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CPAT NEURO > CPAT NEURO > Flashcards

CPAT NEURO Flashcards

1
Q

What does the falx cerebri separate

A

right and left hemispheres

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2
Q

what does the tentorium cerebelli separate

A

forebrain and hindbrain

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3
Q

what are the 5 types of space occupying lesions

A
  1. haemorrhage -extradural, subdural, subarachnoid, intracerebral
  2. tumour
  3. infection
  4. edema.
  5. hydrocephalus (increase csf volume)
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4
Q

what are two conseqences of SOL which continue to grow - uncontrolled

A

midline shift

gyral flattening onto outside of skull. (narrowed sulci)

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5
Q

normally cerebral perfusion means

A

arterial pressure is greater than intracranial pressure causing a net flow into the brain.
if arterial pressure is less than or qual to intracranial pressure, no net flow into brain and brain death.

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6
Q

what is a sub falcine herniation

A

displacement of brain under falx cerebri

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7
Q

what is a transtentorial herniation

A

displacement of brain under tentorium cerebelli into hind brain.

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8
Q

what is a tonsilar herniation

A

displacement of brain through foramen magnum into spinal column.

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9
Q

what are some secondary pathologies of SOLs

A
  • haemorrhage e.g. Duret haemorrhage
  • compression of cranial nerves/arteries
  • edema
  • congestive brain swelling
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10
Q

what is Alzheimers disease characterised by

A

progressive loss of neurons (white matter) and a long disease course with amjor risk factor being age.

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11
Q

what is the characteristic pathologic feature of alzheimers disease

A

protein accumulation - tauopathies

protein inclusions

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12
Q

what are the forms of AD

A

inherited and sporadic/acquired.

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13
Q

what are some symptoms of AD

A

early loss of short term memory, cognitive impairment to e.g. loss of visuospatial skills

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14
Q

what are the macroscopic features of AD

A 
Global atrophy (Except parietal and occipital lobe), widened sulci. 
atrophy begins in hippocampus, proceeds to temporla, then global
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15
Q

what are the microscopic features of AD

A

1/. plaques - extracellular, variable in size and structure, mostly composed of beta amyloid.
2.neurofibrillary tangles - intracellular, in cytoplasm of neurons. major component is hyperphosphorylated tau

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16
Q

what is the evolution of AB plaques

A

diffuse
neuritic (dystrophic neurites, tau +ve)
compact

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17
Q

where are neurofibrillary tangles usually found

A

hippocampus, medial temporal lobe

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18
Q

what do you see when there is overlap between tau (NFTs) and AB (plaques) pathology

A

neuritic plaques - central core of AB surrounded by distorted neuritic tau positive processes and glial cells.

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19
Q

what are the two pathways of amyloid precursor protein proteloysis

A
  1. non amyloidogenic - alpha secretase cuts peptide between AB so the AB fragment cant be formed
  2. amyloidogenic - beta and gamma secretase cut the peptide either side of AB so AB fragment is formed. AB42 is very sticky - causes fibrillisation and plaques
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20
Q

what are the mutations identified in familial AD

A

mutations to APP, preselin 1 and 2 (components of gamma secretase)
no mutations in tau protein yet identified

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21
Q

describe the amyloid cascade hypothesis for sporadic AD

A
  1. dysregulation of APP metabolism causes increase AB
    2 interacts with neuronal receptor or membrane and changes conditions in neuron (ionic homeostasis/oxidative injury)
  2. alterered kinase/phosphatase activity which causes hyperphosphorylated tau which leads to development of NFTs.
    4 neuronal death/dysfunction.
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22
Q

what are risk factors for sporadic AD

A

e4 allele of APOE gene (has probable role in clearance of AB, has been shown in plaques)

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23
Q

what is a problems with the amyloid cascade hypothesis

A
  1. failure of AB therapies to halt cognitive decline (may just need to introduce therapy earlier)
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24
Q

parkinsons disease is apart of what disorder specturm

A

lewy body disorder spectrum (most common lewy body disorder)

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25
Q

what kind of proteinopathy does parkinsons exhibit

A

synucleinopathy - characterised by intra neuronal alpha synuclein inclusions.

