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YR5 Histopathology > Cerebrovascular disease and trauma > Flashcards

Cerebrovascular disease and trauma Flashcards

1
Q

What is cerebral oedema?

A

Excess accumulation of fluid in the brain parenchyma.

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2
Q

What are the two types of cerebral oedema?

A

Vasogenic: Disruption of blood brain barrier.

Cytotoxic: Secondary to cellular injury e.g. hypoxia/ ischaemia.

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3
Q

What is the result of cerebral oedema?

A

Raised intracranial pressure

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4
Q

What are the two types of hydrocephalus?

A

Non-communicating: obstruction of flow of CSF.

Communicating: no obstruction but problems with re-absorption of CSF into venous sinuses.

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5
Q

What is normal ICP?

A

ICP measured in mmHg

7–15mmHg for a supine adult.

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6
Q

What are consequences of raised ICP?

A

Enclosed bony box: Pressure increases because of space occupying lesions, oedema or both.

Increased pressure forces brain against unyielding bony wall of skull + inflexible dural folds.

Results in herniation of brain structures where space is available.

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7
Q

What is the definition of stroke?

A

Clinical syndrome characterised by rapidly developing clinical Sx +/- signs of focal, + at times global loss of cerebral function

with Sx lasting >24h or leading to death, with no apparent cause other than that of vascular origin.

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8
Q

What is a TIA?

A

Warning stroke: should be taken very seriously.

Caused by a clot; blockage is temporary.

Most TIAs last <5m; average ~ 1m.

Unlike a stroke, when a TIA is over, usually no permanent injury to brain.

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9
Q

What is the significance of TIA?

A

1/3 of those with TIA get significant infarct within 5y.

TIA= important predictor of future infarct.

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10
Q

What is a non-traumatic intra-parenchymal haemorrhage?

A

Haemorrhage into substance of the brain: rupture of a small intraparenchymal vessel.

Most common in basal ganglia.

HTN causes > 50% of bleeds.

Presentation with severe headache, vomiting, rapid loss of consciousness, focal neurological signs.

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11
Q

Give 7 features of arteriovenous malformations?

A

Occur anywhere in CNS.

Symptomatic between 2nd- 5th decade (mean 31y)

Present with haemorrhage, seizures, headache, focal neurological deficits.

High pressure: MASSIVE BLEEDING!!!

Seen on angiography.

Morbidity after rupture 53-81%: high in eloquent areas.

Mortality 10-17.6%

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12
Q

What is the treatment of arteriovenous malformations?

A

Surgery

Embolization

Radiosurgery.

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13
Q

What is a cavernous angioma?

A

Well-defined malformative lesion composed of closely packed vessels with no parenchyma interposed between vascular spaces.

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14
Q

What is the pathogenesis/clinical presentation of cavernous angiomas?

A

Can be found anywhere in CNS

Usually symptomatic >50y.

Congenital, pathogenesis unknown.

Present with headache, seizures, focal deficits, haemorrhage.

Low pressure: recurrent bleeds.

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15
Q

What is the treatment of cavernous angiomas?

A

Surgery

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16
Q

What is this?

A

Arteriovenous malformation

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17
Q

What is this?

A

Arteriovenous malformations

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18
Q

What is this?

A

Cavernous angioma

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19
Q

What is this?

A

Cavernous angioma

20
Q

What are subarachnoid haemorrhages?

A

Rupture of a berry aneurysm (present in 1% of gen pop)

80 %: Internal carotid artery bifurcation

20%: within the vertebro-basilar circulation.

21
Q

What is the clinical presentation of subarachnoid haemorrhages?

A

30% of patients have multiple aneurysms.

Greatest risk of rupture when 6-10mm diameter.

Present with sudden onset of severe “thunder clap” headache, vomiting, loss of consciousness.

22
Q

What is this?

A

Berry aneurysm

23
Q

What is the treatment for subarachnoid haemorrhages?

A

Endovascular tx: coils

Blocks blood flow

24
Q

What are infarctions?

A

Tissue death due to ischaemia.

Commonest form of cerebrovascular disease

70-80% of strokes

25
Q

What are risk factors for infarctions?

A

Cerebral atherosclerosis most common cause.

HTN

DM

Smoking

26
Q

Where does the worst atherosclerosis occur?

A

In larger vessels (extra-cerebral arteries)

Thrombosis formation

Often near carotid bifurcation or in basilar artery.

27
Q

Where do emboli occur?

A

Intracerebral arteries.

Usually from heart or atherosclerotic plaques.

