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Neurology SB > Pathology > Flashcards

Pathology Flashcards

1
Q

what type of cells line the ventricular system

A 
Ependyma cells 
(which are a type of Glial cell)
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2
Q

what cells act as the immune system in the brain

A

microglia

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3
Q

what cells act as a myelin sheath

A

oligodendrocytes

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4
Q

what are glial cells derived from

A

neuroectoderm

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5
Q

what are the 4 types of neuronal response to injury/disease

A

Acute neuronal injury
Simple neuronal atrophy
Sub-cellular alterations
Axonal reaction

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6
Q

what cells are most vulnerable to damage in the CNS when hypoxic and why

A

neurones

activation of glutamate receptors results in uncontrolled calcium entry into the cell

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7
Q

what is an axonal reaction

A

a reaction within the cell body that is associated with axonal injury

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8
Q

what is the cells response to axonal injury

A 
increased RNA and protein synthesis	
swelling of cell body
 peripheral displacement of nucleus
 enlargement of nucleolus
 breakdown of myelin sheath
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9
Q

what is the most important histopathological indicator of CNS injury

A

Gliosis

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10
Q

what are features of gliosis

A
  • astrocytes undergo hyperplasia and hypertrophy
  • nucleus enlarges
  • cytoplasmic expansion
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11
Q

what is the role of oligodendrocytes

A

warp around axons of neurones forming myelin sheath

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12
Q

what is injury to oligodendrocytes a feature of

A

demyelinating disorders

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13
Q

what is disruption of the ependymal cells associated with

A

ependymal granulations

local proliferation of sub-ependymal astrocytes
- produce small irregularities on the ventricular surfaces called ependymal granulations

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14
Q

what can cause changes in ependymal cells

A

infectious agents

viruses

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15
Q

how do microglia respond to injury

A
  • proliferate
  • develop elongated nuclei (rod cells)
  • forming aggregates about small foci of tissue necrosis (microglial nodules)
  • congregate around portions of dying neurones (neuronophagia)
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16
Q

how much CO does the brain receive

A

15% of CO

uses 20% of oxygen consumed by the body

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17
Q

what arteries branch off to provide blood supply to the brain

A

internal carotid artery

vertebral artery

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18
Q

what would a haemorrhage in the anterior cerebral artery cause

A
  • frontal lobe dysfunction
  • contralateral sensory loss in foot and leg
  • paresis of arm and foot, relative sparing of thigh and face
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19
Q

what would a haemorrhage in the middle cerebral artery cause

A
  • hemiparesis
  • hemisensory loss
  • aphasia/dysphasia
  • apraxia
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20
Q

what is Vertebrobasilar insufficiency

A

temporary set of symptoms due to ischemia in the posterior circulation of the brain

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21
Q

what does the posterior circulation of the brain supply

A

brain stem
cerebellum
occipital lobe

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22
Q

what conditions would infection in the brain stem cause

A

midbrain - webers syndrome

pons - medial and lateral inferior pontine syndromes

medulla - lateral medullary syndrome

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23
Q

what is the classical presentation of occipital stroke to a posterior artery occlusion

A

Homonymous hemianopia with macular sparing

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24
Q

what would a lack of blood to the cerebellum cause

A

Ataxia
Nystagmous
Intention tremor
Pendular reflexes (abnormal response to stimulus)

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25
Q

what conditions come under the term cerebra-vascular disease

A

Brain ischaemia and infarction
Haemorrhages
Vascular malformations and developmental abnormalities

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26
Q

what pathology can brain ischaemia/infarct cause

A

Global hypoxic-ischaemic damage

Focal infarcts – due to local vascular obstruction

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27
Q

what happens in Hypoxic-ischaemic Damage

A

neurones affected more (as they are more vulnerable than glial cells)

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28
Q

what is meant by ‘watershed’ areas in reference to Hypoxic-ischaemic Damage

A

junctions of arterial territories (arterial border zones) – they are first to be deprived of blood supply during hypotensive episodes

