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PATHOLOGY CAM304 > Pathology of Stroke > Flashcards

Pathology of Stroke Flashcards

1
Q

What is the typical presentation of a cerebrovascular isease:

A
  • Patients present clinically as “stroke”
    : Sudden loss of brain function
    :+/- loss of consciousness
  • Suddenness suggests a vascular cause
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2
Q

Vascular disease in the CNS includes 3 pathologies

A

Occlusion -> infarction
Narrowing -> decreased flow -> infarction
Ruptured vessel- > haemorrhage

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3
Q

2 processes occur in cerebrovascular disease- whatare these?

A
  1. Hypoxia, ischemia, and infarction resulting from IMPAIRED BLOOD SUPPLY & oxygenation of the CNS tissue
  2. HAEMORRHAGE resulting from the rupture of a CNS vessel
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4
Q

Cerebrovascular disease includes:

A

Thrombosis
Embolism
Haemorrhage
Narrowing/occlusion

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5
Q

Cerebrovascular Infarction due to VASCULAR OCCLUSION- causes?

A

Thrombosis or Embolism

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6
Q

Cerebrovascular Infarction due to VASCULAR OCCLUSION-

Arterial Thrombosis - what are the most common sites?

A

Carotid bifurcation
Origin of middle cerebral artery
End of basilar aa

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7
Q

Vascular Occlusion causing CC infarct:
ARTERIAL THROMBOSIS
What are the changes you would see pathologically?

A

Changes in the :
Lumen- changes in blood composition
Wall- mural disease
External compression - very rare

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8
Q

Vascular Occlusion causing CC infarct:
ARTERIAL THROMBOSIS
What disorders could cause a luminal change?

A 
•	Haematological disorders → leading to increased thrombotic tendency
o	Sickle cell disease
o	Polycythemia rubra vera
o	Thombocythaemia
o	Waldenstrom’s
o	PNH
o	TTP
o	Multiple myeloma
o	Circulating lupus anticoagulant
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9
Q

Vascular Occlusion causing CC infarct:
ARTERIAL THROMBOSIS
What disorders could cause a change in the wall?

A

Atheroma (large vessels) – most common! - Diabetes, basilar artery thrombosis, ruptured plaque, pontine infarction

Lipohyalinosis – (small vessels at centre of brain)

Vasculitis - in wall alters endothelium -> atherosclerosis

Arterial dissection
Arterial Vasospasm- Uncommon cause of infarction .Causes:
• Surgical interference
• IV contrast
• Severe head injury
• Ruptured berry aneurysm (occurs day 3 & becomes maximal after 7 days – caused by breakdown products causing the muscle to spasm)

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10
Q

Cerebrovascular Infarction due to EMBOLISM causes?

A

Atrial mural thrombus (most common - MI, valvular disease, afib)
Atheroma carotid

Paradoxical embolus (DVT in legs or pelvis + patent foramen ovale/atrial-septal defect?
Mitral valve vegetations
Ventricular mural thrombus (IE, myocarditis?)
AV vegetations
Atheroma aorta
Pulmonary vein thrombus (uncommon)

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11
Q

Embolic infarctions are clinically what?

A
  • Are often haemorrhagic
  • i.e. embolis comes into artery, extends into smaller vessel & embolus impacts and fragments into smaller pieces → blood flow restored → damaged vessels, endothelial cells leaky → blood goes into neuropil.
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12
Q

YOU CAN have occlusion without infarction; where?

A
  • If there is a collateral blood supply
  • So only (in the brain) if it involves the circle of willis
    o i.e. thrombosis in the circle of willis will not cause infarct (generally – anatomical variation)
  • eg: occlusion in right anterior cerebral artery → no infarct because the anterior communicating artery is a source of collateral blood from the other side
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13
Q

What areas are likely to be occluded?

A

Large vessels- causing infarct- deep vessels.

