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Y3 NEUROLOGY > Pathology > Flashcards

Pathology Flashcards

1
Q

List factors and substances that can damage cells of the CNS

A 
Lack of oxygen (hypoxia)
Trauma
Toxins
Metabolic disturbance
Malnutrition
Infection
Ageing
Genetic mutations
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2
Q

Which component of the CNS is most vulnerable to hypoxia? What key characteristic of this component would suggest acute hypoxic damage?

A

Neurones

Intensely red cytoplasm - ‘RED NEURONE’

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3
Q

Which cells are the “macrophage cells” of the CNS?

A

Microglia - involved in phagocytosis

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4
Q

Axonal injury involves a reaction in which part of the neurone?

A

Reaction within cell body

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5
Q

In which direction does the axon damage in response to injury?

A

Anterograde degeneration of axon distal to site of injury

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6
Q

Which process do astrocytes initiate in response to injury?

A

Reactive proliferation - gliosis - where cells undergo hyperplasia and hypertrophy

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7
Q

Which process if the most important histopathological indicator of CNS injury, regardless of cause?

A

Gliosis

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8
Q

Which cells line the ventricular system?

A

Ependymal cells

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9
Q

The brain receives how much of the cardiac output and how much oxygen, respectively?

A

15%

20%

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10
Q

What is the response of vasculature to the brain in hypotension and hypertension? What is this automatic response called?

A

Constricts in hypertension
Dilates in hypotension
Autoregulation

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11
Q

What are the two main sets of arteries supplying blood to the brain?

A

Branches of internal carotid + vertebral arteries (form anterior + posterior circulations)

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12
Q

Lack of blood supply in the anterior cerebral artery is associated with which dysfunctions?

A

Frontal lobe dysfunction
Contralateral sensory loss in foot + leg
Paresis of arm + foot

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13
Q

Lack of blood supply in the middle cerebral artery is associated with which dysfunctions?

A

Hemiparesis
Hemisensory loss
Aphasia/dysphasia
Apraxia

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14
Q

Lack of blood supply in the posterior cerebral artery (vertebrobasilar) is associated with which cerebellar dysfunctions?

A

Ataxia
Nystagmus
Intention tremor
Pendular reflexes

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15
Q

Lack of blood supply in the posterior cerebral artery (vertebrobasilar) is associated with which occipital lobe dysfunctions?

A

Homonymous hemianopia with macular sparing

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16
Q

When does gliosis occur following a cerebral infarct?

A

1-2 weeks

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17
Q

What is the most common cause of a subarachnoid haemorrhage?

A

Spontaneous rupture of a saccular aneurysm (Berry aneurysm)

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18
Q

List diseases that have increased incidence of Berry aneurysms

A

Polycystic kidney disease
Fibromuscular dysplasia
Coarctation of aorta

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19
Q

Most berry aneurysms occur where?

A 
90% = arterial bifurcations near internal carotid artery
10% = vertebrobasilar circulation
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20
Q

At which diameter do berry aneurysms have greatest risk of rupture?

A

6-10mm

If over 25mm, risk of rupture decreases

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21
Q

Lacunar infarcts can be present in hypertensives. What are they?

A

Small cavities up to 10mm in diameter found in basal ganglia, thalami in pons

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22
Q

What is demyelination?

A

Destruction of myelin sheath surrounding an axon, either due to breakdown or abnormal production

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23
Q

What common disease comes under primary demyelination?

A

Multiple sclerosis

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24
Q

What is the female:male affected ratio for MS?

A

2:1

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25
Q

The external appearance of the brain and spinal cord in MS is usually normal. True/False?

A

True

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26
Q

MS is a grey matter disease. True/False?

A

False

MS is a white matter disease

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27
Q

Describe the morphology of MS

A

Well-demarcated plaques in white matter in a non-anatomical distribution

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28
Q

Describe the colour of MS plaques

A

Active lesions: soft pink

Non-active lesions: firm pearl-grey

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29
Q

What structures do MS plaques commonly affect?

A 
Optic nerve
Periventricular white matter
Corpus callosum
Brainstem
Spinal cord
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30
Q

Where do chronic inactive MS plaques typically occupy?

A

Situated around lateral ventricles

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31
Q

Dementia is always pathological. True/False?

