Week 1 - CNS1 Flashcards

Head Injury, Stroke, Other (minor) (60 cards)

1
Q

Which cells are the first to die when there is lack of oxygen?

A

Neurons

  • continuous O2 demand (whether inactive/functioning)
  • commonest cause = ischaemia/infarction
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2
Q

What are nissl granules and how do they relate to neuronal injury?

A
  • blueish granules in a normal neuron

- in neuronal injury, loss of nissl granules –> RED NEURONS

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3
Q

Why are dead/injured neurons red?

A
  • loss of nissl bodies

- pyknosis of nuclei

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4
Q

What are microglia?

A
  • small sedentary cells
  • not functioning
  • from BM
  • activation –> macrophages
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5
Q

Outline mechanism of neuronal injury

A
  • chemical, physical, ischaemic injury to neurons
  • increased excitatory amino acids (glutamate/aspartate)
  • increased cytokines
  • amino acids + cytokines –> inflammation
  • cell swelling, vacuolisation, loss of nissl granules (red neurons), pyknosis of nuclei
  • decreased glucose utilisation –> increased catecholamines –> further/extensive injury
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6
Q

What processes occur post neuronal injury?

A
  1. microglia –> macrophages –> clearing/phagocytosis of dead neurons
  2. astrocyte activation + proliferation –> GLIOSIS (healing) *NO COLLAGEN SCAR
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7
Q

What is the name of the process by which neuronal tissue heals?

A

gliosis

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8
Q

When is there collagen scar formation in the brain?

A
  • only when there is a chronic abscess

- collagen tissue comes from BV walls

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9
Q

What is a concussion?

A
  • no visible injury
  • microscopic, diffuse neuronal stress/damage
  • spontaneous recovery; no permanent damage
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10
Q

What is a contusion?

A
  • localised

- visible injury (bruise in CNS)

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11
Q

What is a laceration?

A

-visible tear in brain tissue

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12
Q

What are the 2 types of intracranial haemorrhage and their respective subtypes?

A
  1. Traumatic
    - epidural
    - subdural
    - subarachnoid
    - intracerebral
  2. Non-traumatic
    - HTN
    - AV malformation
    - tumours
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13
Q

What is meant by coup & contra-coup injury?

A
  • brain is literally floating in the brain cavity
  • when there is blunt head injury (i.e. MVA), front of head is hit with extreme force causing brain to shift to the front and hit the bone (COUP) –> brain then consequently bounces back and hits the back of the head bone (CONTRA-COUP)
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14
Q

What is diffuse axonal injury?

A

extension of injury to surrounding tissue due to damaged neurons

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15
Q

What are the primary and secondary injuries in blunt head injury?

A

Primary:

  • concussion, contusion, laceration
  • coup + contra-coup
  • diffuse axonal injury

Secondary:

  • inflammation
  • haematoma
  • oedema + infection
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16
Q

What are post-traumatic complications in blunt head injury?

A
  • diffuse neuronal injury –> coma/death

- chronic –> epilepsy + dementia

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17
Q

Describe an epidural haemorrhage

A
  • usually in young
  • arterial vessels (esp. middle meningeal artery)
  • due to severe trauma –> skull fracture usually present
  • blood accumulates between dura and skull causing compression of the brain surface –> “lens” shaped haematoma!
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18
Q

Describe subdural haemorrhage

A
  • usually in elderly (nursing homes), delayed symptoms
  • minor trauma
  • venous rupture in subdural space (BRIDGING VEINS)
  • spreads larger areas as it is less adherent –> spreads over surface of the brain –> “linear/crescent” shaped haemorrhages!
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19
Q

Describe subarachnoid haemorrhage

A
  • usually non-traumatic
  • bleeding in arachnoid space
  • cerebral vessel bleeding usually caused by HTN, atherosclerosis or arteriovenous malformation (AVM)
  • bleeding is sudden with a very severe headache (“thunderclap” headache)
  • blood spreads all over surface and into sulci
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20
Q

What is meant by the lucid interval and in which intracranial haemorrhage type is it seen?

A
  • seen in EPIDURAL haemorrhage
  • severe trauma (often with fracture) leads to loss of consciousness due to concussion which is then regained after a few minutes (LUCID INTERVAL)
  • in this interval, however, the hematoma is still expanding and compressing brain tissue –> eventually leads to unconsciousness again
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21
Q

What usually happens to past bleeds in the brain?

