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Neurology > Neuropathology 1 > Flashcards

Neuropathology 1 Flashcards

1
Q

Name the 3 main cell categories of the CNS.

A

* Nerve * Glial * Microglial

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2
Q

Name the 3 types of glial cells.

A

* Astrocytes * Oligodendrocytes * Ependymal cells

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3
Q

What do ependymal cells do?

A

Line the ventricular system

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4
Q

Name the supporting structures of the CNS.

A

* Blood vessels * Connective tissue * Meninges

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5
Q

What can damage to nerve cells and/or their processes lead to?

A

* RAPID necrosis with sudden acute functional failure (e.g stroke)

* Slow atrophy with gradually increasing dysfunction

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6
Q

Give an example of slow atrophy.

A

Age- related cerebral atrophy

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7
Q

What is the red neurone known as?

A

A neuron with acute neuronal injury

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8
Q

What does the red neurone occur in response to?

A

Injury or Hypoxia

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9
Q

When is the red cell visible?

A

12-24 hours after irreversible insult to the cell

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10
Q

Red cells are reversible

A

FALSE - irreversible

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11
Q

What does acute neuronal cell injury cause?

A

Neuronal cell death

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12
Q

What is the sequence of events in neuronal cell injury?

A

* Shrinking and angulation of nuclei

* Loss of the nucleolus

* Intensely red cytoplasm

* Become eosinophilic

* Dying

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13
Q

Explain how damage occurs.

A

Distal degeneration of the axon and towards cell body in response to damage

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14
Q

Name 3 other responses to injury.

A

* Axonal reactions * Simple neuronal atrophy (chronic degeneration) * Sub-cellular alterations – inclusions

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15
Q

What is the typical pattern of axonal reactions?

A

* Increased protein synthesis - cell body swelling, enlarged nucleolus

* Chromatolysis – margination and loss of Nissl granules

* Degeneration of axon and myelin sheath distal to injury “Wallerian degeneration”

* Increased size of nucleolus due to increased protein synthesis

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16
Q

What is the typical pattern of simple neuronal atrophy?

A

Shrunken, angulated and lost neurons, small dark nuclei, lipofuscin pigment, reactive gliosis

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17
Q

What type of reaction is sub-cellular alterations common in?

A

Neurodegenerative conditions ie. neurofibrillary tangles in Alzheimer’s

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18
Q

What do incisions seem to accumulate with?

A

Ageing

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19
Q

What do you also get inclusions with?

A

Viral infections affecting the brain

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20
Q

Describe the appearance of astrocytes.

A

Star-shaped with multipolar cytoplasmic processes

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21
Q

Where are astrocytes found?

A

Throughout the CNS

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22
Q

What do astrocytic processes do?

A

* Envelop synaptic plates

* Wrap around vessels and capillaries within the brain tp regulate BBB and tone of capillaries

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23
Q

What are the roles of astrocytes?

A

* Ionic, metabolic and nutritional homeostasis

* Work in conjunction with endothelial cells to maintain the BBB

* Main cell involved in repair and scar formation, given the lack of fibroblasts

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24
Q

What is gliosis?

A

An astrocytic response to injury

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25
Q

What is gliosis the most important pathological indicator of?

A

CNS injury, regardless of cause

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26
Q

What happens in gliosis?

A

* Astrocyte hyperplasia and hypertrophy

* Nucleus enlarges, becomes vesicular and the nucleolus is prominent.

* Cytoplasmic expansion with extension of ramifying processes

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27
Q

Describe the appearance of old lesions that have undergone gliosis in the past.

A

Nuclei become small and dark, and lie in a dense net of processes (glial fibrils)

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28
Q

What happens to cells in early gliosis?

A

Hypertrophy and hyperplasia

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29
Q

What do oligodendrocytes do?

A

Wrap around axons, forming the myelin sheath

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30
Q

What are oligodendrocytes sensitive to?