A

True

Neurodegenerative disorder, not just part of ageing!

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32
Q

List diseases classified as primary dementias

A

Alzheimer’s disease
Huntington’s disease
Pick’s disease
Lewy body dementia

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33
Q

What is the female:male ratio for Alzheimer’s disease?

A

2:1

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34
Q

List the genes the can be involved in Alzheimer’s disease

A

Amyloid precursor protein (c21)
Presenilin 1 (c14)
Presenilin 2 (c1)
ApoE (allele e4)

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35
Q

Describe the morphology of Alzheimer’s disease on the brain

A

Cortical atrophy
Widened sulci
Narrowed gyri
Dilated ventricles

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36
Q

Which lobes are particularly affected in Alzheimer’s disease?

A

Frontal
Temporal
Parietal

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37
Q

Which protein forms plaques in Alzheimer’s disease? How are the plaques formed?

A

Amyloid precursor protein forms central core of neuritic plaques
Oligomerisation of aB fibres

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38
Q

What colour does amyloid protein stain?

A

Congo red

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39
Q

Which protein in the brain can become tangled and defective in Alzheimer’s disease? What is it found in?

A

Tau protein

Neurofibrillary tangles

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40
Q

Which area of the brain is affected in Lewy body dementia leading to features of parkinsonism?

A

Substantia nigra

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41
Q

Which protein, when stained, can help detect Lewy bodies?

A

Ubiquitin

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42
Q

What happens to the caudate nucleus in Huntington’s disease?

A

Caudate atrophy with loss of neurons

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43
Q

What are the histopathological landmarks of Pick’s disease dementia?

A 
Swollen neurons (Pick's cells)
Filamentous inclusions (Pick's bodies)
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44
Q

Which lobes does Pick’s disease usually affect?

A

Frontal

Temporal

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45
Q

What is the most common type of secondary dementia?

A

Vascular (multi-infarct) dementia

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46
Q

What is the main cell involved in repair ans scar formation in the CNS?

A

Astrocyte

47
Q

Which cells in the CNS are most sensitive to oxidative damage?

A

Oligodendrocytes

48
Q

Microglia are the main cells involved in the formation of _____ around necrotic and damaged tissue

A

Aggregates

49
Q

Neurones are organised into aggregates. What is meant by the term ‘aggregate’?

A

Nuclei ganglia with columns/ layers and assigned functional domains

50
Q

Subcellular alteration in neurones in response to injury would result in the accumulation of which component of the CNS?

A

Proteins

51
Q

Hypoxia as a result of nervous system injury triggers what process in the cell?

A

Excitotoxicity
Energy failure in cell —> collapse of presynaptic MP —> release of glutamate into synapses —> alters calcium homeostasis —> APOPTOSIS

52
Q

Outline the progress of oedema into haemorrhagic conversion

A

CYTOTOXIC OEDEMA: dying cells accumulate sodium and chloride ions, causing osmosis and the shift of water —> swollen cell
IONIC OEDEMA: BBB dysfunction; shift of sodium and chloride into cells creating an osmotic gradient (more water)
VASOGENIC OEDEMA: BBB becomes more dysfunct allowing larger molecules like albumin to cross (very osmotically active) —> profound oedema
HAEM CONVERSION: BBB lets in RBCs (noxious due to high iron content)

53
Q

During osmosis in the brain tissue, there is an increased in fluid. True/ False?

A

False

Movement of fluid from extracellular to intracellular

54
Q

Cerebral ischaemia and infarction can be classified into two categories. What are they? What are they caused by?

A

Global (generalised reduction in blood flow/ oxygenation) due to severe hypotension
Focal due to vascular obstruction

55
Q

At what MAP are autoregulatory mechanisms unable to compensate, leading to reduced cerebral perfusion?

A

<50mmHg

56
Q

Which area of the brain is particularly sensitive to reduced perfusion and is formed by the bridging of 2 arterial territories on peripheries?

A

Watershed areas

57
Q

If cerebral ischaemia and infarction is severe enough, which pathological process will result?

A

Pan necrosis

58
Q

List the processes of remodelling that occur in hypertension and cerebrovascular disease. Why are these processes significant in cerebral perfusion?

