Test 4: 2: neuropath Flashcards

1
Q

order of the ventricular system of the CNS

A
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2
Q

gray matter in the CNS is organized

A

laminae or nuceli

found on the outside of the brain

inside of the spinal cord

made of neuronal cell bodies and dendrites

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3
Q

white matter of the CNS is organized

A

into tracts

conduction of nerve impulse from grey matter(nuclei or laminae)

made of neuronal axons surrounded by myelin

on inside of brain, outside of spinal cord

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4
Q

nissel substance in the neuron is made from

A

rough ER

where neurotransmitters are being processed into vesicles

golgi

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5
Q

what makes up grey matter

A

neuronal cell bodies
dendrites
glial cells

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6
Q

what makes up white matter

A

axons
axon terminals/synaptic end bulbs

used for conduction of impulse

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7
Q

three type of CNS glial cells

A

astrocytes
microglia
oligodendrocytes

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8
Q

astrocytes maintain —, regulate —, — synapses and can respond to injury

A

blood brain barrier
nutrients
insulate

astrocytosis/gliosis

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9
Q

microglia are the resident — of the CNS, help regulate —

A

macrophage- phagocytosis and antigen presenting

neuron function

microgliosis/gliosis

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10
Q

oligodendrocytes make —, one cell insulates —, can respond to myelin injury by —

A

myelin

one cell- multiple neurons

OPC regeneration

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11
Q

schwann vs oligodendrocytes

A

many schwann one neuron

one oligo= many neurons

makes myelin

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12
Q

— cells make CSF

A

chroid plexus cells

Epithelial-endothelial
border (Blood CSF Barrier)

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13
Q

— cells line the ventricles and move CSF

A

ependymal cells

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14
Q

pachymeniges are the —

A

dura mater

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15
Q

leptomeninges are the —

A

arachnoid mater
subarachnoid space
pia mater

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16
Q

3 components of the blood brain barrier

A

Specialized vascular endothelial cells

Tight junctions and unique basement membranes

Astrocyte foot processes

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17
Q

some functions of the blood brain barrier

A

Protects the brain from pathogens and xenobiotics

Regulates diffusion of hormones and cytokines

Contributes to sustain the delicate CNS homeostasis

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18
Q

2 components of the blood meningeal barrier

A

Specialized vascular endothelial cells

Tight junctions and basement membrane

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19
Q

function of the blood meningeal barrier

A

Same properties as BBB but less restrictive and promote immune responses during injury/infection

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20
Q

3 components of the blood CSF barrier

A

Choroid plexus epithelial cells with tight junctions

Vessels in choroidal stroma are fenestrated

Arachnoid membrane

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21
Q

function of the blood CSF barrier

A

Regulates movement of agents from blood to CSF

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22
Q
A
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23
Q

upper vs lower motor neuron

A

upper do not leave CNS (come from the motor cortex or nuceli in the brain stem and will synapse will lower motor neuron in the spinal cord, activates skeletal muscle

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24
Q

what caused this

A

thiamine deficiency in carnivore

neuronal necrosis
posterior colliculi neuronal cell bodies

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25
Q

what caused this

A

copper deficiency

oligodendroglia dysfunction
diffuse cerebral white mater loss

leukoencephalomalacia: necrosis of the white matter of the brain

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26
Q

another name for necrosis in brain

A

malacia

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27
Q

what type of neoplasm

A

meningioma

cause atrophy of the brain

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28
Q

encephalomalacia

A

encephalomalacia: necrosis of the brain

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29
Q

polioencephalomalacia

A

necrosis of the grey matter of the brain

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30
Q

leukoencephalomalacia:

A

necrosis of the white matter of the brain

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31
Q

myelomalacia

A

necrosis of the spinal cord

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32
Q

poliomyelomalacia

A

necrosis of the grey matter of the spinal cord

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33
Q

leukomyelomalacia

A

leukomyelomalacia: necrosis of the white matter of the spinal cord

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34
Q

thiamine deficiency in ruminants will do what to the brain

A

Polioencephalomalacia of ruminants: necrosis of the grey matter of the brain

laminar cortical necrosis

Clinical signs: facial twitching, grinding teeth, opisthotonos, convulsions, coma

