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Year 5 - Pathology > HISTO: Neuropathology > Flashcards

HISTO: Neuropathology Flashcards

1
Q

What is cerebral oedema including the 2 types? What is the consequence?

A
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2
Q

Where is the CSF produced?

A

Choroid plexus

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3
Q

What is the normal flow of CSF?

A
  • Made in choroid plexus
  • Flows lateral ventricles–> intraventricular foramina –> 3rd ventricle
  • Down the cerebral aqueduct–>4th ventricle
    • The floor of the 4th ventricle is the pons and the roof is the cerebellum
  • Into medulla –>central canal of the spinal cord
    • Most of it exits via a number of foramina in the 4th ventricle into the subarachnoid space
  • Then circulate through subarachnoid space and via arachnoid granulations which pierce the superior sagittal sinus, returning the CSF to the systemic circulation
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4
Q

What are the two types of hydrocephalus?

A
  • Non-Communicating: obstruction to the flow of CSF (usually involving the cerebral aqueduct)
  • Communicating: NO obstruction but is associated with problems in reabsorption of CSF into venous sinuses
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5
Q

What is the normal ICP?

A

7-15 mm Hg for supine adult

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6
Q

What are the main 3 herniation sites for the brain in raised ICP?

A
  • Subfalcine - cortex forced under rigid falx cerebri
  • Uncal/Transtentorial - medial temporal lobe through posterior cerebral fossa/tentorial notch
  • Tonsillar - tonsil of cerebellum pushed through foramen magnum
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7
Q

What is the consequence of raised ICP on brain structure?

A

Herniation

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8
Q

Menti: When the integrity of the blood brain barrier is disrupted the resultant oedema is described as?

A

Vasogenic

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9
Q

Menti: Which of the following types of herniation does not involve the cerebral cortex?

  • Uncal
  • Subfalcine
  • Transtentorial
  • Tonsillar
A

Tonsillar

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10
Q

What is the mortality associated with stroke?

A

3rd biggest cause of death in the UK / largest single cause of severe disability

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11
Q

Define stroke.

A

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

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12
Q

The definition of stroke includes which types of infarction and haemorrhage?

A
  • Includes:
    • Infarct –> cerebral infarction
    • Haemorrhage –>primary intracerebral, intraventricular or sub-arachnoid (most common) haemorrhage
  • Excludes:
    • Subdural haemorrhage
    • Epidural haemorrhage
    • Intracerebral haemorrhage
    • Infarction caused by infection or tumour
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13
Q

What is a TIA? What does it mean for stroke risk?

A
  • Caused by a clot but the blockage is temporary
    • 1/3rd people with TIA get a significant infarct within 5 years
    • I.E. TIA is a predictor of a future infarct
  • Symptoms resolve within 24 hours (most TIAs last < 5 mins)
  • There is usually NO permanent injury to the brain
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14
Q

What is non-traumatic parenchymal haemorrhage? What is the usual cause? Where do they usually occur?

A

Haemorrhage into the substance of the brain (parenchyma) due to rupture of a small intraparenchymal vessel

Hypertension plays a role in >50% of bleeds

Most common in the basal ganglia

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15
Q

How does non-traumatic intra-parenchymal haemorrhage present?

A
  • Severe headache
  • Vomiting
  • Rapid loss of consciousness
  • Focal neurological signs
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16
Q

Where can AVMs occur? When do they become symptomatic?

A
  • Arteriovenous malformations can occur anywhere in the CNS
  • Symptomatic from 2nd and 5th decade (mean = 31 years)
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17
Q

How are AVMs visualised? What is the pressure within these?

A
  • Occur under high pressure and can cause MASSIVE BLEED
    • Morbidity 50-80%; mortality at 15%
  • Can be visualised on angiography
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18
Q

How do AVMs present?

A
  • Haemorrhage
  • Seizures
  • Headache
  • Focal neurological deficits
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19
Q

What are the treatment options for AVMs?

A
  • Surgery
  • Embolisation
  • Radiosurgery
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20
Q

What are cavernous angiomas? What is the pressure within them?

A

“Well-defined malformative lesion composed of closely-packed vessels with no parenchyma interposed between vascular spaces” - similar to an AVM but no brain substance wrapped up amongst the vessels

Occur under lower pressure –> recurrent bleeds

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21
Q

Where do cavernous angiomas occur? When do they occur in life?

A
  • Can be found anywhere in the CNS
  • Usually symptomatic over the age of 50 years
  • Pathogenesis is unknown
22
Q

How do cavernous angiomas present?

A
  • Headache
  • Seizures
  • Focal deficits
  • Haemorrhage
23
Q

How are cavernous angiomas ddiagnosed?

