Neuro 1 Flashcards

1
Q

3 ways a nerve can be injured

A

transect compress/crush stretch

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2
Q

Wallerian degeneration is? causes death of what? why does it matter? mistakes lead to?

A

degeneration of distal component of injured axon, causes death of DISTAL segment, important to localize where injury occured, mistakes can lead to neurofibroma (proliferation of axons without rein nervation)

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3
Q

3 examples of trauma to PNS

A

brachial plexus avulsion eg. HBC, facial nerve paralysis horses, obturator nerve paralysis cows

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4
Q

equine laryngeal hemiplasia also known as? which side? which breeds? cause?

A

roarer’s, left, tall large breeds, Wallerian degeneration of recurrent laryngeal nerve (left is longer)

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5
Q

4 causes of roarer’s

A

direct trauma, toxins, inflammation from guttural pouches, or inherited

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6
Q

who gets colonic agangliosis? what is it also known as

A

American paint horses: white foals with over markings. lethal white foal syndrome

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7
Q

signs of colonic agangliosis/lethal white foal syndrome

A

foals die within a few days of birth and the GIT is functionally obstructed

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8
Q

history finding of lethal white foal syndrome

A

lack of myenteric and submucosal ganglia

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9
Q

myasthenia gravis, acquired, is caused by what

A

immune-mediated Abs against cholinesterase receptors

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10
Q

acqueried myasthenia gravis is linked to what

A

in some cases thymic abnormalities

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11
Q

what type of paralysis is seen with acquired myasthenia gravis? what would be seen at necropsy?

A

flaccid; megaesophagus, hypothyroidism, thymoma

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12
Q

three clinical forms of acquired myasthenia graves

A

generalized, localized, fulminating

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13
Q

cauda equine syndrome is observed in two species, one more than other. what are general C/S and 4 specific ones

A

horse and then similar condition in dogs. slowly progressive signs relating to hind end: hypotonia (decreases rear end sensation), urinary bladder paresis, fecal retention and colic, rear limb weakness and atrophy

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14
Q

history lesion with cauda equine syndrome

A

nodular granulomatous inflammation, fibrosis of giant cells

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15
Q

what does acute polyradiculoneuritis progress to? what scary disease could that resemble?

A

ascending flaccid paralysis. rabies (also both CAN get from raccoons)

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16
Q

cause of acute polyradiculineuritis? target?

A

immune mediated primary demyelination which targets ventral spinal nerve roots and their peripheral nerves

17
Q

vitamin A deficiency cause? effect in neonatal calves and pigs? effect in puppies?

A

defective remodelling of membranous bone. neonatal calves and pigs narrows optic foramina, compressing nerves, causing blindness. deafness in puppies

18
Q

botulism important clinical signs (2). cause?

A

ascending FLACCID paralysis and loss of tongue tone. Clostridium botulinum

19
Q

Gram, spore status, metabolism of Clostridium botulinum?

A

Gram positive spore forming anaerobic

20
Q

compare botulism cause in foals vs adult horses

A

foals ingest and enters through gastric ulcers. adults ingest or less commonly get wound infection

21
Q

pathogenesis of botulism

A

toxin enters blood and goes to NMJ. prevents release of ACh at presynaptic junction. causes flaccid paralysis

22
Q

contrast botulism and tetanus. type of paralysis? entry? where does toxin bind? transport? effect on NTs?

A

botulism=ascending flaccid paralysis. enters either ingestion and gastric ulcers (foals) or ingestion/wound infection (adults). from blood to NMJ and block ACh release. tetanus=spastic paralysis. enters wound. toxin binds to NMJ or sensory nerve, retrograde axoplasmic flow to CNS to block inhibitory transmitters.

23
Q

when are outbreaks of botulism seen in wild ducks

A

spring and summer

24
Q

how do you diagnose botulism? tetanus?

A

clinical diagnosis for both

25
Q

clinical signs tetanus? cause? species?

A

SPASTIC paralysis, prolapse 3rd eyelid, sawhorse stance, seizing. Clostridium tetani. horses.

26
Q

Gram status, spore status, metabolism of tetanus causing agent

A

Clostridium botulism: Gram positive, spore forming, anaerobic

27
Q

pathogenesis of tetanus

A

wound contaminated by C tetani (eg. we see 10-14 days after castration). toxin produced binds at NMJ or sensory nerve. retrograde axoplasmic flow, moves to CNS, blocks release of inhibitory NTs, causing uncontrolled stimulation motor nerves

28
Q

where do you see histo lesions with equine grass sickness?

A

autonomic and enteric ganglia (think of how they are eating grass and we know this is a PNS disease, what 2 ganglia)

29
Q

stringhalt affects which limb? which species and/or breed? clinical signs? which direction? which gait? can we localize the lesion?

A

pelvic limb neuropathy, exaggerated flexion of one or both hindlimb. visible for any gait and direction. is in horses. we don’t know the cause and can’t localize the lesion, no.

30
Q

shivers affects which limb? clinical signs? which direction? which gait? which species or breed? can we localize the lesion?

A

like stringhalt, is a pelvic limb neuropathy, but there are more specific signalment and C/S details. this is in TALL horses. difficulty walking BACKWARDS, only visible at WALK, and is localized to cerebellum

31
Q

tumor time! how can we group all the tutors of the PNS (2 names)

A

peripheral nerve sheath tumours or nerve sheath tumours

32
Q

two big categories of PNS tumors are? which are the ones we are learning about?

A

we are learning about tutors of grossly discernible nerves. there are also tumors of skin and subcutis which are under umbrella of soft tissue sarcomas

33
Q

common location of benign tumors of PNS in dogs?

A

spinal nerves

34
Q

cell of origin for benign tumours of PNS? name for them?

A

Schwann cells. Schwannoma

35
Q

common species for benign tumors of PNS? 2 of them

A

cattle and dogs

36
Q

where do malignant peripheral nerve sheath tumours occur

A

close to spine to cranial nerves

37
Q

infectious tumor of Schwann cell origin that we learned about in a specific Oceanic mammal

A

Tasmanian devil facial tumour