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Z MD1 neurology > histology and pathology > Flashcards

histology and pathology Flashcards

1
Q

what are the types of glial cells? (macroglia)

A
  • astrocytes
  • oligodendrocytes
  • schwann cells
  • ependymal cells
  • satellite cells of ganglia
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2
Q

what are microglia

A

the immune cells of the CNS

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3
Q

what is special about using the silver stain on neural tissue

A

can see the cell processes

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4
Q

explain the histology of the choroid plexus

A

an epithelial cell that line the ventricles

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5
Q

histology of epndymal cells

A

low columnar or cuboidal cells that line the central canal of the spinal cord and the ventricle within the brain - some have cilia to aid CSF flow

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6
Q

function of actin in neurons

A

allows for dynamic assembly/disassembly –> shape changes and movement

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7
Q

function of microtubules in neurons

A

axon transport

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8
Q

difference between dendrite and axon

A

dendrite - receives information from other neurons

axon - main conducting unit for carrying signals to other neurons

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9
Q

if you damage a neuron at random… why is it that the axon is often involved, not the cell body

A

because there is a high proportion of total cell volume in the axons and dendrites compared to the cell body

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10
Q

what is the difference between the electrical activity occurring down dendrites and axons

A

dendrites - passive electrotonic spread

axons - action potential propagated

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11
Q

what is a Nissl body

A

parts of the neuron that is involved in protein production

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12
Q

what are the passive support functions of astrocytes

A
  • NT uptake and degradation (in particular GABA and glutamate)
  • K+ homeostasis
  • neuronal energy supply (take glucose from the blood and give to neurons)
  • maintenance of the BBB
  • injury response and recovery
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13
Q

what are the active functions of astrocytes

A
  • modulation of neuronal function
  • modulation of blood flow
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14
Q

how do astrocytes regulate NT uptake and degradation

A

express glutamate and GABA transporters

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15
Q

what happens when the glutamate and GABA transporters on the glial cells are inhibited and therefore their function removed

A

causes overexcitation of the neurons –> if this happens for a long period of time –> cell will die

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16
Q

excitation of glial cells leads to –>

A

modulations of intracellular Ca levels –> modifies activity of neighboring cells

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17
Q

do glial cells have synaptic vesicles?

A

yes!! - but very small number compared to neurons

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18
Q

what does the release of Ca from glial cells do to neurons?

A

inhibits neurons by hyperpolarising it through release of ATP

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19
Q

what is the mechanism for astrocytes regulating vascular tone

A

the calcium wave propagated by the glial cell causes vasoconstriction

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20
Q

what is the importance of astrocytes regulating blood flow

A

astrocyte can sense what is going on in the synapse and can therefore directly regulate the blood supply to meet the metabolic demand of the synapse

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21
Q

what type of glial cell is responsible for myelination in the CNS and the PNS

A

oligodendrocytes - CNS

Schwann cells - PNS

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22
Q

what is the difference in myelination by oligodendrocytes and Schwann cells other CNS vs PNS

A

oligodendrocytes - extend processes that wrap around parts of several axons

schwann cells wrap around a single axon

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23
Q

what are nodes of ranvier

A

small gaps in the myeination of an axon

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24
Q

function of microglia

A

constantly survey the CNS ensuring all the synapses are working properly and rapidly responding to inflammation or injury

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25
Q

where are perineurium, epineurium and endoneurium

A

perineurium - surrounds each fascicle of axons

epineurium - surrounds a bundle of fascicles

endoneurium - surrounds individual nerve fibres and schwann cells

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26
Q

what are autonomic ganglia

A

house the cell body of post-ganglionic neurons

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27
Q

What is a stroke

A

the development of a focal or global neurological deficit related to a vascular event

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28
Q

what are the 3 pathological processes involved in stroke and what are their prevalences

