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muscle Flashcards

1
Q

myofiber components

A
  • Myofibrils:
  • Actin and myosin filaments
  • Arranged into sarcomeres (striated appearance)
  • Sarcoplasmic reticulum:
  • Sequesters calcium necessary to initiate actin and myosin interaction and contraction
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2
Q

Normal muscle function requires normal PNS
function

A
  • Lower motor neurons
  • Peripheral nerves
  • Neuromuscular junctions
  • Action potential arrives via motor neuron
  • Terminal axons release acetylcholine
  • Acetylcholine binds to acetylcholine receptors on post-
    synaptic myofiber membrane
  • Sodium channels open in myofiber membrane, action
    potential, muscle contracts
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3
Q

muscle dysfunction

A

Myopathy: primary pathology of the muscle
cell
* Neuromuscular disease: includes pathology
of LMN, peripheral nerves, neuromuscular
junction, muscle

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4
Q

clinical signs associated with neuromuscllar disease

A

Muscle atrophy – a decrease in muscle size
Muscle hypertrophy – an increase in muscle size
Muscle swelling – due edema, hemorrhage, inflammation
Weakness and exercise intolerance – direct or indirect decrease in muscle function
Muscle spasm – sudden, intense
Myotonia – a tonic spasm; delayed relaxation of a muscle after an initial contraction
Abnormal movement – lameness
Dysphagia

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5
Q

origin of injury

A

-exogenous: penetrating wound including IM injection
-hematogenous: microorganisms, toxins, immune complexes
-endogenous: excessive contraction, genetic defecfs, nutritional deficiencies

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6
Q

color changes of muscle

A

White / Pallor:
anemia
necrosis ± mineralization
denervation (atrophy)
fibrosis

Red:
congestion
hemorrhage

Black
hemorrhage
melanosis
melanoma

Green eosinophilic inflammation

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7
Q

Responses to Injury (identified grossly)

A

1.Necrosis and regeneration
2.Alteration in myofiber size
* Atrophy
* Hypertrophy
* Hypoplasia
3.Chronic myopathic change:
fibrosis/steatosis

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8
Q

necrosis in response to injury

A
  1. Necrosis and regeneration
    * necrosis is common**
    * wide range of etiologies
    * often segmental
    * regeneration is possible**
    * satellite cells
    * requires intact basal lamina
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9
Q

alteration in myofiber size response to injruy: atrophy causes and types

A

a. Atrophy
* entire muscle or individual myofibers
* potentially reversible
i. Physiologic atrophy: disuse atrophy, aging, cachexia

ii. Denervation atrophy: loss of innervation

iii. Endocrine associated: generalized muscle atrophy, hypothyroidism, hyperadrenocorticism, PPID
* Muscle has lots of hormone receptors

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10
Q

Responses to Injury
2. Alteration in myofiber size

A

b. Hypertrophy
* entire muscle or individual
myofibers
* response to increased workload
* addition of myofibrils
i. Physiologic hypertrophy
ii.Compensatory hypertrophy

c. Hypoplasia
* Piglets get Splay leg
* premature animals
* MDx. Myofibrillar
hypoplasia

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11
Q

Responses to injury
3. Chronic myopathic change

A

Chronic myopathic change
* fibrosis
* steatosis

  • Accompanies variety of myopathic and
    neuropathic conditions e.g. chronic
    inflammation, denervation, degenerative
    myopathy
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12
Q

causes of muscle ischemia

A

-occlusion of major BV ex saddlethrombus in cat
-external pressure: recumbancy disease in large animal
-compartment syndrome: edema reperfusion injury
-widespread vascular injury: trauma

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13
Q

recumbency necrosis (downer cow)

A
  • Recumbency ->vascular occlusion
    ->myonecrosis
  • Myofiber necrosis due to recumbency can occur due to:
    1. Decreased blood flow (artery compression)
    2. Reperfusion injury if she gets up causing massive Ca influx into muscle cells
    3. Increased intramuscular pressure causing compartment syndrome
    4. Combination
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14
Q

compartment syndrome

A

-compression of tissues within a compartment
(nerves, blood vessels, muscle)
* compartment created by
* bone
* thick fascia
* increase in volume / pressure within muscle results in
compression, ischemia, necrosis

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15
Q

nutritional myopathy

A

Selenium/Vitamin E deficiency
➔ decreased antioxidant activity
➔oxidative injury to myofibers
➔Muscle necrosis and mineralization

Risk factors: sample high work load muscles
* neonates (selenium)
* farm animals (soils & plants)
* late winter (vitamin E)

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16
Q

nutritional myopathies of muscle

A

B. Nutritional Myopathies
* Muscle requires & receives a large amount of oxygen
* Therefore, muscle is susceptible to oxidative injury
(cell and tissue damage)
* Selenium (Se) & vitamin E are critical components of
antioxidants in muscle
* Se & vitamin E are derived from the diet

17
Q

Toxic Myopathies

A

-Ionophore antibiotics
* feed additives (for coccidiosis)
* monensin
* Rumensin (Elanco)

-mixing errors, toxic to horses

18
Q

toxic myopathies path (ionophore toxicity)

A

Ingest excess ionophore
➔increased movement of cations across cell membrane
➔disruption of ionic equilibrium
➔calcium overload of skeletal (and cardiac) muscle
➔muscle necrosis (pale areas in muscle)

