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Pathology Flashcards

1
Q

What are the cellular components of the CNS?

A

Neurones
Glial cells: astrocytes, oligodendrocytes, ependymal cells
Microglia
Supporting structures: connective tissue, meninges, blood vessels

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2
Q

What are the 2 ways that neurones will respond to injury?

A

Rapid necrosis with sudden acute functional failure

Slow atrophy with gradually increasing dysfunction - seen in age related cerebral atrophy

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3
Q

When will you see a red neurone?

A

Context of hypoxia/ ischaemia
Visible 12-24 hours after an irreversible insult to the cell
Results in neuronal cell death

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4
Q

What is the pattern to acute neuronal injury?

A

Shrinking and angulation of nuclei
Loss of nucleolus
Intensely red cytoplasm

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5
Q

How will axons respond to injury?

A

Increased protein synthesis; cell body swelling and enlarged nucleolus
Chromatolysis; margination and loss of nissl granules
Degeneration of axon and myelin sheath distal to the injury - wallerian degeneration

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6
Q

What is simple neuronal atrophy?

A

Shrunken, angulated and lost neurones
Small dark nuclei
Lipofuscin pigment
Reactive gliosis

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7
Q

What is gliosis?

A

Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system
Hypertrophy and hyperplasia of astrocytes

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8
Q

What are sub-cellular alterations (inclusions)?

A

Common in neurodegenerative conditions such as neurofibrillary tangles in alzheimer’s
Inclusions appear to accumulate with ageing
Will get inclusions in viral infections

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9
Q

What is the function of an oligodendrocyte?

A

Wraps around axons to form a myelin sheath to facilitate salutatory conduction

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10
Q

What will occur with damage to an oligodendrocyte?

A

Variable pattern of demyelination

Apoptosis

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11
Q

Are oligodendrocytes sensitive to oxidative damage?

A

Yes

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12
Q

What is an astrocyte?

A

Star shaped cell with multipolar cytoplasmic processes

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13
Q

Where can strocytes be found?

A

Present throughout the CNS
Astrocytic process; envelops synaptic plates
Wraps around vessesl and capillaries within the brain

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14
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 - gliosis

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15
Q

Where can you find ependymal cells?

A

Ventricular system

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16
Q

What occurs with disruption to these cells?

A

Local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulations

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17
Q

What is the microglia response to injury?

A

Proliferation

Recruited through inflammatory mediators; forms aggregates around areas of necrotic and damaged tissues

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18
Q

What is the difference between M1 and M2 microglia?

A

M2; anti-inflammatory, phagocytic, more acute

M1; pro-inflammatory, more chronic

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19
Q

What are causes of nervous system injury?

A 
Hypoxia
Trauma 
Toxic insult - exogenous and metabolic disruption within brain releasing noxious substances
Metabolic abnormalities
Nutritional deficiencies
Infections
Genetic abnormalities
Ageing
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20
Q

What can result in hypoxia?

A 
Cerebral ischaemia
Infarct
Haemorrhage
Trauma
Cardiac arrest
Cerebral palsy
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21
Q

What occurs in the brain cells after the onset of ischaemia?

A

Mitochondrial inhibition of ATP synthesis leading to ATP reserves being consumed within a few minutes - underlies rapid loss of consciousness in hypoxia

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22
Q

What occurs in terms of glutamate in excitotoxicity?

A

Glutamate released by depolarising neurone
Uptake of glutamate inhibited at astrocytes
Glutamate storm and excitation
Increased calcium resulting in protease activation, mitochondrial dysfunction and oxidative stress

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23
Q

What results in cytotoxic oedema?

A

Intoxication
Reye’s
Severe hypothermia

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24
Q

What results in ionic oedema?