*there are partical collateralls for distal branches of A.M/P cerebral arteries. No collaterals for deep vessels

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14
Q

Infarct of large vessels

A

Travel in the SUBARACHNOID SPACE- branch and have penetrating vessels that go into the brain.
Anterior, posterior and middle cerebral arteries- > cause a large infarct, surface based which is a wedge

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15
Q

Describe an acute cerebral infact

A
  • Wedge shaped
  • Pale
  • Cerebral swelling - bigger, has pushed the brain over to the other side: septum pellucidum has moved to other side etc
  • Subfalcine & midline shift
  • Deformed ventricles
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16
Q

Section of acute cerebral infarct - histological features

A
  • Neurons show evidence of infarct: Nucleus is dissolving
  • Neutrophil margination
  • Neutrophil emigration
  • Oedema (white spaces)
  • Red cell diapedesis – leaking out through spaces in endothelial cells
  • Neuronal ischaemia (hyperchromasia of nucleus)
  • Occasional macrophages (must be 3 days old to see this)
17
Q

What are the effects of an acute cerebral infarct?

A
  • The whole cerebral hemisphere swells
  • No longer have subarachnoid space
  • Cerebral swelling → TENTORIAL HERNIATION
  • lateral compression of midbrain (by expanding brain & tentorial free edge) →
  • CST signs & decreased consciousness
  • Elongated brainstem (in AP direction) →
  • Capillaries become stretched & they tear →
  • secondary brainstem haemorrhage → respiratory/cardiac arrest
18
Q

If they do not die- > infarct organisation- what happens:

A

Neutrophils: enter periphery of infarct, degenerate & release enzymes →
Dead tissue gradually disintegrates →
Day 3: macrophages enter →
Ingest & remove necrotic debris → cystic spaces
Peripheral surviving astrocytes transform to gemistocytic & fibrous astrocytes → scarring (wall off the area)

Organising infarct – 2 weeks
Lipid in the myelin is breaking down & being consumed by macs – hence yellow appearance
Still wedge shaped
Can see a gelatinous area = early gliosis (astrocytes proliferating to wall off infarct)

Micro:
Macrophages ingesting lipid (necrotic material)
Neuronal necrosis (neurons that have lost their nuclei)
Periphery in gelatinous areas: infarct margin, pink cells with long processes = gemistocytic astrocytes & neuropil oedema

19
Q

What would you see in an old cerebral infarct?

A
  • Dead tissue has been completely resorbed
  • Collapsed cystic space
  • Surface meningeal thickening
  • Middle cerebral artery territory – smaller than represented on diagrams due to collateral circulation from ACA & PCA
20
Q

What are the secondary changes you would see on an old cerebral infarct?

A
  • Wallerian degeneration: entire neuron eventually disappears
  • Leads to fiber tract atrophy
  • Dead tissue resorbed
  • Collapsed cystic space – loss of all the neurons that usually sit in this areas
  • Surface meningeal thickening
  • Sub-pial astrocyte sparing (some astrocytes survive due to Pia blood supply)
  • Hydrocephalus “ex vacuo” – ventricle becomes bigger
  • Thinner corpus callosum (less axons tracking across to other side)
  • Midbain
    o Corticospinal tracts on injured sign, pons etc all atrophied
21
Q

Occlussion of Small Blood Vessels:

A

Penetrating vessels, mainly end arteries

22
Q

What is an occlussion due to thrombosis in a small area called?

A

LACUNAR INFARCT

23
Q

Describe

HOW, WHERE and the importance of Lacunar Infarct

A

How?

  • Increased luminal px (hypertension) →
  • Degenerative changes within walls (liohyalinosis) →
  • Luminal thrombosis →
  • Tiny lacunar infarcts (old)
-	Where are they?
o	Central white matter (centrum semiovale)
o	Basal ganglia
o	Pons
o	Cerebellum
-	Importance of Lacunar Infarction
o	Tiny infarcts but important due to location
o	Profound clinical effects (CST) 
o	No mass effect (no brain swelling)
o	Patient survives
o	Seen at post-mortem as old infarcts
  • What do you see
    o Cystic space with a few BVs crossing it, a few glial fibers going across
24
Q

How does a cerebral haemorrhage occur?

A

Due to rupture of a BV
- in subarachnoid space = subarachnoid haemorrhage and is usually due to trauma
Intracerebral- intracerebral haemorrhage and usually due to underlying vascular disease

25
Q

Describe intracerebral haemorrhage

  • where does it occur?
  • What % of stroke make up ICH?
A

Central white matter, basal ganglia, cerebellum, pons
About 10% of “strokes”
Lesion of vessel → rapidly forming intracerebral haematoma → pressure on brain stem
Space-occupying lesion
Death due to acute brainstem compression

26
Q

WHat are the macrosopic features of ICH?

