Principles and Cerebrovascular Disease Flashcards

1
Q

What is the dura?

A

the tough fibrous outer layer which bridges crevices and is attached to the skull

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2
Q

What is the arachnoid?

A

delicate sealed bag for CSF - bridges crevices - impermeable to salt and water

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3
Q

What ropes across the subarachnoid space?

A

arachnoid trabeculae

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4
Q

Where is the cerebral artery branch?

A

embedded in the pia - susceptible to tearing and damage

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5
Q

What is the pia mater?

A

delicate - next to brain and dips into crevices

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6
Q

What are the main cellular components of the CNS?

A
nerve cells
glial cells
blood vessels
microglia
connective tissue - meninges
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7
Q

What are the glial cells?

A

astrocytes, oligodendrocytes, ependyma

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8
Q

What can damage the cells of the CNS?

A
hypoxia
trauma
toxic insult
metabolic abnormalities
nutritional deficiencies
infections
ageing
genetic abnormalities
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9
Q

What are the neuronal responses to injury?

A

acute neuronal injury
simple neuronal atrophy
sub-cellular alterations
axonal reactions

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10
Q

Why are neurons particularly susceptible to hypoxic damage?

A

due to activation of glutamate receptors -> Ca overload

can’t use anaerobic glycolysis

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11
Q

Why would you be better drowning in cold water?

A

slows metabolic processes and cell death down

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12
Q

What is the axonal reaction?

A

the reaction within the cell body that is associated with injury to the axon

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13
Q

What is the responses to axonal injury?

A
  • increased RNA and protein synthesis
  • swelling of the cell body
  • peripheral displacement of the nucleus
  • enlargement of the nucleolus
  • anterograde degeneration of the axon - distal to site of injury
  • breakdown of myelin sheat
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14
Q

How do astrocytes react to injury?

A

proliferation (gliosis)

reactions leading to cell death or degeneration

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15
Q

What is the process gliosis?

A

where astrocytes undergo hyperplasia and hypertrophy
nucleus is enlarged, becoming vesicular and the nucleolus is prominent
cytoplamsic expansion with extension of ramifying processes

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16
Q

What can be seen on old lesions of gliosis?

A

nuclei become small and dark and lie in a dense net of processes - fibrils
comparable to scar formation

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17
Q

What is injury to oligodendrocytes a feature of?

A

demyelinating diseases

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18
Q

How do oligodendrocytes react to injury?

A

very limited response

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19
Q

where are ependymal cells found?

A

lining the ventricular system

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20
Q

What is disruption of ependymal cells associated with?

A

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

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21
Q

What can produce changes in ependymal cells?

A

infectious agents i.e. viruses

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22
Q

How do microglia respond to injury?

A
  • proliferate
  • develop elongated nuclei
  • forming aggregates about small foci of tissue necrosis
  • congregate around portions of dying neurons
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23
Q

How long does brain need to lose blood supply before there is irreversible damage?

A

4 minutes

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24
Q

How much CO and O2 does the brain receive?

A

15% of CO and 20% of O2

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25
How is blood flow maintained in the brain?
autoregulatory mechanisms
26
Where does the blood supply in the brain come from?
internal carotid arteries and vertebral arteries
27
Why is the circle of willis protective?
occlusion of any one pathway does not stop flow to one area unlike when blood flow is deeper into the brain
28
Where is the circle of willis?
base of the brain
29
What does occlusion to the anterior cerebral artery lead to?
contralateral sensory loss in foot and leg | paresis of arm and foot, relative sparing of thigh and face
30
Where does the anterior cerebral artery lead?
frontal lobe
31
What happens with occlusion to the middle cerebral artery?
hemiparesis hemisensory loss aphasia/dysphasia - loss of language or vocal chord function apraxia
32
what does the brain stem consist of?
mid-brain, pons, medulla
33
What does the brain stem control?
cardio-respiratory centres
34
what do bleeds on the occipital lobe cause?
homonymous hemianopia because of the cross over of optic nerve
35
What does a stroke in the cerebellum cause?
ataxia nystagmous - eye twitch in extreme visual fields intention tremor pendular reflexes - acts like a pendulum when it shouldnt
36
what is the mortality of Cerebrovascular disease?
20% in the first month
37
What are the potential causes of cerebrovascular disease?
brain ischemia and infarctions haemorrhages vascular malformations and developmental abnormalities
38
What may cause hypoxic ischemic damage?
respiratory obstruction, lung and heart disease, epilepsy, cardiac arrest
39
Which groups of neurons are more vulnerable to hypoxic/ischemic damage?
pyramidal cells of hippocampus | purkinje cells of cerebellum
40
What are watershed areas?
junctions of arteries which are the first areas to be deprived
41
When may hypoxic ischemic encephalopathy occur?
in any circumstance that results in global decrease in HbO2 available to the brain
42
What is a stroke?
a sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
43
What are the types of stroke and their commonality?
infarction (84%) or haemorrhage (16%)
44
What is a cerebral infarction?
caused by local interuption of cerebral blood flow due to thrombosis or emboli
45
What is an embolis?
a clot that has broken off
46
What are risk factors for stroke?
atheroma, HBP, serum lipids, obesity, diet, T2DM, heart disease, smoking
47
What is the morphology of a cerebral infarct 4-12 hours later?
brain may appear normal
48
What is the morphology of a cerebral infarct 15-20 hours later?
ischemic neuronal changes develop
49
What is the morphology of a cerebral infarct 24-36 hours later?
inflammatory reaction, extravasion of RBCs and activation of astrocytes and microglia
50
What is the morphology of a cerebral infarct 36-48 hours later?
necrotic area visible macroscopically, becomes swollen and softer than surrounding tissue
51
What is the morphology of a cerebral infarct 3 days later?
macrophages are in the area
52
What is the morphology of a cerebral infarct 1-2 weeks later?
liquification of tissue and gliosis
53
What is the morphology of a cerebral infarct months later?
cavitation and completion of glial scar
54
What is the most common cause of haemorrhage?
spontaneous
55
What is a spontaneous haemorrhage??
rupture of a saccular aneurysm
56
Where do most aneurysms occur?
arise at arterial bifurcation in territory or internal carotid (90%)
57
What are the potential morphologies of aneurysms?
- rupture of berry aneurysm - bleeds into subarachnoid space - intracerebral haematomas adjacent to aneurysm - infarcts of brain parenchymal due to arterial spasms (40%)
58
What are the clinical features of haemorrhages?
-abrupt onset (headache, vomiting, loss of conciousness)
59
What are the signs of a haemorrhage?
bloody CSF, meningeal signs incl. neck stiffness
60
What are the complications of a haemorrhage?
cerebral infarcts, acute hydrocephalus, herniation
61
Why may chronic hydrocephalus develop in patients surviving the initial haemorrhage?
due to organisation of blood in the leptomeninges and or arachnoid granulations with resultant obstruction of CSF flow
62
What does hypertension cause in the brain?
increased atheroma hyaline arteriosclerosis microaneurysms shift in autoregulatory curve to the right
63
What is the pathology of hypertension in the brain?
- lacunar infarcts - intracerebral haemorrhage - multi-infarct dementia - hypertensive encephalopathy