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Neurology > Neurapthology 1 > Flashcards

Neurapthology 1 Flashcards

1
Q

main cellular components of CNS?

A 
nerve cells (neurons)
glial cells (astrocytes, oligodendrocytes, ependymal cells)
microglia (immune function)
supporting structures (connective tissue, meninges, blood vessels)
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2
Q

damage to nerve cells and/or their processes can cause what?

A

rapid necrosis with sudden acute functional failure (stroke etc)
slow atrophy with gradually increasing dysfunction (age related cerebral atrophy, dementia etc)

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3
Q

what is red neurone?

A

descriptive term for acute neuronal injury
occurs in context of hypoxia/ischaemia
visible 12-24 hrs after irreversible insult and results in neuronal cell death

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4
Q

what is seen in red neurone?

A

shrinking and angulation of nuclei
loss of nucleus
intensely red cytoplasm

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5
Q

how else may a neurone react to injury/disease?

A

axonal reactions
simple neuronal atrophy (chronic degeneration)
sub-cellular alteration - inclusions

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6
Q

describe axonal reactions

A

increased protein synthesis > cell body swelling, enlarged nucleus
chromatolysis - margination and los of Nissl granules
degeneration of axon and myelin sheath distal to injry “wallertan degeneration)

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7
Q

describe simple neuronal atrophy?

A

shrunken, angulated and lost neurons, small dark nuclei, lipofuscin pigment, reactive gliosis

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8
Q

describe sub-cellular alterations

A

common in neurodegenerative conditions (e.g neurofibrillary tangles in alzheimers)
inclusions accumulate with ageing
also get inclusions in viral brain infections

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9
Q

function of astrocytes?

A

start shaped cells in CNS with astrocytic processes which envelop synaptic plates and wrap around vessels and capillaries
involved in ionic, metabolic and nutritional homeostasis
work in conjunction with endothelial cells to maintain BBB
main cells involved with repair and scar formation

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10
Q

what is gliosis?

A

astrocyte response to injury
most important histopathological indicator of CNS injury
shows astrocyte hypertrophy and hyperplasia
nucleus enlarges and becomes vesicular and the nucleolus is prominent
cytoplasmic expansion with extension of ramifying processes
in old lesions, nuclei are small and dark and lie in a dense net of processes (glial fibrils)

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11
Q

function of oligodendrocytes?

A

wrap around axons forming myelin sheath in CNS

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12
Q

how do oligodendrocytes respond to damage?

A

limited reaction
variable patterns and degree of demyelination
apoptosis
sensitive to oxidative damage
damage is a feature of demyelinating disorders

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13
Q

function of ependymal cells and how do they react to damage?

A

line ventricular system
limited reaction to injury
- disruption associated with local proliferation of sub-ependymal astrocytes to produce small irregularities on ventricular surface called ependymal granulation

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14
Q

function of microglia?

A

embryologically derived cells which function as a macrophage system (phagocytosis)
important mediators in acute nervous system injury
- M1 = pro-inflammatory, more chronic
- M2 = anti-inflammatory, phagocytic, more acute

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15
Q

microglia response to injury?

A

microglia proliferate
recruited through inflammatory mediators
form aggregates around areas of necrotic and damaged tissues

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16
Q

why is the brain so sensitive to hypoxia?

A

brain consumes 20% of all body resting oxygen consumption

cerebral blood flow can only increase twofold to maintain oxygen delivery, so cant cope well with hypoxia

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17
Q

what happens in the rbain with hypoxia?

A

after onset of ischaemia, mitochondrial inhibition of ATP synthesis leads to ATP reserves being consumed within a few minutes

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18
Q

describe the pathway of excitotoxicity?

A

energy failure (hypoxia) > neuronal depolarization and inhibition of astrocyte reuptake > release and inhibited reuptake of glutamate > glutamate storm and excitation > increased Ca2+ > oxidative stress, protease activation and mitochondrial dysfunction

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19
Q

what are the 3 types of oedema?

A

cytotoxic (intoxication, reye’s, severe hypothermia)
ionic/osmotic (occurs in hyponatraemia and excess water intake/SIADH)
vasogenic (most important) - occurs in trauma/tumours/inflammation/infection/hypertensive encephalopathy

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20
Q

haemorrhagic conversion?

A

complication of ischaemic stroke where bleeding occurs after reperfusion of the blocked artery

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21
Q

cerebral arteries supply what general areas of the brain?

A 
anterior = midline
middle = lateral aspects
posterior = posterior
22
Q

the brain uses how much of cardiac output?

A

15% of cardiac output and 20% of oxygen

23
Q

how is the brain supplied?

A

requires active aerobic metabolism of glucose
autoregulatory mechanisms help maintain blood flow over wide range of blood perfusion pressures at a constant rate by dilation and constriction of cerebral vessels

24
Q

what is cerebrovascular disease?

A

any abnormality of brain caused by a pathological process of blood vessels

25
Q

stroke essentially involves what 2 processes?

A

infarction/ischaemia/hypoxia etc
haemorrhage/blood vessel damage/rupture etc
- underlying link = hypertension

26
Q

global vs focal hypoxic ischaemic damage?

