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Gastrointestinal > Lecture 13– Introduction to neuropathology > Flashcards

Lecture 13– Introduction to neuropathology Flashcards

1
Q

types of neuropathology

A

infections

dementia

increased intracranial pressure

stroke

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2
Q

the CNS is usually sterile. name 3 routes of entry of microorganisms

A
  • Direct spread e.g. middle ear infection, base of the skull
  • Blood borne e.g. sepsis, infective endocarditis (bacterial emboli)
  • Iatrogenic e.g. Ventricular-Peritoneum (hydrocephalus) shunt, surgery, lumbar puncture
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3
Q

Cerebral abscess cause by middle ear infections

A
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4
Q

Acute Meningitis

A
  • Inflammation of the leptomeninges (pia/arachnoid )
  • With or without septicaemia
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5
Q

why is prompt diagnosis life saving in people with acute meninigits

A

disease process moves very quickly

  • Oedema in the brain due to acute inflammation (very quick decline)
  • Inflammatory cell influx
  • Raises ICP = death
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6
Q

Causative organism (various in immunocompromised individuals): neonates

A

E.Coli, L. monocytogenes

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7
Q

Causative organism (various in immunocompromised individuals): 2-5 yrs

A

H. influenza type B (HiB)

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8
Q

Causative organism (various in immunocompromised individuals): 5-30 yrs

A

N. Meningitides

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9
Q

Causative organism (various in immunocompromised individuals): over 30

A

S. Pneumonia

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10
Q

Chronic meningitis

A
  • Chronic clinical course
  • Rare
  • Causative agent: Tuberculosis
    • Granulomatous inflammation
    • Fibrosis of the meninges
    • Nerve entrapment
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11
Q

Complication of meningitis

A
  • Local
    • Death (swelling –> Raised intracranial pressurte (RICP))
    • Cerebral infarction –> neurological deficit
    • Cerebral abscess
    • Subdural empyema (pus within a potential space)
    • Epilepsy
  • Systemic (if associated with septicaemia)
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12
Q

differenc e between encephalitis and meningitis

A
  • Parenchyma not meninges
    • Neuronal cell death by virus
      • Inclusion bodies
    • Temporal lobe
      • Herpes virus
    • Spinal cord motor neurones
      • Polio
    • Brainstem
      • Rabies
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13
Q

encephalitis is usuallly

A

viral and self-limiting (viral flu like illness/ headaches)

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14
Q

ecephalitis brain

A

damage caused lymphocytic inflammatory reaction

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15
Q

what is a prion

A

a proteion (PrP)

  • A normal constituent of synapse
  • Problems when this protein mutates
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16
Q

ways Prions mutate

A
  • Sporadic mutation
  • Familial mutation
  • Ingested mutation
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17
Q

how do mutated Prions (PrPs) cause disease

A
  • Mutated PrP interacts with normal PrP to undergo a post translation conformation changeà PrPs start to aggregate
  • Extremely stable structure
    • Insoluble
    • Causes cell death
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18
Q

vCJD

A

Variant Creutzfeldt-Jakob Disease (vCJD)

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19
Q

Variant Creutzfeldt-Jakob Disease (vCJD)

A

Variant Creutzfeldt-Jakob disease (vCJD) is a prion disease that was first described in 1996 in the United Kingdom. There is now strong scientific evidence that the agent responsible for the outbreak of prion disease in cows, bovine spongiform encephalopathy (BSE or ‘mad cow’ disease), is the same agent responsible for the outbreak of vCJD in humans.

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20
Q

vCJD is different fro

A

classical CJD (e.g. a form of dementia)

  • Each has a unique genetic prion
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21
Q

characteristics of vCJD infection which make it different to classic CJD

A
  • Prolonged incubation period of 15+ year
  • Prions not eradicated by traditional sterilisation
  • More symptoms and effects patients at younger age
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22
Q

comparison table comparing classical CJD and variant CJD

A
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23
Q

is vCJD an infection? Think about Kochs postulates

A

debatable

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24
Q

define dementia

A

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

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25
Q

types of demenita

A
  • Alzheimer’s (50%)
    • Sporadic/ familial
    • Early/late
  • Vascular dementia (20%)
  • Others e.g. Lewy body, rare
26
Q

Alzheimers disease (AD)

A
  • Exaggerated aging process
  • Loss of cortical neurones
    • Brain weight decreases
    • Cortical atrophy (cortex becomes thinner)
      • Increases sulci and gyri definition
  • Due to increased neuronal damage
    • Neurofibrillary tangles
    • Senile plaques
27
Q

ways neuronal damage occurs in AD

A

Neuronal damage in AD

  • Neurofibrillary tangles
  • Senile plaques
  • Amyloid deposition in vessels in centre of plaque
28
Q
  • Neurofibrillary tangles
A
  • Intracellular twisted filaments of tau protein
  • Tau normally binds and stabilises microtubules
  • Tau becomes hyperphosphorylated in AD –> Tauopathy
29
Q

Senile plaques

A

Foci of enlarged axons, synaptic terminals and dendrites

  • Amyloid deposition in vessels in centre of plaque
30
Q

Amyloid deposition in AD

A

Central to pathogenesis

  • E.g. Downs syndrome
    • Trisomy 21
      • 3 mutations on chromosome 21
      • Amyloid precursor protein (APP) gene
      • Presenilin (PS) genes 1 and 2 code for components of secretase enzymes
      • Leads to incomplete breakdown of APP and therefore amyloid is deposited
    • Early onset AD
31
Q

