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Pathology 3 > Neuro 1 - circulation, injury > Flashcards

Neuro 1 - circulation, injury Flashcards

1
Q

types of cells (4)

A
  • neurons
  • oligodendrocytes
  • astrocytes
  • microglia
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2
Q

3 circulatory disorders and injury to the CNS

A
  • raised incracranial pressure
  • circulatory disorders
  • trauma
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3
Q

what can increased ICP lead to and why

A

head pressing due to edema

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4
Q

types of CNS circulatory disorders

A
  • brain swelling and edema
  • thrombosis, ischemia, infarcts
  • hydrocephalus
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5
Q

what is increased ICP

A

limited potential for expansion due to the non-yielding nature of the cranial vault –> results in increased ICP

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6
Q

causes of increased ICP

A
  • focally expanding mass (tumor, abscess)
  • CSF accumulation (ventricular obstruction)
  • vascular congestion (inflammation, trauma, toxin, etc)
  • brain edema
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7
Q

list consequences of intacranial expanding lesion (swelling)/increased ICP

A
  • local deformity (tumor), reduced CSF volume and brain distortion
  • internal herniation
  • ischemic brain necrosis
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8
Q

significance of internal brain herniation

A

results in hemorrhagic infarction of the herniated segment and/or the tissue compressed by the herniated segment

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9
Q

what happens in ischemic brain necrosis

A
  • brain swelling compresses small caliber vessels, esp those entering from meningeal surfaces
  • widespread endothelial damage
  • even if severe swelling is reduced, reperfusion of damaged vessels will cause severe vasogenic edema
  • greater degrees of vascular compression = ischemic brain necrosis
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10
Q

4 locations for brain herniation

A
  • supracallosal subfalcine
  • trantentorial
  • foraminal
  • transcalvarias
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11
Q

supracallosal subfalcine herniation

A
  • falx cerebri (dural septium) –> permanent location
  • falx cerebri = division between hemispheres (part of meninges)
  • cingulate gyrus slips beneath it
  • clinical signs aren’t as defined (seizures, loss of voluntary consciousness)
  • 12:00 on drawing
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12
Q

transtentorial herniation

A
  • tentorium cerebelli (dural septum + bone) –> permanent location
  • occipital cortex slips beneath, compressing midbrain –> displaces it posteriorly
  • 4:00 on drawin
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13
Q

foraminal herniation

A
  • most common
  • herniation of cerebellum may compress and thus disrupt function of respiratory centers in brain
  • permanent location
  • 6:00 on drawing
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14
Q

transcalvarias herniation

A
  • from trauma

- location varies (2:00 on drawi6)ng)

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15
Q

what is brain swelling

A

increase in volume of all or part of the brain

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16
Q

what is brain swelling a potential complication of (6)

A
  • head injury
  • ischemia
  • hemorrhage
  • tumor
  • infection
  • metabolic disease
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17
Q

what is congestive brain swelling

A

enlargement of the brain resulting in elevated ICP caused by an increased diameter of the blood-containing vasculature (cerebrovascular dilation) –> localized or generalized

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18
Q

cause of congestive brain swelling

A

trauma

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19
Q

what is brain edema

A

increased brain tissue water content (of brain parenchyma) within the cell and within the intercellular space

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20
Q

types of brain edema (4)

A
  • vasogenic edema
  • cytotoxic edema
  • hypo-osmoic edema
  • hydrostatic edema
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21
Q

what is neuropil

A

everything in the brain that is not cell body, cell processes, or glia/neuron processes

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22
Q

BBB and permeability with edema

A
  • separation of interendothelial tight junction
  • increased vesicular transport and formation of transendothelial channels
  • biochemical and structural alteration of the endothelial membrane –> increase in permeability
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23
Q

vasogenic edema

A
  • most common
  • from loss of BBB function
  • distribution of edema depends on distribution of affected vessels (localized things like tumor/abscess/hematoma/trauma/infarct or generalized things like trauma/toxins)
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24
Q

cytotoxic edema

A
  • intracellular fluid accumulation with normal vascular permeability
  • damaged ATP-dependent ion pumps (hypoxia, bacterial exotoxin)
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25
Q

histologic changes in vasogenic edema

A
  • polymicrocavitation change, fluid accumulation between cells
  • vacuolization of neuropil
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26
Q

ultrastructural changes in cytotoxic edema

A
  • accumulation of fluid within astrocyte (clear cytoplasm sparse chromatin, vacuolization of cytoplasm)
  • toxin in astrocyte –> cytotoxic edema
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27
Q

hypo-osmotic edema

A
  • rapid osmolarity shifts
  • water intoxication, salt toxicity
  • osmolarity of CSF slightly higher than plasma –> drink lots of water –> liquid moves into brain –> edema
28
Q

hydrostatic edema

A
  • interstitial edema
  • elevated intraventricular hydrostatic pressure that accompanies hydrocephalus
  • abnormal circulation of CSF
29
Q

combination of vasogenic and cytotoxic edema (2 types)

