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Neurology > Week 3- pathology > Flashcards

Week 3- pathology Flashcards

1
Q

Name possible causes of injury to the nervous system?

A 
Hypoxia
Trauma
Infection
Nutritional defects
Toxic insult
Metabolic abnormalities
Genetic abnormalities
Ageing
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2
Q

What two cellular responses does the CNS have to injury?

A

Rapid necrosis- meaning sudden, acute functional failure

Slow atrophy- gradually increasing dysfunction

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3
Q

On histological slides- acute neuronal injury looks like:

A

Blood red nuclei, loss of nucleolus and shrinking and angulation of the nucleus.

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4
Q

What would axonal damage look like histologically?

A

The axon damage causes the nucleus to become larger distally.

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5
Q

Role of astrocytes

A

Sheath the synapse and are important in regulating neurotransmitters. Also important in metabolic coupling in the neurone and regulation of the blood brain barrier.

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6
Q

What surrounds all the capillaries in the brain?

A

Astrocytes.

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7
Q

Gross appearance of astrocytes

A

Star shaped with multipolar cytoplasmic processes.

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8
Q

Term for astrocytes response to injury. Describe the process.

A

Gliosis.

Astrocytes increase in number, size and the size of the nucleus.

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9
Q

When does gliosis occur?

A

Acute injury to astrocytes.

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10
Q

Role of oligodendrocytes?

A

Facilitate saltatory conduction.

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11
Q

Role of microglia

A

Resident macrophage in the CNS. Most important inflammatory cell in the CNS.

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12
Q

Microglial cells response to injury consists of:

A

Proliferate in number and are recruited to the site.

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13
Q

Where are microglia cells made?

A

They are embryonically derived so once in the CNS, they do not leave.

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14
Q

Meaning of hypoxia?

A

Loss of blood supply depriving the tissue of oxygen.

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15
Q

Which pump in the brain consumes a lot of oxygen?

A

The sodium/pottasium ATP ase.

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16
Q

What is excitotoxicity?

A

Pathological process by which neurone are killed by overactivations of receptors causing neurotransmitter build up.

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17
Q

Describe excitotoxicity

A

Energy failure means collapse of the resting membrane potential, leading to depolarisation. This activates neurotransmitter release and glutamate is released into the synaptic cleft. Astrocytes normally circulate glutamate to be re-packaged, however this is an energy (ATP) dependent process. Due to the lack of ATP, glutamate then builds up in the synaptic cleft causing constant excitation. This leads to massive calcium influx which causes protease activation, mitochondrial dysfunction and…

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18
Q

Describe cytotoxic oedema

A

A build up of sodium and chloride in the cell draws water in down an osmotic gradient. This creates a deficit in the extracellular space causing sodium and chloride to move out of the blood and into the extracellular space, and water follows again.

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19
Q

What is vasogenic oedema?

A

Disruption in the blood brain barrier

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20
Q

When does vasogenic oedema occur?

A

Trauma, tumours and inflammation.

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21
Q

What does the term hemorrhagic conversion mean?

A

So much disruption of the blood brain barrier that red blood cells can move across.

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22
Q

What is global hypoxic ischaemic damage?

A

Generalised reduction in cerebral perfusion.

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23
Q

What can cause globalised hypoxic ischaemic damage?

A

Cardiac arrest
Shock
Severe hypotension
Trauma

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24
Q

Which neurones are most sensitive to globalised hypoxic ischaemic damage?

A

The neurones in the hippocampus and neocortex.