Embolic occlusion usually in middle cerebral artery branches.

28
Q

What is the difference between an infarction and haemorrhagic stroke?

A

Infarction:

  • Tissue necrosis (stains)
  • Rarely haemorrhagic
  • Permanent damage in affected area
  • No recovery

Haemorrhage:

  • Bleeding
  • Dissection of parenchyma
  • Fewer macrophages
  • Limited tissue damage (periphery)
  • Partial recovery
29
Q

What is the epidemiology of TBI?

A

Trauma single largest cause of death in <45s.

9 deaths from head injury per 100,000.

Account for 25% of all trauma deaths.

High morbidity:

  • 19% vegetative or severely disabled
  • 31% good recovery
30
Q

What are different classifications of TBI?

A

Non-missile + missile

Non-missile:

  • Acceleration/ deceleration (brain decelerates at different rate to skull)
  • Rotation (midline more susceptible due to rotational forces)

Cause: RTA, falls + assaults

Resulting damage: Focal or diffuse.

31
Q

What are fractures associated with cerebrovascular disease?

A

Fissure fractures often extend into base of skull

May pass through middle ear or anterior cranial fossa

Otorrhea or rhinorrhea

Infection risk

32
Q

What is a contusion in the context of cerebrovascular trauma?

A

Brain in collision with skull.

Surface “bruising”.

If pia mater torn, becomes laceration.

Lateral surfaces of hemispheres, inferior surfaces of frontal + temporal lobes.

Coup = hits front of skull

Contrecoup = rebound hitting back of skull

33
Q

What is diffuse axonal injury in the context of cerebrovascular trauma?

A

Occurs at moment of injury.

Shear + tensile forces affecting axons.

Commonest cause of coma (when no bleed).

Midline structures particularly affected e.g. corpus callosum, rostral brainstem + septum pellucidum.

e.g. rotational blow in boxing

34
Q

Describe the production, flow and absorption of CSF

A

CSF produced by ependymal cells of choroid plexus (mainly in lateral ventricles)

From lateral ventricles, goes through interventricular foramina to 3rd ventricle

Flows down cerebral aqueduct to 4th ventricle

Enters subarachnoid space (via medial + lateral apertures)
Drains back into venous system via arachnoid granulations

35
Q

List 3 different types of brain herniation and their consequences.

A
  • *Subfalcine**: cingulate gyrus pushed under the falx cerebri (not usually clinically significant)
  • *Uncal/ transtentorial:** medial temporal lobe pushed under the tentorium cerebelli – affects midbrain, can cause unconsciousness
  • *Tonsilar:** cerebellar tonsils pushed through foramen magnum. Affects medulla + causes cardiorespiratory failure
36
Q

Which type of herniation does not involve the cerebral cortex?

A

Tonsillar

(Cerebellum going through foramen magnum)

37
Q

What are the inclusions in the definition of stroke?

A

Stroke due to cerebral infarction

Primary intracerebral haemorrhage

Intraventricular haemorrhage

Most cases of SAH

38
Q

What are the exclusions in the definition of stroke?

A

Subdural haemorrhage

Epidural haemorrhage

Intracerebral haemorrhage (ICH)

Infarction caused by infection or tumour.

39
Q

What occurs in AVMs?

A

Blood passes quickly from artery to vein, bypassing the normal capillary networks

Not supplying tissues effectively

40
Q

What is the difference between focal and global cerebral ischaemia?

A

Focal: defined vascular territory, tissue downstream of blockage dies due to lack of blood flow

Global: systemic circulation fails, insufficient blood to brain on a regular basis

41
Q

Where does the anterior cerebral artery supply?

A

Midline of frontal lobes

Superior medial parietal lobes

42
Q

Where does the middle cerebral artery supply?

A

Lateral cerebral cortex

Subcortices

43
Q

Where does the posterior cerebral artery supply?

A

Occipital lobe

Inferior temporal lobe

44
Q

What percentage of patients who experience a TIA will have a significant infarct within 5 years?

A

33%

45
Q

What is the most common cause of non-traumatic intraparenchymal haemorrhages?

A

HTN

46
Q

How may a TBI cause rhinorrhea or otorrhea?

A

Fracture may pass through middle ear or anterior cranial fossa

Loss of CSF through ear or nose

Indicates rupture of CSF barrier= infection risk

47
Q

Give 2 signs of skull fracture

A

Battle sign: haemorrhage over mastoid process post traumatic basilar skull fracture

Panda eyes: base of skull fracture in anterior cranial fossa

YR5 Histopathology (27 decks)

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