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Pathology > Pathology if the CNS > Flashcards

Pathology if the CNS Flashcards

1
Q

what two conditions can cause a significant loss of function to the CNS

A
  • ischemia

- infection

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2
Q

why may a small injury from ischemia or infection to one cell cause loss of function to the whole CNS

A

because the cells in the CNS are connected

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3
Q

list the order of cells of the CNS which are susceptible to injury from most to least

A
  • neurons
  • oligodendrocytes
  • astrocytes
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4
Q

what are the roles of astrocytes in the CNS

A

they maintain the homeostasis of ion channels and ions of the CNS and regulating ionic composition & neurotransmitters

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5
Q

how do astrocytes work in order to maintain homeostasis of components within the CNS

A

by picking up metabolites released in the CNS & picking up GABA & glutamate

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6
Q

what is the role of microglia in the CNS

A

act as macrophages in the CNS by removing infectious elements within the CNS

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7
Q

what is the role of oligodendrocytes in the CNS

A

involved in myelination around the nuclei

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8
Q

list the things which causes actions of neurons to injury in the CNS

A
  • acute neural injury - ‘red neurons’
  • sub-acute and chronic - ‘degenerations’
  • ageing - inclusion bodies, lipofuscin
  • neurodegeneration - alzheimer’s (neurofibrillary tangles)
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9
Q

what is acute damage in the CNS neurons caused by

A

ischemia

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10
Q

which areas of the brain tend to get infarcts and ischemia

A

areas between the main arteries e.g. the anterior cerbral artery - ACA & MCA or between the MCA & PCA
or
in the deeper structures e.g. basal ganglia & thalamus

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11
Q

why are the deeper structures such a basal ganglia & thalamus at risk to ischemia and stroke

A

as there is not any collateral supply to the deeper structures as around the brain you have the meninges surrounding it

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12
Q

what is the ACA, MCA & PCA areas known as

A

the watershed areas

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13
Q

what do the neurons appear as following an infarct with H and E staining

A

damaged cells are stained red (ischemic neurons under stress)

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14
Q

what do the neurons undergo following an infarct

A

necrosis & macrophages/microglia scavenge debris

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15
Q

which structure of the CNS is not as susceptible to ischemia compared to neurons

A

oligodendrocytes

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16
Q

what is the appearance of the nuclei of oligodendrocytes

A

small & round

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17
Q

what is the name of a tumour of the oligodendrocytes

A

oligodendoglioma

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18
Q

what happens as a result of a oligodendoglioma (tumour)

A

proliferation/increase in the number of oligodendrocytes compared to that of normal tissues

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19
Q

what is it called when there is an increase of the number of cells following a oligodendoglioma

A

hyperplasia

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20
Q

what is multiple sclerosis (MS)

A

a demyelinating disease (myelin loss - oligodendrocytes)

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21
Q

over which structure do oligodendrocytes have darker rounder nuclei

A

astrocytes (in H and E staining)

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22
Q

what are astrocytes

A

metabolic buffers and detoxifiers in the brain

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23
Q

what do astrocytes have a similar function to

A

fibroblasts (healing)

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24
Q

what do astrocytes form

A

part of the blood brain barrier

forms a protective structure within the choriocapillaris

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25
Q

why do astrocytes form part of the blood brain barrier

A

to protect the CNS from drugs (which is why it can be very hard to reach the brain)

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26
Q

why is it not useful to carry out chemotherapy if someone has a brain tumour, and what is a more effective alternative

A

astrocytes prevents the job of chemotherapy drugs to reach the CNS in the brain, brain surgery is more effective at removing the tumour

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27
Q

what is gliosis

A

the hypertrophy and hyperplasia of astrocytes in response to stress

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28
Q

what do you get an increase of in astrocyte hyperplasia

A

gliosis

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29
Q

what is the increase in astrocyte as response from

A

ischemic GFAP (glial fibrillary acidic protein)

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30
Q

what happens to the microglia in response to injury

A

proliferates, aggregates around foci of necrosis (as any other macrophage would, i.e. moves to the site of damage to initiate wound healing & repair), phagocytose apoptotic/necrotic neurons

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31
Q

what type of nuclei do microglia have

A

elongated rod like

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32
Q

what is a cerebrovascular disease e.g. stroke caused from

A

hypoxia, ischemia and infarct or haemorrhage

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33
Q

what is the cause of hypoxia, ischemia and infarct of cerebrovascular disease

A

impairment of blood supply and oxygenation of tissue (e.g. from heavy smoking reduces the amount of blood to the CNS)

