Lecture 32: Nervous 1 Flashcards

1
Q

What are the parts of a neuron

A

cell body

axon

dendrite

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2
Q

What are the 3 main functions of a neuron

A

transmit electrical and chemical signals

regulate impulses

axonal transport

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3
Q

What cell type makes up most of the CNS

A

astrocytes

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4
Q

What are the 3 functions of astrocytes

A

regulation

repair

form barrier

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5
Q

What is the glia limitans

A

The foot processes of astrocytes

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6
Q

What are microglia

A

CNS immune cells

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7
Q

What is the function of oligodendrocytes

A

make CNS myelin

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8
Q

What is the functions of the choroid plexus

A

makes CSF

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9
Q

What is the functions of ependymal cells

A

moves CSF through the ventricles

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10
Q

What is the gross appearance and function of CSF

A

clear fluid

protection - absorb shock
transports nutrients and removes waste

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11
Q

What is the pattern of flow of CSF in the CNS

A

lateral ventricle

3rd ventricle

mesencephalic aquaduct

4th ventricle

subarachnoid space

circulates multiple times per day

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12
Q

What are the layers of the meninges

A

dura mater (adhered to periosteum)

subarachnoid space

pia mater (attached to nervous tissue)

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13
Q

What makes up the blood brain barrier? Which is the key element

A

astrocyte foot processes/glia limitans

tight junctions in the endothelium
- this is the key element

blood vessel basement membrane

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14
Q

What are the leptomeninges

A

the arachnoid membrane and the pia mater

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15
Q

What feature of the blood brain barrier is key to its function

A

specialized transport systems in the cells

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16
Q

What features of neurons make them susceptible to injury

A

they have low glucose stores

very susceptible to free radicals

high metabolic rate
- they will die fast

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17
Q

Order, neurons, endothelial cells, and support cells in order of susceptibility to injury

A

high
neuron

support cell

endothelial cell
low

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18
Q

Describe the regeneration capacity of neurons

A

neurons/axons in the CNS have no ability to regenerate
- injury will result in neuro deficit/paralysis

in the PNS there is some ability to regenerate but it requires
- axonal transport
- nerve must be aligned

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19
Q

What is another name for axonal damage

A

wallarian degeneration

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20
Q

What causes wallarian degeneration? What are the gross features

A

many causes
- trauma
- toxin
- compression

reduces axon function and causes axonal swelling and myelin degeneration
- macrophages digest

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21
Q

What is the main mechanism of injury caused by space occupying lesions in the CNS?

A

there is no ability for tissues to expand

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22
Q

What are examples of causes of space occupying lesions in the CNS? What are the clinical consequences?

A

neoplasia
abcess
hemorrhage
hydrocephalus

the clinical effects are dependent on what part of the CNS is affected

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23
Q

How would you describe the ability of the CNS to resist infection

A

poor

if the organism is able to cross the BBB there are few mechanisms to strop it

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24
Q

What cell type facilitates healing in the CNS

A

astrocytes

but they cannot form strong capsules and so they break easily

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25
Q

Describe 2 ways a neuron could die? Why might each occur?

A

apoptosis
- normal proccess
- removing old cells
- can be a feature of disease

necrosis
- multiple cells involved
- will cause inflammation
- it is a response to injury (cerebral ischemia/inflammation/toxin…)

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26
Q

What is the consequence of chronic neuronal loss

A

cerebral cortical atrophy

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27
Q

What is cerebral cortical atrophy? What might cause it?

A

slow and progressive neuronal loss without the presence of inflammation

due to
- aging
- pigment accumulation (ceroid-lipofuscinosis)
- neurodegenerative disease

can occur in any species

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28
Q

What is result of oligodendrocyte damage and what is the consequence?

A

demyelination

causing slower signalling and neurologic signs

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29
Q

What can cause demyelination of oligodendrocytes

A

virus
iscemia
lead toxicity
autoimmune

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30
Q

What is an infarct and what does it look like grossly in the CNS?

A

is it the rapid onset of ischemia
- if slow onset there is compensation with collateral flow

hemorrhagic grey matter
pale/soft white matter

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31
Q

What causes congestive brain swelling? What is the consequence?

A

due to vasodilation
- maybe from trauma

rapid and severe increase in intracranial pressure

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32
Q

What is a subdural hematoma? What does it cause

A

it is focal hemorrhage between the dura and leptomeninges (arachnoid membrane and pia)

causing increase intracranial pressure

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33
Q

What is cytotoxic cerebral edema and what causes it

A

intracellular accumulation of fluid from altered cell metabolism

usually due to ischemia

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34
Q

What is vasogenic cerebral edema and what causes it

A

extracellular fluid accumulation from BBB breakdown

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35
Q

What is hydrostatic cerebral edema and what causes it

A

extracellular fluid accumulation from increased HP

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36
Q

What is hypo-osmotic cerebral edema and what causes it

A

extracellular and intracellular fluid accumulation from reduced OP

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37
Q

What is the gross appearance of cerebral edema

A

flat and swollen gyri and sulci

there can be herniation of the vermis of the cerebellum through the foramen magnum

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38
Q

List the 4 main portals of entry into the CNS

A

direct extension (ear/nasal/osteomyelitis)

hematogenous (septicemia)

leukocyte trafficking

retrograde axonal transport

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39
Q

What type of portal of entry does Strep suis use into the CNS? What are the sequelae?

