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VM742 BOD 3 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

encehpalo

A

brain

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2
Q

myelo

A

spinal cord

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3
Q

polio

A

grey matter

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4
Q

leuko

A

white matter

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5
Q

Why are neurons non-dividing permanent cells?

A

Don’t have centrioles, thus can’t divide

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6
Q

Neuronal regeneration after injury

A

Regeneration as long as cell body intact

Regeneration is better in PNS vs. CNS

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7
Q

Types of glial cells

A

Microglia - resident CNS macrophages

Macroglia - astrocytes (structural), oligodendrocytes (myelinate like schwann cells of PNS)

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8
Q

Anterograde NT movement

A
  • facilitated by kinosin

- away from nucleus toward synapse

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9
Q

Retrograde NT movement

A
  • facilitated by Dynein

- from synapse toward nucleus (e.g. rabies)

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10
Q

White vs. grey matter locations of cerebrum & spinal cord

A

cortex is grey matter (on periphery)

corona radiata is white matter (towards middle)

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11
Q

Histo signs of neuronal damage

A
  • swollen or shrunken (dying) axons
  • chromatolysis, cell body enlargement
  • Ischemic cell change
  • satellitosis (increased glial cells), neuronphagia
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12
Q

Chromatolysis

A

swollen nerve cell body (perikaryon)

w/ loss of nissel substance, displaced nucleus (dispersion)

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13
Q

Ischemic cell change

A

angular neurons w/ clear surrounding spaces (b/c retracting from neuropil)
hypereosinophilic
pyknotic (dark) nuclei
+/- edema

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14
Q

neuropraxia

A

loss of neural function but no accompanying organic lesions

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15
Q

axonotmesis

neurotmesis

A

axonotmesis - axon damaged but myelin sheath is preserved

neurotmesis - entire nerve severed

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16
Q

“wear & tear” pigment

A
  • accumulation of lipofuscin - orange/brown pigment

- inert change occuring w/ aging

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17
Q

intracytoplasmic negri bodies

A

Rabies

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18
Q

Virus with just intranuclear inclusion bodies

A

Herpes

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19
Q

Virus w/ intracytoplasmic and intranuclear inclusion bodies

A 
Canine distemper (morbilivirus)
Paramyxoviruses
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20
Q

Cytoplasmic vacuolization

A

Prion dz

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21
Q

Astrocyte reaction to injury

A

astrocytosis (hyperplasia)
astrogliosis (reactive astrocytes, just processes get enlarged)
gemistocyte - enlarged astrocytes

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22
Q

Oligodendrocyte reaction to injury

A
  • hydropic swelling
  • hypomyelination (myelin is pale, conduction slow)
  • status spongiosus - cavitated myelin
  • May see remyelination or permanent demyelination
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23
Q

Microglia (macrophages) reaction to injury

A

microgliosis (hyperplasia)
microglial nodules (groupings) - perivascular cuffs if around vessel
“gitter cells” - phagocytically active

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24
Q

Schwann cell reaction to injury

A

CNS - wallerian degeneration and/or regeneration

PNS - hypomyelination, demyelination

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25
Q

What happens when the brain swells

A

Swelling –> compression of bv’s –> BBB compromise, rupture –> hemorrhagic stroke (more common)

vessel occlusion –> ischemic stroke

Edema, Herniation

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26
Q

Ischemic stroke

A

thrombus or thromboembolism –> compromise of end arteries (no anastamosis) = entire area of brain loses blood flow, dies

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27
Q

how do electrolytes get into the brain

A

active transport d/t BBB, also affects water regulation

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28
Q

what is the hallmark of cerebrovascular dz

A

sudden loss of neuro function

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29
Q

Atherosclerosis

A

hypothyroid, high dietary fat intake –> hypercholesterolemia –> plaque buildup –> thrombosis, embolism, infarction, ischemic stroke

Cerebral aa. have narrow lumen, yellowish

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30
Q

what type of necrosis happens in the brain

A

liquefactive - b/c majority of components are made of lipids

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31
Q

Grossly, how do you evaluate for brain edema?

