Muscle Flashcards
1
Q
Sarcoplasmic reticulum
A
- Sequesters calcium necessary to initiate actin AND myosin interaction and contraction
2
Q
Satellite cells
A
- Resting myoblasts
- Capable of mitosis
- Can fuse with other satellite cells
- Result in regeneration of myofiber
- *regeneration requires an intact basal lamina (=scaffold, preventions infiltration of fibrous tissue)
3
Q
Normal muscle function requires normal PNS function
A
- LMN
- Peripheral nerves
- NMJs
o AP arrive via motor neuron
o ACh released
o ACh binds to ACh-receptors on post-synaptic myofiber membrane
o Na channels open in myofiber membrane, AP, muscle contracts
4
Q
Myopathy: description
A
- Primary pathology of muscle cell
5
Q
NMJ disease: description
A
- Includes pathology of LMN, peripheral nerves, NMJ, muscle
6
Q
What are some exogenous examples of injurious stimuli?
A
- Penetrating wound including intramuscular injection
- Fractured bones
- External pressure causing ischemia or crushing injury
- Loss of innervation
- Loss of blood supply
7
Q
What are some hematogenous examples of injurious stimuli?
A
- Microorganisms
- Toxins
- Autoantibodies
- Immune complexes
- Hormone and electrolyte abnormalities
8
Q
What are some endogenous examples of injurious stimuli?
A
- Excessive contraction
- Genetic defects
- Nutritional deficiencies (selenium, vit E or both)
9
Q
What can cause a white/pallor colour change?
A
- Anemia
- Necrosis
- Denervation
- Steatosis
- Inflammation
- Parasites
- Osseous metaplasia
10
Q
What can cause red colour change?
A
- Congestion
- Hemorrhage
- Hyperemia
- Myoglobin
11
Q
What can cause black colour change?
A
- Hemorrhage
- Melanosis
- Melanoma
12
Q
What can cause green colour change?
A
- Eosinophilic inflammation
- Putrefaction (gangrene)
13
Q
What can cause tan to brown colour change?
A
- Lipofuscin
14
Q
What are the 3 main responses to injury?
A
- Necrosis and regeneration
- Alteration in myofiber sizes
o Atrophy
o Hypertrophy
o Hyperplasia - Chronic myopathic change: fibrosis/steatosis
15
Q
Necrosis and regeneration
A
- Necrosis is common
- Wide range of etiology
- Often segmental
- Regeneration is possible
- Satellite cells
- Requires intact basal lamina
16
Q
What are some things that can cause muscle necrosis?
A
- Ionophore toxicity
- Ischemia (“downer cow”)
- Clostridial myositis (black leg: C. chavoei, malignant edema: C. septicum)
- Associated with mineralization (chronic): canine X-linked muscular dystrophy
17
Q
Atrophy
A
- Entire muscle or individual myofibers
- Potentially reversible
- Physiologic
- Denervation
- Endocrine associated
18
Q
Physiologic atrophy
A
- Disuse atrophy
- Aging
- Cachexia
19
Q
Denervation atrophy
A
- Loss of innervation: loss of trophic effects
- If unilateral=consider peripheral nerve damage
20
Q
Endocrine associated atrophy
A
- Generalized muscle atrophy
- Hypothyroidism, hyperadrenocorticism, PPID
- Muscle had lots of hormone receptor
21
Q
Hypertrophy
A
- Entire muscle or individual myofibers
- Response to increased workload
- Addition of myofibrils
- Physiologic hypertrophy
- Compensatory hypertrophy
22
Q
Hypoplasia
A
- Piglets
- *splay leg
- Premature animals
- MDx: myofibrillar hypoplasia
23
Q
Chronic myopathic changes: fibrosis and/or steatosis
A
- Accompanies variety of myopathic and neuropathic conditions
- Ex. chronic inflammation, denervation, degenerative myopathy
24
Q
What are the 2 causes of significant ischemia?