A

-remains as hemosiderin (golden/brown pigment)

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22
Q

Describe intracerebral haemorrhage?

A
  • trauma –> contusion
  • increased intracranial pressure with focal deficits
  • profound coma
  • usually rapidly fatal
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23
Q

After how long will neuron cell death be irreversible due to ischaemia?

A

approx. 10mins

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24
Q

How much CO and body O2 does the brain require?

A
  • 20% CO
  • 20% body O2

*despite the brain only being 2% of body weight

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25
What is CVA and what are the 2 broad types?
"Cerebro-Vascular Accident" 1. Ischaemic (thrombotic/embolic) 2. Haemorrhagic
26
What are cerebral venous infarctions usually secondary o?
Infections *99% of strokes involve arteries
27
What are the 3 clinical phases of stroke?
1. Transient - less than 24hrs without cell necrosis 2. Evolving (thrombotic) - progressive increase in Sx. - atheroma --> thrombosis 3. Completed (embolic) - stable Sx. or improvement - no change
28
What are the sensitive areas of the brain in a stroke?
- border zone (watershed zone) - basal ganglia *areas first to get damaged in global ischaemia
29
What is the etiology of global ischaemia?
-decreased O2 -decreased BP -decreased glucose OR -major artery block (carotids)
30
What are the clinical features of global ischaemia?
- mild confusion --> brain death | - acute --> major infarct OR chronic
31
What are watershed zones?
- aka border zones | - border areas between the areas supplied by major arteries (ACA/MCA + MCA/PCA)
32
What is the morphology of global ischaemia?
- watershed zone infarcts | - in chronic form --> lamellar necrosis (lines of necrosis along the cortex - usually seen in ventilator brains)
33
What is a transient ischaemic attack (TIA)?
- focal type of stroke - usually due to small blockage which is cleared off, thrombus that is thrombolysed or a spasm in the blood vessel - resolve <24hrs --> no cell death
34
Which is the commonest type of ischaemic stroke?
embolic
35
Compare commonality and mortality of ischaemic and haemorrhagic strokes
Ischaemic - commonest 80% - mortality 20% Haemorrhagic - less common 20% - mortality 80%
36
What is the most common cerebral artery affected by stroke? and what are the consequences?
MCA --> deep branches - supplies the basal ganglia (thalamus, internal capsule, globus pallidus, putamen) - internal capsule (where half the body motor fibres cross over) - involvement of this area causes internal capsule damage --> HEMIPLEGIA (common presentation)
37
Explain Umbra/Penumbra
Umbra -area of cell death --> central infarct area Penumbra -surrounding area of ischaemic damage/inflammation *PENUMBRA --> recovery follwoing resolution of stroke can lead to improvement (NOT recovery of umbra --> permanent)
38
Outline infarct morphology and progression of the brain
<6hrs: -no visible change (molecular) 1-2days: -red neuron (loss of nissl granules/pyknosis of nuclei 2-14days: -inflammation, neutrophils, haemorrhage, liquefactive necrosis 2wks: -foamy macrophages (clear dead debris forming cavities), activated astrocytes >4wks: -cavity and outer gliosis *NO GRANULATION TISSUE/COLLAGEN SCAR
39
Compare ischaemic vs. haemorrhagic strokes
Ischaemic: - pin point haemorrhages (petichiae-like) over a triangular area of inflammation - swelling - oedema Haemorrhagic: - haematoma/blood in ventricles - surrounding area of inflammation - swelling - oedema
40
Why do you get pinpoint haemorrhages in ischaemic stroke?
- RBCs escaping the dead BV walls | - forms a triangular area due to the BV branches
41
What are the clinical features of left vs. right hemisphere strokes?
Left (dominant): - aphasia - right hemipariesis - right sided sensory loss - right visual field defect - poor right conjugate gaze - dysarthria - difficulty reading, writing or calculating Right (non-dominant): - left visual field defect - left hemipariesis - extinction of left sided stimuli - left sided sensory loss - poor left conjugate gaze - dysarthria - spatial disorientation
42
Describe the features of an ACA stroke
