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Neurology Year 3 > Pathology > Flashcards

Pathology Flashcards

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
Q

Causes of Vasogenic oedema.

A

Breakdown in the BBB

Trauma Tumour Inflammation

26
Q

How does a breakdown in the BBB result in vasogenic oedema?

A

Plasma proteins and insoluble proteins able to cross, water follows via osmosis.

27
Q

Global Cerebral ischaemia is due to.

A

Generalised reduction in blood flow - Hypovolaemic shock cardiac arrest

28
Q

Focal Cerebral Ischaemia is due to.

A

Vascular obstruction

29
Q

Which areas are most susceptible to ischaemia?

A

Neocortex
Hippocampus
Zones between two arterial territories.

30
Q

A cerebral thrombosis is most likely to occur where?

A

Middle cerebral artery

31
Q

A cerebral emboli is most likely to occur from where?

A

Internal carotid or aortic arch.

32
Q

List some risk factors for Cerebral infarction.

A 
Atheroma
Hypertension
Obesity
Diabetes Mellitus
Smoking
Septal Defects
33
Q

0-12 hours post infarct what is to be seen?

A

Little is visible

34
Q

12-24 hours post infarct what is to be seen?

A

Paleness
Softening
Swollen Tissues - oedema
Red neurones

35
Q

24-48 hours post infarct what is to be seen?

A

Recruitment of neutrophils
Haemorrhagic conversion
Activation of microglia

36
Q

What is Haemorrhagic conversion.

A

Post infarct the blood vessels can break down leading to leakage.

37
Q

2-14 days post infarct what is to be seen?

A

M1 Microglia predominant

Reactive Gliosis

38
Q

Several Months post infarct what is to be seen?

A

Cavitation
Liquifaction
Gliotic scar

39
Q

A middle cerebellar artery infarct would present with…

A

Contralateral face and arm weakness

40
Q

Anterior Cerebelar infarct would present with…

A

Weakness and sensory loss in contralateral leg

41
Q

A verterbro basilar artery infarct would present with…

A

Vertigo
Ataxia
Dysarthia
Dysphasia

42
Q

Charcott-Bouchard

A

Micro-aneurysm linked to chronic hypertension

43
Q

Charcott- Bouchard are most likely to be found in….

A

Basillar arteries

44
Q

Hypertension is strongly linked to this form of infarct.

A

Lacunar

45
Q

What are lacunar infarcts?

A

Occlusion of small penetrating vessels.

46
Q

What region of the brain is commonly affected by lacunar infarcts?

A

Basal Ganglia

47
Q

How does someone with hypertensive encephalopathy present?

A 
Headache
Confusion
Fits
Coma
Behavioural changes
48
Q

What would the brain of someone with hypertensive encephalitis appear like.

A

Global and cerebral oedema
Tentorial Herniation
Necrosis

49
Q

Give some risk factors for intracerebral haemorrhage.

A 
Hypertension
Amyloid deposits
Diabetes
Cocaine
Vasculitis
50
Q

List some common vascular malformations.

A

Arteriovenus Malformation
Cavernous Angiomas
Venous Angioma
Capillary Telangectaisia

51
Q

What do AVM look like?

A

Abnormal tortuous vesels

Shunting high pressure blood straight into the venous system.

52
Q

Pathologically what do AVM vessels look like.

A

Hypertrophy of smooth muscle in vessels

Loss of compliance

53
Q

Why do AVM carry the highest risk of intracerebral haemorrhage?

A

High pressure blood with weaker fragile walls.

54
Q

What is the commonest cause of Subarachnoid haemorrhage?

A

Rupture of berry aneurysms

55
Q

Where do berry aneurysm usually appear?

A

Bifurcations within the circle of willis

56
Q

At what size do berry aneurysms carry the biggest risk of bleeding?

A

6-10mm

57
Q

At what size does the risk of rupture for berry aneurysms decrease?

A

> 25mm

58
Q

What is the cause of symptoms in a large berry aneurysm ?

A

Mass effect e.g compression

Neurology Year 3 (29 decks)

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