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425 - sys path > Neuro 1 > Flashcards

Neuro 1 Flashcards

1
Q

what are the 3 classical divisions of the CNS?

A
  1. Sensorimotor division
  2. Autonomic division
  3. Enteric division
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2
Q

What are the 2 areas of nervous tissue in enteric division of PNS? why should we know about them?

A
  1. Myenteric plexus AKA Auerbach’s plexus
  2. Submucous plexus AKA Meissner’s plexus

important to understanding dysautonomias

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3
Q

what part of embryology gives rise to PNS?

A

neural crest

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4
Q

which of ectoderm, mesoderm, and endoderm gives rise to nervous system? what is the exception?

A

ectoderm

microglial cells - come from mesoderm

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5
Q

what cell is responsible for making myelin in the PNS?

A

Schwann cells

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6
Q

what cell is responsible for making myelin in the CNS?

A

oligodendrocytes

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7
Q

what are the 3 ways that nerves can be injured by trauma?

A
  1. transection
  2. compression/crushing
  3. stretching
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8
Q

Describe Wallerian Degeneration.

A

degeneration of the distal component of an injured axon.

the proximal segment dies back to the node of Ranvier, macrophages respond to site of injury, cell body swells b/c of chromatolysis of Nissl substance, myelinating cells guide direction of regenerating axon.

very typical response to axon injury

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9
Q

Why is Wallerian degeneration important in diagnosis?

A

can help you localize where injury occurred histologically

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10
Q

why is Wallerian degeneration important for disease processes?

A

mistakes in process can cause rein nervation of the wrong thing or proliferation of axons w/o reinnervation, which leads to formation of a neurofibroma

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11
Q

What are the clinical signs of equine laryngeal hemiplegia?

A

tall, large breeds, male, 2-7 y/o
paralysis of L side of larynx –> roaring sound during inspiration (esp. w/ exercise)

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12
Q

what is the other name for equine laryngeal hemiplegia?

A

Roarers or recurrent laryngeal neuropathy

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13
Q

what are the gross findings of equine laryngeal hemiplegia?

A

L laryngeal paralysis
neurogenic atrophy of the L dorsal, lateral, and transverse cricoarytenoid muscles

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14
Q

why is the L side of the larynx more affected than the R in equine laryngeal hemiplegia?

A

L recurrent laryngeal nerve is longer than the R

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15
Q

What histo lesion do we have to know for Roarers?

A

Wallerian degeneration of the recurrent laryngeal nerve

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16
Q

what are the causes of roarers?

A
  • direct trauma to nerve
  • extension of inflammation from guttural pouches
  • toxins
  • (inherited)
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17
Q

What dis?

A

equine laryngeal hemiplegia AKA roarers

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18
Q

What is the other name for Colonic Agangliosis?

A

Lethal white foal syndrome

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19
Q

what is the signalment for colonic aganliosis?

A

American paint horses
white foals born to parents with Overo markings.

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20
Q

what are the clinical signs of colonic agangliosis?

A

clinical signs of colic
foals die within a few days of birth
functional obstruction of GIT

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21
Q

what are the gross findings of colonic agangliosis?

A

white foal, lumen of large colon small/narrow, ileum to distal large colon affected

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22
Q

what histo finding do we have to know for colonic agangliosis?

A

lack of myenteric and submucosal ganglia

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23
Q

what are you worried about with this foal?

A

colonic agangliosis AKA lethal white foal syndrome

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24
Q

Diaphragmatic paralysis in camelids:
1. clinical sings?
2. gross lesions?
3. cause?
4. important ddx?

A
  1. young llamas and alpacas, resp distress
  2. none
  3. we dunno
  4. choanal atresia
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25
Q

What are the two types of Myasthenia Gravis? what species are affected?

A

Congenital (less common) and acquired (more common)

dogs (and less commonly cats)

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26
Q

in congenital myasthenia gravis, what is wrong?

A

defect in acetylcholine end plate receptors

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27
Q

in acquired Myasthenia Gravis, what is wrong?

