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Sem 4: Nervous System > 8c.) Neuropathology > Flashcards

8c.) Neuropathology Flashcards

1
Q

The CNS is NOT normally sterile; true or false?

A

FALSE- it is normally sterile

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2
Q

Micoorganisms can gain entry into CNS via 3 routes; state and provide an example for each

A
  • Direct spread: e.g. middle ear infection, base of skull fracture
  • Blood borne: e.g.sepsis, infective endocarditis
  • Iatrogenic: post surgery, via ventriculoperitoneal shunt, lumbar puncture
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3
Q

What is meningitis?

A

Inflammation of the leptomeninges (pia mater & arachnoid) with or without septicaemia

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4
Q

State the causative orangisms fo meningitis in:

  • Neonates
  • 2-5yrs
  • 5-30yrs
  • >30yrs
  • Immunocompromised
A
  • Neonates= E.coli, Listeria monocytogenes
  • 2-5yrs= Haemophilius influenza type B
  • 5-30yrs= Neisseria meningitidis (types) “meningococcus”
  • >30yrs= Streptococcus pneumoniae
  • Immunocompromised= various organisms e.g. fungi
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5
Q

What is chronic meningitis?

What organism is typically responsible for chronic meningitis?

A
  • Meningitis that lasts at least a month
  • Mycobacterium tuberculosis
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6
Q

State some consequences/features of chronic meningitis

A
  • Granulomatous inflammation
  • Meningeal fibrosis
  • Cranial nerve entrapment
  • Bilateral adrenal haemorrhage (Waterhouse-Friederichsen syndrome) can occur as a complicatoin

***Waterhouse-Friederichsen syndrome= adrenal gland failure due to bleeding into the adrenal glands. Usually caused by a severe meningococcal, or other severe, infection in the blood

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7
Q

Describe the presentation of Waterhouse-Friderichsen syndrome

A

Abrupt onset of fever

Petechiae/DIC

Cardiogenic shock (when haemorrhage into adrenal glands)

And then other vague symptoms:

Malaise

Headache

Dizziness

Joint pain

Myalgia

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8
Q

State some complications of meningitis; include local complications (5) and systemic complications

A

Local

  • Death due to raised ICP
  • Cerebral infarction (stroke)
  • Cerebral abscess
  • Subdural empyema
  • Epilepsy (due to direct irritation of brain)

Systemic

  • If it becomes systemic it will now be meningitis + septicaemia. Septicaemia can lead to organ failure
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9
Q

State some symptoms of meningitis

A
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10
Q

Is encaphalitis usually bacterial or viral?

A

Viral

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11
Q

What is encephalitis?

A

Inflammation of brain parenchyma- usually a viral cause

*NOTE:can occur as a complication of meningitis

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12
Q

Encephalitis is inflammation of the brain parenchyma usually caused by a virus; how does the virus cause brain inflammation/what does the virus do?

A
  • Virus kills neurones causing inflammation
  • Intracellular viral inclusions present (indicating viral replication)
  • Often there is lymphocytic infiltrate
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13
Q

State what virus typically causes encephalitis in each of these regions of CNS:

  • Temporal lobe
  • Spinal cord
  • Brainstem
A
  • Temporal lobe: herpes viruses (most commonly)
  • Spinal cord: polio (now eradicated)
  • Brainstem: rabies (very rare)
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14
Q

What is prion and where is it usually found?

A

Prion is a protein (referred to as PrP) that is found in synapses (its function is unknown but it is normal)

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15
Q

Discuss whether PrPsc is stable

A
  • PrPsc is extremely stable
  • Resistant to disinfectants, irradation and not susceptible to immune attack as it is essentially a self protein (just a mutated one)
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16
Q

PrP (prion protein) can transform into PrPsc, an abnormal form of the protein, via 3 mechanisms; state these

A
  • Sporadic mutation
  • Familial inheritance of a mutated gene
  • Following ingestion of PrPsc (e.g. can be ingested through meat if contaminated say from BSE (bovine spongioform encephalopathy)
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17
Q

Describe how PrPsc causes damage to brain

A

PrPsc forms aggregates which destroy neurones and cause brain to take on spongiform (sponge-like) appearance

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18
Q

What are prion diseases?