A

Oxidative damage

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31
Q

What is oligodendrocyte damage a feature of?

A

Demyelinating disorders

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32
Q

Describe the reaction of oligodendrocytes to injury.

A

Reaction to injury is relatively limited: - variable patterns of demyelination - variable degrees of demyelination - apoptosis

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33
Q

The reaction of ependymal cells to injury is ______

A

LIMITED

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34
Q

What is disruption of ependymal cells often associated with?

A

A local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surface, termed ependymal granulations

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35
Q

What can produce changes in ependymal cells?

A

Infectious agents, including viruses

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36
Q

How are microglial derived?

A

Embryologically

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37
Q

Where are microglia made?

A

Bone marrow

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38
Q

What do microglia function as?

A

* A macrophage in phagocytosis

* Mopping up injured neuronal cells

* Anti-inflammatory

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39
Q

Outline the role of microglia in response to injury.

A

* Microglia proliferate.

* Recruited through inflammatory mediators.

* Form aggregates – around areas of necrotic and damaged tissues

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40
Q

Name the 2 important mediators in the acute response to injury in the NS.

A

M2 – anti-inflammatory, phagocytic, more acute

M1 – pro-inflammatory, more chronic

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41
Q

What is the most important base line of neuronal injury?

A

HYPOXIA

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42
Q

Give examples of pathologies that can lead to hypoxia of the brain.

A

* Cerebral ischaemia

* Infarct

* Hameorrhages

* Trauma

* Cardia arrest

* Cerebral palsy

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43
Q

What % of total body resting oxygen does the brain consume?

A

20%

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44
Q

To maintain oxygen delivery, by how much can cerebral blood flow increase?

A

2 fold

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45
Q

After the onset of ischaemia, what leads to the ATP reserves being consumed within a few minutes?

A

Mitochondrial inhibition of ATP synthesis

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46
Q

Outline the steps of hypoxia.

A
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47
Q

How can cytotoxic oedema occumulate?

A

Independantly or via pre-morbid processes

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48
Q

Suggest situatins in which cerebral cytotoxic oedmea may occur.

A

* Intoxication

* Reye’s

* Severe hypothermia

* Ischaemia

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49
Q

What happens to dying cells?

A

They accumulate more Na and Cl, thus there is a shift of water form the extracellular space into the cell causing the cells to swell

NOTE: the brain doesnt get bigger as there isnt more water, just the water is shifting location

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50
Q

What is another name for ionic oedema?

A

OSMOTIC oedema

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51
Q

What does ionic oedema occur in?

A

Hyponatraemia + excess water intake ie. in SIADH

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52
Q

When does vasogenic oedema occur?

A

* Trauma

* Tumours

* Inflammation

* Infection

* Hypertensive encephalopathy

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53
Q

When does haemorrhagic conversion occur?

A

Occurs when endothelial integrity is completely lost and blood can enter the extracellular space

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54
Q

In what condition does haemorrhagic conversion occur?

A

Ischaemic strokes

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55
Q

What arteries of the brain are most important?

A

Anterior, middle and posteror cerebral arteries

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56
Q

What problems may arise due to ischaemia of the anterior cerebral artery territory?

A

* trunk + legs – sensory and motor abnormalities
* Frontal lobe dysfunction
* Higher cognitive dysfunction

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57
Q

What areas may be damaged in ischaemia of the area supplied by middle cerebral artery territory?

A

Major bulk of the sensory and motor cortex

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58
Q

What may ischaemia of the posterior cerebral artery terriroty result in?

A

Problem in occipital lobes, leading to homonymous hemianopia with visual field defect in both eyes on the same side as the lesion

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59
Q

What % of the cardiac output does the brain recieve?

A

15%

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60
Q

What % of oxygen consumed from the body does the brain use?

A

20%

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61
Q

To function, what does the brain require?

