Neuropathology Flashcards

1
Q

What are the 3 routes by which microorganisms can gain entry to the CNS?

A
  1. Direct Spread from a physical breach- e.g. middle ear infection, base of skull fracture
  2. Blood-borne - sepsis, infective endocarditis
  3. Iatrogenic (by medical professionals) - e.g. V-P shunt, surgery, lumbar puncture
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2
Q

What is meningitis, what are the consequences of it if left untreated?

A

Meningitis is inflammation of the leptomeninges (pia + arachnoid mater). Can occur with/ without septicaemia

Untreated causes rapid influx of oedema, neutrophil influx causes pus → raises ICP leading to death if not quickly treated

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3
Q

What are the main causative organisms of meningities in the age groups:

Neonates

2-5 years

5-30 years

Over 30s

A

Neonates - E.coli, L. monocytogenes

2-5 years - H. influenzae type B (HiB) - vaccinated against

5-30 years - N. Meningitides types A,B+C

Over 30s - S.pneumoniae

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4
Q

What organism causes chronic meningitis?

What are the effects of having chronic meningitis?

A

Mycobacterium Tuberculosis

  • Granulomatous inflammation
  • Fibrosis of the meninges
  • Nerve entrapment
    • facial nerve palsy
    • headache
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5
Q

What are the some the local and systemic complications of meningitis

A

Local:

  • Death (swelling raises ICP)
  • Cerebral infarction → neurological deficit
  • Cerebral abcess
  • Subdural empyema → chronic pus
  • Epilepsy

Systemic: if associated with speticaemia

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6
Q

What is Encephalitis?

A

Inflammation of the parenchyma (not the meninges) in the brain - affects neuronal cell bodies

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7
Q

What type of microorganisms cause encephalitis affecting different areas of the brain:

  • Neuronal cell death
  • Temporal lobe
  • Spinal cord motor neurones
  • Brain Stem
A

Mainly viral not bacterial

  • Neuronal cell death - inclusion bodies (build up of virus)
  • Temporal lobe - Herpes Virus
  • Spinal cord motor neurones - Polio
  • Brain Stem - Rabies
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8
Q

How do you treat encephalitis?

A

Often self limiting in young patients as long as they’re not immunocompromised

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9
Q

What are prions?

A

Prions are proteins we all have that are a part of synpases

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10
Q

What is prion disease?

A
  • Mutation in prion proteins that are either sporadiac, familial or ingested
  • Mutated PrP interacts with normal PrP to induce post translational conformational change
  • Makes an extremely stable striucture that aggregates and cannot be elimited
  • Causes neuronal death and holes in grey matter → spongiform encephalopathies
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11
Q

Name some types of spongiform encephalopthies

A
  • Scrapie in sheep
  • BSE in cows
  • vCJD- Variant Creutzfeld- Jacob Disease - strongly associated with BSE
  • Kuru in tribes of New Guinea
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12
Q

There are 2 forms of vCJD, classic and variant. What are the different clinical features of each?

A
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13
Q

Why is prion diease not classed as infection?

A
  • Infectious agents should not be found in healthy organisms which prions are
  • Microorganisms must be isolated and grown in pure culture- proteins cannot be grown
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14
Q

What is dementia?

Name the most common types

A

Aquired global impairment of intellect, reason and personality without impairment of conciousness

  • Alzehimer’s (50%)- Sporadic/ Familial, Early/ Late
  • Vascular dementia (20%)
  • Lewy body
  • Pick’s disease (Fronto-temporal dementia)
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15
Q

What happens to the brain in Alzheimer’s Disease?

A
  • Brain undergoes an exggerated aging process
  • Loss of cortical neurones
    • decreased brain weight- greater sulci/ gyri definition
    • cortical atrophy (thinner cortex)
  • Neurofibrillary tangles and senile plaques cause increased neuronal damage
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16
Q

What are neurofibrillary tangles?