A

immune-mediated antibodies against cholinesterase receptors

–> results in immune complexes of the neuromuscular junction, decreased receptor density

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28
Q

some cases of acquired myasthenia gravis are linked with what?

A

thymic abnormalities

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29
Q

what are the 3 clinical forms of acquired myasthenia gravis?

A
  1. generalized form: weakness of appendicular muscles with exercise, also megaesophagus
  2. localized form: face, esophagus, pharyngeal muscles
  3. fulminating form: rapidly developing and sustained weakness
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30
Q

what type paralysis is seen with acquired myasthenia gravis?

A

flaccid paralysis

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31
Q

what might you see at necropsy for an individual with myasthenia gravis?

A

megaesophagus, thymoma, or hypothyroidism

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32
Q

what secondary condition/cause of death might send animals with myasthenia gravis to necropsy?

A

aspiration pneumonia

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33
Q

what species does cauda equina syndrome affect?

A

primary horses, sometimes dogs

34
Q

what are the clinical signs of Cauda Equina Syndrome?

A

slowly progressive clinical signs related to hind end
1. hypotonia, decreased sensation of the tail, anus, and perineum
2. urinary bladder paresis with sabulous cystitis
3. fecal retention and colic
4. rear limb weakness and atrophy chronically

35
Q

what are the gross lesions of cauda equina syndrome?

A

mild edema and hemorrhage
enlargement of nerves

36
Q

what histo lesions do we have to know for cauda equina syndrome?

A

nodular granulomatous sinflammation
fibrosis

37
Q

what is cauda equina syndrome?

A

neuritis of the cauda equina

38
Q

these are caudal spinal cords from horses. the one on the L is normal, the one on the L has a pathology. The horse that the R one came from displayed signs of colic, fecal retention, urinary bladder paresis, and hypotonia of the hind end. what is the pathology?

A

cauda equina syndrome

39
Q

what is the other name for acute polyradiculoneuritis?

A

Coonhond paralysis

40
Q

what are the clinical signs of a dog with acute polyradiculoneuritis?

A

dog 1-2 wks after being bit by racoon
hyperesthesia, weakens, ataxia
progresses of ascending flaccid paralysis
death from resp paralysis possible

41
Q

what is the cause of acute polyradiculoneuritis?

A

immune mediated primary demyelination with possible microbial trigger

racoon bite

42
Q

what is targeted in acute polyradiculoneuritis?

A

ventral spinal nerve roots and their associated peripheral nerves

43
Q

based on the clinical signs and history of acute polyradiculoneuritis, what other disease should you be worried about?

44
Q

vitamin A deficiency is an indirect cause of what? how?

A

peripheral neuropathy

defective remodelling of membranous bone can result in CNS and PNS abnormalities

45
Q

How does vitamin A deficiency cause blindness in neonatal calves and pigs?

A

causes narrowing of the optic foramina and compression of the optic nerves

46
Q

What does vitamin A deficiency cause in:
1. neonatal calves and pigs?
2. puppies?

A
  1. blindness
  2. deafness
47
Q

what does vitamin B deficiency (riboflavin) cause in chickens?

A

curled-toe paralysis (demyelinating neuropathy)

48
Q

this poor little dude has this lesion. what is one differential for the reason?

A

vitamin B (riboflavin) deficiency

49
Q

what are the clinical signs of Botulism? signalment?

A

signalment: horses, ducks, sometimes cattle

ascending flaccid paralysis (paralysis of diaphragm can cause death)
loss of tongue tone (good to look for)

50
Q

what is the cause of botulism?

A

Clostridium botulinum
Type A, B, or C in NAm

51
Q

briefly describe Clostridium botulinum

A

gram positive, spore forming, anaerobic bacteria

52
Q

describe how botulism is different in foals vs adult horses

A

foals ingest it, gets through gastric ulcers
adults may ingest or less commonly get wound infection

53
Q

tell me the pathogenesis of botulism

A
  1. toxin enters blood and moves to the neuromuscular junction
  2. moves into presynaptic junction and prevents release of acetylcholine
  3. leads to flaccid paralysis
54
Q

why is botulism diagnosis difficult?