A
  • shifted midline
  • hemispheres not symmetrical
  • Gyri more flattened, sulci less deep
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32
Q

Edema in the brain

A

Often d/t trauma

excess fluid accum in CNS parenchyma –> edema

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33
Q

4 different types of edema

A

Vasogenic
Cytotoxic/cellular
Interstitial/hydrostatic
Osmotic

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34
Q

Vasogenic edema

A

most common type, worst type
usually a trauma, mass, inflamm, hemorrhage
bbb compromise or trauma –> vascular injury –> fluid accum EXTRAcellularly in cerebral WHITE matter

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35
Q

Cytotoxic/cellular edema

A

usually less severe, most commonly d/t ischemia & hypoxia
na/k pump failure –> ionic disruption –> INTRAcellular fluid accum in both white AND grey matter

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36
Q

Interstitial/hydrostatic edema

A

increased ventricular pressure –> ependymal barrier breach –> fluid accum in periventricular white matter

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37
Q

Osmotic edema

A

protein loss in blood (via GI, kidney, skin) –> hypoosmolar plasma –> intracellular but some extracellular fluid accum

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38
Q

What types of edema usually result in herniation?

A

vasogenic

cytotoxic

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39
Q

Places the brain can herniate

A
  • cerebellar vermis through foramen magnum
  • through tentoial notch (btwn cerebrum & cerebellum)
  • parahippocampal gyral herniation under falx cerebri
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40
Q

How is trauma to the skull described

A

plane of trauma
mechanism of trauma
where hemorrhage will develop

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41
Q

Planes of trauma

A

axial - head on
angular - to L or R (most common)
rotational - while rolling, multiple places damaged

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42
Q

coup hemorrhage

A

hemorrhage develops at site of impact

e.g. fall and hit head

43
Q

contrecoup hemorrhage

A

hemorrhage develops opposite site of trauma, e.g. blow to head

44
Q

epidural hemorrhage

A

meningeal a. damage = hemorrhage above dura (most external CT layer)

45
Q

cortical hemorrhage

A

hemorrhage in cortex

46
Q

subcortical white matter hemorrhage

A

hemorrhage deeper than cortex

47
Q

subdural hemorrhage

A

hemorrhage btwn dura and leptomeninges (arachnid + pia mater)

48
Q

subarachnoid hemorrhage

A

hemorrhage underneath arachnoid layer

49
Q

deep intracerebral hemorrhage

A

worst kind, deepest hemorrhage

50
Q

concussion

A

temporary loss of consciousness - mental process affected

51
Q

contusion

A

brain bruising, usually assoc’d w/ blood vessel rupture, trauma

52
Q

common fracture when horses rear over backward

A
  • basisphenoid fracture
  • lacerates cerebellar and vertebral aa.
  • hemorrhage dominant lesion, may affect brainstem, can die quickly
53
Q

Hansen type 1 spinal cord trauma

A

rapid annulus rupture –> sudden pain/paresis, maybe death

hemorrhage likely visible

54
Q

Hansen type 2 spinal cord trauma

A
  • more common
  • weakening annulus –> slow bulge –> chronic compression of cord
  • white matter lesion only (wallerian degen of axons)
  • animal has chronic painful back, proprioceptive deficits, decreased pain perception
55
Q

Wallerian degeneration aka secondary demyelination

A
  • white matter lesion
  • axons constricted, myelin breaks down
    macrophages degrade myelin, spaces left are “digestion chambers”
  • axonal damage occurs before myelin degeneration
  • see accum of galactocerebroside & psychosine
  • hansen type II spinal dz, copper in pigs
56
Q

What nervous system components are most sensitive to ischemia? Least?