A
  • Intracerebral haematoma
  • Compression of surrounding structures
  • No central structure
  • Brain shift
  • May rupture through brain into →
    o Subarachnoid space or ventricular system
27
Q

What are the Microcsopic features of ICH?

A
  • Expanding hematoma
  • Neutrophils around edge
  • 3 days: macs come in & ingest blood clot
  • Weeks/months: Organised cyst with pigmented lining due to haemociderin
    o Blood breakdown → haemotoidin or haemociderin
    o Eventually all blood disappears → pigmented lining
28
Q

Inctracerebral haemorrhages are caused by two things-

A

Primary (hypertensive) ICH

Secondary ICH

29
Q

PRIMARY INTRACEREBRAL HAEMORRHAGE

A

HTN causes a number of abnormaities of the vessel wal; accellerated atherosclerosis in large aas, hyaline arteriosclerosis in smaller aa and in severe instances -> proliferative change and necrosis. Arteirolar walls are affected by hyaline change and are pressumabily weaker than normal vessels AND threfore more vulnerable to rupture

  • older people, benign HTN and diabetes mellitus
  • Cause infarct in: central white matter, pons and the cerebellum
30
Q

Secondary INTRACEREBRAL HAEMORRHAGE
who?
Causes?

A

Consider if: person is young, no history of HTN, sit is somewhere other than the white matter in brain, pons or cerebellum.

  • Coagulation disorders
    o Anticoagulant therapy; haemopoieitic disorders; coagulation factor deficiencies
-	Weakening of vessel wall (mural weakening) →
o	Vessel wall damage
•	BERRY ANEURYSM
•	Infective aneurysm - Complicate 3% cases of IE; Small; 20%  multiple; 65% rupture within several weeks; ICH, SAH
•	Congophilic angiopathy
•	Arteritis
•	Cerebral metastases
•	Systemic amyloidosis
o	Vascular malformation
•	Aterial-venous malformation
•	Microscopic
o	Numerous vessels embedded within brain tissue
o	Marked variation in wall thickness
o	Gliosis +/- haemosiderin
o	Arteries, veins & hybrid vessels
•	Cavernous angioma
•	GBM
31
Q

SUBARACHNOID HAEMORRHAGE - aetiology

A

Due to extension of intracerebral haemorrhage

Direct bleeding into subarachnoid space
o Abnormal vascular structure: AVM: Cavernous angioma: Infective aneurysm: Arteritis
o Coagulation disorders: Anticoagulant therapy: Haemopoietic disorders: Coagulation factor deficiencies

  • Ruptured berry aneurysm (most common)- anterior circulation - near major branch points- most common at branch of ACA and anterior communicating artery
32
Q

Describe a BERRY ANEURYSM

A

o Vessels in circle of Willis arise as separate vessels & then unite: but in some people they don’t properly unite & there is a defect which bulges & forms an aneurysm

33
Q

BERRY ANEURYSM- gradually enlarges

A

o Present ~40y.o with rupture→ ruptured aneurysms often associated with atheroma & HTN)
o May present earlier then 40 if there is a:
• AVM
• Coartcation of aorta → HTN
• Adult polycystic kidney disease → HTN
• Connective tissue disorder (EDS, MS, PXE) → weak vessel wall
• Fibromuscular dysplasia ipsilateral internal carotid artery

34
Q

What are MICRO ft

A
  • Microscopic
    o Aneurysmal wall has fibrous tissue, myxoid change & atheroma
  • Most aneurysms bulge into subarachnoid space & hence give a subarachnoid haemorrhage; burrowing aneurysms can burrow into the brain causing intracerebral haemorrrhage
    o Rarely berry aneurysm becomes attached to arachnoid → subdural haemorrhage
    o SAH : 10-15% are multiple aneurysms
  • Burrowing berry aneurysm
    o 14-40% burrow into brain & rupture
    o Intracerebral haemorrhage (ICH) or IVH +/- SAH
35
Q

What is the order for treatment of STROKE

A

→ Imaging
→ SAH or ICH or Infarct
→ SAH → berry aneurysm or vascular malformation or bleeding disorder
→ ICH→ primary or secondary (vascular malformation, tumour – angiography)
→ Infarct → lacunar or large vessel

PATHOLOGY CAM304 (16 decks)

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