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Clinical neuroscience > L11 - Neuropathology > Flashcards

L11 - Neuropathology Flashcards

1
Q

How do microorganisms gain entry to the CNS

A

Direct spreads:

  • middle ear infections
  • basilar skull fractures

Blood bourne:

  • sepsis
  • infective endocarditis

Iatrogenic:

  • VP shunt
  • surgery
  • lumbar puncture
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2
Q

Meningitis

A

Inflammation of the leptomeninges
With or without septicaemia
Non blanching rash

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3
Q

Effects of meningitis

A

Rapid oedema
Blood vessel congestion’s
Invasion by neutrophils
Raised intracranial pressure

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4
Q

Causative organism of meningitis in neonates

A

Ecoli

Monocytogenes

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5
Q

Causative organism of meningitis in 2-5 year olds

A

Haemophilus influenzae type B

Rare due to vaccines

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6
Q

Causative organism of meningitis in 5 - 30 yr olds

A

Neisseria meningitidis

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7
Q

Causative organism of meningitis in over 30 yr olds

A

Streptococcus pneumoniae

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8
Q

What causes chronic meningitis

A

Mycobacterium tuberculosis
Causes granulomatous inflammation
Fibrosis of meninges due to chronic inflammation
Nerve entrapment

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9
Q

Complications of meningitis

A 
Death
Cerebral infarcts
Cerebral abscess 
Subdural empyema
Epilepsy
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10
Q

Encephalitis

A

Neuronal cell death by virus
Inclusion bodies aggregate
Parenchyma affected
Lymphocytic inflammatory reaction

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11
Q

Causes of encephalitis

A

Temporal lobe:
- herpes virus - shingles can cause epilepsy

Spinal cord motor neurones:
- polio

Brainstem
- rabies

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12
Q

How to treat encephalitis

A

Normally self limiting in younger patients

Can cause death

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13
Q

Prions

A

Normal protein constituent of synapses

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14
Q

Prions disease

A
  1. Mutated prion protein can come in to contact with normal prion proteins
  2. Normal prion proteins undergo a post translational confirmation change into the mutated form
  3. Mutated prions aggregate inside cells and are difficult to remove
  4. Cell apoptosis - neurones in brai.
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15
Q

How are mutated prions obtained

A

Sporadic mutation
Familial condition
Ingested

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16
Q

What can prions disease cause?

A

Spongiform encephalopathies:

  • scrabies - sheep
  • kuru
  • bovine spongiform encephalopathy- cows
  • variant creutzfeld Jacob disease - vCJD
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17
Q

Difference between variant and classic CJD

A

Variant:

  • younger age of death (28)
  • longer duration of illness (13- 14months)
  • prominent psychological/ behavioural changes
  • painful dyesthesiasis
  • delayed neurological signs
  • presence of florid plaques
  • accumulation of protease resistant prions

Classic CJD:

  • older age of death (68)
  • shorter duration (4-5 months)
  • dementia
  • early neurological signs
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18
Q

Dementia

A

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

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19
Q

Alzheimer’s disease

A

Exaggerated ageing process

Cortical atrophy due to increased neuronal damage by neurofibrillary tangoes and senile amyloid plaques

20
Q

Neurofibrillary tangles

A

Intracellular twisted filaments of Tau proteins
Tau proteins become hyperphosphorylated and insoluble
The build up of irregular tau proteins cause cell death

21
Q

Tau protein

A

Normally binds and stabilises microtubules

22
Q

Senile plaques

A

Foci of enlarged axons and dendrites fused together that aggregate

Amyloid deposition in the vessel in the middle of the plaque, reduced blood flow to the brain and can cause ischaemia

23
Q

How was amyloid discovered to be involved in Alzheimer’s disease

A

People with Down’s syndrome - trisomy 21 has early onset Alzheimer’s disease

They were found to have mutations of:

  • amyloid precursors protein gene
  • presenilin genes 1 and 2

Therefore there was incomplete breakdown of the amyloid precursor protein and increased amyloid deposition