A

· Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family of rare progressive neurodegenerative disorders that affect both humans and animals. Mutated prion protein forms aggregates and destroys neurones

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19
Q

Discuss whether prion diseases are classed as an infection?

A

Not classed as an infection as only fulfils one of Koch’s postulates (criteria fof infec). Since it is a protein it can’t be cultured hence it can’t fulfil two of the postulates.

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20
Q

Can PrPsc cause interact with normal PrP and cause it to become PrPsc?

A

Yes!

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21
Q

State some examples of spongioform encephalopathies

A
  • BSE (bovine spongioform encephalopathy) a.k.a. mad cows disease
  • Variant Creutzfeld-Jacob disease (vCJD)
  • Scrapie in sheep
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22
Q

What is CJD (creutzfeld-Jacob disease)?

A

A prion disease that causes brain damage that worsens rapidly over time

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23
Q

Variant CJD has been linked with BSE; true or false?

A

True

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24
Q

Compare classic CJD with variant CJD

A

Essential difference is that vCJD compared to classic CJD tends to have a much higher prion load associated with it, patients develop disease and die at younger age and it has more prominent psychiatric features

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25
Q

What is dementia?

A

Acquired global impairment of intellect, reason and personality without impairment of consciousness

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26
Q

There are numerous types of dementia, which will be studied at a later date, but state the most common form of dementia

A

Alzheimer’s disease (50%)

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27
Q

What happens to brain weight in Alzheimer’s disease?

A

Loss of cortical neurones leading to cortical atrophy and decreased brain weight

28
Q

Describe the pathophysiology of Alzheimers disease

A

Plaques

  • Amyliod precursor protein in membrane- thought it helps growth & repair after injury
  • When its broken down & recycled, if the wrong enzymes do this the degradations products are insolube called amyloid beta
  • Amyloid beta aggregate to form plaques outside neurones- can get in way of neuron to neuorn signalling
  • Can also casue inflammation which can damage other neurones
  • Deposit around blood vessels weakening their walls and increases risk haemorrhage

Tangles

  • TAU protein normally binds & stablises microtubules
  • Kinase phosphorylates TAU
  • TAU changes shape
  • Aggregates with other TAU proteins to form neurofibrillary tangles
29
Q

What is the normal intracranial pressure?

A

0-10mmHg

30
Q

State the effect of coughing and straining on intracranial pressure

A

Can rise intracranial pressure to ~20mmHg

**HOWEVER, this is only significant if the increase in mainted for several minutes

31
Q

State 3 compensatory mechanisms to maintain normal intracranial pressure (if it gets too high)

A
  • Reduce blood volume
  • Reduce CSF volume
  • Spatial- brain atrophy if intracranial pressure is chronically elevated
32
Q

Cerebral blood flow can be maintained as long as ICP remains less than…?

A

60mmHg

33
Q

Describe 3 possible consequences of a space occupying lesion (e.g. a tumour) in the brain

A
  • Deformation or destruction of surrounding brain
  • Displacement of midline structures resulting is loss of symmetry & midline shift
  • Brain herniation (when brain protrudes through a structure/wall that normally contains it)
34
Q

State three types of herniation you need to be aware of

A
  • Subfalcine herniation
  • Tentorial hernation
  • Tonilar herniation
35
Q

Describe a subfalcine herination (also known as a cingulate hernation)

A
  • Cingulate gyrus is pushed under the free edge of the falx cerebri
  • Ischaemia of medial parts of frontal & parietal lobes & corpus callosum due to compression of the anterior cerebral artery which can get pinched by the herniated brain
36
Q

What does this image show?

A

Subfalcine (cingulate) herniation

37
Q

Describe tentorial herniation

A
  • Medial part of temporal lobe, typically the uncus, pushes down through tentorial notch
38
Q

Describe two possible conequences of tentorial herniations

HINT: think about what structures may be compressed

A
  • Compress ipsilateral oculomotor nerve - ipsilateral 3rd nerve palsy
  • Compress cerebral peduncle- causing contralateral UMN signs
39
Q

A tentorial herniation can be complicated by a….?