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29
Q

what is the definition of a stroke

A

sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours

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30
Q

what are the 2 types of stroke

A

infarction

haemorrhage

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31
Q

what are the subtypes of stroke

A

infarction

  • thrombotic
  • embolic

haemorrhage

  • intracerebral
  • subarachnoid
  • bleeding into infarct
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32
Q

what causes a cerebral infarction

A

local interruption of cerebral blood flow due to thrombosis or emboli

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33
Q

what is the risk factors of a cerebral infarction

A 
Atheroma
Hypertension
Serum lipids, obesity, diet
Diabetes mellitus
Heart disease
Diseases of neck arteries
Drugs
Smoking
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34
Q

what is the presentation of the brain between 4-12hrs, 15-20hrs and 24-36hrs after a cerebral infarction

A

4-12 = brain may appear normal

15-20 = ischaemic neuronal changes develop, defined margin between ischaemic and normal brain

24-36 = inflammatory reaction, extravasation of RBC. Activation of astrocytes and microglia

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35
Q

what is the presentation of the brain between 36-48hrs, day 3 and 1-2 weeks after a cerebral infarction

A

36-48 = necrotic area visible macroscopically, becomes swollen and softer than surrounding tissue

3 days = macrophages infiltrate into the area

1-2 weeks = stiffening of tissue and gliosis

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36
Q

what is the most common cause of a spontaneous SAH

A

rupture of a saccular aneurysm (i.e. Berry Aneurysm)

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37
Q

where do saccular aneurysm commonly occur

A

90% at arterial bifurcation of internal carotid artery

10% in vertebro-basilar circulation

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38
Q

what else can happen in a rupture of a Berry aneurysm apart from SAH

A

may also get intracerebral haematomas

infarcts of brain parenchyma

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39
Q

what are the symptoms of a SAH

A 
abrupt onset 
severe headache
vomiting 
LOC
meningeal signs 
CSF grossly bloody
no precipitating factor often
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40
Q

what are acute complications of SAH

A

cerebral infarcts (4-9 days), acute hydrocephalus, and herniation

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41
Q

what effect does hypertension have on the brain

A

increased amount of atheroma
hyaline arteriosclerosis
microaneurysms

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42
Q

what can complicate a case of severe hypertension

A

hypertensive encephalopathy

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43
Q

what is hypertensive encephalopathy

A

upper limit of autoregulation is exceeded by forced cerebral hyperperfusion, induced by eclampsia or malignant-phase hypertension.

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44
Q

what is ‘auto regulation’ and what happens when this fails

A

mechanisms help to maintain blood flow at a “constant” rate

hypoxic brain damage likely

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45
Q

what pathology is seen in hypertension and the brain

A
  • Lacunar infarcts
  • Intracerebral haemorrhage and haematoma formation – ruptured aneurysms
  • Multi-infarct dementia
  • Hypertensive encephalopathy
46
Q

what is demyelination

A

Preferential destruction of myelin sheath around axon

Relative preservation of axons themselves

47
Q

what causes demyelination

A

Diseases of myelin or oligodendrocyte/Schwann cell

48
Q

what does myelin allow for

A

rapid conduction of electrical impulses along cell membranes.

disruption of myelin sheath leads to disruption of electrical conductivity within the CNS

49
Q

what is a primary demyelinating disorder

A

MS

50
Q

what are examples of secondary demyelinating disorder

A
  • central pontine myelinosis
  • sub-acute sclerosing panencephalitis
  • AIDS
  • axonal degeneration
51
Q

what are other causes of demyelinating disorders

A

Metabolic

Toxic - cyanide, CO, solvents

52
Q

what is the morphological appearance of MS

A

External appearance of brain and spinal cord usually normal

Cut surface - multiple areas of demyelination, termed “plaques”

Well-demarcated plaques in white matter

May act as SOL

53
Q

what matter does MS affect

A

white matter

54
Q

how might plaques differ in appearance

A

acute lesions tend to be soft/pink

older lesions are firmer/pearly grey

55
Q

what areas can MS affect

A

occur at any site in the CNS

commonly seen in CN II, periventricular white matter, corpus callosum, brain stem and spinal cord

56
Q

what are the types of MS plaques

A

Acute active plaques
Chronic (inactive) plaques
Chronic active plaques
Shadow plaques

57
Q

what is the appearance of acute active plaques

A

demyelinated plaques that are yellow/brown, with an ill-defined edge which blends into surrounding white matter

58
Q

what is the appearance of inactive plaques

A

centre of an inactive plaque contains little or no myelin.

