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Pathology Term 4 > Week 1 - CNS1 > Flashcards

Week 1 - CNS1 Flashcards

Head Injury, Stroke, Other (minor)

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
Q

What is CVA and what are the 2 broad types?

A

“Cerebro-Vascular Accident”

  1. Ischaemic (thrombotic/embolic)
  2. Haemorrhagic
26
Q

What are cerebral venous infarctions usually secondary o?

A

Infections

*99% of strokes involve arteries

27
Q

What are the 3 clinical phases of stroke?

A
  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
Q

What are the sensitive areas of the brain in a stroke?

A
  • border zone (watershed zone)
  • basal ganglia

*areas first to get damaged in global ischaemia

29
Q

What is the etiology of global ischaemia?

A

-decreased O2
-decreased BP
-decreased glucose
OR
-major artery block (carotids)

30
Q

What are the clinical features of global ischaemia?

A
  • mild confusion –> brain death

- acute –> major infarct OR chronic

31
Q

What are watershed zones?

A
  • aka border zones

- border areas between the areas supplied by major arteries (ACA/MCA + MCA/PCA)

32
Q

What is the morphology of global ischaemia?

A
  • watershed zone infarcts

- in chronic form –> lamellar necrosis (lines of necrosis along the cortex - usually seen in ventilator brains)

33
Q

What is a transient ischaemic attack (TIA)?

A
  • 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
Q

Which is the commonest type of ischaemic stroke?

A

embolic

35
Q

Compare commonality and mortality of ischaemic and haemorrhagic strokes

A

Ischaemic

  • commonest 80%
  • mortality 20%

Haemorrhagic

  • less common 20%
  • mortality 80%
36
Q

What is the most common cerebral artery affected by stroke? and what are the consequences?

A

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
Q

Explain Umbra/Penumbra

A

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
Q

Outline infarct morphology and progression of the brain

A

<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
Q

Compare ischaemic vs. haemorrhagic strokes

A

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
Q

Why do you get pinpoint haemorrhages in ischaemic stroke?

A
  • RBCs escaping the dead BV walls

- forms a triangular area due to the BV branches

41
Q

What are the clinical features of left vs. right hemisphere strokes?

A

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
Q

Describe the features of an ACA stroke

A
  • 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
Q

What is abulia?

A
  • slowness and prolonged delays to perform actions

- usually result of ACA stroke

44
Q

Describe the features of a PCA stroke?

A

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
Q

What is the major risk factor for haemorrhagic strokes?

A

HTN

46
Q

What are Charcot-bouchard microaneurysms?

A
  • 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
Q

What are slit haemorrhages?

A
  • type of hypertensive haemorrhage
  • microhaemorrhages with or without aneurysm
  • usually heal as a slit with hemosiderin pigment
  • common in basal ganglia
48
Q

What are lacunar infarcts?

A
  • type of hypertensive haemorrhage
  • areas of old infarcts covered by clear fluid
  • “lacunes” –> like lakes
  • brainstem –> pale healed old infarcts
49
Q

What can occur as a result of chronic hypertension in hypertensive encephalopathy?

A

vascular dementia

50
Q

What is acute hypertensive encephalopathy?

A
  • condition usually seen in malignant HTN (>130 diastolic)
  • increased intracranial tension (ICT)
  • headache
  • confusion
  • vomiting
  • convulsions
  • -> COMA
51
Q

What are berry aneurysms?

A

-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
Q

What does a ruptured berry aneurysm cause?

A

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
Q

What are arterio venous malformations (AVM)?

A
  • 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
Q

What is the most common cause of stroke in young patients?

A
  • 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
Q

What is the pathogenesis of MCA deep branches - haemorrhagic CVA?

A
  • hypertensive arteriolosclerosis/microaneurysms
  • haemorrhage in deep penetrating branches of MCA
  • blood tears through basal ganglia, putamen, internal capsule (HEMIPLAGIA) and enters ventricles
56
Q

What is the result of oedematous swelling of the brain after stroke?

A
  • narrowing of sulci
  • flattening of gyri
  • loss of demarcation of gray and white matter
  • herniation –> midline shift and compression of lateral ventricles
57
Q

Haematoma in the basal ganglia region extending to ventricles is typically seen in?

A

haemorrhagic stroke

58
Q

What are the microscopic features of healing in stroke?

A
  • foamy macrophages in cavity clearing/phagocytosing debris
  • surrounding activated, large astrocytes
  • gliosis (fibrils)
59
Q

Central pontine haemorrahge typically occurs in patients with?

A

cerebellar herniation

60
Q

What are differentials of the “unconscious pt.”?

A

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)

Pathology Term 4 (6 decks)

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