A
- Occlusion or failure of a major artery
- Widespread failure of intramuscular vessels
- (external pressure)
- (compartment syndrome)
25
Q
Downer cow (recumbency to vascular occlusion to myonecrosis): steps
A
- Decreased blood flow (artery compression)
- Reperfusion injury causing massive Ca influx into muscle cells
- Increased intramuscular pressure causing compartment syndrome
- *combination
26
Q
Compartment syndrome
A
- Compression of tissues within a compartment
- Compartment created by
o Bone or thick fascia - *increase in volume/pressure within muscle=compression, ischemia and necrosis
27
Q
**What is the pathogenesis of Selenium/Vit E deficiency?
A
- Decreased antioxidant activity
- Oxidative injury to myofibers
- Muscle necrosis and mineralization
28
Q
**What are the risk factors to nutritional myopathies?
A
- Neonates: selenium
- Farm animals: soils and plants
o Late winter: vitamin E - *highest workload muscles are affected=tongue in neonates for suckling
29
Q
**Ionophore antibiotics
A
- Feed additive
o Coccidostate, feed efficiency, weight gain - Monensin: rumensin
- *problems associated with:
o Mixing errors
o ‘accidental feeding’=horses
30
Q
**Excess ingestion of ionophores: pathogenesis
A
- Increased movement of cations across cell membrane
- Disruption of ionic equilibrium
- Calcium overload of skeletal (and cardiac) muscle
- Muscle necrosis
31
Q
What are the 3 types of exertional myopathies?
A
- Exertional rhabdomyolysis: horses and working dogs
- Capture myopathy: wildlife
- Malignant hyperthermia: swine
*often underlying myopathy (selenium deficiency and defect in CHO metabolism)
32
Q
Equine exertional rhabdomyolysis
A
- Equine polysaccharide storage myopathy, or high grain diet or lack of regular exercise
- Altered CHO metabolism in muscle
- Insufficient energy production by muscle cells
- Muscle necrosis and oxidative injury
- Edema within nonexpendable fascia
- Ischemia
- Compartment syndrome
- Myoglobin release
- 8 Myoglobinuric nephrosis
33
Q
Capture myopathy
A
- ‘stress’, catecholamines, acidosis, hyperthermia
- Muscle necrosis
- Myoglobin release
- Myoglobinuric nephrosis
34
Q
Malignant hyperthermia (porcine stress syndrome)
A
- Genetic defect of calcium-release channel (ryanodine receptor-ryr1) of skeletal muscle sarcoplasmic reticulum
o Halothane anesthesia or stress
o Uncontrolled Ca release
o Excess muscle contraction
o Hyperthermia
o Death - *autosomal recessive disorder in pigs (autosomal dominant in dogs and humans)
35
Q
Traumatic myopathies: examples of causes
A
- External trauma
o Iatrogenic: surgical incision and injection site
o Laceration, crush, burn, gunshot, etc. - Excessive stretching
- Forceful contraction
36
Q
What is the most common muscle to rupture in dogs and cats?
A
- Diaphragm (ex. hit by a car)
37
Q
Myositis ossificans
A
- Rare
- Metaplastic bone formation
o Previous trauma, fibrosis (injection, exercise) - DDx: extra-skeletal osteosarcoma
38
Q
What are some congenital and inherited myopathies?
