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3 - Pathology > Stroke > Flashcards

Stroke Flashcards

1
Q

Hypoxia

A

Oxygen deficiency which causes cell injury by reducing aerobic oxidative respiration

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2
Q

Ischaemia

A

Reduced tissue blood flow

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3
Q

Infarct (ion)

A

A localized area of ischemic tissue necrosis (death), usually coagulative necrosis

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4
Q

Liquefactive necrosis

A

Hypoxic ischaemic necrosis that occurs in the CNS

Digestion of dead tissue into a liquid mass - tissue outline not preserved

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5
Q

What is stroke?

A

Cerebrovascular disease encompassing:
Ischaemic Stroke - those that cause hypoxic ischaemic infarction of the brain
Intracerebral (intraparenchymal) and subarachnoid haemorrhages - hemorrhagic stroke

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6
Q

List the most common types of ischaemic stroke.

A

Global cerebral ischaemia (hypoxic ischemic encephalopathy)

Focal cerebral ischaemic (ischemic infarction) caused by thrombosis or embolism

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7
Q

List the common causes of haemorrhagic stroke.

A 
Hypertensive intraparenchymal haemorrhage 
Ruptured aneurysm (subarachnoid haemorrhage)
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8
Q

Which is most common - an ischaemic or hemorrhagic stroke?

A

Ischaemic

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9
Q

List the subtypes of the focal ischaemic stroke.

A

Embolic (from thrombosis elsewhere) - infarct can be reperfused = hemorrhagic infarct
Thrombotic - due to cerebral atherosclerosis = infarct usually pale

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10
Q

What causes global cerebral ischaemia?

A

Decrease in cerebral perfusion e.g. cardiac arrest, shock, severe hypotension
Same effect as severe respiratory depression (generalized hypoxia)

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11
Q

What is the clinical outcome of a generalized hypoxia ischaemic stroke?

A

Depends on the severity of the insult

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12
Q

Which parts of the brain are more vulnerable to ischaemic injury?

A

Hippocampus
Purkinje cells of the cerebellum
Watershed areas

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13
Q

What are the watershed areas of the brain?

A

Border Zone or Watershed areas lie between arterial perfusion territories (i.e. at the most distal reaches of arterial blood supply)

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14
Q

What causes focal ischaemic strokes?

A

Obstruction of blood supply to a localized area of the brain
Vascular occlusion may be the result of embolism to the brain (usually from a thrombus = thromboembolism) or thrombosis of cerebral vessels due to atherosclerosis

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15
Q

What are the most common blood vessels occluded in a local ischaemic stroke?

A

Large vessels - most commonly the Middle Cerebral Artery

Small penetrating vessels (those supplying the basal ganglia, thalamus and internal capsule)

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16
Q

Where do sources of emboli come from?

A

Heart:
- Mural thrombus complicating MI
- Thrombosis complicating AF
- Thrombosis complicating valvular diseases
Aorta and Carotid Arteries
- Thrombosis developing over atheromatous plaques
Paradoxical emboli
- Thromboemboli from the venous circulation may pass through a cardiac septal defect into the arterial circulation and embolize to the brain

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17
Q

Name the two types of infarcts, based on the haemorrhage within the infarct.

A

Haemorrhagic (red) infarct

Non-hemorrhagic (bland) infarct

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18
Q

What is a hemorrhagic (red) infarct?

A

Typically associated with embolic events
Multiple, sometimes confluent petechial haemorrhages
Due to reperfusion of damaged tissue through collateral circulation or following fibrinolysis of thromboembolic material in the occluded vessel and leakage of blood through necrotic vessels

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19
Q

What is a non-haemorrhagic infarct associated with?

A

Thrombosis

20
Q

Name the different management techniques for infarcts.

A

Thrombolytic therapy is used in thrombotic cases

This is contraindicated in Haemorrhagic infarcts

21
Q

What is the penumbra?

A

This is the area which lies around the ischaemic area and is potentially reversible if circulation is restored

22
Q

Which artery supplies the internal capsule?

A

Upper halves of anterior and posterior limbs are supplied by the MCA.

23
Q

Describe the gross appearance of an infarct that has occurred 0-6 hours before a patients death.

A

Undetectable macroscopically (except if haemorrhagic)

24
Q

What happens to the gross appearance by 48 hours?