A

hematogenous

suppurative meningitis
fibrinous peritonitis
interstitial pneumonia

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40
Q

What portal of entry does HPAI use into the CNS? What are the sequelae?

A

leukocyte trafficking

causing meningoencephalitis

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41
Q

What are the defense mechanisms of the CNS

A

skin
meninges
BBB
glia limitans
microglia

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42
Q

How do pathogens enter the BBB

A

they disrupt the BBB

allow other inflammation cells in and also increase tissue compromise

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43
Q

What type of pathogen causes suppurative inflammation

44
Q

What type of pathogen causes granulomatous inflammation

A

fungi
protozoa
soma bacteria

45
Q

What type of pathogen causes lymphoplasmacytic inflammation

A

virus
protozoa

46
Q

What type of pathogen causes eosinophilic inflammation

47
Q

Define encephalo-

48
Q

Define -leuko

A

white matter

49
Q

Define malacia

50
Q

Define -myelo

A

spinal cord

51
Q

Define -meningo

52
Q

Define poliencophalomyelitis

A

inflammation of grey matter in brain and spinal cord

53
Q

Define meningoencephalitis

A

inflammation of meninges and brain

54
Q

What are the portals of entry of bacteria causing a brain abscess

A

direct extension and hematogenous

55
Q

What are the clinical consequences of brain abscesses? What is the mechanism of injury

A

it is location dependent

the mechanism of injury is due to tissue destruction and space occupying damage

result in abnormal mentation
ataxia
head tilt
circling
blind
cardiac and/or resp dysfxn

56
Q

What are the gross lesions of a brain abscess

A

single or multiple

a center of necrosis with a thin capsule
- the capsule can be fibrotic if it is near the meninges

can have herniation of the cerebellum through the foramen magnum

57
Q

Where are brain abscesses located usually and why?

A

usually occur at the grey-white matter interface because there is increased blood flow and the vessels turn horizontally

58
Q

What might cause brain abscesses in small ruminants

59
Q

What brain lesion does Strep equi equi cause and what is its route of entery

A

brain abscess

hematogenous

60
Q

What is the main manifestation of spinal cord/vertebral abscesses

A

discospondyliosis

due to bacterial emboli lodging between vertebrae > they extend and spread to the intervertebral discs causing abscess which compresses the spinal cord

61
Q

What is ependymitits and choroid plexitis

A

inflammation of the ependymal cells and/or choroid plexus

62
Q

What is the route of entry for bacteria causing ependymitis and choroid plexitis

A

hematogenous

direct

enter CSF

63
Q

Whhat are the lesions associated with ependymitis and choroid plexitis

A

purulent CSF

hemorrhage/hyperemia

spread to meninges

hydrocephalus if the flow is obstructed

64
Q

What causes meningitis? Give 2 example. How do they enter

A

bacteria
- e coli
- streptococcus

hematogenous
direct extension
leukocyte trafficking

65
Q

What causes neonatal septicemia? How does it enter the body? How does it spread to CNS

A

bacteria

oral intrauterine
umbilical
post surgical
inhale
failure of passive transfer

spread to CNS hematogenously

66
Q

What are the clinical consequences of neonatal septicemia

A

fibrosuppurative inflammation on serosa

cause
- meningitis
- arthritis
- synovitis
- polyserositis

result in vascular leakage of fibrin

67
Q

What are the gross lesions of neonatal septicemia

A

congestion
hemorrhage
opacity of meninges
fibrin in the ventricles

68
Q

What are the 4 main agents that cause neonatal septicemia in calves

A

e coli
strep
pasturella
mannheimia

69
Q

What are the 3 main agents that cause neonatal septicemia in foals

A

e coli

strep

staph

70
Q

What are the 3 main agents that cause neonatal septicemia in lambs

A

e coli

pasturella

mannheimia

71
Q

What are the 4 main agents that cause neonatal septicemia in pigs

A

haemophilus parasuis

e coli

strep

staph

72
Q

What is the causative agent of glassers disease and what are the clinical manifestations?