A

infarction - 75%

haemorrhage - 20%

subarachnoid haemorrhage - 5%

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29
Q

risk factors for cerebral infarction

A

age

hypertension

cardiac disease

hyperlipidaemia

DB

hypercoagulability states

smoking

obesity

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30
Q

definition of cerebral infarction

A

necrosis of cerebral tissue in a particular vascular distribution due to vessel occlusion or severe hypoperfusion

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31
Q

what are the mechanisms of cerebral infarction

A
  • pump failure
  • systemic hypotension
  • narrowed vessel lumen
  • occlusion by embolus
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32
Q

pathogenesis of large artery, small vessel and venous occlusion leading to cerebral infarction

A

large artery - embolic>thrombotic

small vessel - thrombotic>embolic

venous - thrombotic

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33
Q

common sites of atherosclerosis in the circle of willis

A
  • internal carotid termination
  • proximal middle cerebral artery
  • vertebral arteries
  • basilar artery
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34
Q

how does the Circle of Willis offer some protection from stroke

A

because of the anastomoses between anterior and posterior circulation - only works up to a point

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35
Q

what is an endarterectomy

A

where are surgeon goes in a removes the thickened intima and some of the media of an atherosclerotic vessel to try and prevent the formation of thrombus/embolus –> stroke

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36
Q

what happens macroscopically a few hours after a stroke

A

the brain can start to swell due to cytotoxic oedema and adjacent vasogenic oedema –> herniation –> death

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37
Q

what happens microscopically to the neurons of the brain after stroke

A
  • initially swell up
  • then become hypereosinophilic
  • shrink
  • nucleus become pyknotic and then eventually disappears
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38
Q

what happens macroscopically a few days-weeks after stroke

A

the infarcted tissue becomes necrotic (liquefactive)

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39
Q

what happens macroscopically a few months-years after stroke

A

eventually a cystic space becomes of what was the tissue

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40
Q

what causes haemorrhagic stroke

A

when the vessel becomes occluded and then becomes reperfused very quickly with blood –> haemorrhagic infarction

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41
Q

how can hypertension lead to stroke

A

hypertension –> hyaline arteriolosclerosis of the small vessels of the brain (particularly deep vessels) –> narrowing and ballooning

42
Q

what are lacunar infarcts

A

small infarct due to hypertension

43
Q

what is the main reason for people to die after stroke

A

due to the consequences of their incapacitation after their stroke

  • pneumonia
  • CVD
  • pulmonary thromboembolism

(can also die from cerebral swelling and the stroke involving vital centres)

44
Q

causes of intracerebral haemorrhage

A

hypertensives small vessel disease

amyloid angiopathy blood disorders

coagulopathy

tumour

vasculitits

vascular malformation

drugs

45
Q

what is the difference in effect on the type of stroke, between hypertensive small vessel disease and amyloid angiopathy small vessel disease

A

hypertensive - tends to involve deep cerebral structures like the basal ganglia and brainstem

amyloid angiopathy - tends to involve superficial cortical areas

46
Q

what is amyloid angiopathy

A

deposition of Abeta amyloid in the walls of the superficial supratentorial blood vessels

47
Q

causes of non-traumatic subarachnoid haemorrhage

A
  • rupture of saccular aneurysm in the COW
  • rupture of other types of aneurysm
  • extension of intracerebral hemorrhage
48
Q

risk factors for developing saccular aneurysm

A
  • female
  • PCKD
  • coarctation of the aorta
  • type 3 collagen deficiency
  • HT
  • smoking
  • alcohol
49
Q

where are the favoured sites for berry/saccular aneurysm of the COW

A
  • bi/trifurcation of the MCA
  • junction of the ICA and posterior communicating artery
  • anterior communicating artery (tend to be more anterior circulation)
50
Q

why does a surgeon want to go in and clip a berry aneurysm

A

because the blood from the rupture is spasmogenic of the cerebral vessels –> can lead to further infarction

51
Q

how do you get concussion

A

follows sudden change in the momentum of the head

52
Q

what is concussion

A

instantaneous loss of consciousness, temporary respiratory arrest and loss of reflexes

53
Q

what is a “closed” brain injury

A

when movement (change in momentum) or compression (tumour/haemorrhage) of neural and vascular structures with the skull

54
Q

what are the secondary effects of traumatic brain and spinal cord injury

A

ischaemia and hypoxia - tend to be acute

cerebral swelling –> raised ICP

infection and epilepsy - usually delayed

55
Q

what is the term describing a skull fracture with splintering of the bone?