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26
Q

what are the clinical features of PD

A

bradykinesia, tremor, ridgidity

may also exhibit stooped posture and asymmetric motor dysfunction.

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27
Q

treatment for PD

A

L-DOPA

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28
Q

what are the macroscopic features of PD

A

loss of cells in susbtantia nigra which contain a pigment called neuromelanin. loss of this pigment. neuromelanin is thought to be involved in handling the oxidisable biproducts of dopamine.

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29
Q

microscopic features of PD

A

loss of dopaminergic neurons and neuromelanin, nigral lewy bodies (inclusions in dopaminergic neurons)

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30
Q

what are the main component of lewy bodies

A

alpha synuclein (fibrillar)

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31
Q

how is PD staged

A

by the spread of lewy bodies. (Braak staging)
early stages - medullar and olfactory region
mid stages - midbrain and pons
late stages - neocortices (dementia)

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32
Q

what is the lewy body pathogenesis of PD

A

excess alpha synuclein forms oliogmers then fibrils then lewy bodies which eventually kills cell.

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33
Q

dopaminergic output in PD

A

In normal brain, dopamine activate the direct over indirect (reduced GPi output) and promotion of movement
With Parkinson’s disease there is loss of > 50% dopamine (DA) input to striatum
So indirect pathway favoured, thalamic inhibition increased, movement retarded
What about Tremor? – not only striatum deficit, may also involve cerebellum, red nucleus

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34
Q

describe monogenic forms of PD

A

rare, incolve mutatations in LRRK2, PINK1, Parkin - all invovled in mitochondrial function.

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35
Q

describe sporadic forms of PD

A

combinatino of genetic susceptibility ( from common polymorphisms) and environmental factors on a background of aging.

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36
Q

describe an example of environmental induced PD

A

MPTP )biproduct of methadone) crosses BBB and is converted into MPP+ by monoamine oxidase. MPP+ is a complex 1 inhibitor - this prevents oxidative phosphorylation and damages dopaminergic neurons.

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37
Q

what might be protective factor against PD

A

nicotine - by preventing alpha synuclein defibrilisation.

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38
Q

how is PD treated

A

LDOPA, deep brain stimulation.

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39
Q

what is multiple system atrophy

A

parkinsonism with autonomic dysfunction. alpha synuclein in oligodendricytes, cytoplasmic not intraneuronal protein inclusions.

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40
Q

what are the three types of stroke

A
  1. ischemic - large artery atherothrombosis, embolism
  2. haemorrhagic
  3. unknown
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41
Q

what are the main sites of larger artery atherothrombi

A
  1. extracranial vessels (most common) - internal carotid artery near common carotid bifurcation
  2. intracranial vessels - origin of middle cerebral artery and ends of basilar artery
42
Q

what are the two major zones of injury during cerebral ischemia

A
  1. core ischemic zone
  2. ischemic penumbra - mild to moderate ischemic tissue remains viable for much longer due to blood supply from collateral arteries.
43
Q

when does neuronal electrical failure develop during brain ischemia

A

at 30% cerebral blood flow, causes loss of sensation , movement, speech

44
Q

when does neuronal membrane failure develop

A

at 5% cerebral blood flow - neurons die.

45
Q

what are the molecular events occuring in acute ischemia

A
  1. glutamate release - in excess is toxic. causes increase in intracellular Ca, stimulates reactive intermediates leading to membrane and DNA damage.
  2. decreased energy production - leads to failure of ionic pumps, mitochondrial injury and production of free radicals.
  3. ischemic reperfusion injury - leukocyte infiltration etc causes damage.
46
Q

what are macro features of acute brain infarct (< 2 days)

A
  1. softening/loss of tissue
  2. swelling and edema
  3. infiltration of neutrophils
  4. ischemic red cell neuronal change
47
Q

what are macro features of subacute brain infarct (days-weeks)

A
  1. liquefication and cavitation
  2. foamy macrophages filled with myelin (lipid)
  3. reactive astrocytes form glial scar
48
Q

what are macro features of remote brain infarct (weeks +)

A
  1. cavitation
  2. glial scar
  3. haemosiderin laden macrophages
49
Q

what kind of stroke is a small penetrating artery occlusion

A

atherothrombotic stoke

50
Q

where do small penetrating artery occlusions occur

A

lenticulostriate arteries coming off the middle cerebral arteries - these arteries are very susceptible to changes in bp.