A
  • neurons, oligodendrocytes (grey matter) - most
  • astrocytes - moderately
  • microglia, b.v. - fairly resistant
57
Q

Dz’s that cause primary focal cerebrovascular dz

A
  • atherosclerosis
  • fibrocartilaginous embolism in spinal cord causing hansen type 1 embolus
  • feline ischemic encephalopathy
58
Q

feline ischemic encephalopathy

A
  • cuterebra larvae migration

- see vessel necrosis, edema, gitter cells on histo

59
Q

DZ’s causing multisystemic cerebrovascular dz

A
  • vascular wall dz
  • intravascular (thombi, emboli)
  • global cardiac ischemia d/t cardiac arrest
60
Q

Viruses causing vascular wall dz

A 
SHV (suid)
IBR
EHV 1 & 5
MCF (malignant catharral)
EVA (EQ viral arteritis)
FIP - pyogranulomatous inflamm around vessels
61
Q

Malacic/nutritional diseases

A

PEM
Salt poisoning
Nigropallidal encephalomalacia
Mycotoxic leukoencephalomalacia (moldy corn)

62
Q

PEM (polioencephalomalacia)

A

softening of deep lamina of cerebrocortical grey matter in cattle, sheep, goats

63
Q

Causes of PEM

A
  • Thiamine deficiency (heat, thiaminases (plants/meat), or diet insufficiency)
  • sulfur/sulfate being reduced by bacteria causing ATP depletion, cell death
64
Q

How does thiamine (B1) deficiency differ in carn vs. rum

A

carn - midbrain/brainstem nuclei dz, usually diet deficiency (caudal colliculi, periventricular nuclei)
rum - cerebrocortical grey matter

65
Q

gross signs of PEM

A
  • swollen, edematous, necrotic areas are discolored yellow, bilateral dz
  • dead grey matter will fluoresce under a Wood’s lamp
66
Q

clin signs of PEM

A

bilateral vestibular dz - animal can’t right self

vs. circling is unilateral dz

67
Q

salt poisoning

A
  • pigs
  • water deprivation + high salt diet –> hypernatremic/hypertonic blood dehydrates brain, slow to equilib
  • water returns, blood becomes hypotonic, dilutes sodium –> cns dehydration, cerebral and osmotic edema
68
Q

clin signs

A

sitting like a doggo, head drawn up

69
Q

Gross lesions of salt poisoning

A

herniation, moderate edema/swelling

70
Q

histo lesions of salt poisoning

A

edema
laminar cortical necrosis
eosinophilic meningoencephalitis

71
Q

nigropallidal encephalomalacia

A

EQ

  • softening of substantia nigrus, globus pallidus –> bilateral caviation
  • prolonged, high % ingestion of yellow star thistle or russian knapweed (often in a dry summer)
72
Q

mycotoxic leukoencephalomalacia (aka moldy corn poisoning)

A

poorly stored corn = fungus growth

mycotoxins –> swelling, softening, hemorrhage of subcortical white matter

73
Q

Things that affect grey matter

A

Thiamine deficiency
Sulfur or lead toxicity
salt poisoning

74
Q

4 Main molecular level insults to the brain

A

Acidosis
Free radical formation
Apoptosis
Excitotoxicity

75
Q

Excitotoxicity

A

overactivation of glutamate receptors –> constant depolarization –> high Ca into cells, excess E –> excess enz activation –> cell structure damage —> neuron damage and death

76
Q

Causes of excitotoxicity

A 
stroke
traumatic brain injury
CNS neurodegenerative dz
hypoglycemia
status epilepticus
77
Q

4 portals of pathogen entry into the CNS

A

Hematogenous - most common
Direct Extension
Leukocyte trafficking (retroviruses)
Retrograde axonal transport (rabies)

78
Q

Examples of hematogenous entry

A 
Thrombotic meningoencephalitis (TME) - bov
Polyserositis - pigs
C. pseudotb - sheep
79
Q