A

A secondary brainstem haemorrhage (duret haemorrhage)

40
Q

What is a duret haemorrhage?

A

A brainstem (midbrain & pons) haemorrhage secondary to tentorial herniation

41
Q

What is the usual mode of death for those with large brain tumous or severe intracranial haemorrhages?

A

Tentorial hernation which leads to duret haemorrhage (which is often fatal)

42
Q

What does this image show?

A

Tentorial herniation

43
Q

What does this image show?

A
44
Q

Describe a tonsilar herniation

A

Cerebellar tonsils pushed into the foramen magnum compressing the brainstem

45
Q

Brain tumours are common; true or false?

A

False- they are rare

46
Q

State an exampe of a benign brain tumour

A

Meningioma (arises from meninges)

47
Q

State an example of a malignant brain tumour

A

Astrocytoma

48
Q

Describe how astrocytomas can spread

A
  • Direct spread along white matter pathways
  • Spread to distant parts of CNS via CSF
49
Q

Aside from meningiomas and astrocytomas, state 3 other brain tumours (which arise from nervous tissue)

A
  • Neurofibroma: from Schwann cells of peripheral or cranial nerve
  • Ependymoma: from ependymal cells lining ventriular system
  • Neuronal tumours: from neurones (extremely rare)
50
Q

Brain tumours don’t have to arise form nervous tissue; state 2 other causes of brain tissue that are of non-nervous tissue origin

A
  • Lymphomas
  • Metastases
51
Q

What is the most common cause of brain tumour?

A

Metastases

52
Q

What is a stroke?

A

A sudden event producing a disturbance of CNS function due to vascular disease (blood supply to brain is interupted)

53
Q

State some risk factors for stroke

A
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes
54
Q

Stroke could be caused by…. (2 broad causes)

A
  • Embolism: heart due to AF, atheromatous debris from carotids, thrombus over ruptured plaque, aneuysms
  • Thrombosis
55
Q

Which is the most common cause of stroke; embolism or thrombosis?

A

Embolism

56
Q

State the two broad categories of stroke including which is more common

A
  • Cerebral infarction- 85%
  • Cerebral haemorrhage- 15%
57
Q

Cerebral infarcts can be divided into types; state and describe each type

A
  • Regional: in the territory of a named cerebral artery
  • Lacunar: occlusion of small arteries, affected area less than 1cm. Commonly associated with hypertension
58
Q

What 2 structures are lacunar infarcts commonly associated with?

A
  • Basal ganglia
  • Internal capsule
59
Q

Cerebral haemorrhages are usually spontaneous; true or false?

A

True

60
Q

Intracerebral haemorrhages make up 10% of all strokes; state some factors associated with intracerebral haemorrhages

A
  • Increased age
  • Hypertensive vessel damage
  • Amyloid deposition in vessels
61
Q

What are Charcot-Bouchard aneurysms?

A

Aneuryseums in small arteries in cortex or basal ganglia

**Can cause intracerebral haemorrhage

62
Q

Subarachnoid haemorrhages can be caused by the rupture of berry aneurysms; what is a berry aneursym?

A

Aneuryseum found at branch points in circle of Willis

63
Q

Blood in subarachnoid space can cause secondary spasm of cerebral arteries; true or false?

A

True

64
Q

State some factors associated with subarachnoid haemorrhages

A
  • Male
  • Hypertension
  • Atherosclerosis
65
Q

State some symptoms of subarachnoid haemorrhages

A
  • Thunderclap headache
  • May be preceded by sentinel headache
  • Loss of consciousness
  • Often instantly fatal
66
Q

Describe why downs syndrome is associated with Alzheimers

A

In patients with downs syndrome alongside trisomy 21 also found 3 mutations on chromosome 21 which are related to amyloid precursor protein hence increasing probability of amyloid plaques

67
Q

Astrocytomas are malignant briefly state how the diferent grades behave

A
  • Low grade: slow growing but difficult to remove
  • High grade (e.g. glioblastoma)
  • Spread along nerve tracts and through subarachnoid space so often present with spinal secondary mets (but won’t met outside of CNS)

Sem 4: Nervous System (21 decks)

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