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34
Q

what is the cause of a haemorrhage of cerebrovascular disease

A

resulting from rupture of CNS vessel e.g. blood vessel can cause aneurysm of the brain

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35
Q

what does the type of cerebrovascular disease injury depend on

A
  • presence of collateral blood supply (e.g. if it was the watershed region or deeper within the structures or if its more peripheral)
  • duration of ischemia
  • magnitude and time-course of the reduction in flow (acute vs chronic) i.e. how long the amount of oxygen to the brain was restricted, determines how much damage was done to the brain
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36
Q

what is global cerebral ischemia

A

general reduction in cerebral perfusion (i.e. blood supply is cut off via):

  • cardiac arrest - brain dead
  • shock - loss of blood = fall in BP and volume (decreased capacity to get oxygen to brain)
  • severe hypotension - watershed infarcts
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37
Q

what is focal cerebral ischemia caused by

A
  • embolus (travel in the blood & get lodged in a BV)
  • thrombosis of artery (thinning of artery)
  • vasculititis (inflammation of the artery)
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38
Q

what is the appearance of an acute infarct in the brain under the microscope

A

pale region = blood supply is reduced there

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39
Q

what happens as a first sign in tissues 12-24 hours following an infarct under the microscope

A

appearance of ‘red nuclei’ due to necrosis
releasing glutamate, GABA and calcium as they lose the ability to maintain/regulate their own homeostasis, neurotransmitters, ions become toxic to surrounding tissues

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40
Q

what happens 1-2 days following an infarct to the CNS under the microscope

A

neutrophils marginate/emigrate from blood vessels in the surrounding areas and perfuse the area to deal with the acute inflammation (clearing it up)

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41
Q

once neutrophils have approached the area of infarction in the CNS, what do they recruit

A

macrophages

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42
Q

10-14 days following an infarction to the CNS, what occurs

A

macrophages & microglia will come into the area & initiate wound healing

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43
Q

how do macrophages and microglia initiate wound healing following an infarct to the CNS

A

by laying down collagen fibres and phagocytosing necrotic tissues

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44
Q

which cell of the CNS deals with scarring and repairing the wound from an infarct to the CNS and how

A

astrocytes, by laying down collagen granulation tissue & trying to reorganise the damaged area

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45
Q

what is the result of scarring of the damaged area of the brain following infarction

A

the scarred part of the brain won’t function too well

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46
Q

what causes a haemorrhagic infarct ‘red’ in the CNS

A
  • an embolus
    either a cardiac or thrombus set free from the artery (from the heart) to create an embolism which causes an infarct
  • fat or bone marrow embolism secondary to fracture
  • blood leaks from collateral vessels or through necrotic capillaries
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47
Q

what causes a non haemorrhagic infarct ‘pale/bland/anaemic’

A
  • a thrombosis (thinning of the arteries)
    arterial block
    thrombosis of atherosclerotic plaque
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48
Q

which therapy is warranted < 3 hours following a non haemorrhagic infarct to the CNS and why

A 
thrombolytic therapy (drug can be given to break down the thrombosis & restore function to the area)
to preserve the penumbra
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49
Q

what is the penumbra region and why is it at risk following a non haemorrhagic infarct to the CNS

A

region on border of infarct that is as risk of necrosis (due to release of neurotransmitters & microglia & astrocytes to the area)

50
Q

which type of infarct can be given treatment and which one cannot

A

a white non haemorrhagic infarct caused by a thrombosis can be given treatment
but a haemorrhagic infarct caused by an embolis cannot

51
Q

what are the two classes of infarct to the CNS

A
  • haemorrhagic ‘red’

- non haemorrhagic ‘white’

52
Q

what are retinal microglia

A

surveyors of the environment of the retina and check for any diseases or pathology by dynamic movements of their processes, allowing the neural parenchyma to be completely sampled every few hours with very little movement of the microglial somata

53
Q

what do microglial cells of the retina react to

A

injury

54
Q

what appearance do the RPE cells have in a young retina

A

hexagonal shape cells

55
Q

in a younger retina, where is the microglia located

A

limited to the outer plexiform layer and above in the inner plexiform layer & ganglion cell layer, maybe one odd microglia cell found in the RPE