A

Blurring of gray/white matter interface
Infarct is pale, soft, swollen, ill-defined
Extensive vasogenic edema due to disruption of BBB and passage of fluid into extracellular space

25
Q

What happens to the gross appearance from 2-10 days.

A

Area of brain infarct becomes gelatinous and friable

Infarct has well defined border

26
Q

What happens to the gross appearance from 10 days to 3 weeks?

A

Tissue breaks down and liquefies leaving cystic spaces (fluid-filled cavities) lined by dark grey tissue (gliosis)

27
Q

Describe why a brain edema follows an infarct.

A

Tissue necrosis triggers inflammation
Inflammation & loss of structural integrity of blood vessels = disruption of BBB
Increase in vascular permeability and extravasation of fluid = Vasogenic Edema
Edema may be severe enough to increase ICP and brain herniation

28
Q

Describe the histological appearance in the early stage (12-24 hours).

A

Cytoplasmic eosinophilia and nuclear pyknosis = red, dead, neurons
Neutrophilic infiltrates are evident early on, subside after about 48 hours

29
Q

Describe the microscopic appearance of the subacute stage (24 hours to 2 weeks)

A

Tissue necrosis, macrophage infiltrates, vascular proliferation and starting gliosis

30
Q

Describe the microscopic appearance of the repair stage (2 weeks onwards)

A

Removal of necrotic tissue by macrophages, leaving a cystic space surrounded by gliosis

31
Q

What additional features does the haemorrhagic infarct show microscopically?

A

Blood extravasation and resorption

32
Q

What is gliosis the indicator for?

A

CNS injury

33
Q

What characterizes gliosis?

A

Hypertrophy and hyperplasia of mainly astrocytes - main glial cells = astrogliosis
Form a dense web that surrounds lesions in the CNS

34
Q

Which blood vessels does hypertension affect?

A

Deep penetrating arteries and arterioles that supply the basal ganglia and hemispheric white matter and brainstem

35
Q

What does hypertension lead to in cerebral arterioles?

A

Hyaline atherosclerosis - thickening of their walls and narrowing of their lumens = predisposition to vascular occlusion and rupture

Also potentiates cerebral atherosclerosis = predisposition to thrombosis

36
Q

What causes hyaline atherosclerosis?

A

Plasma protein leakage across injured endothelial cells and extracellular matrix deposition by vascular smooth muscle cells
= response to HTN

37
Q

What does rupture of larger calibre penetrating vessels lead to?

A

Large intracerebral (intraparenchymal) haemorrhages

38
Q

What does rupture of small-caliber penetrating vessels leads to?

A

Small, slit haemorrhages

39
Q

What are lacunar infarcts?

A

Small infarcts due to vascular occlusion

40
Q

What are minute aneurysms?

A

Charcot-Bouchard micro-aneurysms = may be the site of rupture and bleeding in the basal ganglia - due to HTN

41
Q

What is the most common cause of non-traumatic deep brain parenchymal haemorrhages?

A

HTN

42
Q

What do hypertensive intraparenchymal haemorrhages commonly involve?

A

Basal ganglia (50-60% of cases)
Thalamus
Pons
Cerebellum

43
Q

What are Duret Haemorrhages and what causes them?

A

Linear haemorrhages seen in the midline of midbrain and pons in cases of uncal herniation
Tearing of the penetrating veins and arteries supplying the upper brainstem during progression of transtentorial herniation

44
Q

What is the most common cause of a SAH?

A

Non-traumatic (spontaneous) rupture of a saccular berry aneurysm in a cerebral artery

45
Q

What is the most common symptom of a SAH?

A

Severe thunderclap headache of sudden onset
Usually signs of meningeal irritation too - photophobia, positive Kernigs, neck stiffness, headache
Also signs and symptoms of raised ICP

46
Q

What may also cause a SAH?

A 
Extension of traumatic haematoma 
Rupture of HTN intracerebral haemorrhage into the ventricular system 
Vascular malformations
Hematologic disturbances
Brain tumours
47
Q

What causes saccular “berry” aneurysms?

A

Congenital defect in arterial wall
Not present at birth, but develop at young age
Occur at arterial branching points

HTN also a risk factor for developing berry aneurysms and increases risk of rupture

3 - Pathology (7 decks)

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