A

comminuted

56
Q

what does blood/CSF from the nose/ears suggest

A

that there may be a basal fracture

57
Q

how do you get extradural and subdural haematomas?

A

extradural - rupture of MMA

subdural - rupture of subdural veins

58
Q

why are older people less likely to get extradural haemorrhages and more likely to get subdural haemorrhages?

A

because with aging - the dura becomes more tightly attached to the skull (less potential to accumulate blood here), and also because the brain starts to atrophy with aging and therefore there is more stretch placed on the subdural veins - more easily ruptured

59
Q

what is a contrecoup

A

a contusion that has occurred on the opposite side of the brain to that of the site of impact

60
Q

what is the typical clinical sign of a basal contusion?

A

ansomnia or loss of smell

61
Q

what does the brain look like macroscopically when recovered from a contusion?

A

the crests of the gyri collapse down and become yellowish (due to the action of macrophages)

62
Q

what part of the brain is particularly vulnerable to axonal injury

A

corpus callosum

63
Q

what macroscopic feature suggests that there is axonal injury

A

small spotty haemorrhages (due to small BVs being ruptured along with the axonal injury)

64
Q

what is the histological feature of axonal injury

A

axonal spheroids/swellings

65
Q

what are the macroscopic features of the longterm effects of diffuse axonal injury

A
  • corpus callosum atrophy
  • thin white matter
  • large lateral ventricles
66
Q

why is a spinal cord injury not localised to just the site of impact?

A

because the spinal cord gets squished both proximally and distally so that it further damages itself

67
Q

what are 4 long term sequelae of brain trauma

A

infections

hydrocephalus

epilepsey

chronc traumatic encephalopathy

68
Q

what happens in chronic traumatic encephalopathy

A
  • brain atrpohy due to neuronal loss
  • abnormal deposition of Tau protein
  • diffuse deposition of A-beta plaques in cortex
69
Q

what is the mechanism leading from increased CSF to brain death

A
  • expulsion of as much CSF and venous blood as possible
  • IC pressure starts to rise
  • herniations of brain tissue occur through dural openings
  • as ICP approaches arterial pressure, brain perfusion ceases
70
Q

what are potential causes for increased intracranial pressure

A

trauma

tumour

infarction

haemorrhage

infection

cerebral oedema

overproduction/obstruction to flow/absorption of CSF

71
Q

2 main subtypes of cerebral oedema

A

vasogenic

cytotoxic

72
Q

what is vasogenic cerebral oedema due to

A

BBB disruption with increased vascular permeability

73
Q

what is cytotoxic cerebral odema due to

A

increased intracellular fluid secondary to neuronal, glial or endothelial cell membrane injury

74
Q

which type of cerebral oedema is responsive to steroid treatment

A

vasogenic

75
Q

what are the 5 potential sites of obstruction of CSF

A
  • foramen of monro (interventricular foramen)
  • 3rd ventricle
  • aqueduct of Sylvius (cerebral aqueduct)
  • foramina of Luschka and Magendie
  • basal cisterns/subarachnoid space
76
Q

what are the 3 major sites of herniation of the brain due to raised IC pressure from subdural haematoma

A
  • subfalcine herniation of cingulate gyrus
  • transtentorial herniation of medial temporal lobe
  • transforaminal herniation of cerebellar tonsil
77
Q

what is Duret?