Causes: thiamine deficiency, high sulfur diets, water deprivation

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35
Q
A

Polioencephalomalacia of ruminants-necrosis of the grey matter of the brain

  • Laminar cortical necrosis
  • Clinical signs: facial twitching, grinding teeth, opisthotonos, convulsions, coma
  • Causes: thiamine deficiency, high sulfur diets, water deprivation
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36
Q

what can cause ventricular dilation (hydrocephalus)

A

Excessive formation of CSF

Obstruction of CSF flow within ventricular system or subarachnoid space

Lack of resorption

Focal or diffuse loss of parenchyma → ventricles expand and CSF fills the space
( hydrocephalus ex-vacuo)

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37
Q
A

hydrocephalus (ventricular dilation)

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38
Q

what causes this

A

cerebellar herniation with compression of brainstem breathing centers leading to death

hemorrhage or edema or tumor can cause this

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39
Q

what happens during neuronal degeneration

normal on top
A

chromatolysis
peripheralization of nucelus
neuronal swelling

increased glial cells

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40
Q

what happen to neurons during acute neuronal necorsis

A

shrunken
angular
pink (hypereosion)

increased glial cells

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41
Q

what happens during degeneration of axons

A

swelling and spheroid formation

digestion chambers (phagocytosis of axon debris)

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42
Q

what disease

A

neuronal ceroid lipofuscinosis

Accumulation of lipofuscin (oxidation of fatty acids)

  • Likely mitochondrial defect (not lysosomal defect)

storage disease

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43
Q

what disease in the brain that causes neuronal vacuolization

A

Transmissible spongiform encephalopathies

(mad cow= bovine spongiform encephalopathy)

Accumulation of misfolded prion proteins (PrP)

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44
Q

what causes this neuronal vacuolization

A

Hepatic encephalopathy

Ammonia toxicity: changes in transport of amino acids and electrolytes into neurons
disrupting function and causing cytoxic/intracellular edema

Astrocytosis (Type II, aka Alzheimer’s type II – arranged in pairs and small clusters)

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45
Q

What are some things that cause necrosis of neurons

A

ischemia, hypoglycemia, seizures, viral infection, or toxins

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46
Q

hypertrophy and hyperplasia of astrocytes is called

A

astrocytosis

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47
Q

astrocytes can respond to injury by laying down —

A

astrocytic fibers
glial scars

(fibrosis like)

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48
Q

Neuronophagia

A

glial nodules

glial cells surround dying neuron

accumulation of mononuclear cells, oligodendrocytes,
microglia, and neutrophils or astrocytes, around or at the site of a neuronal cell body

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49
Q

what common infection causes secondary demyelination

A

canine distemper

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50
Q

why are primary demyelination rare

A

deadly

Leukodystrophies (genetic enzyme defects; rare)

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51
Q

what is happening

A

demyelination (white mater)

(luxol-fast blue stain)
Caused by damage to the oligodendrocytes (CNS) or Schwann cells (PNS)
Remyelination is very poor in the CNS, but usually successful in the PNS

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52
Q

what neural tube defect

A

spina bifida

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53
Q

what neural tube defect

A

meningeocele

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54
Q

Agyria (lissencephaly)

A

Complete lack of the normal number and thickness of
cerebral hemispheric gyri

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55
Q

similar to Chiari type I malformation in people

A

Caudal occipital malformation (COMS)

common in Small breed dogs (Cavalier King Charles Spaniels)

Congenital malformation of caudal occipital region of skull → overcrowding of caudal fossa →
compression of the brainstem and cerebellum at the level of the foramen magnum (arrowhead)
Syringomyelia: accumulation of fluid within the spinal cord (aka syrinx) (arrow)

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56
Q

Syringomyelia:

A

accumulation of fluid within the spinal cord (aka syrinx)

can be caused by Caudal occipital malformation (COMS)

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57
Q

what went wrong?

c

A

cerebellar hypoplasia

congenital defect
or
Viral: Feline panleukopenia virus, bovine viral diarrhea virus, border disease virus, and classical swine fever virus.

