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Neurology > Pathology > Flashcards

Pathology Flashcards

1
Q

cellular responses to injury

A

rapid necrosis

slow atrophy

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2
Q

what is Nissl substance

A

large granular body in neurons - RER

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3
Q

when is a red neuron found

A

in acute neuronal injury

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4
Q

how does a red neuron arise

A

hypoxia/ischaemia

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5
Q

when are red neurons visible

A

12-48 hours after irreversible insult to cell

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6
Q

why is a red neuron called what it is

A

intensely red cytoplasm

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7
Q

list other neuronal responses to injury

A

axonal
chronic degeneration
sub cellular alterations - inclusions

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8
Q

What is Wallerian degeneration

A

axonal response to injury where there is degeneration of myelin and axon distal to site of injury

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9
Q

give an example of subcellular alterations / inclusions

A

neurofibrillary tangles in Alzheimers

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10
Q

What is the main cell involved in repair and scar formation

A

astrocytes

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11
Q

what is gliosis

A

astrocyte damage

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12
Q

what are the early stages of gliosis

A

hyperplasia and hypertrophy of astrocytes

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13
Q

what is the most important histopathological indicator of CNS injury regardless of cause

A

gliosis

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14
Q

what does damage to oligodendrocytes result in

A

demyelination

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15
Q

what are oligodendrocytes sensitive to

A

hypoxia

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16
Q

Ependymal cells have a limited response to injury, true or false

A

true

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17
Q

M2 microglia are anti/pro inflammatory

A

ANTI inflammatory

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18
Q

causes of nervous system injury

A 
hypoxia 
trauma 
toxins 
metabolic abnormalities 
nutritional deficiencies 
infections 
genetics 
ageing
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19
Q

Why is excitotoxicity important

A

important mediator of neuronal injury

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20
Q

what is excitotoxicity

A

hypoxia leads to reduced ATP production and so reduced energy followed by neuronal depolarisation
glial cells fail to reuptake glutamate resulting in a glutamate storm
this excites post synaptic GluR resulting in rapid Ca2+ accumulation in post synaptic neuron

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21
Q

what are the 3 outcomes of Ca2+ accumulation in excitotoxicity

A

protease activation
mitochondria dysfunction
oxidative stress

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22
Q

what is cytotoxic oedema

A

accumulation of Na and Cl in the CELL resulting in a shift of water to the cell also

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23
Q

causes of cytotoxic oedema

A

alcohol intoxication
Reye’s
hypothermia

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24
Q

what is ionic/osmotic oedema

A

movement of Na, Cl and water into interstitium

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25
Q

causes of ionic oedema

A

SIADH

increased water uptake

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26
Q

what is vasogenic oedema

A

disruption of BBB resulting in larger molecules like albumin bringing in water

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27
Q

causes of vasogenic oedema

A 
trauma 
tumours
inflammation 
infection 
encephalopathy
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28
Q

what is haemorrhagic conversion

A

BBB is majorly disrupted that RBCs enter

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29
Q

in global hypoxic ischaemic damage, what does the MAP fall below

A

50mmHg

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30
Q

define stroke

A

sudden disturbance of cerebral function of vascular origin that causes symptoms lasting more than 24 hours

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31
Q

what can cause cerebral infarction

A

thrombus from atherosclerosis - commonly MCA

embolus - from internal carotid artery or from the heart

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32
Q

what type of necrosis occurs in the brain

A

liquefactive necrosis

33
Q

consequences of hypertension in the brain

A

lacunar infarct strokes
vascular dementia
ruptured aneurysms and intra-cerebral haemorrhage
hypertensive encephalopathy

34
Q

what are lacunar infarcts

A

small infarcts in deep cerebral white matter, basal ganglia or pons

35
Q

what type of necrosis do you get in blood vessels

A

fibrinoid necrosis

36
Q

what is hypertensive encephalopathy

A

HTN and raised ICP
brain herniation
global cerebral oedema
petechiae

37
Q

what illicit drugs can cause intra cerebral haemorrhage

A

cocaine

alcohol

38
Q

what is amyloid angiopathy

A

accumulation of abnormal B sheet proteins resulting in stiffened vessels and HTN

39
Q

cellular constituents of CSF

A 
clear fluid 
No WBC
low protein 
no RBCs 
glucose >2.2
40
Q

what is hydrocephalus

A

accumulation of excessive CSF in ventricular system of brain

41
Q

3 main causes of hydrocephalus

A

obstruction of CSF flow
decreased CSF resorption
CSF overproduction

42
Q

hydrocephalus calssification

A

communicating

non-communicating

43
Q

what is non-communicating hydrocephalus

A

obstruction to CSF flow withIN the ventricular system

44
Q

what is communicating hydrocephalus

A

obstruction to CSF flow OUTwith the ventricular system

45
Q

what is hydrocephalus ex vacuo and in which degenerative condition is it seen in

A

loss of brain parenchyma resulting in secondary ventricular dilatation and increase in CSF
Alzheimer’s disease