24
Q

Presenilin genes

A

Codes for components of the secretase enzyme that normally breaks down amyloid plaques

25
Q

Normal intracranial pressure

A

0-10 mmHg
Normally above 0
Coughing and straining e.g. the Valsava manoeuvre can increase ICP to 20 mmHg

26
Q

Compensatory mechanism to maintain ICP

A

Reduced blood volume
Reduced CSF volume
Brain atrophy

27
Q

ICP at which vascular mechanisms can maintain cerebral blood flow

A

Below 60 mmHg

28
Q

Types of space occupying lesions in the brain

A

Tumour
Haemorrhage
Oedema

29
Q

Effects of space occupying lesions

A

Deformation and destruction of the brain around the lesion
Asymmetry
Displacement of midline structures
Herniation

30
Q

Types of brain herniation

A

Subfalcine
Central
Tentorial
Tonsillar

31
Q

Subfalcine herniation

A

Cingulate gyrus pushed under the falx cerebri
Compression of the anterior cerebral artery
Ischaemia of medial parts of the frontal and parietal lobe and corpus callosum leading to an infarct
Can be secondary to stroke

32
Q

Tentorial herniation

A

The uncus or medial part of the parahippocampal gyrus herniated through the tentorial notch of the tentorijm cerebellum

  • damages the ipsilateral occulomotor nerve - down and out pupil
  • occlusion of the posterior cerebral artery and superior cerebellar artery causing ischaemia and infarction

Often fatal due to secondary haemorrhage into the brainstem - Duret haemorrhage

33
Q

Tonsilar herniation

A

Cerebellar tonsils are pushed down through the foramen magnum and compresses the medulla

Causes the Cushing’s reflex:
Early sign - raised BP - hypertension
Compression of respiratory centre - irregular breathing
Reflex bradycardia - low HR - low pulse

34
Q

Benign brain tumours

A

Meningioma - can get sudden development of epilepsy

- grow outwards and is not invasive

35
Q

Malignant brain tumour

A

Astrocytoma - spreads along nerve tracts and through the subarachnoid space

  • can include spinal cord as secondary
  • can occur in all ages but grade 1 commonly in younger patients and has a better prognosis
36
Q

Metastasising tumours

A

More common

  • Lymphoma
  • renal cell carcinoma
37
Q

Stroke

A

Sudden event producing a CNS disturbance due to a vascular disease

38
Q

Categories of stroke

A

Cerebral infarction - 85%

Cerebral haemorrhage -15%

39
Q

Risk factors of stroke

A

Hypertension
Hyperlipidaemia
Diabetes

40
Q

Causes of embolism

A
  • Heart - atrial fibrillation or mural thrombus
  • atheromatous debris - carotid atheromatous
  • thrombus over ruptured atheromatous plaque
  • aneurysm
41
Q

Types of infarct

A

Regional - dependent on what artery infarcted

Lacuna:

  • small less that 1cm
  • associated with hypertension
  • commonly affects the basal ganglia
42
Q

Types of cerebral haemorrhage

A

Intracerebral haemorrhage - 10% of strokes

Subarachnoid haemorrhage - 5%

43
Q

Intracerebal haemorrhage

A

Associated with chronic hypertension
Charcot - Bouchard aneurysms - affecting the lenticulostriate vessels of the basal ganglia
Associated with amyloid deposition around the cerebral vessels in the elderly
Can have an inherited disposition
- blow out haemorrhage

44
Q

Subarachnoid haemorrhage

A 
Rupture of berry aneurysms 
Thunderclap headache 
Sentinel headaches - small bleeds before major event 
Loss of consciousness 
Often instantly fatal
45
Q

Berry aneurysms

A

Aneurysms that commonly occur at the burfications of the circle of Willis

46
Q

Risk factors of subarachnoid haemorrhages

A

Male
Hypertension
Atheromatous
Poly cystic ovary disease

Clinical neuroscience (20 decks)

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