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58
Q

what virus can cause cerebellar hypoplasia

A

Feline panleukopenia virus, bovine viral diarrhea virus, border disease virus, and classical swine fever virus.

59
Q

brain= what is this showing

A

cerebellar hypoplasia

loss of purkinje and granular cells

caused by genetic or viral ( feline panleukopenia virus, bovine viral diarrhea virus, border disease virus, and classical swine fever virus.

60
Q

cerebellar abiotrophy is caused by —

A

genetic or idiopathic

born normal then losses purkinje cells and granular cells

accelerated degeneration

61
Q

cerebellar abiotrophy vs cerebellar hypoplasia

A

both are loss of purkinje and granular cells in the brain

hypoplasia: caused by virus- born abnormal

abiotrophy: unknown cause- born normal then accelerated degeneration

62
Q

atherosclerosis in animals is related to —

A

hypothyroidism and DM

Mini Schnauzers predisposed

63
Q

Feline ischemic myelopathy and encephalopathy is associated with

A

Hypertension, Hypertrophic cardiomyopathy, Chronic renal failure

ventral spinal artery most common

64
Q

Fibrocartilaginous embolism (FCE) is caused by

A

Intervertebral disc emboli (fibrocartilaginous emboli) → occlusion of small blood vessels → infarct → necrosis (myelomalacia) → Macrophages remove necrotic debris

history: dogs very active then acute onset of disuse of back legs

65
Q
A

vascular anomalies

Hemangiomas, arteriovenous malformations

benign but can rupture and squish things around it

66
Q

intervertebral discs

A

Nucleus pulposus (NP): central
gelatinous proteoglycan-rich substance

Annulus fibrosus (AF):
surrounding concentric fibrous lamellae comprised of collagen and elastin

67
Q

hansen type I herniation

A

Extrusion of nucleus pulposus material into the
spinal canal, resulting in spinal cord compression

acute causes full paralysis

68
Q

hansen type II herniation

A

Protrusion of the annulus fibrosus into the spinal
canal, resulting in spinal cord compression

69
Q

patients with IVDD usually have hansen type —. Will often present with impaired motor function or complete loss of voluntary movement in both hind limbs (—)

A

type 1

paraplegia

acute onset

small dogs (Dachshund, Lhasa Apso, Shih Tzu)

70
Q

IVDD caused by hansen type — leads to onset of symptoms that is slow and progressive

A

type II

paraparesis→ paraplegia

71
Q

storage disease
Cellular catabolism: degradation of macromolecules
in vesicular compartments (i.e. —) to smaller molecules to be reused or excreted (aka: —)

A

lysosomes

autophagy

72
Q

storage disease is caused by problem with enzymes caused by

A

genetic mutation resulting in dysfunctional enzyme

ingestion of substance that interferes with enzyme function (swainsonine- plant with alkaloid enzyme inhibitor)

73
Q

Degenerative Myelopathy occurs in what type of dogs

A

german shepherd
corgi

74
Q

Degenerative Myelopathy causes —

A

Late onset (≥7 years), progressive Weakness and ataxia due to spinal cord lesions

Spheroids and demyelination in dorsal funiculi

  • SOD1 mutation has been found in corgis (and other breeds)
75
Q

corgis with SOD1 mutation get —

A

degenerative myelopathy

76
Q
A

neuroaxonal dystrophy

77
Q

neuroaxonal dystrophy affects — dogs and — horses

A

Rottweilers, Papillons, Chihuahuas, Collie sheepdogs,
Jack Russell Terriers

Quarterhorse (and others: Morgans, Appaloosa,
Lusitano, Haflinger…)