A
- Arthrogryposis
- Double muscling
- Muscular dystrophies
39
Q
Arthrogryposis
A
- Persistent congenital flexure
- Often a neuromuscular disease
- *in utero infection or toxin ingestion OR genetic defect
o NS lesion
o Failure of innervation/denervation of skeletal muscle
o Atrophy, persistent flexure, myopathic change/steatosis
40
Q
Double muscling
A
- Congenital muscular hyperplasia
- Cattle, dogs, children
- *defect in myostatin gene
o Lack of myostatin=hormone produced by skeletal muscle that INHIBITS muscle growth
o Increased number of myofibers
41
Q
Muscular dystrophies
A
- Group of heterogenous diseases
- Inherited
- Progressive: muscle weakness and wasting
- Degenerative: necrosis, regeneration, fibrosis and steatosis
42
Q
X-linked muscular dystrophy (Duchenne’s Type)
A
- X-linked recessive mutation in dystrophin gene
o Decreased dystrophin (cytoskeletal protein in muscle)
o Repeated necrosis and regeneration of skeletal muscle
o Necrosis of cardiomyocytes and fibrosis
o Progressive weakness, muscle atrophy, splaying of distal legs
43
Q
What are some neuromuscular junction disorders?
A
- Myasthenia gravis
- Botulism
- Tick paralysis
44
Q
What is the pathogenesis of acquired (immune-mediated) myasthenia gravis?
A
- THYMOMA: loss of self tolerance
o Autoantibody against ACh receptors on muscle
o Damage of receptors and blockage of ACh binding
o Prevents muscle contraction
o Episodic weakness and collapse
o Megaesophagus
45
Q
Botulism
A
- C. botulinum spores in soil or GI tract of animal
o Spores germinate under anaerobic/alkaline conditions (within GI tract, soil/rodent in spoiled feed) - Produces a neurotoxin
o Absorbed by animal through alimentary system
o Irreversibly blocks ACh release at myoneural junctions - Flaccid paralysis
- Respiratory paralysis=death (no gross lesions)
o No denervation atrophy (it’s at the NMJ) - HORSE SENSITIVE
46
Q
Tick paralysis
A
- Dermacentor or Ixodes tick attach to animal
o Tick produces toxin that blocks ACh release form axon terminals
o Flaccid paralysis
o Tick removal=recovery
47
Q
Do you expect denervation atrophy with NMJ disorders?
A
- NO=no gross lesions
48
Q
**Clostridial myositis
A
- Farm animals: black leg
o C. chauvoei - Horse: malignant edema
o C. septicum, others - *myonecrosis with hemorrhage and emphysema, acute, multifocal
- *need to have lesion (C. chauvoei is normally in muscle)
49
Q
**Clostridial myositis: ingestion of Clostridal spores during grazing
A
- Spores pass through intestinal mucosal barrier and enter circulation
- Dissemination to tissues (especially striated muscle and liver)
- Spores multiple in low oxygen environment
- Toxin production
- Hemorrhage, edema, necrosis of adjacent myofibers
- Systemic dissemination of toxin (toxemia)
- Death
50
Q
Masticatory myositis of dogs
A
- Antibodies to unique type 2M myosin of masticatory muscles
- Acute inflammation of temporalis and masseter
- Chronic atrophy
- **always bilateral
- *immune-mediated myositis
51
Q
Polymyositis of dogs
A
- Bilateral temporalis/masseter involved AND muscles throughout the body
- *immune-mediate inflammation of skeletal muscle
o Severe, generalized muscle atrophy +/- megaesophagus
52
Q
Neoplasia
A
- Primary neoplasia of striated muscle
o Rhabdomyoma
o Rhabdomycosarcoma
o Arise from intramuscular pluripoteintial stem cells - Primary neoplasia of supporting connective, adipose, vascular or neural tissue
o Ex. hemangiosarcoma
53
Q
Neospora caninum
A
- Mom can be a chronic carrier
- In utero transmission to fetus
- Peripheral NS and skeletal muscle are invaded by protozoa, including ventral spinal roots
- Denervation atrophy
54
Q
Sarcocystis spp.
A
- Usually incidental
- Rarely cattle may have a hypersensitivity
o Multifocal green areas (eosinophilic myositis)
55
Q
Trichinella spiralis
A
- Zoonotic nematode
- Encysted larvae may not be visible grossly
- Dead, encysted larvae, visible as calcified, white, 1mm nodules