Astrocytic proliferation and gliosis are prominent.

59
Q

how do shadow plaques appear

A

Border between normal and affected white matter is not clearly defined.

Abnormally thinned out myelin-sheaths can be identified, especially at the outer edges.

60
Q

what is the appearance of chronic plaques

A

well-demarcated grey/brown lesions in white matter, classically situated around lateral ventricles

61
Q

to summarise what are the main histological features of MS

A

Demyelination
Inflammation
Gliosis (astrocytic gliosis particularly)

62
Q

dementia is subdivided into primary and secondary - what are examples of both

A

primary/organic dementia
- Alzheimer’s. diffuse levy body disease, huntington’s disease, Pick’s disease

secondary - vascular, metabolic, infection, trauma

63
Q

what is the most common cause of dementia in the elderly

A

Alzheimer’s disease (AD)

64
Q

what genetic condition has increased incidence of AD

A

Down’s Syndrome - Trisomy 21

65
Q

what are genetic links for familial AD

A

amyloid precursor protein (APP) gene found on chromosome 21,

presenilin 1 gene on chromosome 14

presenilin 2 gene on chromosome 1

66
Q

what is the macroscopic pathology of AD

A
  • decreased size and weight of brain (cortical atrophy)
  • widening of sulci
  • narrowing of gyri
  • compensatory dilatation ventricles, 2° hydrocephalus
67
Q

what lobes are affected in AD

A

frontal, temporal and parietal

68
Q

what is the microscopic pathology of AD

A

neurofibrillary tangles
Aß amyloid plaques (senile plaques)
amyloid angiopathy
extensive neuronal loss with astrocytosis

69
Q

what stain is used to look for amyloid collections

A

congo red

it goes Apple-green birefringence in the presence of amyloid

70
Q

what are the neurofibrillary tangles seen in AD mainly composed of

A

TAU protein

71
Q

what is the hallmark features of dementia with lewy bodies (DLB)

A

progressive dementia with hallucinations and fluctuating levels of attention

72
Q

what type of features can develop in DLB

A

features of Parkinson’s disease

73
Q

what are the pathological features of DLB

A

Degeneration of the substantia nigra
Remaining nerve cells contain abnormal structures called Lewy bodies
Degeneration of the cortical areas of the brain

74
Q

how can degeneration of the cortical areas of the brain with formation of lewy bodies be detected

A

immunochemical staining for the protein ubiquitin.

75
Q

what is the inheritance pattern of Huntington’s disease (HD)

A

Autosomal dominant

huntingtin gene of chromosome 4

76
Q

what is the pathological appearance of HD

A

loss of neurons in caudate nucleus and cerebral cortex accompanied by reactive fibrillary gliosis

77
Q

what is Pick’s disease

A

progressive dementia commencing in middle life (usually between 50 and 60 years) characterised by slowly progressing changes in character and social deterioration leading to impairment of intellect, memory and language

78
Q

pathology of Picks disease

A

Extreme atrophy of cerebral cortex in frontal and temporal lobes
Neuronal loss and astrocytosis
Pick’s cells (swollen neurons) Pick’s bodies (intracytoplasmic filamentous inclusions)

79
Q

what are symptoms in Pick’s disease related to

A

damage to frontal and temporal lobe

80
Q

what is multi-infarct dementia

A

deterioration in mental functioning due to changes or damage to the brain tissue from hypoxia or anoxia (lack of oxygen) as a result of multiple blood clots within the blood vessels supplying the brain.

