Test 4: 1: skeletal PNS Flashcards
muscle cell make up
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
myofibril surrounded by —
Fascicles surrounded by —
muscle surrounded by —
endomysium
perimysium
epimysium
— are cells in muscles that cen divide and reform mature myofibers
satellite cell
live between in the plasma membrane and the basal lamina
motor unit makes up
motor neuron and all of the myofibers(muscle cells) it innervates
Motor neuron releases —from
synaptic vesicles to trigger muscle contraction
acetylcholine
what are some blood values that indicate muscle damage
Creatinine kinase (CK)
* Lactate dehydrogenase (LDH)
* Aspartate aminotransferase (AST)
* Alanine aminotransferase (ALT)
— is the Loss of myofilaments (actin & myosin) causing the myofibers (muscle
cells) to decrease in size
atrophy
decrease in diameter of entire muscle and individual myofibers
3 common causes of atrophy
denervation
disuse
malnutrition
denervation is loss of connection with –
peripheral nerves
— type of atrophy Leads to patchwork myofiber atrophy
denervation
why type of muscle atrophy does not show muscle regeneration?
denervation
disuse
common causes of muscle atrophy denervation
Wallerian degeneration
* Secondary to trauma to the peripheral nerve
Axonal degeneration
Demyelination (rare)
— cells proliferate at the motor end plate of the denervated fiber to cause reinnervation after wallerian degeneration
Schwann cell
caused by collateral sprouting or axon regrowth
hypertrophy with increase in myofibrils
disuse atrophy is due to — mechanical load leading to — atrophy
low
diffuse
disuse atrophy activates the — pathways
catabolic
-cage rest, cast ect.
what can cause hypertrophy of muscle cells
increased workload
compensatory hypertrophy- cells increase in size to make up for the loss of other myofibers
degeneration of muscle fibers cause —
multifocal/regional hydropic swelling and fatty changes
reversible but can lead to necrosis
can be caused by toxins
muscle necrosis
Loss of striations and hypereosinophilic cytoplasm
Inflammatory cells infiltrate within 24-48 hours
* Macrophages and neutrophils clean up debris
necrosis of muscle cell causes loss of — and — cytoplasm
striations
hypereosinophilic
inflammatory cells come in and clean up
satellite cells start regeneration
necrosis with intact basal lamina leads to –
necrosis with destroyed basal lamina lead to —
regeneration
fibrosis
— will fuse together to make new myofiber
satellite
basal lamina needs to be intact for regeneration to occur
metastatic mineralization is caused by
excess Vit D
vit D toxicity
hyperparathyrodism
dystrophic mineralization is caused by
necrosis
dead cell can’t control how calcium comes into cell
Fibrodysplasia ossificans progressiva in cats causes —
mineralization of skeletal muscle leading to bone formation
X-linked muscular dystrophy is caused by mutation in — that lead to —
dystrophin
dystrophin needed to anchor muscle cell membranes to basement membrane
without this, cells undergo necrosis, mineralization and fibrosis
x linked musclar dystrophy attacks — muscle
skeletal and cardiac
mutation in anchoring gene dystrophin
what are some symptoms of x linked muscular dystrophy
Golden retrievers, Rottweilers
* Diffuse muscle atrophy, splaying of limbs, weakness
x linked in dogs and cats
autosomal recessive in sheep
two possible causes of equine extertional ehabdomyolysis
oxidative damage
from vit E or selenium deficiency
Metabolic/electrolyte imbalance (hypokalemia- low potassium)
— in horses is triggered by exercise and leads to acute myofiber necrosis
equine extertional rhabdomyolysis
vitE or selenium deficiency
Metabolic/electrolyte imbalance (hypokalemia)
Diet change to one high in — and low in — improves clinical signs in many horses (with or without EPSSM)
Equine Polysaccharide Storage Myopathy
fat and fiber
starches and sugars
Some horses with Equine Polysaccharide Storage Myopathy demonstrate exertional rhabdomyolysis
Eq uine Exertional Rhabdomyolysis causes marked elevation in — and —, —uria and acute —
CK and AST
myoglobinuria- pigmented urine
renal failure
symptoms of equine Exertional Rhabdomyolysis
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
difference between histo of Equine Exertional Rhabdomyolysis
and Equine Polysaccharide Storage Myopathy
exertional- necrosis
poly- degeneration of myofibers
some horses with Equine Polysaccharide Storage Myopathy have a mutation in
skeletal muscle
glycogen synthase 1 (GYS1)
what kind of stain for Equine Polysaccharide Storage Myopathy
PAS
makes polysaccharides dark red
masticatory myositis effects what kind of dogs
Young large breed dogs predisposed (German
shepherds, Rottweilers)
Masticatory myositis is caused by autoantibodies to
Type 2M
myosin isotype and myositigen (myosin-
binding protein)
