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22 fall: path > Test 4: 1: skeletal PNS > Flashcards

Test 4: 1: skeletal PNS Flashcards

1
Q

muscle cell make up

A

myofilaments (actin and myosin) form together to make

myofibril, a bunch of myofibrils form together to make

myofiber/muscle cell surrounded by endomysium, many group together to make

fascicles surrounded by perimysium, many to form muscle surround by epimysium

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2
Q

myofibril surrounded by —
Fascicles surrounded by —
muscle surrounded by —

A

endomysium
perimysium
epimysium

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3
Q

— are cells in muscles that cen divide and reform mature myofibers

A

satellite cell

live between in the plasma membrane and the basal lamina

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4
Q

motor unit makes up

A

motor neuron and all of the myofibers(muscle cells) it innervates

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5
Q

Motor neuron releases —from
synaptic vesicles to trigger muscle contraction

A

acetylcholine

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6
Q

what are some blood values that indicate muscle damage

A

Creatinine kinase (CK)
* Lactate dehydrogenase (LDH)
* Aspartate aminotransferase (AST)
* Alanine aminotransferase (ALT)

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7
Q

— is the Loss of myofilaments (actin & myosin) causing the myofibers (muscle
cells) to decrease in size

A

atrophy

decrease in diameter of entire muscle and individual myofibers

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8
Q

3 common causes of atrophy

A

denervation
disuse
malnutrition

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9
Q

denervation is loss of connection with –

A

peripheral nerves

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10
Q

— type of atrophy Leads to patchwork myofiber atrophy

A

denervation

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11
Q

why type of muscle atrophy does not show muscle regeneration?

A

denervation

disuse

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12
Q

common causes of muscle atrophy denervation

A

Wallerian degeneration
* Secondary to trauma to the peripheral nerve

Axonal degeneration

Demyelination (rare)

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13
Q

— cells proliferate at the motor end plate of the denervated fiber to cause reinnervation after wallerian degeneration

A

Schwann cell

caused by collateral sprouting or axon regrowth

hypertrophy with increase in myofibrils

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14
Q

disuse atrophy is due to — mechanical load leading to — atrophy

A

low
diffuse

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15
Q

disuse atrophy activates the — pathways

A

catabolic

-cage rest, cast ect.

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16
Q

what can cause hypertrophy of muscle cells

A

increased workload

compensatory hypertrophy- cells increase in size to make up for the loss of other myofibers

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17
Q

degeneration of muscle fibers cause —

A

multifocal/regional hydropic swelling and fatty changes

reversible but can lead to necrosis

can be caused by toxins

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18
Q
A

muscle necrosis

Loss of striations and hypereosinophilic cytoplasm

Inflammatory cells infiltrate within 24-48 hours
* Macrophages and neutrophils clean up debris

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19
Q

necrosis of muscle cell causes loss of — and — cytoplasm

A

striations

hypereosinophilic

inflammatory cells come in and clean up
satellite cells start regeneration

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20
Q

necrosis with intact basal lamina leads to –

necrosis with destroyed basal lamina lead to —

A

regeneration

fibrosis

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21
Q

— will fuse together to make new myofiber

A

satellite

basal lamina needs to be intact for regeneration to occur

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22
Q

metastatic mineralization is caused by

A

excess Vit D

vit D toxicity
hyperparathyrodism

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23
Q

dystrophic mineralization is caused by

A

necrosis

dead cell can’t control how calcium comes into cell

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24
Q

Fibrodysplasia ossificans progressiva in cats causes —

A

mineralization of skeletal muscle leading to bone formation

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25
Q

X-linked muscular dystrophy is caused by mutation in — that lead to —

A

dystrophin

dystrophin needed to anchor muscle cell membranes to basement membrane

without this, cells undergo necrosis, mineralization and fibrosis

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26
Q

x linked musclar dystrophy attacks — muscle

A

skeletal and cardiac

mutation in anchoring gene dystrophin

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27
Q

what are some symptoms of x linked muscular dystrophy

A

Golden retrievers, Rottweilers
* Diffuse muscle atrophy, splaying of limbs, weakness

x linked in dogs and cats
autosomal recessive in sheep

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28
Q

two possible causes of equine extertional ehabdomyolysis

A

oxidative damage
from vit E or selenium deficiency

Metabolic/electrolyte imbalance (hypokalemia- low potassium)

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29
Q

— in horses is triggered by exercise and leads to acute myofiber necrosis

A

equine extertional rhabdomyolysis

vitE or selenium deficiency

Metabolic/electrolyte imbalance (hypokalemia)

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30
Q

Diet change to one high in — and low in — improves clinical signs in many horses (with or without EPSSM)

Equine Polysaccharide Storage Myopathy

A

fat and fiber

starches and sugars

Some horses with Equine Polysaccharide Storage Myopathy demonstrate exertional rhabdomyolysis