19
Q

Equine exertional rhabdomyolysis (exertional myopathy)

A

-equine polysaccharide storage myopathy**, high grain diet, lack of regular exercise

➔altered carbohydrate metabolism in muscle
➔insufficient energy production by muscle cells
➔muscle necrosis and oxidative injury**
➔ edema within nonexpendable fascia
➔ ischemia
➔compartment syndrome
➔myoglobin release (red tinge to muscle)
➔releases from muscle to kidney–>myoglobinuric nephrosis**

20
Q
  1. Capture myopathy in wildlife
A

-exertional myopathy
-capture and / or restraint of wild animals
➢ ‘stress’, catecholamines, acidosis,
hyperthermia
➢ muscle necrosis
➢ myoglobin release
➢ myoglobinuric nephrosis

21
Q

Malignant hyperthermia

A
  • Genetic defect of calcium-release channel (ryanodine receptor-ryr1)**
    of skeletal muscle sarcoplasmic reticulum
    ➢Halothane anesthesia or stress
    ➢Uncontrolled Ca release
    ➢Excess muscle contraction
    ➢Hyperthermia
    ➢Death
  • Autosomal recessive disorder in pigs (autosomal dominant in dogs and humans)

-porcine stress syndrome: white, pale, wet muscle. myonecrosis

22
Q

Myositis ossificans (traumatic myopathies)

A
  • Rare
  • Metaplastic bone formation
  • Previous trauma, fibrosis
  • Injection
  • Exercise
  • DDx extraskeletal osteosarcoma
23
Q

Congenital and Inherited Myopathies
1. Arthrogryposis

A
  • persistent congenital flexure
  • often a neuromuscular
    disease

path:
In utero infection or toxin ingestion or genetic defect
➢Nervous system lesion
➢Failure of innervation/denervation of skeletal muscle
➢Atrophy, persistent flexure, myopathic change/steatosis

24
Q

Muscular dystrophies

A

-congenital and inherited myopathy
* group of heterogeneous diseases
* inherited
* progressive
* muscle weakness and wasting
* degenerative
* necrosis
* regeneration
* fibrosis and steatosis

25
Q

X-Linked Muscular Dystrophy (Duchenne’s Type)

A

X-linked recessive mutation in dystrophin gene
➢Decreased dystrophin, cytoskeletal protein in muscle
➢Repeated necrosis and regeneration of skeletal muscle
➢Also, necrosis of cardiomyocytes and fibrosis
➢Progressive weakness, muscle atrophy, splaying of distal limbs

26
Q

Pathogenesis of Acquired (Immune-mediated)
Myasthenia Gravis

A

Thymoma, loss of self-tolerance
➢Autoantibody against acetylcholine receptors on muscle
➢Damage of receptors and blockage of acetylcholine binding
➢Prevents muscle contraction
➢Episodic weakness and collapse
➢Megaesophagus

27
Q

Botulism

A

-Clostridium botulinum spores in soil or GI tract of animal
➢Spores germinate under anaerobic/alkaline conditions
➢Within GI tract
➢Soil/rodent carcass in spoiled feed

➢C. botulinum produces neurotoxin**
➢Toxin absorbed by animal through alimentary system
➢Toxin irreversibly blocks acetylcholine release at myoneural junctions
➢Flaccid paralysis
➢Respiratory paralysis = death
* horses sensitive

28
Q

tick paralysis

A

-Dermacentor or Ixodes tick attach to animal
➢Tick produces toxin that blocks acetylcholine release from axon terminals
➢Flaccid paralysis
➢Tick removal = recovery

29
Q

clostridial myositis (inflammatory bacterial infection) path

A

Ingestion of Clostridial spores during grazing
➔spores pass through intestinal mucosal barrier and enter circulation
➔dissemination to tissues (especially striated muscle and liver)
➔ spores multiply in low oxygen environments (i.e. trauma, horses:
penetrating trauma)
➔ toxin production
➔ vascular damage
➔ hemorrhage, edema, necrosis of adjacent myofibers
➔ systemic dissemination of the toxin (toxemia)
➔death

30
Q

Clostridial myositis causes

A
  • Farm animals – black leg= Clostridium chauvoei
  • Horses – malignant edema= Clostridium septicum,
31
Q

masticatory myositis of dogs

A

-immune mediated myositis
Antibodies to unique type 2M myosin of masticatory muscle
➢Acute inflammation (edema, pain) of temporalis and masseter
➢Chronic atrophy
always bilateral

if other muscles in body involved: polymyositis

32
Q

neoplasia

A
  • Primary neoplasia of striated muscle
  • Rhabdomyoma
  • Rhabdomyosarcoma
  • Arise from intramuscular pluripotential
    stem cells
  • Primary neoplasia of supporting
    connective, adipose, vascular, or
    neural tissue
  • Hemangiosarcoma
33
Q

parasitc

A
  • Protozoal myopathy
  • Neospora caninum (dogs, cattle)
  • Sarcocystis spp. (farm animals, horses)
  • Nematodes
  • Trichinella spiralis (pigs, bear
34
Q

neospora canium dogs

A

➢In utero transmission to fetus
➢Peripheral nervous system and skeletal muscle are
invaded by protozoa, including ventral spinal roots
➢ Denervation atrophy

sys path (13 decks)

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