78
Q

what part of the CNS does neuroaxonal dystrophy attack

A

Brainstem (cuneate and gracilis nuclei),
Thoracic spinal cord nuclei

forms spheroids

leads to intermittent weakness of hind legs

79
Q

encephalitis

A

inflammation of the brain

80
Q

polioencephalitis:

A

inflammation of the grey matter of the brain

81
Q

leukoencephalitis:

A

inflammation of the white matter of the brain

82
Q

myelitis:

A

inflammation of the spinal cord

83
Q

4 ways for infection to get into nervous system

A

blood
local extension
direct penetration
retrograde axonal flow (listeria, rabies, herpes)

84
Q

rabies is caused by —

A

Lyssavirus (Rhabdoviridae)

85
Q

rabies cellular tropsim is for —

A

neurons

uses retrograde axonal flow to travel to brain through nerves

86
Q

how to test for rabies

A

Direct fluorescent antibody test (dFA, IF)

87
Q

rabies histo will show perivascular —, — inclusion bodies in the neurons

A

cuffing

intracytoplasmic (negri bodies)

88
Q

canine distemper virus is caused by

A

Morbillivirus (Paramyxoviridae)

89
Q

how to transmit canine distemper

A

respiratory secretions

90
Q

what cells do canine distemper attack

A

epithelium(conjunctiva), lymphoid (macrophages and lymphocytes)

91
Q

clinical signs of canine distemper virus

A

respiratory: Conjunctivitis, rhinitis, and bronchopneumonia
GI:Diarrhea and vomiting
CNS: nervous, Seizures, cerebellar or vestibular ataxia

92
Q

histo of canine distemper virus shows — inclusion bodies in — cells

A

Intracytoplasmic AND intranuclear

astrocytes, neurons, choroid plexus epithelium

93
Q

what happens to the white matter with canine distemper virus

A

demyelination of the cerebellum, midbrain, brainstem, optic nerves, spinal cord

leukoencephalitis

94
Q

canine distemper does what to gray matter

A

Neuronal necrosis with gliosis and perivascular cuffing of lymphocytes and macrophages

95
Q

histo of arbovirus such as EEE

A

Pe rivascular cuffing by lymphocytes and plasma cells And neutrophils!

with glial nodules (neuronophagia)

96
Q

caprine arthritis and encephalitis virus is spread by

A

direct contact

through milk leading to persistent infection

97
Q

what cells does caprine arthritis and encephalitis virus attack

A

macrophages

98
Q

clinical signs of caprine arthritis and encephalitis virus in young goats

A

Nervous system disease = hind limb lameness and ataxia with
paresis that progresses over several weeks to paralysis
* Usually fatal

99
Q

clinical signs of caprine arthritis and encephalitis virus in adult goats

A

arthritis
pneumonia
encephalomyelitis

100
Q

caprine arthritis and encephalitis virus histo shows

A

Perivascular cuffing by lymphocytes and macrophages with malacia particularly in the white matter of the subependymal cerebrum, brainstem, and beneath the pia in spinal cord

101
Q

FIP is caused by —

A

enteric coronavirus is mutated inside a cat to feline infectious peritonitis virus

102
Q

how is FIP spread

A

fecal oral

most common in young cats

103
Q

FIP attacks what cell types

A

intestinal epithelium and macrophages

104
Q

clinical signs of FIP

A

varied (aggression, rage, hiding/withdrawal), convulsive disorders, nystagmus, head tilt or circling

Pathological findings: Hydrocephalus, granulomatous meningitis, choroid plexitis, ependymitis, and vasculitis (immune complex)

105
Q

— is a DNA virus that causes vasculitis leading to thrombosis in horses

A

Equine herpesviral myeloencephalopathy

Equine herpesvirus-1 and 4 (Alphaherpesvirinae)

106
Q

what type of cells do equine herpes attack

A

epithelium, endothelium and neurons

lives forever in neurons- waiting

107
Q

equine herpesviral myeloencephalopathy is caused by vasculitis with — leading to secondary ischemia and axonal —.