Examples of direct extension entry

A
  • penetrating trauma - mid/inner ear infections, osteomyelitis, sinusitis
  • mycoplasmosis in cows
  • pasteurellosis
80
Q

signs of acute bacterial infection

A

suppurative encephalitis, myelitis, encephalomyelitis

81
Q

signs of chronic bacterial infection

A

caseous necrosis, CT capsule formation

82
Q

Listeriosis/circling dz (L. monocytogenes)

A

sheep, often <3 yo
brain stem lesions (adults - encephalitic form)
head tilt, circling

83
Q

4 forms of Listeriosis

A

abortive
ocular
systemic infection
nervous

84
Q

Histo signs of listeriosis

A

microabscesses
perivascular cuffing
stain purple on gram stain

85
Q

Thrombotic meningoencephalitis (H. somni)

A

birds, bovids

vasculitis AND thrombosis –> vascular necrosis in cerebrum, lungs, heart, larynx

86
Q

Characteristics of viral encephalitis

A

perivascular cuffing, glial nodules
gitter cells, reactive astrocytes
neuronphagia, demyelination
inclusion bodies

87
Q

Signs of Equine encephalitis infection

A

vasculitis, thrombosis
polioencephalomyelitis (grey matter softening of brain and spinal cord)
neutrophilic reaction

88
Q

Signs of fungal encephalitis

A

pyogranulomatous to granulomatous inflamm w/ intrahistiocytic organisms

89
Q

Protozoa that cause neural infection

A

Sarcocystis neurona
Neospora caninum
Toxoplasma gondii

90
Q

Sarcocystis neurona

A

EPMyelitis/myeloencephalitis
opossums - definitive host, EQ - dead end host
non-suppurative asymmetric spinal cord lesions - cervical and lumbar enlargements

91
Q

Neospora caninum

A
  • multisystemic infection –> multifocal infarctions, abortion
  • brain, heart, kidneys of fetus
  • dogs intermediate hosts, EQ/rum ingest
  • banana shaped organisms
92
Q

Causes of myelinopathies

A

BVDV, border dz/pestiviruses, ovine progressive pneumonia, canine distemper

93
Q

Primary demyelination

A

Removal of normal myelin by macrophages d/t inflammatory response, then axon degenerates

94
Q

Dz’s that cause primary demyelination

A

canine distemper
visna (sheep) & caprine arthritis encephalitis
coonhound paralysis
globoid cell leukodystrophy (krabbes-like dz)

95
Q

GCLD (globoid cell leukodystrophy)

A

abnx storage of galactocerebroside & psychosine in oligodendrocytes & schwann cells –> primary demyelination

96
Q

prosencephaly

A

abnx closure of rostral neural tube = anterior brain doesn’t form

97
Q

porencephaly

A
  • Cyst/cavity in cerebral hemisphere of brain separate from ventricular system
  • Can progress to hydraencephaly
98
Q

Lissencephaly/agyria

A
  • cerebral hemispheres are smooth possibly d/t neurons not migrating during development
  • lab animals & poultry don’t have sulci/gyri normally
99
Q

cerebellar hypoplasia

A

usually viral etiology - in utero infection w/ canine parvo, feline panleuko/parvo, pestiviruses (BVD, CSF)

100
Q

hydrocephalus

A
  • ependymal cell and choroid plexus cell issues = increased fluid accum, increased ICP
  • if in utero, dome calvarium at birth
101
Q

hydrocephalus is usually congenital, what is one acquired cause?

A

intrauterine infection of bluetongue in lambs –> hydraencephaly (end stage of hydrocephalus)

102
Q

Cereoid-lipofuscinosis

A

storage dz causing bronze-colored brain

Tibetan terriers

103
Q

most common brain tumor in cats

A

meningioma, space-occupying & assymetric

high grade = hemorrhage

104
Q

2 metastatic tumors causing brain lesions

A

hemangiosarcoma

mammary carcinoma

VM742 BOD 3 (3 decks)

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