A

Active metabolism of glucose

62
Q

The brain maintains blood flow over a wide range of ______ pressures?

A

PERFUSION

63
Q

What do ‘autoregulatory’ mechanisms do?

A

Help to maintain blood flow at a ‘constant’ rate by dilatation and constriction of cerebral vessels

64
Q

What is ‘cerebrovascular disease’?

A

Any abnormality of brain caused by a pathological process of blood vessels

65
Q

Cerebrovascular disease is the _rd most common cause of death

A

3rd

66
Q

What is cerebrovascular disese the commonest cause of?

A

Adult disability

67
Q

Cerebrovascular disease is a medical emergency with a high mortality that is also treatable

A

TRUE

68
Q

Give examples of different types of cerebrovascular disease.

A

* Brain ischaemia and infarction.
* Haemorrhages i.e strokes.
* Vascular malformations.
* Aneurysms

69
Q

Cerebrovascular disease involved 2 processes. What are they?

A

1 – hypoxia, ischaemia and infarction, resulting from impairment of blood supply and oxygenation of tissue
2 – haemorrhage, resulting from rupture of CNS vessels

70
Q

What is the overlapping process (both hypoxia and haemorrhage) that causes cerebrovascular disease?

A

HYPERTENSION

71
Q
A

Infarction that is a few days old

72
Q
A

SAH

73
Q

What is GLOBAL hypoxic ischaemic damage?

A

Generalised reduction in blood flow/oxygenation - when there is systemic compromise to circulation which cannot be compensated for by CNS autoregulatory mechanisms

74
Q

Give examples of global hypoxic ischaemic damage.

A

* Cardiac arrest

* Severe hypotension

75
Q

What is the main cause of severe hypotension?

A

Trauma with hypovolaemic shock

76
Q

What is focal ischaemia typically due to?

A

Vascular obstruction

77
Q

Describe simply what global ischaemia entails.

A

A generalised reduction of cerebral perfusion

78
Q

When does global ischaemia occur?

A

MAP <50 mmHg

79
Q

What happens when MAP <50 mmHg?

A

Autoregulatory mechanisms can no longer compensate

80
Q

Suggest situations in which MAP <50 mmHg.

A

* Cardiac arrest

* Shock/severe hypotension

* Trauma

81
Q
A
82
Q

What areas of the brain are particulary sensitive to hypoxic damage?

A

Watershed areas -

* these are 2 areas between arterial territories (i.e parieto-occipital)

* these are areas at the periphery of vascular territories and contain neurones particularly sensitive to hypoxia as they are the most distant from the heart, and least well supplied

83
Q

What cells are more sensitive - neurones or glial cells?

A

Neurones

84
Q

What type of neurones are the most sensitive?

A

NEOCORTEX + HIPPOCAMPUS

85
Q

What does severe ischaemia lead to?

A

Pan-necrosis

86
Q

What is a stroke?

A

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

87
Q

What type of stroke is most common?

A

Infarction - thrombotic

88
Q

What is cerebral infarction caused by?

A

Interruption of cerebral blood flow, due to thrombosis or emboli

89
Q

What is the peak age of incidence of a cerebral infarct?

A

70 yo

90
Q

In what geneder is cerebral infarct most common?

A

MEN

91
Q

What is thrombosis?

A

An atherosclerotic segment

92
Q

Where does thrombosis most often occur?

A

The middle cerebral artery

93
Q

What does an embolic infarct arise due to?

A

Atheroma in the internal carotid artery, and aortic arch.
or
From heart

94
Q

Outline the main risk factors for a cerebral infarction.

A

Atheroma

  • Intracranial vessels
  • Extracranial vessels

Hypertension

Risk factors for atheroma anywhere in intra and extracranial vessels

  • Also causes changes in cerebral vessel walls

Serum lipids, obesity, diet

Diabetes mellitus – changes to small vessels that makes them less compliant and more likely to form atheroma

Heart disease

Diseases of neck arterie

Smoking

95
Q

LOOK AT THE TABLE FOR MICROSCOPIC AND MACROSCOPIC APPEARANCE OF CEREBRAL INFARCTION

A
96
Q

What happens after 48 hours of cerebral infarction?