Normal ICP

A
  • 0-10mmHg
  • Coughing and straining increase to 20 mmHg
  • Only significant if the increase maintained for several minutes
32
Q
  • Compensation mechanisms to maintain normal pressure
A
  • Reduce blood volume
  • Reduced CSF volume
  • Spatial- brain atrophy
33
Q
  • Vascular mechanisms maintain cerebral blood flow as long as ICP <
A

60 mmHg

34
Q

What causes ICP

A

Expanding lesion (SoL)

  • Tumour, haemorrhage, oedema
35
Q

SoL cause

A
  • Deformation or destruction of the brain around the lesion
  • Displacement of midline structures- loss of symmetry
  • Brain shift resulting in internal hernia (tentorium cerebelli)
36
Q

define hernia

A

a protrusion of an organ or part of an organ through wall that normally contains it

37
Q

types of herniation

A

subfalcine

tentorial

tonsilar

38
Q

subfalcine herniation

A

It is generally caused by unilateral frontal, parietal or temporal lobe disease that creates a mass effect with medial direction of the ipsilateral cingulate gyrus beneath the free edge of the falx cerebri due to raised intracranial pressure.

  • Occurs same side as mass
    • Contralateral leg weakness
39
Q
A
40
Q
A
41
Q

what can result due to subfalcine herniation

A
  • Ischaemia of medial parts of the frontal and parietal lobe and corpus callosum due to compression of anterior cerebral artery–> infarction
42
Q

tentorial herniation

A
  • Uncus (medial part of the Para hippocampal gyrus) gets forced through the tentorial notch as the brain swells
    • Damage to the oculomotor nerve on the same side (clinical sign- down and out eye)
    • Occlusion of blood flow in posterior cerebral and superior cerebellar arteries
  • Frequently fatal because of secondary haemorrhage in the brainstemà duret haemorrhage
    • Common cause of death in those with large brain tumours
43
Q

tonsilar herniation

A
  • Cerebellar tonsils pushed into the foramen magnus compressing the brainstem
  • Suppressing cardiorespiratory centres
  • High BP low pulse (Cushings reflex)
  • ‘Coning’
44
Q

homeostatic response which worsens brain damage during RICP

A

Herniation will cause increase in BP to increase blood supply to the brain–> becomes even more swollen

45
Q

primary tumours

A
  • rare
  • benign (usually)
  • malignant
46
Q

benign primary tumour

A
  • Meningeal origin –> meningioma
47
Q

malignant primary tumour

A
  • Astrocyte origin –> astrocytoma (grade 1 –> grade 4)
    • Younger the patient usually lower grade
    • grow very rapidly
    • cause death via increased ICP
    • spread along nerve tracts and through sub arachnoid space often presents with a spinal secondary
      • will never metastasise out of the CNS
  • others
    • neurofibroma (NF)
    • ependymoma
    • neuronal e.g. medulloblastoma
48
Q
A
49
Q

Secondary tumours, metastasis most common

*

A
50
Q

meningioma

A
  • Doesn’t grow into the brain
  • Common presenting sign - epilepsy
51
Q

stroke- a vascular disease

A
  • A disease of blood vessels supplying the brain
  • Sudden event producing a disturbance of CNS function due to vascular disease
  • Common
  • Clinical features depends on site and type of lesion
  • 2 categories
52
Q

2 categories of stroke

A
  • Cerebral infarction – 85%
    • Embolism (most common)
    • Thrombosis
  • Cerebral haemorrhage – 15%
    • Spontaneous i.e. non-traumatic
    • Intracerebral haemorrhage 10% of all stroke
    • subarachnoid haemorrhage- 5%
53
Q
A
54
Q

cerebral infarction- embolism (most common)

A
  • Heart- AF, mural thrombus
  • Atheromatous debris (carotid atheroma)
  • Thrombus over ruptures atheromatous plaque)
  • Aneurysm
55
Q

cerebral infarction- thrombosis

A

over atheromatous plaque

56
Q

Cerebral haemorrhage – Intracerebral haemorrhage

A
  • Produced SOL
  • May be inherited
  • Deposition of amyloid around cerebral vessels in the elderly
  • Charcot-bouchard aneurysm
  • Associated with hypertensive vessel damage
57
Q

cerebral haemorrhage- subarachnoid haemorrhage

A
  • Subarachnoid haemorrhage 5% of all strokes
    • Rupture of berry aneurysms (bifurcation of circle of willis)
    • Pathogenesis poorly understood
      • More common in males
      • Hypertension
      • Atheroma
      • Linked to other diseases e.g. polycystic kidney disease
    • Sudden severe headache- thunderclap
    • Seninel headache
    • Loss of consciousness
    • Often instantly fatal
58
Q

berry aneursysm

A
59
Q

intracerebral haemorrhage

A
60
Q

Risk factors for atherosclerosis

A
  • Hyperlipidaemia
  • Hypertension
  • DM
61
Q

Types of infarct

A
  • Regional
    • Named cerebral artery or carotid
  • Lacunar e.g. basal ganglia
    • Less than 1cm
    • Associated with hypertension
    • Commonly affects the basal ganglia

Gastrointestinal (35 decks)

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