A
  • common
  • primary endothelial injury –> vasogenic edema + decreased tissue perfusion –> tissue hypoxia –> cytotoxic component
  • primary astrocytic insult –> cytotoxic edema + tissue volume expansion –> vascular compression/low flow –> endothelial injury from loss of laminar blood flow –> vasogenic component
30
Q

status spongiosus

A

extracellular or intracellular edema of white matter affecting mostly oligodendrocytes

31
Q

spongiform changes

A

-vacuolation observed in neurons and its processes in the transmissible spongiform encephalopathy (prion diseases)

32
Q

intramyelinic edema

A
  • histo: status spongiosus (white matter) –> holes
  • uncommon, reflecting toxic insult to oligodendrocytes
  • fluid accumulation within myelin lamella –> resultant vacuoles are sharply demarcated
33
Q

what is it when you have increased water content in brain interstitium

A

brain edema

34
Q

causes of hemorrhage in animals

A
  • trauma
  • infection and clotting disorders
  • degeneration of the vascular wall
  • arterio-venous malformations (uncommon)
  • hypertention (only great apes)
  • aneurysms (rare)
35
Q

what happens in “brain vascular accident”

A

vessel rupture –> bleeding –> expansion –> edema, compression, necrosis

36
Q

what is ischemia

A

reduction in blood flow to a region

37
Q

metabolism of brain tissue and ischemia

A
  • nervous tissue has high metabolic rate

- regional variations in metabolic rate (developing tissue/cell vulnerability) –> measure blood flow

38
Q

selective vulnerability to ischemia and selective neuronal death

A
  • specific neuron population
  • not all cell types are equally vulnerable to ischemic insults
  • neurons more susceptible than glia or vascular cells, some neurons more susceptible than others
39
Q

neurons most susceptible to ischemia

A
  • large pyramidal cells of layers 3, 5, 6 in cerebral cortex, hippocampal pyramidal cells, and purkinje cells in cerebellum
  • neonate: more involvement of brain stem nuclei than in adult
40
Q

time limit of ischemia

A

2-3 minutes of oxygen deprivation is all that neurons can tolerate (depends on energy sensitivity)

41
Q

causes of diminished tissue perfusion

A
  • embolism
  • thrombosis (secondary to endothelial damage; vasculitis)
  • trauma
  • external compression
42
Q

what is infarction

A
  • territorial death of nervous tissue die to lack of blood supply
  • gross appearance: red or pale (depends on whether reperfusion takes place)
43
Q

causes of infarction

A
  • thrombi
  • emboli
  • idiopathic
  • feline ischemic encephalopathy
  • septic emboli
  • edema
44
Q

major consequence of hemorrhage

A

-increased ICP due to space occupying nature of lesion and destruction of functional tissue

45
Q

feline ischemic encephalopathy

A
  • cause of infarction
  • affects animals of all ages, both sexes
  • acute onset with variable signs: ataxia (cerebellum), circling (ears), seizures, blindness, postural deficits
  • mild improvement over first few days then typically remain stable
46
Q

pathology of infarction

A
  • usually unilateral ischemic necrosis, typically involving territory of middle cerebral artery
  • boundary or border zone infarcts: distal regions of vascular territories particularly vulnerable to reductions in BP and blood flow
  • can be bilateral, probably won’t be symmetric
47
Q

ischemic changes over time

A
  • 0-12hrs: no changes in routine light microscopy
  • 12hrs: pink neurons
  • 12-24hrs: neutrophils
  • 1-3d: macrophages
  • 1-2wks: reactive astrocytes
  • months: cavitation
48
Q

spinal cord infarction info

A
  • fibrocartilaginous disc emboli
  • dogs, cats, horses, swine, humans
  • acute onset of sudden hemiparesis or flaccid paraplegia (signs depend on occlusion site)
  • little recovery
  • in dogs, more common in chondrodysplastic or large breeds
49
Q

pathology of spinal cord infarction

A
  • usually in lumbar and thoracic segments
  • unilateral infarct of cord involving both gray and white matter
  • sometimes can localize disc material within arteries and veins
  • how the disc material gains access to vasculature is unclear
50
Q

what is malacia

A

softness of nerve tissues

51
Q

principal effect of vascular compressive spinal cord lesion

A

reduction of blood supply –> extent of injury function of rapidity in which mass compromises vascular supply and degree of compromise