A 
Increased atherosclerosis
Arteriosclerosis
Fibrinoid necrosis of BV walls
Charcut-Bouchard (micro-aneurysms)
INCREASED BP NEEDED TO PERFUSE BRAIN
59
Q

List the long term consequences of prolonged hypertension

A 
Lacunar infarcts
Multi-infarct demetia (multiple lacunar infarcts)
Aneurysm formation and rupture
Intracerebral haemorrhage
Hypertensive encephalopathy
60
Q

What are the types of intracranial haemorrhage?

A

Spontaneous

Traumatic

61
Q

What is the typical appearance of intracerebral haemorrhage?

A

Massive black spot on white matter of basal ganglia

62
Q

List the causes of intracranial haemorrhage

A 
Hypertension
DM
Vaculitis
Coagulation disorders
Amyloid angiopathy
Amyloid deposits (ageing)
Drugs
Aneurysms/ vascular malformations
Heart surgery
SAH
63
Q

What is the pathogenesis of amyloid angiopathy that can lead to ICH?

A

Lack of compliance of small blood vessels

64
Q

What is the pathogenesis of AV malformation that can lead to ICH?

A

Shunting from an artery to a vein and the brain cannot cope with the high pressure in the artery

65
Q

SAH can lead to what emergency clinical condition in affecting the brain?

A

Hydrocephalus (blood in subarachnoid space, creates haematomas, leading to increased ICP)

66
Q

CSF should be clear and acellular. List the limited number of cells found in CSF.

A

Lymphocytes
Monocytes
Glucose
Protein

67
Q

Which cells in particular should not be found in CSF?

A

RBCs

Neutrophils

68
Q

What are the 3 mechanisms in which CSF can accumulate in the ventricular system? Give examples for each

A 
Obstruction (e.g. inflam, pus, tumours)
Reduced reabsorption (post SAH, meningitis)
Overproduction (choroid plexus tumour)
69
Q

What are the two types of hydrocephalus?

A

Non-communicating (obstruction of CSF flow in ventricular system)
Communicating (outside ventricular system)

70
Q

Define ‘hydrocephalus ex vacuo’

A

Dilatation of ventricular system and compensatory increase in CSF secondary to loss of brain parenchyma

71
Q

Brain herniation can result due to raised intracranial pressure. Describe a subfalcine herniation

A

Cingulate gyrus pushed under falx cerebri, resulting in limb weakness

72
Q

Which structures are particularly at risk in a subfalcine herniation?

A

Anterior cerebral arteries

Paramedian cortex

73
Q

Brain herniation can result due to raised intracranial pressure. Describe a transtentorial herniation

A

Medial temporal lobe squeezed under tentorium

74
Q

Which structures are particularly at risk in a transtentorial herniation?

A

CN III
Posterior cerebral artery
Cerebral peduncle
Upper brainstem (later)

75
Q

Brain herniation can result due to raised intracranial pressure. Describe a cerebellar tonsillar herniation

A

Cerebellar tonsils forced through foramen magnum

76
Q

Which structures are particularly at risk in a tonsillar herniation?

A

Brainstem

CSF outflow

77
Q

Brain herniation can result due to raised intracranial pressure. Describe a transcalvarial herniation

A

Outside skull forced through fracture

78
Q

List types of space occupying lesions that can increase ICP. Which is most common?

A

Primary tumour
Metastatic tumour (most common)
Abscess
Haematoma

79
Q

How do patients with SOLs typically present?

A

Headaches (worse in morning)
Vomiting
Seizures
Visual defects inc. papilloedema

80
Q

Why do patients with SOLs have headaches worse in the morning?

A

Hypercapnia develops overnight

81
Q

CNS tumours can occur in all age groups. In which age group are CNS tumours the most common solid malignancy?

A

Childhood

82
Q

The most common malignant primary tumour in adults is…

A

Astrocytoma

83
Q

The most common malignant primary tumour in children is…

A

Medullablastoma

84
Q

The most common benign primary tumour is…

A

Meningioma

85
Q

Abscesses will present with symptoms of SOL and which other clinical sign?

A

Fever

86
Q

How are abscesses diagnosed and managed?