A
  • Found in Alzheimer’s Disease
  • Intracellular twisted filaments of Tau protein
  • Tau, normally binds and stabilies microtubules
  • Tau becomes hyperphospharylated and starts to aggregate
  • Cell can’t function and produce energy → death
17
Q

What are senile plaques?

A
  • Plaques found in Alzheimer’s Disease
  • Foci of englarged axons, synaptic terminals and dendrites
  • Amyloid deposition in vessels in the centre of the plaque- buolds up around blood vessels causing ischemia
  • Look like balls of cotton wool
18
Q

What is the link between amyloid deposition and chromosome 21?

A
  • Down’s syndrome (trisomy 21) will have early onset AD
  • Mutation in 3 genes on trisomy 21 throught to be ivolved
  • Amyloid precursor protein (APP) gene
  • Presenlin genes 1 and 2 make secretase (enzyme that breaks down amyloid)
  • Leads to incomplete breakdown of APP and amyloid is deposited
19
Q

What is normal brain ICP?

A

0-10 mmHg

(may increase to 20mmHg during coughing and straining)

20
Q

What compensatory mechanisms happen to maintain noraml brain ICP?

A
  • Recued blood volume
  • Reduced CSF volume
  • Spatial → brain atrophy (if raised ICP is chronic)

Mechanisms work as long as ICP is <60 mmHg

21
Q

If ICP raises too much it will cause herniation. What are the different types of herniation?

A
  • Subfalcine
  • Tentorial
  • Tonsilar
22
Q

Explain what happens in a subfalcine herniation

A
  • The cingulate gyrus on the same side of the SoL is pushed under the free edge of the falx cerebri
  • Causes ischemia of medial parts of the frontal & parietal lobes and the corpus callosum due to compression of the anterior cerebral artery → infarction
23
Q

What happens in tentorial herniation?

A
  • The uncus (medial part of the parahippocampal gyrus) is pushed through the tentorial notch
  • Can cause damage to the occulomotor nerve (on the same side)
  • Occlusion of blood flow in posterior cerebral and uperior cerebrallar arteries
  • Frequently fatal due to secondary haemorrhage into the brainstem (Duret Haemorrhage- of the midbrain & pons)
24
Q

What happens in tonsilar herniation?

A
  • Cerebellar tonsisl are pushed into the foramen magnum compressing the brainstem
  • Early on- blood can’t get to brain so systemic blood pressure rises to compensate
  • After time- brainstem herniation depresses cardio respiratory centres
  • Cushing’s reflex : High BP and Bradycardia
25
Q

How common are tumours of the brain?

A

Primary tumours are rare, will more commonly see secondary tumours from other sites

26
Q

Which tumours commonly metastasise to the brain?

A
  • Renal Cell Carcinoma
  • Malignant Melanoma
27
Q

What is a menangioma?

A

A benign tumour of meningeal origin

Often found incidentally- can present as new onset epilepsy

28
Q

What is an astrocytoma?

A

A maligant tumour of astrocyte origin (Grades 1-4)

Lower grades more common in younger people, in adults usually very aggressive 3-4 month survival

Won’t metastasise outside the CNS → spread along nerve tracts and through sub arachnoid space often present as spinal accessory

29
Q

What is a stroke?

A

A sudden event producing a distrubance of CNS function due to Vascular disease

2 broad categories: Cerebral infarction 85%

Cerebral haemorrhage 15%

30
Q

What types of infarct can you get in stroke?

A

Regional - names agter the cerbral artery or carotid

Lacuna - less than 1cm, associated with hypertension, commonly affects the basal ganglia

31
Q

How do subarachnoid haemorrhages occur?

A

Rupture of berry aneurysms usually at bifuraction points of the circle of Willis

Pathogenesis poorly understood; male sex, hypertension, atheroma, links to other disease

32
Q

What symptoms would you associate with a subarachnoid haemorrhage?

A
  • Severe sudden onset headache - thunderclap
  • Sentinal headaches (small bleeds before main headache)
  • Loss of conciousness
  • Often instantly fatal