56
Q

in an older/aged retina, where is the microglia located

A

more microglia found at the RPE as it breaks through the OPL, as also found at the sub retinal space as well as in the outer segments of the retina

57
Q

what do microglia secrete

A

neuroprotective substances (implicated in alzheimer’s & ARMD through reduced surveillance & protection)

58
Q

what are neuroprotective substances which the microglia secretes important for

A

the maintenance of the health of the neural retina

59
Q

as well as microglia not remaining in the OPL and migrating to the RPE, what does an old retina lack in compared to a young retina and what does this result in

A

ramification (is reduced)
therefore not able to protect the retina as well as there are less branches of the microglia and therefore less able to search & touch surrounding neural tissues

60
Q

in order to carry our surveillance, what has to occur in the microglia structure over time

A

growth and extension of the microglia axons which occurs in young and old microglia

61
Q

although both young and old microglia axons can grow and extend the same over time, what difference is there with the axons which has an advantage in surveillance in younger microglia

A

younger microglia axons have larger movements which are also more frequent and older microglia axons have slower movements so are slower at detecting movements

62
Q

at what rate does a laser burn in a young compared to an old microglia accumulate

A

both accumulate at the same rate

63
Q

as the young and old microglia can accumulate at a laser burn at the same rate, what difference to they have following the accumulation

A

dispersal and healing in a younger microglia is quicker, and slower in an aged microglia i.e. slower to phagocytose & repair the damaged tissue

64
Q

what does a crush of the optic nerve cause

A

glaucoma

65
Q

what does a crush of the ONH cause a loss of

A

RGCs

66
Q

what is identified as the ending of the disc of the ONH

A

limit of bruch’s membrane found my modern imaging

67
Q

what can finding the limit of bruch’s membrane help with

A

finding the cup disc ratio much better as it promotes the disc margins

68
Q

what does the ophthalmic artery branch down to

A

central retinal artery

69
Q

where does the ONH get their supply from

A

central retinal artery

70
Q

whittles branched off the ophthalmic artery

A

short & long posterior ciliary arteries

71
Q

where does the long posterior ciliary artery go to and why

A

to the front of the eye, to supply that region

72
Q

what is the lamina cribrosa

A

holes in the sclera through which axons of the RGCs pass in sheaths

73
Q

what type of fit do the sheaths of RGCs that go through the lamina cribrosa have

A

tight fit

74
Q

how does IOP cause damage to the sheaths of the RGCs in the lamina cribrosa

A

by creating more pressure

75
Q

which theory does the damage of the sheaths of the RGCs in the lamina cribrosa created by IOP =

A

trauma/mechanical theory of glaucoma

76
Q

what strengthens the lamina cribrosa

A

collagen

77
Q

what is the type of collagen fibres we have in our lamina cribrosa important for

A

mechanical strength & how flexible the lamina cribrosa is

78
Q

in relation to the collagen fibres of the lamina cribrosa, how can a rigid lamina cribrosa cause more trauma to RGCs which pass through

A

eye movements around the rigid lamina cribrosa

79
Q

what factor determines the type of collagen we have in our lamina cribrosa which can determine susceptibility to glaucoma

A

genetic factor

80
Q

how can the ONH be more vulnerable to hypoxia, inflammation & glaucoma

A

if a smoker or diabetic

81
Q

list the potential things which can cause glaucoma

A
  • pathogenesis
  • age
  • hypoxia
  • trauma
  • genetics (afro Caribbean/diabetes)
82
Q

what does early signs of glaucoma show in visual fields

A

small isolated/localised scotomas

83
Q

as glaucoma progresses, what do the small localised scotomas become

A

merge and become an arcuate scotoma

84
Q

what does the arcuate scotoma in more advanced glaucoma respect

A

the horizontal line

85
Q

what type of visual field defect can a tumour if it is in the retina cause

A

visual field defect can be anywhere in the retina as it does NOT respect the horizontal or the vertical midline

86
Q

if the tumour is post chiasmatic, what will it respect in terms of visual fields

A

the horizontal midline

87
Q

if the tumour is pre chiasmatic, what will it respect in terms of visual fields

A

the vertical midline

88
Q

which visual field areas are lost, when theres a loss of RGCs

A

areas above and below the horizontal midline (i.e. glaucoma)

