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Histopathology > Cerebrovascular disease and trauma > Flashcards

Cerebrovascular disease and trauma Flashcards

1
Q

Define cerebral oedema

A

•Excess accumulation of fluid in the brain parenchyma

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2
Q

What are the 2 main types of cerebral oedema?

A
  • Vasogenic – disruption of the blood brain barrier (fluid leakage from capillaries into parenchyma)
  • Cytotoxic – secondary to cellular injury e.g.hypoxia/ischaemia
  • Usually due to damage at the astrocyte end-foot processes
  • AQA4 is found in the brain (and is used to transport water)
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3
Q

What is the result of cerebral oedema?

A

•Result is raised intracranial pressure•

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4
Q

What are the mechanisms of reducing oedema?

A
  • Repairing the BBB
  • Fluid can be reaborbed into the ventral or the subarachnoid space
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5
Q

How would a oedematous brain look post-mortem/CT scan

A

Swelling in the brain is shown on radiology by a loss of gyri

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6
Q

Describe the normal flow of CSF.

A
  • The choroid plexus (mainly in the lateral ventricles) pumps out the CSF
  • CSF flows from the lateral ventricles, through the intraventricular foramina into the 3rd ventricle
  • CSF flows down the cerebral aqueduct into the 4th ventricle
    • The floor of the 4th ventricle is the pons and the roof is the cerebellum
    • CSF flows down into the medulla and further down into the central canal of the spinal cord
      • Relatively little CSF volume will go down the spinal cord because most of it exits via a number of foramina in the 4th ventricle into the subarachnoid space
    • CSF will then circulate through the subarachnoid space and via the arachnoid granulations which pierce the superior sagittal sinus, thereby returning the CSF to the systemic circulation
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7
Q

What Is hydrocephalus?

A

A blockage of normal CSF flow

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8
Q

What are the 2 types of hydrocephalus?

A
  • TWO forms of hydrocephalus:
    • Non-Communicating: obstruction to the flow of CSF (usually involving the cerebral aqueduct)
      • I.E. neonatal = some of the choroid plexus getting stuck in the cerebral aqueduct and blocking CSF flow
    • Communicating: NO obstruction but is associated with problems in reabsorption of CSF into venous sinuses
      • This can be caused by infection (e.g. meningitis)
      • Inflammation of the meninges can impinge and interfere with the normal flow of CSF to be reabsorbed
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9
Q

What is normal ICP?

A

•ICP is measured in mmHg and, at rest, is normally 7–15mmHg for a supine adult

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10
Q

What happens during increased ICP?

A
  • Enclosed bony box- pressure can increase because of localised (space occupying) lesions, oedema or both
  • Increased pressure forces brain against unyielding bony wall of skull and inflexible dural folds
  • This results in herniation of brain structures where space is available
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11
Q

What are the tree herniations sites? Why do they occur?

A
  • THREE sites of brain herniation:
    • Subfalcine → singular cortex forced under rigid falx cerebri
    • Uncal (transtentorial) - relatively rare. Supratentorial trauma →herniation ofmedial temporal lobe through tentorial notch
    • Tonsillar → tonsil of cerebellum pushed through foramen magnum
      • Can occur if lumbar puncture on raised ICP
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12
Q
A
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13
Q

Describe the epidemiology of strokes.

A
  • Stroke is the third biggest cause of death in the UK and the largest single cause of severe disability
  • Each year more than 110,000 people in England will suffer from a stroke
  • This costs the NHS over £2.8 billion
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14
Q

Define stroke.

A

A stroke is a clinical syndrome characterised by rapidly developing clinical symptoms and/or signs of focal, and at times global loss of cerebral function, with symptoms lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin

  • This definition includes stroke due to cerebral infarction,primary intracerebral haemorrhage, intraventricular haemorrhage and most cases of subarachnoid haemorrhage
  • It excludes subdural haemorrhage, epidural haemorrhage, intracerebral haemorrhage (ICH) or infarction caused by infection or tumour
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15
Q

What is a transient ischaemic attack?