51
Q

what can occlusion of a small penetrating artery lead to

A

infarcts in striatum, internal capsule, basal ganglia, thalamus, brain stem - can be catastro[hic

52
Q

what is small penetrating artery occlusion associated with

A

arterial hypertenstion

53
Q

what does small penetrating artery occlusion often present as

A

transient ischemic attacks - may be clinically silent

54
Q

describe an embolic stroke

A

the dislodging of a thrombus causing an emboli to move and lodge in vessel in brain.

55
Q

what do embolic strokes usually present as

A

haemorhagic due to blood reflowing into area after lysis of emboli but damage to vessels leading to haemorrhagic embolic stroke. different to haemorhagic stroke.

56
Q

where do most embolic strokes occur

A

middle cerebral artery territory

57
Q

what are the most common sites for haemorhagic strokes

A

sub cortical structures - cerebellum, basal ganglia, brain stem.

58
Q

what is a histologically feature of small vessel haemorrhagic stroke

A

slit haemorrhage lined with hemosidering laden macrophages

59
Q

what is the major risk factor for strokes in subcortical regions

A

hypertension

60
Q

what is a micro feature of lobar haemorhage

A

beta amyloid build up.

61
Q

describe subarachnoid haemorrhage

A

occurs due to rupture of BV outside of brain on surface, usually caused by ruptured berry anuerism. sudden onset, thunderclap headaches, high mortality,

62
Q

describe a berry aneurisum

A

stretched blood vessel which forms a pocket of blood. thin wall highly susceptible to rupture.

63
Q

where to berry anuerisms usually occur

A

at areas where there is a change of blood flow from laminar to turbulent.

64
Q

describe the stroke subtype - global ischemia

A

caused by infarcts between arterial territories

65
Q

when are boundary zone infarcts seen

A

global ischemia when there is abrupt hypotension followed by rapid recovery.

66
Q

where are global ischemic infarcts usually seen

A

between middle and anterior cerebral arteries and middle and posterior cerebral arteries.

67
Q

what are the two kinds of primary traumatic brain injury

A

concussion, diffuse and focal

68
Q

what are some examples of diffuse traumatic brain injury

A

global ischemia, diffuse vascular injury, brain swelling

69
Q

what are some examples of focal brain injury

A

haemorrhage

70
Q

describe diffuse brain injury

A

APP immunostaining - amyloid precursor protein indicative of axonal damage caused by injury.

71
Q

focal brain injury: traumatic haemorrhage - what types

A

extradural - skull fracture
subdural
chronic subdural
subarachnoid (fatal, a result of major trauma)

72
Q

what is traumatic intracerebral haemorhage

A

intraparenchymal haemorrhage, similar presentation as stroke but due to trauma. coupe and contre coupe injury. symmetrical injury to other side of brain.

73
Q

secondary injury from TBI.

A

secondary damage due to inflammatory processes, glutamate buildup, ROS, BBB damage - leads to vascular and cytotoxic edema and swelling, most often COD.

74
Q

what does raised intracerebreal pressure lead to

A

as intracerebral pressure rises and approaches arterial pressure, cerebral perfusion pressure decreases. at 30% blood flow electrical failure
15% blood flow =cell death

75
Q

what are characteristic signs of secondary injury FROM TBI

A

damage first in CAI neurons of hippocampus, characteristic red neuron look.

76
Q

what is treatment from secondary injury from TBI

A

monitor ICP, monitor brain o2, drainage, craniotomy.

77
Q

describe subdural haemorrhage

A

bridging veins between arachnoid into dura are thinner and more suscptible to rupture following trauma.