A

CT/MRI
Aspiration for culture
Antibiotics

87
Q

List the two main types of skull fracture

A

Linear (diastatic fracture)

Compound (full thickness scalp laceration (depressed))

88
Q

What is a surface contusion?

A

Bruise to brain

89
Q

What are the two types of surface contusions?

A

Coup: impact on brain

Contra-coup: Opposite side that the brain hits off

90
Q

What are the two theories explaining why contra-coup injuries are worse than coup?

A

Dense CSF moves to impact coup first

Low pressure cavitation bubbles gravitate to contra-coup side

91
Q

Intracranial haematoma can be divided into two sub-categories. What are they?

A

Extradural (80%)

Intradural (20%) - subdural, intracerebral

92
Q

Intracranial haematomas typically arise due to a fracture to what area of the skull? What artery is affected?

A

Squamous portion of temporal bone

Middle meningeal artery

93
Q

What are the two subdivisons of subdural haematoma? What is their aetiology?

A

ACUTE: History of trauma, usually head injury in elderly
CHRONIC: Associated brain atrophy

94
Q

Which T cell factors influence the pathogenesis of MS?

A

TH1: IFNg macrophages
TH17: recruit and activate damaging leukocytes

95
Q

What humeral factor influences the pathogenesis of MS?

A

Oligoclonal IgG bands on CSF

96
Q

Define ‘dementia’

A

Acquired and persistent generalised disturbance of higher mental functions in otherwise fully alert person

97
Q

Outline the pathogenesis of dementia

A

Progressive loss of neurones, typically affecting functionally related neuronal groups

98
Q

List diseases classified as secondary dementias

A

Multi-infarct (vascular) dementia
Infection (HIV, syphillus)
Trauma
Metabolic

99
Q

Which form of dementia is the most common cause of dementia in the elderly?

A

Alzheimer’s

100
Q

Define ‘Alzheimer’s dementia’

A

Insidious impairment of higher intellectual function, with alterations in mood and behaviour

101
Q

Outline the pathogenesis of amyloid angiopathy

A

Extracellular eosinophillic accumulation forms B pleated sheets from aB fibres that disrupt the BBB (leads to oedema and hypoxia)

102
Q

Define ‘Lewy Body dementia’

A

Progressive dementia with hallucinations and fluctuation of attention/ cognition

103
Q

What clinical sign distinguishes Lewy Body dementia from Alzheimer’s?

A

Memory is affected later in Lewy Body dementia

104
Q

Idiopathic parkinsonism is otherwise defined as…

A

Parkinson’s Disease

105
Q

Define ‘Hintingdon’s disease’

A

Relentlessly progressive neuropsychiatric disorder, occuring between the ages of 30-50yo

106
Q

List the clinical symptoms of Huntingdon’s disease. Highlight the classical feature.

A 
CHOREA
Myoclonus
Clumsiness
Slurred speech
Depression
Irritability
Apathy
107
Q

Outline the inheritance pattern of Huntingdon’s Disease

A

Gene on chromosome 4p

Increase in CAG repeats corresponds to severity of diasease

108
Q

Define ‘Picks Disease’

A

Progressive dementia, typically occuring in 50s-60s characterised by change in character and social deterioration leading to impairment of intellect, memory and language

109
Q

List the clinical symptoms of Picks Disease, corresponding to damage to the frontal and temporal lobes

A

Personality and behavioural change
Speech and communication problems
Changes in eating habits
Reduced attention span

110
Q

Define ‘multi-infarct dementia’

A

Disorder involving deterioration in mental function due to cumulative damage to the brain via hypoxia from multiple blood clots in BVs of the brain

111
Q

Multi-infarct dementia is more common in males than females. True/ False?

A

True

112
Q

What clinical sign distinguishes multi-infarct dementia from Alzheimer’s?

A

Abrupt onset
Stepwise progression
History of hypertension or stroke
Evidence of stroke on CT/ MRI

113
Q

Morphologically, multi-infarct dementia can be classified into two types depending on the size of the infarcts. What is the aetiology of these types of infarcts?

A

LARGE: atheroma of large cerebral arteries causing thromboembolism
SMALL (LACUNAR): Longstanding hypertension

114
Q

What is the primary location where Alzheimer’s disease starts within the brain?

A

Nucleus of Meynert

Y3 NEUROLOGY (22 decks)

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