52
Q

nature of mass in vascular compression spinal cord lesions

A
  • herniated interverterbral disc material
  • epidural abscess/neoplasm
  • displaced vertebral body (subluxation)
53
Q

what part of the cord is usually compressed and why

A

since most of the compression of the spinal cord originates in the vertebral disc or body, most tend to compress the ventral aspect of the cord

54
Q

what is wallerian degeneration

A

degeneration of distal part of axon (from compression) –> hallmark of the response of the nerve fiber to a compression (axon and myelin around axon degenerates, macrophages come to remove debris)

55
Q

causes of extramedullary spinal cord compression (7)

A
  • canine degenerative intervertebral disc disease
  • equine cervical vertebral instability/stenotic myelopathy (young thoroughbreds)
  • equine cervical static stenosis (QH)
  • cranioventral malformation of arab
  • canine lumbar discospondylitis (brucella canis)
  • epidural abscesses
  • spinal neoplasia
56
Q

what is hydrocephalus

A
  • consequence of a structural anomaly which is either acquired or heritable, congenital or post-natal in development
  • underlying defect is increase in CSF volume reflecting imbalance in rate of production and resorption
57
Q

2 types of hydrocephalus (list)

A
  • communicating hydrocephalus

- noncommunicating hydrocephalus (internal hydrocephalus)

58
Q

communicating hydrocephalus

A
  • CSF may accumulate in subarachnoid space and ventricular system
  • physical alteration of arachnoids granulations is such that CSF absorption occurs at a slower rate
  • uncommon, generally acquired
59
Q

noncommunicating hydrocephalus

A
  • results from decreased CSF resorption (stuck in 1 chamber)
  • most common congenital anomaly of dogs
  • more commonly, accumulation may be restricted to venitricular system
  • for CSF to reach arachnoid villi from origin in choroid plexus of lateral ventricles, efficient passage through 3 foramina/ducts must be unhindered (interventricular forames, mesencephalic aqueduct, lateral apertures of 4th ventricle)
60
Q

interventricular foramen

A
  • due to large size of opening, obstruction is uncommon
  • causes are generally masses in the vicinity (ipsilateral choroid plexus, foramen thalamic neoplasm)
  • unilateral or bilateral (symmetric or asymmetric)
61
Q

mesencephalic aqueduct

A
  • highly susceptible to alterations, decreasing CSF flow due to small diameter of channel and length
  • hereditary malformations often result in congenital hydrocephalus
  • inflammatory lesions where there is ependymal destruction
  • reparative processes restrict the diameter of the duct (canine parainfluenza, FIP, mass)
62
Q

consequences of hydrocephalus (3)

A
  • hydrostatic edema
  • herniation (cerebellum)
  • atrophy
63
Q

CNS trauma

A
  • generally holds poor prognosis
  • lack of neuron regenerative abilities
  • hemorrhage increases ICP due to fixed volume of cranial vault and inability of CSF to compensate for space occupying lesions
  • local hemorrhage –> vasoconstructive effect on brain vasculature –> infarction
64
Q

concussion

A
  • loss of consciousness following transient deformation of axonal processes (temporary)
  • structural changes not present, reversible
  • when structural changes are present, lesion is a diffuse axonal injury characterized by axonal degeneration and necrosis
65
Q

contusion

A
  • structural changes are present
  • coup: stationary head is struck by moving object –> lesion on same side as trauma
  • contrecoup: moving head strikes a stationary object –> lesion on opposite side of trauma
66
Q

laceration/avulsion

A
  • cutting or tearing of parenchyma; frequently involves fracture of bone encasement of the CNS
  • displacement of bone fracture margins
  • penetrating wound
  • stretching/rupture of optic nerve
  • contusion may have laceration component

Pathology 3 (11 decks)

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