A

Phagocytosis by macrophages

97
Q

What happens after 1 week of cerebral infarction?

A

Reactive gliosis begins

Astrocyte hypertrophy and hyperplasia

98
Q

What happens after a few weeks of a cerebral infarct?

A

Gliotic scar

99
Q

Describe an OLD, cerebral infarct.

A

Eventually, a cystic gapremains as a permanent marker of the site of an old infarction.

(below shows where there has been a middle cerebral artery infarct)

100
Q

What does the image show?

What is it a sign of?

A

Cystic gap

A sign that there has been a middle cerebral artery infarct

101
Q

What does this show?

A

Gliotic scar

102
Q

What does this show?

A

An infarct after 48 hours

103
Q

When is this post infact?

What does it show?

A

1 week

Reactive gliosis

104
Q

What is disrupted in a haemorrhagic infarct?

A

BBB

105
Q

What may occur in a haemorrhagic infarct?

A

Haemorrhagic conversion

106
Q

Explain how thrombolysis can be implicated in a haemorrhagic infarct

A

An occluded vessel may be reperfused by thrombolysis.
This, however, may lead to leakage through a damaged capillary bed following lysis of the embolus.

107
Q

What process does this show?

A

Haemorrhagic infarct

108
Q

How may a stoke, due to carotid artery disease present?

A

* Contralateral weakness or sensory loss.
* If dominant hemisphere – there may be aphasia or apraxia

109
Q

How may a stroke, due to a problem in the middle cerebral artery present?

A

With weakness predominantly in the contralateral face and arm

110
Q

How may a stroke, due to a problem in the middle cerebral artery present?

A

With weakness and sensory loss in the contralateral leg

111
Q

What are the features of vertebra-basilar artery disease?

A

Vertigo, ataxia, dysarthria and dysphasia.
àcomplex ‘brain stem syndromes.’

112
Q

What is the other name given to microaneurysms?

A

Charcot - Bouchard

113
Q

What does hyaline atherosclerosis result in?

A

Thinning and weakening of small vessel walls, making them more prone to occlusion and to rupture

114
Q

What is associated with the development of micro-aneurysms?

A

Chronic hypertension

115
Q

Where do microaneurysms particulary occur?

A

In small MCA branches, most commonly within the basal ganglia

116
Q

What does rupture of small branches of MCA result in?

A

Intracerebral haemorrhage

117
Q

What is the consequence of hypertension in the brain?

A

Lacunar infarcts

118
Q

Who gets hypertensive encephalopathy?

A

Severely hypertensive patients

119
Q

Outline the process that leads to the development of hypertensive encephalopathy.

A

Upper limit of autoregulatory mechanism is saturated, and the BBB becomes incapable of resisting movement of plasma proteins like albumin and water àvasogenic oedema

120
Q

List the symptoms of hypertensive encephalopathy.

A

* Headache

* Vomitng

* Fits

* Confusion

* Coma

121
Q

What are the symptoms of hypertensive encephalopathy due do?

A

RAISED ICP

122
Q

What does the pathology of hypertensive encephalopathy reveal?

A

Global cerebral oedema.
Tentorial and tonsillar herniation.
Petechiae.
Arteriolar fibrinoid necrosis.

123
Q

What can increasing numbers of lacunar infarcts contribute to?

A

Multi-infarct dementia

124
Q

What can a small lacunar infarct of the internal capsule result in?

A

Extensive motor weakness, including effecting the face, arm and leg

125
Q

What can intracranial haemorrhage be due to?

A

Spontaneous or trauma

126
Q

Give the 3 sub-types of spontaneous intracranial haemorrhage.

