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Clinical Neuroscience > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

The CNS is normally sterile.

What are 3 ways microorganisms can gain entry

A

Direct spread (From middle ear, basal skull fracture, ethmoid bone)

Blood-borne: (Sepsis, Infective endocarditis)

Iatrogenic: (Post neurosurgery, lumbar puncture)

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2
Q

Describe the pathophysiology of Meningitis (Potentially life threatening)

A
  • Inflammation of leptomeninges
  • May have septicaemia

(Non-balancing rash is a sign of meningococcal septicaemia, not meningitis)

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3
Q

Which organisms cause Meningitis in;

  • Neonates
  • 2-5 years old
  • 5-30 years old
  • 30+
  • Immunocompromised patients
A

Neonates: E. coli, L. monocytogenes

2-5: H. influenza
5-30: N. meningitidis
30+: S. pneumoniae

Immunocompromised: Various organisms (E.g fungi)

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4
Q

Describe 5 features of Chronic Meningitis

A
  • Caused by M. tuberculosis
  • Granulomas
  • Meningeal fibrosis
  • Cranial nerve entrapment
  • Bilateral adrenal haemorrhage (Waterhouse-Friederichsen syndrome) as a complication
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5
Q

List 5 complications of Meningitis

A
  • Death due to raised ICP
  • Cerebral infarction
  • Cerebral abscess
  • Subdural Empyema
  • Epilepsy (due to direct irritation of brain)

(Systemic complication- Septicaemia)

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6
Q

Encephalitis is usually viral and causes inflammation of brain parenchyma

Describe the pathophysiology

A

Virus kills neurones causing Inflammation and presence of Intracellular viral inclusions

Lymphocytic infiltrate is typical

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7
Q

Which parts of the CNS are affected by;

  • Herpes
  • Polio (Eradicated)
  • Rabies
A
  • Herpes affects Temporal lobe
  • Polio affects Spinal cord
  • Rabies affects Brainstem
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8
Q

Prion protein (PrP) is a normal protein found in synapses

What can cause PrP to transform into PrPsc (abnormal form)

A
  • Sporadic mutation
  • Familial inheritance of mutated gene
  • Ingestion of PrPsc
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9
Q

List 3 features of PrPsc

A
  • Able to convert PrP into PrPsc by protein-protein interactions (induce a conformational change)
  • Extremely stable (Resistant to radiation, disinfectants)
  • Not susceptible to immune attack (is essentially a ‘self’ protein)
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10
Q

How does PrPsc cause damage?

A

PrPsc aggregates cause neuronal death, leading to ‘holes’ in grey matter

(Brain takes on a spongiform/ sponge-like appearance)

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11
Q

List 5 Spongiform Encephalopathies

A
  • Scrapie (in sheep)
  • BSE (in cows, ‘mad cow disease’)
  • Kuru (in some tribes due to cannibalism)
  • CJD (Creutzfeld Jacob disease)
  • vCJD (Variant CJD)
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12
Q

Variant CJD is strongly linked to BSE.

How does it differ from ‘classical’ CJD?

A

Higher prion load associated with;

  • Earlier age at death
  • More prominent psychiatric/ behavioural symptoms
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13
Q

In Dementia, is consciousness impaired?

A

No

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14
Q

Describe the Pathophysiology of Alzheimer’s

A

Loss of cortical neurones-> Cortical atrophy and reduced brain weight

Damage caused by Neurofibrillary Tangles and Amyloid Plaques

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15
Q

Describe what Neurofibrillary tangles are

A

Intracellular twisted filaments of Tau protein

Tau normally binds and stabilises microtubules, becomes hyperphosphorylated in in Alzheimer’s

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16
Q

Describe what Amyloid Plaques are

A
  • Foci of enlarged axons, dendrites and synaptic terminals

- Amyloid deposition in vessels in centre of plaque

17
Q

What is Trisomy 21 associated with?

How?