A

T2-weighted “Target Sign” – black ring around lesion (AVM has no ring) – no brain parenchyma ​

24
Q

What is the treatment for cavernous angioma?

A
  • May not be necessary
  • Surgery
25
Q

What is sub-arachnoid haemorrhage? What is the cause of these in most cases?

A

Rupture of berry aneurysms (1% of general population, congenital)

26
Q

Where do subarachnoid haemorrhages usually occur?

A
  • 80% occur at the internal carotid bifurcation
  • 20% occur within the vertebrobasilar circulation
  • 30% of patients will have multiple berry aneurysms
27
Q

What size of SAH is at highest risk of rupture?

A

HIGHEST risk of rupture when 6-10 mm in diameter

28
Q

How do SAH present?

A
  • Sudden-onset severe headache
  • Vomiting
  • Loss of consciousness
29
Q

What is the treatment of SAH?

A

Endovascular coiling - stops blood flow in the aneurysm

Clipping is sometimes also done with craniotomy.

30
Q

What is the most common form of cerebrovascular disease? What is the most common cause of this?

A

Cerebral infarction

Cerebral atherosclerosis

31
Q

Where does atherosclerosis usually affect the cerebal vessels?

A
  • Atherosclerosis can particularly badly affect the larger, extracerebal vessels = carotid bifurcation** or the **basilar artery
  • Can also be from emboli from the heart (i.e. AF) –> middle cerebral artery branches
32
Q

What % of stroke are due to infarction?

A

70-80%

33
Q

What are 3 main risk factors for stroke?

A
  • HTN
  • DM
  • Smoking
34
Q

What is the difference between focal and global cerebral ishcaemia?

A
  • Focal cerebral ischaemia – due to lack of blood flow to a particular vascular territory
  • Global cerebral ischaemia – when the systemic circulation fails
35
Q

Where is the supply of the ACA, MCA and PCA?

A
36
Q

What are the differential diagnoses for infarcts?

A
  • Tissue necrosis (stains)
  • Rarely haemorrhagic
  • Permanent damage in the affected area
  • No recovery
37
Q

What are the differential diagnoses for haemorrhage?

A
  • Bleeding
  • Dissection of parenchyma
  • Fewer macrophages
  • Limited tissue damage (periphery)
  • Partial recovery
38
Q

Menti: What percentage of patients who experience a TIA will get a significant infarct within 5 years?

  • 10
  • 25
  • 33
  • 50
A

33% - about a third will go on to have a stroke within 5 years unless whatever caused the stroke is modified in some way

39
Q

Menti: What is the most common cayuse of non-traumatic intraparenchymal haemorrhage?

A

Hypertension

40
Q

What is the largest cause of trauma death in young people (<45yrs)?

A

TBI - traumatic brain injury

Accounts for 25% of all trauma deaths

High morbidity

  • 19% in a vegetative or severely disabled state
  • 31% good recovery
41
Q

How is head trauma classified?

A

Focal or diffuse OR

  • Non-missile
    • Acceleration/deceleration
    • Rotation - around midline puts pressure on midline brain structures
    • RTA, falls and assaults
  • Missile i.e. missile most commonly caused by firearms.
42
Q
A
43
Q

What is shown?

A
  • Battle sign – basilar skull fracture – bruise over mastoid process; takes 1 day to appear
  • Racoon eyes – basal skull fracture – takes 1 day to appear
44
Q

Where do skull fractures affect usually? What can be seen when there is loss of CSF due to fracture?

A
  • Fissure fractures often extend into the base of the skull
  • May pass through the middle ear or anterior cranial fossa

Can cause otorrhoea and rhinorrhoea (i.e. loss of CSF through the ear or nose)

  • Increases risk of infection (because you have ruptured the containment of the CSF, which could act as a route of infection into the cranial cavity
45
Q

What is a contusion? When is it a laceration?

A

Contusion = brain collides with the internal surface of the skull

If this causes rupture of the pia mater, it is called laceration

46
Q

What are two common locations for contusions?

A

Due to direct contact with the skull:

  • Lateral surfaces of the hemispheres
  • Inferior surfaces of frontal and temporal lobes
47
Q

What is the consequence to the other side of the brain when there is rebound of the brain after direct impact on the opposite site?

A

Contrecoup damage

48
Q

What is diffuse axonal injury?

A

When shearing and tensile forces cause damage to the axons

Occurs at the moment of injury

49
Q

What are the consequences of diffuse axonal injury?

A

Coma - DAI is the MOST COMMON cause of coma when there is no bleed

Cognitive and degenerative problems - potentially due to persistent inflammation

50
Q

Which locations in the brain are most affected by diffuse axonal injury?

A

Midline structures are particularly affected e.g.

  • corpus callosum,
  • rostral brainstem
  • septum pellucidum

Year 5 - Pathology (89 decks)

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