Pathology Flashcards

(58 cards)

1
Q

What are common causes of acute neuronal injury?

A

Hypoxia

Ischaemia

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2
Q

What is the descriptive term used for neurones affected by acute neuronal injury?

A

Red Neurones

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3
Q

How soon after the acute injury do “Red Neurones” appear?

A

12-24 hours

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4
Q

On examination what do the neurones post injury look like?

A

Shrinking and angulation of nuclei
Loss of nucleolus
Red cytoplasm
Eosinophilia

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5
Q

How do axons appear post injury?

A

Swelling of the cell body and nucleolus.

Degeneration of axon and myelin sheath distal to the injury.

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6
Q

Chronic Degeneratie neuronal atrophy appears how?

A

Shrunken small dark nuclei

Reactive Gliosis

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7
Q

How do oligodendrocytes react to injury?

A

Loss of myelin sheath
Conduction is reduced
Axons are exposed to injury

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8
Q

What are oligodendrocytes susceptible to?

A

Oxidative stress e.g hypoxia

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9
Q

Astrocytes undergoing scar formation and repair can be described as undergoing what?

A

Gliosis

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10
Q

How does early gliosis appear?

A

Hyperplasia
Hypertrophy
Nucleus enlargement

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11
Q

How does late gliosis appear?

A

Translucent nuclei

Shrunken and dark lying within a dense mass

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12
Q

What are ependymal cells susceptible to?

A

Limited reaction to injury

Usual site of tumour formation or infection

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13
Q

Microglia

A

CNS Macrophage

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14
Q

How do microglia appear on inspection?

A

Form aggregate around area of necrotic or damaged tissue.

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15
Q

M2 - Microglia

A

Anti inflammatory phagocytic cells - More Acute

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16
Q

M1 - Microglia

A

Pro Inflammatory more chronic

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17
Q

List some common causes of Hypoxia.

A
Cerebral Ischaemia
Infarct
Haemorrhage
Trauma 
Cardiac Arrest
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18
Q

What proportion of the bodies intake of oxygen is used by the brain?

A

20%

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19
Q

By how many times can cerebral blood flow increase to match the demand before supplies of ATP are used up?

A

2x

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20
Q

What s excitotoxicity?

A

Energy Failure- Hypoxia or hypoglycaemia

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21
Q

What is the Pathophysiology behind excitoxicity?

A

Neuronal depolarisation and re-uptake of transmitters inhibited.
Glutamate is released and builds up.
Glutamate storm
Ca2+ build-up proteases activated.
Mitochondria dysfunction and oxidative stress.

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22
Q

List the types of oedema affecting the brain.

A

Cytotoxic
Ionic
Vasogenic
Haemorrhagic Conversion

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23
Q

Causes of Cytotoxic oedema

A

Intoxication

Severe hypothermia

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24
Q

Causes of Ionic oedema

A

Hyponatraemia

Excess water intake

25
Causes of Vasogenic oedema.
Breakdown in the BBB | Trauma Tumour Inflammation
26
How does a breakdown in the BBB result in vasogenic oedema?
Plasma proteins and insoluble proteins able to cross, water follows via osmosis.
27
Global Cerebral ischaemia is due to.
Generalised reduction in blood flow - Hypovolaemic shock cardiac arrest
28
Focal Cerebral Ischaemia is due to.
Vascular obstruction
29
Which areas are most susceptible to ischaemia?
Neocortex Hippocampus Zones between two arterial territories.
30
A cerebral thrombosis is most likely to occur where?
Middle cerebral artery
31
A cerebral emboli is most likely to occur from where?
Internal carotid or aortic arch.
32
List some risk factors for Cerebral infarction.
``` Atheroma Hypertension Obesity Diabetes Mellitus Smoking Septal Defects ```
33
0-12 hours post infarct what is to be seen?
Little is visible
34
12-24 hours post infarct what is to be seen?
Paleness Softening Swollen Tissues - oedema Red neurones
35
24-48 hours post infarct what is to be seen?
Recruitment of neutrophils Haemorrhagic conversion Activation of microglia
36
What is Haemorrhagic conversion.
Post infarct the blood vessels can break down leading to leakage.
37
2-14 days post infarct what is to be seen?
M1 Microglia predominant | Reactive Gliosis
38
Several Months post infarct what is to be seen?
Cavitation Liquifaction Gliotic scar
39
A middle cerebellar artery infarct would present with...
Contralateral face and arm weakness
40
Anterior Cerebelar infarct would present with...
Weakness and sensory loss in contralateral leg
41
A verterbro basilar artery infarct would present with...
Vertigo Ataxia Dysarthia Dysphasia
42
Charcott-Bouchard
Micro-aneurysm linked to chronic hypertension
43
Charcott- Bouchard are most likely to be found in....
Basillar arteries
44
Hypertension is strongly linked to this form of infarct.
Lacunar
45
What are lacunar infarcts?
Occlusion of small penetrating vessels.
46
What region of the brain is commonly affected by lacunar infarcts?
Basal Ganglia
47
How does someone with hypertensive encephalopathy present?
``` Headache Confusion Fits Coma Behavioural changes ```
48
What would the brain of someone with hypertensive encephalitis appear like.
Global and cerebral oedema Tentorial Herniation Necrosis
49
Give some risk factors for intracerebral haemorrhage.
``` Hypertension Amyloid deposits Diabetes Cocaine Vasculitis ```
50
List some common vascular malformations.
Arteriovenus Malformation Cavernous Angiomas Venous Angioma Capillary Telangectaisia
51
What do AVM look like?
Abnormal tortuous vesels | Shunting high pressure blood straight into the venous system.
52
Pathologically what do AVM vessels look like.
Hypertrophy of smooth muscle in vessels | Loss of compliance
53
Why do AVM carry the highest risk of intracerebral haemorrhage?
High pressure blood with weaker fragile walls.
54
What is the commonest cause of Subarachnoid haemorrhage?
Rupture of berry aneurysms
55
Where do berry aneurysm usually appear?
Bifurcations within the circle of willis
56
At what size do berry aneurysms carry the biggest risk of bleeding?
6-10mm
57
At what size does the risk of rupture for berry aneurysms decrease?
>25mm
58
What is the cause of symptoms in a large berry aneurysm ?
Mass effect e.g compression