A
  • Alzheimer’s

- Amyloid Precursor Protein (APP) gene is found on this chromosome (hence extra dose of gene)

18
Q

What are 2 gene mutations associated with Alzheimer’s

A
  • APP gene

- Presenelin gene (Produce secretase which breaks down APP)

19
Q

What is the normal ICP?

What can coughing/ sneezing raise it to?

A

0-10mmHg

10-20mmHg

(Only significant if raised for several minutes)

20
Q

Suggest 2 mechanisms to compensate for raised ICP

Up to what ICP can cerebral flow be maintained?

A
  • Reduced blood and CSF volume
  • Brain atrophy if chronically elevated

Upto 60mmHg

21
Q

Suggest 3 effects of a Space Occupying Lesion in the brain

A
  • Deforms/ destroys around lesion
  • Displacement of midline structures
  • Can cause brain herniation
22
Q

Describe a Subfalcine herniation as well as its possible effects

(One of the first herniations to occur)

A
  • Cingulate Gyrus pushed under Falx Cerebri

- Herniated brain can become ischaemic due to compression of ACA

23
Q

Describe a Tentorial herniation as well as its possible effects

A
  • Medial Temporal Lobe (Uncus, typically) pushed through Tentorial Notch

Compression of;

  • Ipsilateral CNIII-> CNIII Palsy
  • Ipsilateral Cerebral Peduncle-> Contralateral UMN signs in limbs

Occlusion of Posterior Cerebral and Superior Cerebellar arteries

24
Q

Duret haemorrhages are associated with Tentorial Herniation

What is it?

A

Secondary brainstem haemorrhage

25
Q

What is a Tonsilar herniation?

A

Cerebellar tonsils pushed into Foramen Magnum-> Brainstem compression

26
Q

Name a Benign brain tumour

A

Meningioma

27
Q

List 5 Malignant brain tumours

not including Metastases which are the most common of all brain tumours

A
  • Astrocytoma
  • Neurofibroma (Schwann cells)
  • Ependymoma (Ependymal cells)
  • Neuronal tumours (Neurones)
  • Lymphoma
28
Q

List some features of Astrocytomas

A
  • Low grade, slow growing, difficult to remove
  • High grade ones known as Glioblastoma Multiforme
  • Direct spread along white mater pathways
  • Can also spread to distant CNS via CSF
29
Q

Strokes are more frequent in the elderly.

List 4 risk factors

A
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes
30
Q

Strokes can be caused by an Embolism or Thrombus

What are the 2 broad categories of Stroke?
What percentage of all strokes do they each make up?

A
  • Cerebral Infarction (85%)

- Cerebral Haemorrhage (15%)

31
Q

Compare the 2 types of cerebral infarction

A

Regional;

  • Large
  • Worse prognosis

Lacunar;

  • Small
  • Associated with hypertension
  • Commonly affect Basal Ganglia and Internal Capsule
32
Q

Cerebral haemorrhages are usually spontaneous.

What are the 2 types of cerebral haemorrhage?

A
  • Intracerebral haemorrhage (10% of all strokes)

- Subarachnoid haemorrhage (5% of all strokes)

33
Q

List features of Intracerebral haemorrhage

A
  • Associated with Age, Hypertensive vessel damage and Amyloid deposition in vessels
  • Charcot-Bouchard aneurysms seen
  • May be inherited
  • Produces a Space Occupying Lesion
34
Q

List features of Subarachnoid haemorrhage

A
  • Rupture of Berry aneurysms, usually at branching points in Circle of Willis
  • Blood in Subarachnoid space-> Spasm of cerebral arteries
35
Q

What are 4 associations/ risk factors of Subarachnoid haemorrhage

A
  • Male
  • Hypertension
  • Atherosclerosis
  • Other diseases (CT disorders, Polycystic Kidney disease)
36
Q

List 4 symptoms of Subarachnoid haemorrhage

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

Clinical Neuroscience (19 decks)

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