89
Q

what do RGCs undergo with high IOP

A

apoptosis

90
Q

what does TGD-beta stand for

A

transforming growth factor beta

91
Q

what two things increase with increased IOP with signs of microglia & macrophages from damage to the ONH

A

TGF-beta & collagen-1

92
Q

what type of eyes is transforming growth factor beta highly expressed in

A

glaucomatous compared to non glaucomatous eyes (showing pinkish blobs/hue in glaucoma ONH)

93
Q

what is TGF beta secreted by and what does this mean

A

macrophages so immune reaction against ONH (which is damaged from elevation in IOP)

94
Q

list the things that can cause infections of the CNS

A
  • haematogenous spread - artery/veins
  • traumatic - infection secondary to trauma (e.g. brain injury from orbital cellulitis) or congenital malformation or meninges
  • local - sinuses, teeth, osteomyelitis
  • peripheral nervous system to CNS (zoster, rabies) feed back into CNS
95
Q

when can infections spread to the body/CNS especially

A

when in a coma as can’t speak if they are getting symptoms

96
Q

what is acute meningitis

A

inflammation of CSF + pia mater & arachnoid mater, known as the leptomeninges

97
Q

what can be the three types of causes of acute meningitis and give examples

A 
- acute pyrogenic:
bacterial = E. Coli (young), N. meningitidis (adult) stereptococci (old)
- aseptic:
viral
- chronic: 
tuberculosis
98
Q

what are the neurological symptoms and systemic signs of an acute pyrogenic ‘bacterial’ CNS infection

A

shown via spinal tap:

  • CSF cloudy
  • high neutrophils number
  • increase protein concentration
  • decreased glucose
  • bacterial culture positive
99
Q

why is there decreased glucose in an acute pyrogenic ‘bacterial’ CNS infection

A

as the bacteria eats the glucose up

100
Q

what are the fever & neurological symptoms of an acute aseptic ‘viral’ CNS infection

A

shown via spinal tap:

  • lymphocytes in CSF (CSF = non cloudy)
  • protein elevation mild high
  • glucose normal
  • usually self-limiting
101
Q

what causes the infection of the brain called viral meningoencephalitis

A

brain + meninges
- many ‘arboviruses’ = arthropod borne virus
- mosquito vectors
leads to seizures, ocular palsies, coma, death

102
Q

what does viral meningoencephalitis lead to

A

seizures, ocular palsies, coma, death

103
Q

what is HSV-1

A

herpes simplex virus, retrograde infection through trigeminal to temporal lobes

104
Q

which herpes virus is NOT sexually transmitted

A

herpes simplex virus -1 (HSV-1)

105
Q

what are the symptoms of herpes simplex virus -1

A
  • cold sores
  • change in mood, memory and behaviour (as frontal lobe impaired)
  • temporal & frontal lobes (infection can get into CNS and effect)
106
Q

what type of population is herpes simplex virus -1 most common in

A

children

107
Q

what do 10% of herpes simplex virus -1 sufferers have

A

previous exposure

108
Q

what type of herpes is herpes simplex virus -2

A

genital herpes (sexually transmitted)

109
Q

how many % of children acquire herpes simplex virus -2 and how

A

50% during birth if mother is infected

110
Q

what do herpes simplex virus -2 sufferers develop

A

encephalitis (viral meningitis)

111
Q

what two things does viral encephalitis show in HSV-2

A
  • perivascular cuffs of leukocytes

- microglial nodules - clusters of reactive astrocytes + microglia & rod nuclei

112
Q

what are microglial nodules common in

A

viral infections

113
Q

what is a motor neuron disease the degeneration of which neurons

A

upper and lower neurons

114
Q

what is a motor neuron disease mutations in

A

super-oxide dismutase

115
Q

which part of the spinal chord does a motor neuron disease thin

A

anterior/motor (ventral) roots

116
Q

what does a motor neuron disease cause atrophy in

A
  • precentral gyrus (motor cortex)
  • anterior horn neurons
  • motor ventral column of spine (in motor neuron disease)
117
Q

what can be associated in the late stages of a motor neuron disease

A

ocular palsies

118
Q

what does a motor neuron disease cause the atrophy of

A

ventral motor column of CNS/spine

119
Q

what does alcoholism cause in the CNS/brain

A

cerebellar degeneration (wiped out)

120
Q

what symptoms and why, does cerebellum degeneration due to alcoholism cause

A

staggering, as it is involved in fine movement

Pathology (20 decks)

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