause damage ?

A

PrPsc- aggregates which destroy neruones and

cause the grey matter to take on a sponge-like (spongiform) appearance

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18
Q

Name 2 Spongiform Encephalopathies

A 
Scrapie in sheep
BSE in cows (‘mad cow’ disease)
Kuru in New Guinean tribes (due to cannibalism and
ingestion of PrPsc)
Creutzfeld Jacob disease (CJD)
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19
Q

What is vCJD ? what is it linked with ? difference between vCJD and CJD?

A

Strongly linked to BSE through ingestion of
prions] higher
prion load associated with earlier age (28) at
death and more prominent psychiatric
symptoms
look at table in lecture

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20
Q

what are Koch’s Postulates ?

A

the Microorganism must be found in abundance in the suffered
Must be isolated and grown in culture
cultured organism must cause disease in healthy individuals
Reisolated from inoculated and identified as same as original host

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21
Q

define dementia

A

Acquired global impairment of intellect, reason and personality without
impairment of consciousness

22
Q

what is the main cause of dementia ?

what are other causes ?

A

Alzheimer’s

vascular, lewy body and Picks

23
Q

define Alzheimer’s

what is its appearance

A

loss of cortical neurones
decrease in brain weight
cortical atrophy
narrow gyri and wide sulci

24
Q

what causes Alzheimier’s ?

A

neurofibrillary tangles and amyloid

plaques

25
Q

what are Neurofibrally tangles ?

A

Intracellular twisted filaments of Tau that has been hyperphosphorylated
- normally bind to stabilise microtubules

26
Q

what are senile plaques ?

A

Foci of enlarged axons, synaptic terminals
and dendrites
Amyloid deposition in centre of plaque
associated with vessels- central to pathogenesis

27
Q

what syndrome is associated with early onset AD?

what mutations specifically ?

A 
Trisomy 21
Down's
APP 
Presenilin -secretase gene
leads to incomplete breakdown of APP = amyloid disposition
28
Q

what is normal range of ICP ?

A

0-10mmHg

• Coughing/straining can increase it to 20mmHg

29
Q

What are compensatory mechanisms for ICP?

what is the limit for vascular mechanism ?

A

Reduce blood volume
reduced CSF
brain atrophy = chronic
<60mmHg

30
Q

what do SoLs do to the brain?

A

Deforms or destroys surrounding brain
Displaces midline structures – loss of symmetry, midline shift
Herniation

31
Q

what is a subfalcine herination?

A

Cingulate gyrus is pushed under the free edge of the

falx cerebri

32
Q

what can subfalcine herination lead to ?

A

ischaemic due to

compression of anterior cerebral artery leading to infarction

33
Q

what is a tenotrial herination?

A

Medial temporal lobe (classically the uncus) pushed

down through the tentorial notch

34
Q

why are tentorial herinations often fatal ?

A

sedondary heamorrhage into brianstem (Duret) leads to resp and CVS control problems
common mode of death in those with large tumours and IC heamorrhage

35
Q

what are the symptoms of tentorial herination ? why?

A

ipsilateral third
nerve palsy contralateral UMN signs in limbs-
compress ipisilateral oculomotor nerve and
ipsilateral cerebral peduncle

36
Q

name 1 benign and 1 malignant Brain tumour

A

Meningioma

Astrocytoma

37
Q

where do astrocytomas usually mets to ?

A

spread along nerve through sub arch space to spine - hard to remove

38
Q

what is the most common cause of brain tumours ?

A

metastasis

39
Q

Name 2 ways tumours can spread in the brain ?

A

white matter pathways

CSF

40
Q

what is Neurofibroma

A

tumour of Schwann cells of

peripheral or cranial nerve

41
Q

what are tumours of ependymal cells lining

ventricular system?

A

Ependymoma

42
Q

what tumours can arise from Non-CNS tissues?

A

mets

Lymphomas

43
Q

what is a stroke ?

A

A sudden event producing a disturbance of CNS function due to vascular
disease

44
Q

name 2 sources an embolism may come from

A

Heart (due to AF, mural thrombus)
Atheromatous debris (carotids)
Thrombus over ruptured plaque
Aneurysm

45
Q

where would a thrombus form in a stroke if it did not embolise from somewhere ?

A

cerebral arteries

46
Q

what s a lacuna stroke ?

A

Small (less than 1cm area affected)
Associated with hypertension
Commonly affect basal ganglia and internal capsule

47
Q

what is seen and associated with intracerebral haemorrhage leading to stroke ?

A

ncreased age, hypertensive vessel
damage and amyloid deposition in vessels
Charcot-Bouchard aneurysms are seen May be inherited
Produces a space occupying lesion

48
Q

what causes subarachnoid haemorrhage ?

A

Rupture of berry aneurysms, usually found at
branch points in circle of Willis
 Blood in subarachnoid space can cause secondary
spasm of cerebral arteries

49
Q

what are some risk factors for subarachnoid haemorrhage?

A

Male
• Hypertension
• Atherosclerosis

50
Q

what are some symptoms of Subarachnoid haemorrhage?

A

Thunderclap headache
• May be preceded by a ‘sentinel’ headache
• Loss of consciousness
• Often instantly fatal

Nervous system (20 decks)

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