A

Hyponatraemia

Excess water intake; SIADH

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25
What results in vasogenic oedema?
``` Trauma Tumours Inflammation Infection Hypertensive encephalopathy ```
26
Which areas of the brain does the anterior cerebral artery supply?
Midline portions of the frontal lobes and superior medial parietal lobes.
27
Which areas of the brain does the middle cerebral artery supply?
Portion of the frontal lobe and the lateral surface of the temporal and parietal lobes, including the primary motor and sensory areas of the face, throat, hand and arm, and in the dominant hemisphere, the areas for speech
28
Which areas of the brain does the posterior cerebral artery supply?
Occipital cortex
29
What is global hypoxic ischaemia?
Generalised reduction in blood flow/ oxygenation
30
What can cause global hypoxic ischaemic damage?
Cardiac arrest | Severe hypotension; trauma with hypovolaemic shock
31
What can cause focal cerebral ischemia?
Vascular obstruction
32
What is a watershed area?
Zone between 2 arterial territories e.g. parieto-occipital
33
Which neurones are particularly sensitive to hypoxic ischaemic damage?
Neocortex - cerebellum | Hippocampus
34
What is a stroke?
Sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
35
What can cause a cerebral infarction?
Interruption of cerebral blood flow due to thrombosis or emboli
36
What artery most commonly become thrombotic?
Middle cerebral artery
37
Where will emboli arise from commonly that affect the brain?
Atheroma in internal carotid and aortic arch
38
What are risk factors for a stroke?
``` Atheroma Hypertx Serum lipids, obesity, diet DM Heart disease Diseases of neck arteries Drugs Smoking ```
39
What is the location, distribution and extent of parenchymal damage determined by in cerebral infarction?
Arterial territory of affected artery Timescale of occlusion Extent of collateral circulatory relief Systemic perfusion pressure
40
What will be seen macroscopically 12-24hrs after a cerebral infarction?
Pale, soft, swollen with ill defined margins between injured and normal brain
41
What will be seen macroscopically 2-14 days after a cerebral infarction?
Brain becomes gelatinous and friable | Reduction in surrounding tissue oedema demarcating the lesion
42
What will be seen macroscopically several months after a cerebral infarction?
Increasing liquefaction apparent | Eventual formation of cavity lined by dark grey tissue
43
What will be seen microscopically 12-24 hours after a cerebral infarction?
Red neurone, oedema (cytotoxic and vasogenic) with generalised cell swelling
44
What will be seen microscopically 24-48hrs after a cerebral infarction?
Increasing neutrophils Extravasation of red blood cells (haemorrhagic conversion) Activation of astrocytes and microglial cells
45
What will be seen microscopically 2-14 days after a cerebral infarction?
Microglia become predominant cell type Myelin breakdown Reactive gliosis begins from as early as 1 week
46
What will be seen microscopically several months after a cerebral infarction?
Ongoing phagocytosis brings increasing cavitation and surrounding gliotic scar formation
47
What is a haemorrhagic infarct?
BBB disruption Hemorrhagic conversion Thrombolysis resulting in occlusion of vessel, usually by an embolus, with reperfusion and leakage through a damaged capillary bed following lysis of the embolus
48
What results from a middle cerebral artery lesion?
Weakness predominantly in contralateral face and arm
49
What results from anterior cerebral artery lesion?
Weakness and sensory loss in contralateral leg
50
What results from vertebrobasilar artery disease?
Vertigo Ataxia Dysarthria Dysphasia
51
What results from a carotid artery lesion?
Contralateral weakness or sensory loss | If dominant hemisphere; aphasia or apraxia
52
What does hypertension in the brain result in?
Extra and intracranial vascular disease Vascular remodelling: accelerated atherosclerosis, arteriosclerosis, fibrinoid necrosis of vessel walls Lacunes Micro-aneurysms; charcot-bouchard
53
What is charcot-bouchard?
Result of chronic hypertension occuring in small middle cerebral artery branches within the basal ganglia resulting in rupturing leading to an intracerebral haemorrhage
54
What is a lacunar infarct?
Occlusion of small penetrating arteries that provide blood to the brain's deep structures such as the basal ganglia
55
What is hypertensive encephalopathy?
Global cerebral oedema, tentorial and tonsillar herniation, petechiae and arteriolar fibrinoid necrosis
56
What are the types of spontaneous intracranial haemorrhages?
Intracerebral haemorrhage Subarachnoid haemorrhage Haemorrhagic infarct
57
What are the types of traumatic intracranial haemorrhages?
``` Extra-dural haematoma Subdural haematoma Contusion Intracerebral haemorrhage Subarachnoid ```
58
What can cause an intracerebral haemorrhage?
``` Hypertx Aneurysms Systemic coag disorders Anticoaga Vascular malformations Cerebral myloid angiopathy Open heart surgery Neoplasms Vasculitis Diabetes Drugs: cocaine, alcoholism ```
59
What are common locations for an intracerebral haemorrhage?
Basal ganglia Thalamus Cerebral white matter Cerebellum
60
What will be seen morphologically with an intracerebral haemorrhage?
``` Asymmetric distortion Various shifts and herniations Well demarcated intraparenchymal haematoma Softening of adjacent tissue Surrounding oedema ```
61
Why will amyloid angiopathy result in intracerebral haemorrhage?
Accumulation of amyloid can cause a plaque, making the blood vessel very stiff and resistant to changes to BP - can easily rupture
62
What are the different types of vascular malformations?
Arteriovenous malformation Cavernous angioma Venous angioma Capillary telangiectasia
63
What is an AVM?
Abnormal tangle of blood vessels connecting arteries and veins, which disrupts normal blood flow and oxygen circulation
64
Why can an AVM result in a bleed?
Veins have a much higher pressure than they are anatomically structured for resulting in bursting and bleeding
65
What is a cavernous angioma?
Blood vessel abnormality characterized by large, adjacent capillaries with little or no intervening brain. The blood flow through these vessels is slow
66
Will AVMs form aneurysms?
Yes
67
What is the most common cause for a subarachnoid haemorrhage?
Saccular/ berry aneurysm
68
What genetic assoc do subarachnoid haemorrhages have?
PKD | Collagen gene abnormalities
69
Why does hydrocephalus occur in subarachnoid haemorrhage?
Lack of CSF flow; can be acute or progress to chronic
70
What are risk factors for a SAH?
Smoking Hypertx Kidney disesae
71
What are the symptoms of SAH?
Severe headache Vomiting Loss of consciousness

Neurology (48 decks)

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