81
Q

what causes multi-infarct dementia

A

successive, multiple cerebral infarctions cause increasingly larger areas of cell death and damage

82
Q

what are people with multi-infarct dementia prone to

A

anxiety and depression as they are aware of their mental deficits

83
Q

multi-infarct dementia can be difficult to distinguish from AD, what is more suggestive of multi-infarct dementia

A

Abrupt onset
Stepwise progression
History of hypertension or stroke
Evidence of stroke will be seen on CT or MRI

84
Q

what are the 2 types of causes of head injury

A

missile

non-missile

85
Q

what happens in a non-missile injury

A

Sudden acceleration/deceleration of head

Brain moves within cranial cavity and makes contact with bony protrusions.

86
Q

what are causes of a non-missile brain injury

A

RTAs
Falls
Assaults

87
Q

what are the different types of fractures seen in the skull

A

fissure fracture
depressed fracture
compound fracture
base of skull fractures

88
Q

what occurs at the moment of injury and what can it cause if severe

A

diffuse axonal injury

coma/vegetative state

89
Q

what are causes of diffuse axonal injury

A 
trauma
raised ICP
progression of inflammatory disease
progression od dementia
hypoxia
90
Q

what is the pathological time scale of axonal injuries

A

2-4 hrs - focal axonal accumulation of APP

12-24 - axonal swelling

24hrs - 2weeks - axonal swelling

2weeks - 5months - glial reaction

5months - years - degeneration and loss of myelinated fibres

91
Q

when is a traumatic extradural haematoma often a complication

A

fracture in temparoparietal region that involves middle meningeal artery

92
Q

what can happen is a extradural haematoma is left untreated

A

midline shift – compression and herniation

associated brain damage often minimal

93
Q

what are causes of raised ICP

A 
SOL
Oedema
Increased CSF (hydrocephalus)
Increased venous volume
physiological 
- hypoxia, hypercapnia, pain
94
Q

what are the effects of raised ICP

A

Intracranial shifts and herniations
Distortion and pressure on cranial nerves and vital neurological centres
Reduced level of consciousness
Impaired blood flow

95
Q

where are the common sites for herniations

A

falcine/cingulate
uncal
tonsillar
transcalvarium

96
Q

clinical signs of Raised ICP

A

papilloedema
nausea and vomiting
headache
neck stiffness

97
Q

what are examples of SOL

A

tumours (primary or mets)
abscess (single/multiple)
haematoma
localised swelling

98
Q

what are causes of a single abscess

A
  • otitis media
  • sinusitis
  • nasal/facial/dental infections
  • skull fractures
  • penetrating injury
  • neurosurgical procedures
99
Q

what are causes of multiple abscess

A
  • septicaemia
  • acute bacterial endocarditis
  • bronchiectasis
  • lung abscess
  • cyanotic heart disease
  • IV drug use
100
Q

what causes focal oedema

A

present as a result of other pathological lesions, such as infarcts, can also lead to an increase in intracranial pressure.

101
Q

what is generalised cerebral oedema

A

Increased water content of the brain (either intracellular or extracellular)

102
Q

what commonly causes extradural haemorrhages

A

rupture of meningeal arteries

skull fractures

103
Q

what happens in an extradural haemorrhage

A

compress the subjacent dura and flatten gyral crest of underlying brain

104
Q

what can be complications of an extradural haemorrhage

A

uncal gyral/cerebellar tonsillar herniation

death.

105
Q

what causes subdural haemorrhages

A

disruption of bridging veins that extend from the surface of the brain into subdural space

106
Q

what is a subdural haemorrhage

A

Collections of blood between the internal surface of dura mater and arachnoid mater

107
Q

what are features of an acute subdural haemorrhage

A

clear history of trauma
unilateral or bilateral
associated with other traumatic lesions

gyral contours preserved
swelling of cerebrum on side of haematoma

108
Q

what are features of a chronic subdural haemorrhage

A

associated with brain atrophy

composed of liquefied blood/yellow-tinged fluid

109
Q

what are Sx of a chronic subdural haemorrhage

A

altered mental status

focal neurological deficits

110
Q

what are astrocytes

A

star shaped glial cells

111
Q

what are the functions of astrocytes

A

provide support to blood brain barrier

role in repair and scarring

provision of nutrients

maintenance of ion balance

Neurology SB (23 decks)

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