46
Q

causes of raised ICP

A

tumour / SOL
hydrocephalus
oedema

47
Q

consequences of raised ICP

A

brain herniations
CN palsies
visual distrubances

48
Q

list some causes of SOL

A

tumour
abscess
haemorrhage
oedema

49
Q

what is the most common primary malignant tumour in:
adults
children

A

adults - astrocytoma

children astrocytoma and medulloblastoma

50
Q

what is the most common primary benign tumour in:
adults
children

A

adults - meningioma

children - craniopharyngioma

51
Q

medulloblastoma is radio/chemosensitive

A

radiosensitive

52
Q

what is demyelination

A

preferential damage to myelin sheath with relative preservation of axons

53
Q

examples of primary demyelination in the CNS

A

MS
acute disseminated encephalomyelitis
acute haemorrhagic leukoencephalitis

54
Q

secondary causes of demyelination in CNS

A

viral - JC virus
metabolic
toxic

55
Q

describe MS plaques

A

well demarcated
irregularly shaped
vary in size
non-symmetrical distribution

56
Q

commonly affected areas by MS plaques

A 
lateral ventricle area
corpus callosum 
optic nerves and chiasm 
brainstem 
ascending and descending tracts 
cerebellum 
spinal cord
57
Q

describe the histology of active plaques in MS

A

perivascular inflammatory cells
microglia
ongoing demyelination

58
Q

describe the histology of inactive plaques in MS

A

gliosis
little remaining myelinated axons
reduced number of oligodendrocytes and axons

59
Q

macroscopically, what colour are active plaques

A

yellow/brown

ill defined edge

60
Q

macroscopically, what colour are inactive plaques

A

grey/brown

well demarcated

61
Q

what is the immunopathology of MS

A

lymphocytic infiltration
oligoclonal bands in CSF
HLA DRB1
Th1 and Th27 cells

62
Q

is dementia a normal part of the ageing process

A

no it is always pathological

63
Q

list primary causes of dementia

A

Alzheimer’s
Lewy body dementia
Frontotemporal dementia/Pick’s disease
Huntington’s disease

64
Q

list secondary causes of dementia

A 
vascular/multi infarct
infection 
trauma 
metabolic 
drugs and toxins 
SOLs
65
Q

what is the most common cause of dementia in the elderly

A

Alzheimer’s disease

66
Q

genetics of Alzheimer’s disease

A

APP
presenalin 1+2
trisomy 21
ApoE4

67
Q

macroscopic appearance of Alzheimer’s disease

A

cortical atrophy - frontal, parietal, temporal lobes
widened sulci and narrowed gyri
hydrocephalus ex vacuo

68
Q

microscopic features of Alzheimer’s disease

A

simple neuronal atrophy
gliosis
neurofibrillary tangles
amyloid plaques/neuritic plaques

69
Q

what are neurofibrillary tangles

A

intracellular bundles of Tau protein

70
Q

what is amyloid angiopathy

A

extracellular eosinophilic accumulation of Abeta sheets

71
Q

appearance of amyloid with congo red stain

A

apple green birefringence

72
Q

features of Lewy body dementia DLB

A

progressive
hallucinations
fluctuating levels of attention

73
Q

all DLB get PD but not all PD get DLB, true or false

74
Q

what are lewy bodies

A

a-synuclein aggregrates + ubiquitin

75
Q

what is frontotemporal dementia FTD also known as

A

Pick’s disease

76
Q

onset of FTD

A

early <65 yo

77
Q

symptoms of FTD

A

social disinhibition
personality change
rapidly progressive

78
Q

atrophy of what happens in FTD

A

frontal and temporal lobes

79
Q

what are Pick’s bodies

A

intracytoplasmic filamentous inclusions seen in Pick’s disease

Neurology (25 decks)

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