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31
Q

Eq uine Exertional Rhabdomyolysis causes marked elevation in — and —, —uria and acute —

A

CK and AST

myoglobinuria- pigmented urine

renal failure

32
Q

symptoms of equine Exertional Rhabdomyolysis

A

Sudden onset of stiff gait, reluctance to move, pain and discomfort, +/- swelling of affected muscles

  • Not always associated with exhaustive exercis

Affected muscles: gluteal, femoral, and lumbar
groups

33
Q

difference between histo of Equine Exertional Rhabdomyolysis
and Equine Polysaccharide Storage Myopathy

A

exertional- necrosis

poly- degeneration of myofibers

34
Q

some horses with Equine Polysaccharide Storage Myopathy have a mutation in

A

skeletal muscle
glycogen synthase 1 (GYS1)

35
Q

what kind of stain for Equine Polysaccharide Storage Myopathy

A

PAS
makes polysaccharides dark red

36
Q

masticatory myositis effects what kind of dogs

A

Young large breed dogs predisposed (German
shepherds, Rottweilers)

37
Q

Masticatory myositis is caused by autoantibodies to

A

Type 2M
myosin isotype and myositigen (myosin-
binding protein)

38
Q

masticatory myositis attacks what muscles

A

muscles used to chew

(masseter, temporal, and
pterygoid)

caused by autoantibodies to Type 2M myosin

autoimmune

39
Q

what do you see on histo of masticatory myositis

A

Multifocal, polyphasic necrosis with inflammation
* Lymphocytic and eosinophilic
inflammation

autoimmune
autoantibodies to Type 2M myosin isotype

40
Q

what breed of dogs get polymyositis

A

Adult dogs of various breeds
* Young Newfoundlands and Boxers

autoimmune

Affected dogs do not have antibodies to type 2M myosin
* BUT serum autoantibodies bind to unidentified sarcolemmal antigen

41
Q

symptoms of polymyositis of dogs

A

Variable clinical signs depending on muscles affected
* Overall muscle weakness, stiff gate, muscle atrophy, regurgitation, +/- pain
* Paraneoplastic syndrome with thymoma

unknown autoimmune disorder- NOT type 2M myosin (Masticatory myositis)

42
Q
A

Extraocular muscle myositis

RARE

not painful

effects young female golden retrievers

unknown cause

histo- Multifocal polyphasic necrosis with lymphocytic inflammation of the extraocular rectus and oblique muscles

autoimmune

43
Q

— effects the extraocular rectus and oblique muscles of young female golden retrievers

A

Extraocular muscle myositis

rare, unknown cause

autoimmune

44
Q

Immune mediated myositis of horses is associated with — bacteria

A

Streptococcus equi– associated purpura
hemorrhagica

immune response to immune complexes of IgA and strep M proteins

cause hemorrhagic necrosis of muscle due to vascular injury

45
Q

blood work of immune mediated myositis of horses will show

A

Immune-complexes of IgA and
streptococcal M protein

Markedly increased CK and AST and muscle weakness and pain

caused by immune response to strep equi infection

46
Q

histo of immune mediated myosistis of horses will —

A

Vasculitis and fibrinoid necrosis of vascular walls with hemorrhagic infarcts within affected muscles

  • Inflammatory infiltrates not seen within muscle

caused by immune response to immune complexes of IgA and strep equi M protein

47
Q

benign or malignant
rhabdomyoma

A

benign
rare
common in larynx of young dogs

can cause respiratory distress depending on position of tumor

48
Q

embryonal, botryoid and alveolar rhabdomyosarcoma occur in — dogs and are found where in the body

A

young

NOT extremities- bladder, tongue and face

49
Q
A

infiltrative lipoma

benign but can be difficult to remove

50
Q

axons are surrounded by —
fascicles are surrounded by
— surrounds nerves

A

endoneurium
perineurium
epineurium (contiguous with the dura mater)

51
Q

— cells myelinates axons of nerves

A

schwann cells

also help with regeneration

52
Q

endoneurial fibroblasts make — and act as —

A

collagen
phagocytes (during axon damage)

53
Q

the blood nerve barrier is made of

A

Tight junctions of endoneurial blood vessels

Perineurium (surrounds nerve fasicle and contains blood vessels)

  • Regulated movement of substances from blood to endonerium

NOT very strong barrier

54
Q
A

wallerian degeneration

55
Q

what causes wallerian degeneration

A

trauma or compression of axon leading to loss of distal segment

leads to build up of proteins, debris and neurofilamatent and chromatolysis of the neural cell body, as well as spheroid formation

chromatolysis can be resolved if axon reattaches/fixes itslef

56
Q

swelling of degenerating axon is called

A

spheroid

Anterograde and retrograde axonal flow is halted → accumulations of neurofilaments, mitochondria and debris

happens with wallerian degeneration

57
Q

if endoneurial sheath is intact what will happen to axon after wallerian degeneration