A

haemophilus parasuis

finbrinosuppurative polyserositis, polyarthritis, meningitis

= neonatal septicemia

73
Q

What damage does hepes cause to the CNS? What is its mechanism of damage

A

necrosis of neurons and glial cells and vascular endothelium

inflammation is the main mediator of damage

74
Q

How does herpes enter the CNS

A

retrograde axonal transport mainly

also hematogenous and leukocyte trafficking

it remains latent in the trigeminal ganglia and can reactivate

75
Q

What is the causative agent/disease manifestation of herpes in horses, bovine, and pigs

A

horse: EHV1

bovine: malignant cattarhal fever or infections bovine rhinotracheitis

pig: pseudorabies

76
Q

How does rabies enter the body? What does it infect?

A

enter via bite

infects brain and non-nervous tissue like salivary glands synchronously

77
Q

What are the clinical signs of rabies? How do they differ for large animals?

A

aggression
irritable
anorexia
hydrophobia
paralysis

LA: lameness and colic

78
Q

What is the 6 steps of rabies pathogenesis

A

bite and replicate in muscle

enter peripheral nerves

retrograde transport to dorsal root ganglia

enter spinal cord and ascend

enter bran via ascending and descending fibres

spread via cranial nerves to the eyes and salivary glands

79
Q

What are the gross lesions of rabies infection

80
Q

What are the histo lesions of rabies infection

A

non suppurative meningoencephalitis

inclusion bodies

neuronal cell death

81
Q

What sample is needed for rabies diagnosis

A

brain and brainstem (intact)

82
Q

What are 3 main types of fungi that cause CNS disease

A

aspergillus

candida

mucor

83
Q

What is 1 type of algae that causes CNS disease

A

blue-green algae aka prototheca

84
Q

What parts of the body does blastomyces dermatitidis infect

A

skin
lung
bone
sometimes CNS

85
Q

What parts of the body does Coccidioides immitis infect

A

skin
lung
bone
sometimes CNS

86
Q

What parts of the body does Histoplasma capsulatum infect

A

skin
lung
bone
sometimes CNS

from bat feces

87
Q

What parts of the body does cryptococcus neoformans/gatti infect? What species is most affected?

A

cats mainly (also dogs and horses)

has a tropism for the CNS

88
Q

What are the hosts associated with neospora caninum

A

definitive host = canid
intermediate host = herbivores

canids ingest infected tissue of herbivores

89
Q

How does neospora caninum enter the CNS and what kind of lesions does it cause?

A

leukocyte trafficking

causes multifocal necrosis and pyogranulomatous inflammation

90
Q

What is the clinical manifestation of neospora caninum in puppies and horses respectively

A

puppies:
- polymyositis
- myocarditis
- dermatitis

horses
- meningoencephalitis

91
Q

What are the hosts associated with toxoplasma gondii

A

definitive host: felids
intermediate hosts: wide range

92
Q

How does toxoplasma gondii enter the CNS? What is its pathogenesis

A

hematogenous spread

endothelial infection leads to vascultits
- causes hemorrhage and necrosis
- resulting in inflammation

93
Q

What are the clinical consequences of toxoplasma gondii infection in animals in utero and in older animals

A

in utero: cause necrosis in CNS

older: causes inflammation and polyradiculoneuritis

94
Q

What is myasis

A

insect larvae infection

95
Q

What are 3 examples of parasites that can cause myasis

A

oestrus ovis (sheep nasal bot)

hypodermic bovis
- migrate and enter spinal cord or cause inflammation in the spinal cord if anthelminth kill it

cuterebra: rabbits and rodents usually

96
Q

What is the mechanism of damage to the CNS of cestodes (tapeworms)

A

migrate and form cysts causing space occupying damage

97
Q

What animal is most affected by tania multiceps? What form causes the damage? How does it enter the CNS?

A

sheep mainly

the larvae - coenuris cerebralis
- hematogenous spread to the CNS
- encyst and cause space occupying damage

98
Q

Nematodes can cause CNS problems. What is more severe aberrant migration of the nematode or migration in aberrant host?

A

migration in the aberrant host

99
Q

What are the lesions associated with nematode damage

A

linear or serpentine tracts of necrosis and hemorrhage

might see the visible parasite

100
Q

Give 2 examples of nematodes causing CNS problems. What species do they affect?

A

Baylisasceris procyonis - raccoons

angiostrongylus cantonensis - rats

101
Q

What are prions? What type of disease do they cause?

A

proteinaceous infectious particles

transmissible spongiform encephalopathies

102
Q

How are prions transmitted

A

ingestion of CNS material

or CWD is also transmitted via saliva, blood, and urine

103
Q

How do prions enter the CNS

A

leukocyte trafficking

hematogeous

104
Q

What are the lesions associated with prions

A

no gross lesions - no inflammation

they will accumulate in neurons - vacuolate neurons

105
Q

Give 3 examples of prion disease

A

scrapies

BSE

CWD