masticatory myositis attacks what muscles
muscles used to chew
(masseter, temporal, and
pterygoid)
caused by autoantibodies to Type 2M myosin
autoimmune
what do you see on histo of masticatory myositis
Multifocal, polyphasic necrosis with inflammation
* Lymphocytic and eosinophilic
inflammation
autoimmune
autoantibodies to Type 2M myosin isotype
what breed of dogs get polymyositis
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
symptoms of polymyositis of dogs
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)
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
— effects the extraocular rectus and oblique muscles of young female golden retrievers
Extraocular muscle myositis
rare, unknown cause
autoimmune
Immune mediated myositis of horses is associated with — bacteria
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
blood work of immune mediated myositis of horses will show
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
histo of immune mediated myosistis of horses will —
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
benign or malignant
rhabdomyoma
benign
rare
common in larynx of young dogs
can cause respiratory distress depending on position of tumor
embryonal, botryoid and alveolar rhabdomyosarcoma occur in — dogs and are found where in the body
young
NOT extremities- bladder, tongue and face
infiltrative lipoma
benign but can be difficult to remove
axons are surrounded by —
fascicles are surrounded by
— surrounds nerves
endoneurium
perineurium
epineurium (contiguous with the dura mater)
— cells myelinates axons of nerves
schwann cells
also help with regeneration
endoneurial fibroblasts make — and act as —
collagen
phagocytes (during axon damage)
the blood nerve barrier is made of
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
wallerian degeneration
what causes wallerian degeneration
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
swelling of degenerating axon is called
spheroid
Anterograde and retrograde axonal flow is halted → accumulations of neurofilaments, mitochondria and debris
happens with wallerian degeneration
if endoneurial sheath is intact what will happen to axon after wallerian degeneration
Axonal sprouting and segmental
remyelination of the proximal axonal spheroid stump by Schwann cells
(regrows and reestablishes neuromuscular junction)
successful regeneration on the PNS depends on
- 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
The time course of Wallerian degeneration varies in the peripheral (—) and central (—) nervous systems.
faster
slower
some causes of axonal degeneration
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
— is Metabolic derangement of the entire neuron
axonal degeneration
myelin sheath breaks down at same time (looks similar to wallerian degeneration)
caused by inherited, metabolic or toxic diseases
segmental demyelination if usually caused by
toxin
can be inflammatory, or compression
loss of myelin sheath leaving an intact bare axon
Polyneuritis equi (Cauda Equina Syndrome) is caused by
unknown but maybe immune mediated
symptoms of Polyneuritis equi (Cauda Equina Syndrome)
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
histo of cauda equina syndrome (polyneuritis equi)
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
aquired myasthenia gravis is caused by
Auto-antibodies to acetylcoline receptors and blocks function
prevents contraction of muscle
treat with anti-acetylcholinesterase therapy (flood area with AcH)
how to treat acquired myasthenia gravis
anti-acetylcholinesterase therapy
(flood area with AcH by preventing enzyme that breaks down AcH)
congenital myasthenia gravis is caused by — in — dogs
decreased number of ACh receptors
Jack Russell terriers, springer spaniels, smooth haired fox terriers
treat will anti-cholinesterase therapy
how does botulism work
Clostridium botulinum
releases toxin that enters neuron and prevents release of acetylcholine leading to flaccid paralysis
how does tetanus work
Clostridium tetani
Tetanospasmin travels
retrograde along peripheral
nerves and preferentially binds
to inhibitory interneurons
prevents release of inhibitory neurotransmitter leading to spastic/rigid paralysis
what causes tetanus
Clostridium tetani
- Ubiquitous G+ spore-forming
anaerobe in soil
— causes flaccid paralysis
— causes rigid paralysis
botulism
tetanus
Equine Laryngeal hemiplegia
Progressive degeneration of axons of left recurrent laryngeal nerve
leads to airway obstruction and stridor
some causes of Equine Laryngeal hemiplegia
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
peripheral nerve sheath tumors originate from
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
— tumors have no widely accepted grading scheme to distinguish benign from malignant
(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