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25
What can prolonged neuronal damage lead too?
Coma or persistent vegetative state.
26
Neurons are more sensitive than glial cells to global hypoxic ischaemic damage?- T or F
True
27
What two forms of clots can cause a stroke?
Atherosclerotic- cholesterol depositation in the arterial walls ruptures blocking an artery supplying the brain Embolic- from clotted blood in the ICA and aortic arch
28
Which blood vessel is most commonly affected by stroke?
Middle cerebellar artery.
29
What are lacunar infarcts?
This is the most common type of stroke associated with blockage of the small penetrating vessels that supply the deep structures of the brain.
30
Name some cerebral consequences of hypertension
Stroke Intracerebral haemorrhage and ruptured aneurysms Hypertensive encepholopathy
31
What is the most common cause of sub-arachnoid haemorrhage?
Secular aneurysm (berry aneurysm)
32
Damage to oligodendrocytes causes
Interruption in neuronal conduction (their job is to facilitate saltatory conduction- when they are damaged this doesn't happen).
33
Describe damage to myelin and axons in demyelinating disorders?
Myelin sheath becomes damaged however the axon is preserved.
34
Name some primary demyelinating disorders?
Multiple sclerosis (Acute disseminated encephalomyelitis Acute hemorrhagic leukoencephalitis)
35
Name some secondary causes of demyelination?
Viral-progressive multifocal leukoencephalopathy Metabolic- central pontine myelinosis Toxic-CO, organic solvents, cyanide
36
Describe multiple sclerosis (generally)
Most common demyelinating disorders. Autoimmune attack of the myelin sheath leads to distinct neurological deficits separated in time and space. (anatomically unrelated sites being affected by the same thing)
37
Who is likely to get MS?
More common in males. | Rare in children and in people over the age of 50.
38
Clinically diagnosing MS?
See atleast two distinct neurological deficits separated in time and space.
39
Clinical features of MS (how will it present/can it present)
Optic nerve lesions- unilateral visual impairment Spinal cord lesions- motor or sensory deficit in trunk and limbs. Spasticity / bladder dysfunction. Brain stem lesions- cranial nerve signs, ataxia, nystagmus, internuclear ophthalmoplegia
40
Which area of the brainstem would be involved to cause internuclear ophthalmoplegia? What are the clinical signs?
The medial longitudinal fasciulus. The affected side can't adduct normally (look medially), therefore the other eye which can develops nystagmus.
41
On MRI, what would you see in a MS patient?
Areas of hypersensitivity- bright white. | May show signs of atrophy (e.g. sulci becoming more pronounced).
42
MS affects which- the white matter or the grey matter?
The white matter due to it only affecting myelinated neurones which live in the white matter.
43
Describe morphologically an MS plaque
Well circumscribed, irregular shaped, glassy appearing lesion. Not anatomically symmetrical.
44
Histology of plaques from MS
Start as a very active lesion. With time- recruitment of microglia (resident macrophages of the CNS) and ongoing demyelination. It then progressive to inactive plaques where gliosis occurs. Oligodendrocytes reduce in number.
45
What are thought to be environmental triggers/predispositions for MS?
Vitamin D deficiency | Latitude- further north- more likely.
46
Why is MS considered an immune mediated disease?
Lymphocytic infiltration has been shown on histology. Also presence of oligoclonal bands in CSF fluid (not specific to MS).
47
Name some degenerative disorders affecting the cerebral cortex?
Alzheimer's disease | Picks disease
48
Degenerative disorders affecting the basal ganglia
Parkinsons disease
49
Name some causes of raised intracranial pressure?
``` Hydrocephalus Tumours/space occupying lesions Diffuse lesion in the brain (oedema) Physiological (hypoxia, hypercapnia, pain) Increased venous volumes ```
50
What is hydrocephalus?
Accumulation of CSF in the ventricular system of the brain.
51
Where is CSF produced?
In the choroid plexus of the lateral and 4th ventricles.
52
What absorbs CSF?
The arachnoid granules.
53
Three broad causes of hydrocephalus?
Obstruction of outflow, overproduction, under-absorption.
54
What is the commonest cause of obstruction of outflow of CSF?
A tumour in the midline obstructing the interventricular duct.
55
What is meant by a communicating obstruction?
Obstruction to the outflow of CSF comes from outside the ventricular system.
56
What is meant by a non-communicating obstruction?
Obstruction to the outflow of CSF from inside the ventricular system.
57
What is hydrocephalus ex vacuo?
Compensatory enlargement of the CSF spaces e.g. enlargement of the ventricles in association with brain volume loss.
58
What are the (general) consequences of raised intracranial pressure?
Can cause herniations and intracranial shifts. Distortion and pressure is put on cranial nerves and vital neurological centres. Also impaired blood flow which clinically presents as a reduced level of consciousness.
59
What is a subfalcine herniation?
The brain is forced underneath the falx cerebri. This displaces the singular gyrus and can also compress the anterior cerebellar artery. This will present as problems with weakness and sensory loss.
60
What is a tentorial herniation?
The brain is forced over the tentorium cerebelli. Causes compression of the 3rd cranial nerve and parasympathetic fibres causing pupillary dilation and impaired ocular movement.
61
What is a cerebellar herniation?
The cerebellar tonsils are forced down through the foramen magnum causing compression of the brainstem structures.
62
What clinical symptoms would a patient with raised ICP have?
Headache Stiffness Nausea/vomiting Papillaoedema
63
Primary tumours in the brain are common. True or false?
False- primary tumours are rare, however metastases are fairly common.
64
Where are tumours in the brain likely to be in children?
Below the tentorium cerebelli whereas in adults they are likely to be above.
65
What cancers commonly metastasise to the brain?
Breast, bronchus, kidney, thyroid and colon.
66
Where are metastases often seen in the brain?
At the boundary between the grey and white matter.
67
What cells are primary brain tumours most often of origin?
Glial cells.
68
Most common childhood tumour
Polycystic astrocytoma
69
Second most common childhood tumour
Medulloblastomas.
70
Describe the placement of medulloblastomas and their treatment prospects?
Found in the midline of the cerebellum. | Very radiosensitive. However if untreated- outlook is dismal.
71
Describe the macroscopic appearance of abscesses. What causes them?
They are in an oedematous fibrous capsule with central necrosis. Usually due to an underlying cause e.g. chronic otitis media.
72
Symptoms of abscesses
Fever and symptoms of raised ICP e.g. headache. | Also symptoms of underlying cause.
73
Investigations into abscesses? Treatment
CT or MRI to diagnose. | Then aspiration.
74
If a weapon (causing blunt injury) is in contact with the head for longer- what do you think will happen?
Due to the time of contact being longer- the acceleration-deceleration (change in speed) time is also longer. This means the force won't be as large as it would be with smaller contact time.
75
Describe the primary and secondary injury process in blunt trauma?
Primary injury- immediate local damage to the neurons. The only thing you can do is preventative measures. Secondary injury- haemorrhage, oedema, cytotoxicity. Potentially treatable.
76
Describe the coup and contra coup in skull fractures?
Coup- occurs to the brain on the side of the impact. | Contracoup- diametrically opposite the point of impact.
77
Which injuries tend to be worse in skull fractures- coup or contra coup?
Contracoup tend to be worse. Denser CSF moves to impact, forcing brain to the opposite side.
78
What types of skull fractures can you get?
Linear- straight sharp fracture line that may cross sutures. Compound- associated with full thickness scalp lacerations Depressed

Neurology (19 decks)

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