A

brainstem haemorrhages due to brainstem herniation

78
Q

what are the outcomes of a CNS neuron that has been injured

A
  • neuron dies
  • adjacent neuron retracts its processes
  • adjacent neuron can “sprout” and make new local connections
  • little/no regeneration
79
Q

what happens up to 2 weeks post-injury of a PNS neuron

A
  • the nucleus in the cell body becomes peripheral
  • loss of Nissl substance
  • Wallerian degeneration
  • (muscle fibre atrophy - if motor neuron)
80
Q

what is the fancy name for loss of Nissl substance

A

chromolysis/chromatolysis

81
Q

what is Wallerian degeneration

A
  • degeneration of axon and myelin sheath below the site of injury
  • debris phagocytosed by macrophages
82
Q

what happens at 3 weeks post injury of a PNS neuron

A
  • Schwann cells proliferate –> forming a compact cord - Growing axons penetrate the Schwann cell cord and grow at a rate of 0.5-3mm/day
83
Q

what happens at 3 months post injury to a PNS nerve

A

successful regeneration with the electrical activity restored and (muscle fibre regeneration if a motor neuron)

84
Q

how does a neuroma form

A

from unsuccessful regeneration of a PNS neuron - axon misses its target and keeps growing and growing due to the GF and therefore bundles up at the end = neuroma

85
Q

what makes a crush injury to a neuron better than a cut injury

A

the alignment is still intact and the Schwann cells and ECM are continuous in a crush injury

86
Q

what is the difference between Schwann cells and oligodendrocytes in nerve injury

A

oligodendrocytes - inhibitory to nerve regrowth

Schwann cells - stimulatory of nerve regrowth

87
Q

what is the thought behind giving tPA for stroke

A

minimizes the extent of the primary damage to the neurons (as while the blood clot is there the primary damage is still occurring)

88
Q

what is primary injury to a neuron

A

physical damage causing cell loss

89
Q

what causes secondary injury to neurons

A
  • ischaemia
  • Ca influx
  • lipid peroxidation and free radical production
  • glutamate excitotoxicity
  • BBB breakdown
  • immune cell infiltration/microglia activation
  • cytokines, chemokines, metalloproteases
90
Q

what happens due to Secondary injury of neurons

A
  • axonal degeneration
  • demyelination
  • apoptosis
  • astrocytic gliosis and glial scar
  • also syrinx (cavity) formation, meningeal fibroblast migration
91
Q

general things you can research and work on to promote CNS repair

A
  • neuroprotection of surviving cells
  • axonal regeneration and functional integration
  • regrowth of surviving neurons and remyelination
  • modulate astrocytic gliosis - neural stem cells
92
Q

what stops axonal regeneration in the CNS

A
  • lack of trophic support to encourage axons to regrow
  • inhibited by the injury environment (astrocytic gliosis, glial scar, myelin inhibitors, developmental guidance molecules)
93
Q

what happens during astrocytic gliosis (7)

A
  • upregulate astrocyte cytoskeletal proteins
  • hypertrophy
  • proliferate
  • secrete cytokines and GFs
  • secrete ECM
  • upregulate expression of developmental axon guidance molecules
94
Q

what does a glial scar do

A

forms a barrier between undamaged tissue and injury site - prevents regrowth of axons through injury site

95
Q

what is the importance of Rho kinase in CNS neuron regeneration

A

it is a common mediator of inhibition of the growth of axons

  • therefore if you can inhibit Rho kinase - may be beneficial
96
Q

how do neurons die in the CNS

A

by apoptosis and necrosis

97
Q

where are the two main places in the adult brain with neural stem cells

A

the subventricular zone of the lateral ventricle the subgranular zone of the dentate gyrus in the hippocampus

98
Q

what is the importance of Epo trials for neural regeneration

A

helps promote the neural stem cells in the lateral ventricle to survive

99
Q

what are the things that inhibit CNS neural regeneration

A
  • astrocyte gliosis
  • myelin inhibitors
  • upregulation of developmental axon guidance molecules
100
Q

what are the things that may help promote neural regeneration

A
  • neuroprotection
  • modulate gliosis
  • promote axonal regeneration by blocking inhibitory molecules
  • activation or transplantation of stem cells

Z MD1 neurology (17 decks)

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