A

Intracerebral haemorrhage.
Sub-arachnoid haemorrhage.
Haemorrhagic infarct

127
Q

Give the 5 sub-types of traumatic intracranial haemorrhage.

A

Extra-dural haematoma.
Sub-dural haematoma.
Contusion – surface bruising.
Intracerebral haemorrhage.
Sub-arachnoid.

128
Q

List the contributing factors to intracerebral haemorrhage.

A

* Hypertension – small vessel disease, stiff and lack of compliance

*Aneurysms

*Systemic coagulation disorders

* Anticoagulation

* Vascular malformations

* Amyloid deposits (cerebral amyloid angiopathy)

* Open heart surgery

* Neoplasms

* Vasculitis (infectious and non-infectious)

129
Q

Where is the most common site for intracerebral haemorrhage to occur?

A

Basal ganglia

130
Q

Where do intracerebal haemorrhages also occur?

A

Thalamus.
Cerebral white matter.
Cerebellum.

131
Q

Describe the morphology of an intracerebral haemorrhage on the cut surface.

A

* Asymmetrical distortion.
* Various shifts and herniations are common.
* Well-demarcated in intra-parenchymal haematomas.
* Softening of adjacent tissue.
* Surrounding oedema.

132
Q

What does amyloid angiopathy occur in?

A

Alzheimer’s disease.
Age-related change

133
Q

Describe the process of amyloid angioapthy.

A

Beta amyloid forms tightly packed beta pleated sheets which are deposited within cerebral and meningeal vessels.
As a result, these vessels become less compliant and less able to deal with localised increased pressure, and can ruptureas a result àforming a lobar intracerebral haemorrhage

134
Q

Name the 4 major types of vascular malformation.

A

* Arteriovenous

* Cavernous

* Venous

* Capillary telangactes

135
Q

As well as bleeding, what else can vascular malformations cause clinically?

A

Headaches, seizures and focal neurological deficits

136
Q

Technically, what are AVM’s?

A

SOL’s

137
Q

Where do AVM’s most commonly arise?

A

In cerebral hemispheres in MCA territory

138
Q

Describe the vessels in AVM’s.

A

Large

Abnormal

Tortuous

139
Q

Shunting can occur from an artery to a vein. What are the effects of this?

A

Vein undergoes smooth muscle hypertrophy.
àtherefore not compliant, and ruptures easily.
Also forms aneurysms which rupture

140
Q

What is the most common cause of SAH?

A

Rupture of a saccular aneurysm (Berry aneurysm)

141
Q

Where do 90% of SAH’s occur?

A

In the territory of the ICA

142
Q

Where do 10% of SAH’s arise?

A

In vertebra-basilar circulation

143
Q

Where do SAH’s arise?

A

Arterial bifurcations

144
Q

Where is blood in an SAH?

A

In the subarachnoid space

145
Q

What may be seen pathologically in an SAH?

A

* Intracerebral haematomas, adjacent to aneurysms.
* Infarcts of brain parenchyma may also develop due to arterial spasm (40%) of cases.
* Mass effect of haematoma and features of raised ICP

146
Q

What are the 3 main risk factors to SAH?

A

* Smoking

* Hypertension

* Kindey disease

147
Q

The onset of an SAH is?

A

ABRUPT

148
Q

What are the symptoms of SAH?

A

Severe headache.
Vomiting.
Loss of consciousness.
Meningeal signs, including neck rigidity

149
Q

What are people with SAH at risk of?

A

Hydrocephalus

150
Q

SAH is very severe. What percentage of people die within 1 week?

A

50%

151
Q

Who gets SAH?

A

Women > men

Usually over 50 years old

152
Q

What is Reye’s syndrome?

A

* Swelling in the liver and brain

* Affects children and teenagers recovering from a viral infection, most commonly the flu or chickenpox

* Causes cytotoxic cerebral oedema

Neurology (42 decks)

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