A
  • TIA is a warning stroke that should be taken very seriously
  • TIA is caused by a clot; the blockage is temporary
  • Most TIAs last less than five minutes; the average is about a minute. Unlike a stroke, when a TIA is over, there is usually no permanent injury to the brain
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16
Q
A

Non-traumatic intra-parenchymal haemorrhage

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17
Q

What is the prognosis of a TIA¿

A
  • Unlike a stroke, when a TIA is over, there is usually no permanent injury to the brain
  • 1/3 of those with TIA get significant infarct within 5 years
  • REMEMBER: TIA important predictor of future infarct
18
Q

What is a Non-traumatic intra-parenchymal haemorrhage?

A

•Haemorrhage into the substance of the brain - rupture of a small intraparenchymal vessel

19
Q

Where does bleeding in the brain most commonly occur?

A

•Most common in basal ganglia

20
Q

What is the risk factor of Non-traumatic intra-parenchymal haemorrhage?

A

•Most common in basal ganglia•Hypertension > 50% of bleeds

21
Q

How do Non-traumatic intra-parenchymal haemorrhage present?

A

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

22
Q

Where do arteriovenous malformations appear? When and how do they present? When can it be seen? What is the morbidity and mortality associated with it? What is the treatment?

A
23
Q
A

Left to right:

  • artery
  • veins
  • vessel with fibrotic wall
24
Q

What is a cavernous angioma? Where can they be found? When and how does it present? What is the pathophysiology? What is the treatment?

A
25
Q

What is a subarachnoid haemorrhage? How common are they? What cause them? When is the greatest risk of rupture? How does it present?

A
26
Q

How do we treat aneurysms?

A
  • Rarely - clipping
  • Endovascular coiling - stops the rupture
27
Q

What is the commonest cause of stroke?

A

Infarction - 70-80% of strokes

28
Q

Define infarction.

A

•Tissue death due to ischaemia - lack of blood flow (not just hypoxia)

29
Q

What causes infarction?

A

•Cerebral atherosclerosis most common cause•hypertension, diabetes, smoking are major risks factors

30
Q

What are the types of ischamia?

A

•

a) Focal cerebral ischaemia: defined vascular territory
b) Global cerebral ischaemia: systemic circulation fails

31
Q

What are the worst types of artherosclerosis? Where does it often occur? What does it cause? What are other causes?

A
  • Worst atherosclerosis in larger vessels (extracerebral arteries) – thrombosis
  • Often near carotid bifurcation or in basilar artery
  • Other cause - emboli (intracerebral arteries)
  • Usually from heart or atherosclerotic plaques•Embolic occlusion usually in middle cerebral artery branches
32
Q

What are the vascular territories?

A

MCA supplies the OUTSIDE, ACA supplies the middle & front

33
Q
A

Midldle cerebral artery occlusion

34
Q

What is the differential diagnosis of infarcts and haemorrhages?

A
35
Q

Describe the epidemiology of Traumatic brain injury.

A
  • Trauma single largest cause of death in people under 45
  • 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
36
Q

What are the types of head trauma?

A
  • Non-missile and missile (fire-arms)
  • acceleration/deceleration
  • rotation around the midline (pressure on brain structures)
  • RTA, falls and assaults
  • Focal or diffuse
37
Q

How do fissure fractures present?

A
  • Fissure fractures often extend into base of skull
  • May pass through middle ear or anterior cranial fossa
  • Otorrhea or rhinorrhea
  • Infection risk
38
Q
A

Battle sign - indicative of skill fracture

39
Q

What are contusions? What happens? What areas of the brain are susceptible?

A
40
Q

What is countercoup?

A
  • Rebound of the brain after a direct impact can cause contrecoup damage to the opposite side of the brain (coup = damage to the area of collision)
41
Q

Define diffuse axonal injury. What does it cause?

A
42
Q
A

DAI in corpus callosum

Histopathology (14 decks)

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