A

thrombosis, edema and hemorrhage

spheroids

108
Q

most common cause of bacterial meningitis

A

E. coli, Streptococccus spp.
* Plus Pasteurella, Salmonella in young large animals

109
Q

pachymeningitis

A

Inflammation of dura mater

pachymeninges is another name for dura mater

110
Q

how does listeria cause encephalitis

A

large animal eats food containimated with Listeria monocytogenes

Break in oral mucosa → invasion of Listeria locally and into trigeminal nerves → travel retrograde up axon to the brainstem→ suppurative encephalitis with microabscesses in the brainstem

can cause abortion and mastitis

111
Q

Infectious thrombotic meningoencephalitis (ITME) is caused by —

A

Histophilus somni
Cattle

112
Q

how does Histophilus somni in cattle cause Infectious thrombotic meningoencephalitis (ITME)

A

toxin from bacteria causes pneumonia that leads to vasculitis then thrombosis and hemorrhage

grossly causing multifocal random hemorrhage

113
Q

cat brain

A

Cryptococcus neoformans (and C. gatii)

yeast

can infect dogs,cats and horses

causes suppurative to granulomatous meningoencephalitis with large areas of necrosis (“pseudocysts”) that contain numerous yeast

114
Q

Cryptococcus neoformans (and C. gatii) will cause the formation of — meningoencephalitis with areas of —

A

suppurative to granulomatous

necrosis (“pseudocysts”) that contain numerous yeast

115
Q

— is an good example of local extension from the nose into the brain in cats

A

Cryptococcus neoformans (and C. gatii)

causes nose deformaty and then Suppurative to granulomatous meningoencephalitis with large areas of necrosis (“pseudocysts”) that contain numerous yeast

116
Q

three protozoa that cause infections in the CNS

A

Toxoplasma gondii
* Can infect nearly any mammalian species
* Definitive host is cat

Neospora caninum
* Disease in dogs, cattle, deer
* Definitive host is dog

Sarcocystis neurona
* Equine Protozoal Myeloencephalitis (EPM)
* Definitive host is opossum, other wildlife

117
Q

Equine Protozoal Myeloencephalitis (EPM)
is causes by

A

Sarcocystis neurona

a protozoa, definitive host opossum

118
Q

protozoal infection of the brain will present as —

A

organism moving through tissue will cause necrosis

Multifocal granulomatous, (eosinophilic), necrotizing encephalitis

can rarely see the organism surrounded by glial cells

119
Q

EPM can look similar to

A

equine herpes virus

weakness and acute ataxia

EPM is caused by sarcocystic neurona and has no long lasting infection

120
Q

three types of meningoencephalomyelitis of unknown origin (MUO)

A

Granulomatous meningoencephalomyelitis (GME)- any breed, caudal CNS- brainstem and spinal cord

necrotizing meningoencephalomyelitis (NME)- small dogs, cerebral

necrotizing encephalitis (NE)- small dogs, cerebral

121
Q

Bromethalin toxicity attacks the —

A

attacks electron transport chain

Uncouples oxidative phosphorylation in mitochondria

leads to edema

Decreased ATP synthesis and dysfunction of ATP-dependent Na/K pump → accumulation of Na (and water) in cells → cytotoxic cerebral edema → cerebral edema, including intramyelinic edema, myelin splitting, and axonal swelling (white matter vacuolation)

type of nonanticoagulant rodenticide

122
Q

Bromethalin toxicity will cause — in the brain

A

white matter edema

rodent killer that attacks electron transport chain

123
Q

yellowstar thistle toxicity in horses will cause malacia in the — and the —

A

pastures containing Centaurea solstitialis (yellow star thistle) or C. repens (Russian knapweed)