A

no gross or histo lesions, it’s a clinical diagnosis
should swab wound/save feed
can culture in rare cases

55
Q

you have this downed cow in the field. note the tongue. what is cause of acute death is top of your ddx list?

56
Q

tell me about botulism in wild ducks

A

there are outbreaks of botulism in wild ducks in the summer and spring

57
Q

what are the clinical signs of tetanus?

A
  1. spastic paralysis and hyperesthesia
  2. prolapse of 3rd eyelid, sawhorse stance, seizing
58
Q

common signalment of tetanus? how to prevent?

A

horses
vaccination! we do that

59
Q

when do you usually see tetanus? what is the incubation period?

A

post-castration
10-14 days

60
Q

what is the cause of tetanus?

A

Clostridium tetani

61
Q

tell me about Clostridium tetani

A

gram positive, spore forming, anaerobic bacteria

62
Q

tell me about the pathogenesis of tetanus

A
  1. wound contaminated by Clostridium tetani
  2. anaerobic environment of wound allows toxin production
  3. toxin binds at local neuromuscular junction or sensory nerve
  4. retrograde axoplasmic flow allows it to move to the CNS where it blocks release of inhibitory neurotransmitters
  5. uncontrolled stimulation of motor nerves
  6. release of spinal motor neurone from inhibitory influences
63
Q

what is the difference b/t tetanus and botulism in the way that it travels through the body?

A

botulism enters the blood
tetanus doesn’t enter the blood

64
Q

why is tetanus diagnosis difficult?

A

no gross or histo lesions (except maybe the wound)
perhaps a hx of castration
can culture from wound in rare cases

65
Q

what is an important ddx for the clinical signs of tetanus?

A

strychnine toxicity

66
Q

Equine Grass Sickness:
1. AKA?
2. gross and histo lesions?

A
  1. equine dysautonomia
  2. no gross, histo = autonomic and enteric ganglia lesions
67
Q

what is the cause of equine grass sickness?

A

consumption of stressed pasture grass with recent rapid growth or sudden onset of cold weather

68
Q

what is stringhalt?

A

pelvic limb neuropathy in horses
a type of neuromuscular gait abnormality

69
Q

what are the clinical signs of stringhalt?

A

exaggerated rapid flexion of one or both hindlimbs

70
Q

Horse keeps doing this. what are you thinking?

A

Stringhalt

71
Q

What is shivers?

A

pelvic limb neuromuscular lameness in tall horses

72
Q

what are the clinical signs of shiverS?

A

difficulty walking backwards
hyperflexed/abducted limbs with tremoring while moving backwards
only visible at walk

73
Q

where is the anatomic location of shivers?

A

cerebellum

74
Q

how are tumors of the PNS grouped together?

A

peripheral nerve sheath tumors or nerve sheath tumors

75
Q

what are the two big categories of peripheral nerve sheath/nerve sheath tumors?

A
  1. tumors that arise from grossly discernible nerves
  2. tumors that arise in the skin and subq – fall under the category of soft tissue sarcomas
76
Q

what are the common locations for benign PNS tumors?

A

spinal nerves, specifically the brachial plexus in dogs
cranial nerves (trigeminal)

77
Q

what are the cells of origin for benign PNS tumors and the tumor names?

A

Schwann cells = Schwannoma
Fibroblasts = neurofibroma
Perineurla cells = perineuroma

78
Q

what species are benign PNS tumors most common in ?

A

dogs and cattle

79
Q

Malignant peripheral nerve sheath tumors occur where?

A

close to spine or cranial nerves

80
Q

Tasmanian Devil Facial Tumor:
1. what is it?
2. transmission?
3. cell of origin?

A
  1. infectious tumor affected Tasmanian devils (no virus assoc.)
  2. fighting/biting
  3. Schwann cell
81
Q

what is the lesion and what is the cell of origin?

A

Tasmanian devil Facial tumor
Schwann cell

425 - sys path (38 decks)

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