A

global = generalised reduction in blood flow/oxygenation
(e.g cardiac arrest, severe hypotension)
focal (e.g vascular obstruction)

27
Q

describe global hypoxic ischaemic damage/

A

generalised reduction in cerebral perfusion
autoregulatory mechanisms cant compensate
watershed areas are vulnerable
neurons more sensitive than glial cells
can lead to pan-necrosis if severe

28
Q

definition of stroke?

A

sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hrs

29
Q

what causes cerebral infarction and who is it most common in?

A 
interruption of cerebral blood flow due to thrombosis or embolization
thrombosis
- atherosclerosis
- usually in middle cerebral artery
embolic
- from atheroma in internal carotid and aortic arch
- travels from heart
more common in men over 70
30
Q

what can influence the end result of cerebral infarct?

A

arterial territory of affected artery
timescale of occlusion
extent of collateral circulatory relief
systemic perfusion pressure

31
Q

when is damage first seen after cerebral infarct and what is seen?

A

12 hrs
12-24 hrs =
pale soft and swollen with ill defined margins
red neurones, oedema and swelling

32
Q

what is seen 24-48 hrs after stroke?

A

increasing neutrophils, extravasation of red blood cells and activation of astrocytes and microglia

33
Q

what is seen 2-14 days after stroke>

A 
brain becomes gelatinous and friable
reduction in surrounding tissue oedema demarcates the lesion
microglia are predominant
myelin breakdown
reactive gliosis
34
Q

what is seen several months after stroke?

A

increasing liquification
formation of cavity lined by dark grey tissue
ongoing phagocytosis increases cavitation and surrounding gliotic scar formation

35
Q

what is haemorrhagic infarct?

A

where, in context of infarct, the blood brain barrier is damaged and deteriorates allowing blood to leak through after reperfusion following the infarct stroke
further disrupts damage of infarct

36
Q

hypertension can cause what types of vessel remodelling?

A

accelerated atherosclerosis
arteriolosclerosis - thick, stiff and weak walls
fibrinoid necrosis of vessel walls if severe
formation of lacunes
microaneurysms

37
Q

how can a vascular lesion be localised?

A

carotid artery disease = contralateral weakness/sensory loss, aphasia or apraxia if dominant hemisphere
middle cerebral artery = weakness in contralateral face and arm
anterior cerebral artery = weakness and sensory loss in contralateral leg
vertebrobasilar artery = vertigo, ataxia, dysarthria and dysphasia

38
Q

4 consequences of hypertension?

A

lacunar infarcts
multi-infarct dementia
ruptured aneurysms and intra-cerebral haemorrhage
hypertensive encephalopathy

39
Q

what are lacunar infarcts?

A

atheroma, embolism of small penetrating vessels leads to occlusion
vessels which supply basal ganglia etc
when multiple, contribute to multi-infarct dementia

40
Q

hypertensive encephalopathy findings?

A 
severe hypertension
symptoms of raised ICP
global cerebral oedema
tentorial and tonsillar herniation
arteriolar fibrinoid necrosis
petechiae
41
Q

2 types of intracranial haemorrhage, spontaneous includes what?

A

intracerebral haemorrhage
sub-arachnoid haemorrhage
haemorrhagic infarct

42
Q

types of traumatic intracranial haemorrhage?

A 
extra-dural haematoma
sub-dural haematoma
contusion (surface bruising)
intracerebral haemorrhage
sub-arachnoid
43
Q

what can contribute to causing an intracranial haemorrhage?

A 
hypertension
aneurysms
systemic coagulation disorders
anticoagulation
vascular malformations
amyloid deposits
open heart surgery
neoplasms
vasculitis
44
Q

what morphology is seen in intracerebral haemorrhage?

A 
asymmetry
shifts/herniations are common
intraparenchymal haematomas
softening of adjacent tissue
surrounding oedema
45
Q

what is amyloid angiopathy and how can it cause haemorrhage?

A

accumulation of beta-beta sheets sticking together to form a plaque
causes vessels to become stiff and rigid so cant respond to changes in BP so likely to rupture

46
Q

name 4 types of vascular malformations

A

arteriovenous malformations
cavernous angiomas
venous angiomas
capillary telangectases

47
Q

what happens in an AVM?

A

abnormal torturous vessels - usually occurring in middle cerebral arteries in cerebrum
causes shunting from artery to vein which causes vein to undergo smooth muscle hypertrophy or aneurysms which can rupture
veins not made to cope with the pressure so can rupture easily

48
Q

what commonly causes subarachnoid haemorrhage?

A

usually spontaneous
most common = rupture of saccular aneurysm
most are in internal carotid
arise in arterial bifurcations (circle of willis)

49
Q

describe the morphology seen in subarachnoid haemorrhage?

A 
presence of berry aneurysm
blood in the subarachnoid space
may see
- intracerebral haematomas
- infarcts of brain parenchyma
- mass effect of haematoma and features of raised ICP
- hydrocephalus
50
Q

clinical features of subarachnoid haemorrhage?

A

severe headache
vomiting
loss of consciousness
usually no history of a precipitating factor
risk factors = smoking, hypertension, kidney disease

Neurology (53 decks)

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