A

Axonal sprouting and segmental
remyelination of the proximal axonal spheroid stump by Schwann cells

(regrows and reestablishes neuromuscular junction)

58
Q

successful regeneration on the PNS depends on

A
  • Intact endoneurium
  • Site of injury: more distal lesions (farther from cell body)
    = better recovery
  • Distance between severed ends: closer = better recovery
  • Amount of damage and debris at injury site: less injury and debris = better recovery
59
Q

The time course of Wallerian degeneration varies in the peripheral (—) and central (—) nervous systems.

A

faster
slower

60
Q

some causes of axonal degeneration

A

Inherited: Degenerative myelopathy

Metabolic: Peripheral neuropathy associated with diabetes (hypothyroidism,
hypoglycemia, insulinoma)
* Diabetes: distal axonopathy with degeneration/demyelination & regeneration/remyelination likely
due to impairment of axonal transport secondary to decreased glucose

Toxic: plant toxins, metals (lead, arsenic, mercury), organophosphates
* Karwinol Toxin from fruit seeds of coyotillo shrub (Karwinskia humboldtiana)
* Small ruminants in southwestern US
* Induces direct axonal injury and subsequent demyelination in peripheral axons (and CNS, too)
* Subsequent denervation atrophy of skeletal muscle

61
Q

— is Metabolic derangement of the entire neuron

A

axonal degeneration

myelin sheath breaks down at same time (looks similar to wallerian degeneration)

caused by inherited, metabolic or toxic diseases

62
Q

segmental demyelination if usually caused by

A

toxin

can be inflammatory, or compression

loss of myelin sheath leaving an intact bare axon

63
Q

Polyneuritis equi (Cauda Equina Syndrome) is caused by

A

unknown but maybe immune mediated

64
Q

symptoms of Polyneuritis equi (Cauda Equina Syndrome)

A

ataxia, pain, dropped tail, urinary incontinence, fecal retention and muscle loss
* Nerve roots are thickened and fusiform and usually discolored yellow
* Granulomatous inflammation and abundant fibrosis

65
Q

histo of cauda equina syndrome (polyneuritis equi)

A

inflammation inside and around nerves with areas of fibrosis

Nodular aggregates of granulomatous inflammation
surrounding nerves at the nerve roots

Expansion of perineurium and epineurium by fibrosis

66
Q

aquired myasthenia gravis is caused by

A

Auto-antibodies to acetylcoline receptors and blocks function

prevents contraction of muscle

treat with anti-acetylcholinesterase therapy (flood area with AcH)

67
Q

how to treat acquired myasthenia gravis

A

anti-acetylcholinesterase therapy

(flood area with AcH by preventing enzyme that breaks down AcH)

68
Q

congenital myasthenia gravis is caused by — in — dogs

A

decreased number of ACh receptors

Jack Russell terriers, springer spaniels, smooth haired fox terriers

treat will anti-cholinesterase therapy

69
Q

how does botulism work

A

Clostridium botulinum

releases toxin that enters neuron and prevents release of acetylcholine leading to flaccid paralysis

70
Q

how does tetanus work

A

Clostridium tetani

Tetanospasmin travels
retrograde along peripheral
nerves and preferentially binds
to inhibitory interneurons

prevents release of inhibitory neurotransmitter leading to spastic/rigid paralysis

71
Q

what causes tetanus

A

Clostridium tetani

  • Ubiquitous G+ spore-forming
    anaerobe in soil
72
Q

— causes flaccid paralysis

— causes rigid paralysis

A

botulism

tetanus

73
Q
A

Equine Laryngeal hemiplegia

Progressive degeneration of axons of left recurrent laryngeal nerve

leads to airway obstruction and stridor

74
Q

some causes of Equine Laryngeal hemiplegia

A

Trauma to the nerve

Extension of inflammation from the guttural pouches → transection of axon

Congenital axonal transport defect?

degeneration of axons of left recurrent
laryngeal nerve

75
Q

peripheral nerve sheath tumors originate from

A

Schwann cells, fibroblasts, or perineural cells

Schwannomas (Schwann cells) - most common in dog (also cat, horse, cattle)
Perineuriomas (perineurial cells) – reported in cattle
Neurofibroma (Schwann cells and perineurial fibroblasts) – reported in dogs

76
Q

— tumors have no widely accepted grading scheme to distinguish benign from malignant

A

(Peripheral) Nerve sheath tumors

Malignant tumors = more anaplastic features, high mitotic index, presence of necrosis, aggressive local growth and invasion into adjacent normal tissue, and potential for metastasis

22 fall: path (46 decks)

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