- paralysis of contralateral foot + leg - sensory loss in toe, foot and leg - impairment of gait and stance - abulia (slowness and prolonged delays to perform actions) - flat affect, lack of spontaneity, slowness, distractibility - cognitive impairment such as preservation + amnesia - urinary incontinence
43
What is abulia?
- slowness and prolonged delays to perform actions | - usually result of ACA stroke
44
Describe the features of a PCA stroke?
Peripheral (cortical) - homonymous hemianopia, memory deficits, preservation (repeat response) - visual deficits --> cortical blindness, lack of depth perception, hallucinations Central (penetrating) - thalamus --> contralateral sensory loss, spontaneous pain, mild hemi - cerebral peduncle --> CN III palsy with contralateral hemiplegia - brain stem --> CN palsies, nystagmus, pupillary abnormalities
45
What is the major risk factor for haemorrhagic strokes?
HTN
46
What are Charcot-bouchard microaneurysms?
- type of hypertensive haemorrhage - microscopic aneurysms of small arterioles - dilatation with formation of thrombosis or haemorrhage - usually in basal ganglia/brainstem region - putamen (60%) --> commonest location!*
47
What are slit haemorrhages?
- type of hypertensive haemorrhage - microhaemorrhages with or without aneurysm - usually heal as a slit with hemosiderin pigment - common in basal ganglia
48
What are lacunar infarcts?
- type of hypertensive haemorrhage - areas of old infarcts covered by clear fluid - "lacunes" --> like lakes - brainstem --> pale healed old infarcts
49
What can occur as a result of chronic hypertension in hypertensive encephalopathy?
vascular dementia
50
What is acute hypertensive encephalopathy?
- condition usually seen in malignant HTN (>130 diastolic) - increased intracranial tension (ICT) - headache - confusion - vomiting - convulsions - -> COMA
51
What are berry aneurysms?
-common non traumatic ICH -anterior 95%; congenital -usually multiple, due to medial degeneration -HTN = cause; rupture due to sudden raise in BP (straining/stress) --> haemorrhage CLINICAL: -headache, dizziness, increased ICT, meningeal irritation (blood in meninges), LOC, seizure, *classic stroke = rare * rarely with genetic disorder: - polycystic kidney disease - neurofibromatosis - marfan's syndrome
52
What does a ruptured berry aneurysm cause?
SUBARACHNOID HAEMORRHAGE - thunderclap headache - meningeal irritation --> LOC, increased ICT, stiff neck, vomiting (DDx. for meningitis BUT here it is sudden!) - blood all over surface, ventricles and in sulci
53
What are arterio venous malformations (AVM)?
- common congenital vascular malformation - embryonic disorganisation (NOT a real tumour) --> irregular blood vessels - common in CNS - typically located in outer cerebral cortex underlying white matter - can bleed in HTN pts. - produce intracranial haemorrhages - depending on size can be asymptomatic, cause seizures or classic haemorrhagic stroke
54
What is the most common cause of stroke in young patients?
- patent foramen ovale (PFO) - bypass of emboli from RA --> LA --> LV --> systemic circ (cerebral vessels) --> embolic stroke due to bypass of emboli (PARADOXICAL EMBOLISM)
55
What is the pathogenesis of MCA deep branches - haemorrhagic CVA?
- hypertensive arteriolosclerosis/microaneurysms - haemorrhage in deep penetrating branches of MCA - blood tears through basal ganglia, putamen, internal capsule (HEMIPLAGIA) and enters ventricles
56
What is the result of oedematous swelling of the brain after stroke?
- narrowing of sulci - flattening of gyri - loss of demarcation of gray and white matter - herniation --> midline shift and compression of lateral ventricles
57
Haematoma in the basal ganglia region extending to ventricles is typically seen in?
haemorrhagic stroke
58
What are the microscopic features of healing in stroke?
- foamy macrophages in cavity clearing/phagocytosing debris - surrounding activated, large astrocytes - gliosis (fibrils)
59
Central pontine haemorrahge typically occurs in patients with?
cerebellar herniation
60
What are differentials of the "unconscious pt."?
AEIOU DAHMS mnemonic: A --> apoplexy (stroke) E --> epilepsy/seizure I --> infections, injury (head), meningitis O --> organophosphate poisoning U --> uremic come D --> DM (HONK/DKA); hypoglycemia A --> alcohol poisoning, anaphylaxis H --> heat stroke, hysteria M --> methylaclohol, malingering, medicine (sedatives/opioids) S --> strychnine, snake bite (anaphylaxis)