124
Q

— deficiency will lead to malacia of the caudal colliculi or the rostal midbrain/caudal brainstem nuceli and cerebral cortex in carnivores

A

thiamine

in ruminants will attack the grey matter

125
Q

deficiency in — will cause this in lambs and kids

A

copper

swayback

Bilaterally symmetrical cavitation of the cerebral white matter
(congenital)

Wallerian degeneration in
dorsolateral and ventromedial tracts of spinal cord (delayed)

126
Q

— are tumor of meninges

A

meningiomas

most common intracranial tumor in cats and dogs, rare in horses

more common rostrally

most benign Grade 1, grade III very rare

127
Q

meningiomas are most common in

A

Most common intracranial neoplasm in cats and dogs

  • Very rare in horses and ruminants

usually benign but cause compression of brain

128
Q

4 subtypes of meningioma tumors

A

histologically different but behave similarly- benign

129
Q

tumor of gilial cells are

A

Astrocytomas Oligodendrogliomas

short faced breeds some cat, cattle and horses

Grossly well demarcated BUT infiltrative histologically

130
Q

— type of brain cancer is Grossly well demarcated BUT infiltrative
histologically

A

glioma

Astrocytomas Oligodendrogliomas

131
Q

what type of tumor

A

intraventricular tumor

Choroid plexus tumors
* Papilloma or Carcinoma
* Golden retriever predisposed
* Reported sporadically in horses and cattle

132
Q

what type of intraventricular tumor is common in golden retrievers

A

choroid plexus tumor

133
Q

type of intraventricular tumor

A

Ependymoma
* Uncommon tumors in dogs, cats,
horses, cattle

134
Q

name some metastatic neoplasia in brain of dog

A

Hemangiosarcoma, carcinoma, malignant melanoma

135
Q

common metastatic brain cancers of cats

A

Mammary adenocarcinoma, lymphoma

136
Q

paraparetic

A

partial paralysis of the lower limbs.

137
Q

You perform a physical exam and you find dimpling of the skin overlying the lumbar region of the spinal column (image), an easily expressed bladder, absent anal sphincter tone, and analgesia to the skin of the perineum.

Given the signalment of the patient and the location of the lesion, what do you think is the most likely disease process —
, most likely specific type of disease —?

A

congenital

neural tube defect

138
Q

On histologic examination of the spinal cord you see the changes depicted below:

What area of the spinal cord does this represent —?

What characteristic pathologic change to neurons are the arrows pointing to?

A

white matter

axonal swelling (spheroids)

139
Q

What is the pathogenesis of this lesion?

A

Degeneration of the nucleus pulposus, annulus fibrosis and/or dorsal longitudinal ligament —> extrusion or herniation of disc material into spinal canal –> trauma to spinal cord and occlusion of blood vessels –> demyelination –> leukomalacia, hemorrhage (and poliomalacia if severe enough)

140
Q

What is the name of this disease?

A

IVDD
Intervertebral disc disease

141
Q

What serologic test(s) will you submit with the serum sample you collected antemortem, given the nature and distribution of the gross lesions in the spinal cord?

Equine herpes virus 1 and 4

Sarcocytis neurona

Equine Eastern Encephalitis virus

West Nile virus

A

Equine herpes virus 1 and 4

Sarcocytis neurona

142
Q

a six year old thoroughbred gelding presents to you with signs of weakness over the past week that have now progressed to severe ataxia

On histologic examination of the spinal cord you find the changes below:

What etiologic agent is responsible for this disease?

What is the disease called?

A

Sarcocystis neurona

Equine protozoal myeloencephalitis (EPM)

143
Q

What disease process do you suspect this represents?

what neoplasm does this most likely represent?

A

neoplasia

Peripheral nerve sheath tumor

Anatomic location and Gross: Multiple masses arising at the spinal nerve roots

Histology: Slender, fusiform cells arranged in bundles and plexiform nodules with bland oval nuclei.