78
Q

what are some examples of sports related TBI

A
  1. concussion
  2. second impact syndrome - accumulative effect of multiple concussions - impaired attention, poor memory, depression
  3. post concussive syndrome - associated with single concussive event, leads to dizziness, impaired attention and poor memory
79
Q

describe chronic traumatic encephalopathy(CTE)

A

caused by repetitive mild TBI or concussions, causes atrophy in white matter structures e.g. corpus collosum and causes NFT (no AB plaques like AD). may also see neuronal white matter loss in cerebellum and substantia nigra.

80
Q

where are NFTS often seen in CTE

A

at the bottom of sulcus - change in tissue densisty

81
Q

what are the amcroscopic features of CTE

A

diffuse brain volume loss, cavum septum pellucidum, cavum vergae, loss of white matter in corpus collosum.

82
Q

what the microscopic features of CTE

A

degeneration of SNc, neuronal loss in cerebelllum, NFTS in cortex (Tauopathy)

83
Q

what is creutzfeld jacob disease

A

an infectious, degenerative disease caused by a prion. also known as a transmissible spongiform encephalopathy.

84
Q

what is the infectious protein in CJD

A

PrPsc - misfolded protein which survives very very long and hard to destroy. has as extended incubation period. begins as asymptomatic but then shows rapid degeneration.

85
Q

what is sporadic CJD

A

most common form of CJD, unsure etiology, short duration, dementia, ataxia, wide posture. atrophy, spongiform encephalopathy due to a loss of cells/ neurons, increased vacuolation pattern, florid plaques.

86
Q

what is the prion hypothesis

A

normal PRPC has 3% beta sheet. a conformational change causes it to switch to PRPSC which has 43% beta sheet. is resistant. comes into contact with normal protein and causes it to switch to PRPSC form which is infective.

87
Q

what is iatrogenic CJD

A

induced CJD e.g. pituitary hromone exrtacts used to treat dawrfism, transplants etc.

88
Q

what is MS

A

demyelinative disease, chronic inflammatory autoimmune disease of CNS. lesions can occur in any parts of cns including spinal cord.

89
Q

risk factors for MS

A

gender - females, distance from equator.

HLADR2 halotype. MHC on chromosome 6P21 involved in presenting peptide to antigens.

90
Q

what is the EAE model for MS

A

an immune rection against murine muelin basic protein induces MS

91
Q

what is the course of MS

A

remitting relapsing

92
Q

how is MS diagnosed

A

MRI - paraventricular lesions/plaques, other lesions sites include optic nerve, brain stem, cerebellum, spinal cord. shows well defined grey firm plaques in white matter.

93
Q

what are the microscopic features of MS

A

myelin loss cause punched out lesions oftern around small veins, myelin debris in macrophages, loss of oligodendricytes. perivascular cuffing - perivascular inflammatory cells including lymphocytes, plasma cells, macrophages. reactive astrocytes.

94
Q

what is pathogenesis of MS

A
  • loss of myelin - slow/no neurotransmission
  • asonal loss
  • axonal destruction in chronic plaques (lack of support from oligodendricytes)
  • loss of brain volume over time.
95
Q

describe alcohol related brain damage

A

brain atrophy, white matter loss, minor neuronal loss in frontal cortex (not motor cortex)

96
Q

what is the pathogenesis of alcohol related brain damage

A
  • gluatamate toxicity and or oxidative damage
  • decreased neurogenesis
  • hepatic encephalopathy (NH3 and inflammation)
  • malnutrition e.g. vitb12 deficiency
  • polydrug use
97
Q

what is wenicke korsakoff syndrome

A

caused by thiamine (VITB12) deficiency, usually caused by chronic alcoholism.

98
Q

what are the acute presentations of wernicke korsakoff syndrome

A

oculomotor abnormalities, cerebellar dysfuntcion, confusion.

99
Q

what are the histological features of acute wernicke korsakoff syndrome

A

periventricular haemorrhage, endothelial hypertrophy

100
Q

what are the chronic presentations of wernicke korsakoff syndrome

A

may have retrograde amnesia (korsakoff psychosis

101
Q

what are the histological features of chronic wernicke korsakoff syndrome

A

mamillary body shrinkage due to neuron loss, also neurons loss in anterior thalamus and anterior cerebral vermis - lose ability to recall memories, make new memories.

CPAT NEURO (1 decks)

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