Muscoloskeletal system Flashcards
(49 cards)
1
Q
neuropathic changes
A
determined by the effect or the absence of the nerve supply
2
Q
myopathic changes
A
reserved for diseases in which the primary change takes place in the muscle cell
3
Q
neuromuscular disease
A
encompasses disorders involving lower motor neurons, peripheral nerves, neuromuscular junctions, and muscles
4
Q
ways to classify skeletal muscle fibers (3)
A
- rates of contraction (fast or slow)
- rates of fatigue (fast or slow)
- types of metabolism (oxidative, glycolytic, mixed)
5
Q
2 types of muscle fibers
A
- type 1 (lots of mitochondria, oxidative metabolism, slow contracting, slow fatiguing)
- type 2 (fewer mitochondria, glycolytic metabolism, fast contracting, easily fatigued)
6
Q
rigor mortis
A
- muscle contractile apparatus is still active immediately following death
- ATP necessary for release of actin from myosin (interaction that results in the sliding of myofilaments and contraction of muscle)
- following death, absence of adequate ATP production causes the muscle fibers to undergo sustained contraction)
7
Q
clinical signs of muscle disease (7)
A
- atophy
- hypertrophy
- swelling
- weakness
- spasm
- abnormal gait
- esophageal dysfunction
8
Q
necrosis/degeneration of muscle findings
A
- segmental hypercontraction (larger diameter, darker staining)
- homogenous eosinophilia (hyalinization) and pallor of cytoplasm with loss of striations and the adjacent muscle nucleus
- myofiber fragmentation with floccular or granular cytoplasm
- creatine kinase and aspartate aminotransferase increases
9
Q
different levels of myocyte degeneration
A
- myofibrils alone or myofibrils and sarcoplasm
- myofibrils and myonuclei
- myofibrils, myonuclei, and satellite cells
- myofibrils, myonuclei, satellite cells, and basal lamina
10
Q
what is myocyte degeneration triggered by
A
increased intracellular calcum (either from influx of extracellular Ca or from release of intracelular stores of Ca)
11
Q
what infiltrate areas of myofiber necrosis
A
macrophages followed by other leukocytes
12
Q
what is activation and division of satellite cells triggered by
A
necrosis of adjacent myofiber segments
13
Q
what determines outcome of myocyte degeneration
A
integrity of basal lamina –> keept myonuclei, satellite cells, and myoblastic cells inside, keeps fibroblastic cells out, allows phagocytic cells entry/exit
14
Q
what happens if basal lamina is intact
A
- macrophages dissolve and remove debris
- satellite cells enlarge and divide
- cell membrane of damaged segment disppears
- satellite cells move into space vacated by damaged myofiber
- satellite cells differentiate into myoblasts
- myoblasts increase in number until critical mass is reached then begin to fuse and elongate along long axis of damaged myofiber
- when cell membranes of fused myoblasts contact intact myofiber, cell membranes fuse
- myofiber differentiates into mature muscle
15
Q
what happens if basal lamina is not intact but satellite cells are not damaged
A
- satellite cells and damaged fibers not contained by basal lamina
- nuclei from damaged ends of myofibers divide
- ends of damaged myofiber bulge
- many nuclei result (muscle giant cells)
- gaps larger than 2-4mm heal by fibrosis
16
Q
what is atrophy
A
- reduction in size (muscle fiber diameter or cross sectional area)
- causes are denervation, disease, cachexia
- rapid progress
17
Q
what is hypertrophy
A
- increase in muscle fiber diameter or cross-sectional area by additional of myofilaments
- physiologic hypertrophy is a normal process
- compensatory hypertrophy is nonspecific and occurs secondary to decreased number of functional myofibers or interference with normal metabolic processes
18
Q
6 types of muscle diseases
A
- degenerative (circulatory, nutritional, toxic, exertional, traumatic)
- inflammatory (myositis)
- congenital/inherited
- endocrine/electrolyte/neuropathic
- neuromuscular junction disorders
- neoplasia
19
Q
circulatory degenerative muscle disease
A
- “downer syndrome”
- muscle ischemia initiated by external pressure
- good condition; cows most frequent
- pressure within muscles exceeds venous and arterial pressure
- muscles dark and hemorrhagic (acute); pale (chronic)
20
Q
nutritional degenerative muscle disease
A
- principal deficiencies are selenium and vitamin E
- result is loss of antioxidant defense mechanisms
- high O2 requirement and high contractile activity make striated muscle sensitive to oxidative injury
- selective, segmental degeneration of contractile components; basal lamina and satellite cells INTACT
21
Q
nutritional myopathy info
A
- vitamin E/selenium-containing enzymes are physiologic antagonists to free radicals
- in absence of protection, cellular membranes modified by free radicals, altering ability to maintain ion gradients
- mitochondrial calcium overload leads to Ca-induced hypercontraction of myofibrils and degeneration of myofibers
22
Q
who is affected by nutritional myopathy
A
- pigs and herbivores primarily
- usually young animals; may occur in utero
- clinical signs may be precipitated by physical activity
23
Q
lesions of nutritional myopathy
A
- affected muscle is pale
- marked mineralization of skeletal/cardiac muscle
- pale, irregularly opaque, yellow to creamy white
- large muscles of thigh, shoulder
- tongue and neck muscles in young animals
- lesions bilaterally symmetrical
- may develop myoglobinuria
24
Q
pigs and nutritional myopathy
A
- spontaneous disease where intensive pig rearing is practiced
- skeletal lesions less common than hepatic necrosis and myocardial necrosis and hemorrhage
- most common at 6-20wks of age
- iron injections
- gross lesions difficult to detect
- mortality may be high
25
toxic degenerative disease of muscle
- phytotoxins, chemical toxins, pharmacological agents
- may be difficult to distinguish from nutritional myopathies
- segmental skeletal muscle or myocardial lesions
- don't act by destroying vitamin E/selenium, not inhibited by addition of these nutrients
- generally more lethal than nutritional deficiencies
- unremarkable and nonspecific lesions - less often associated with mineralization of tissues
26
monensin toxicity info
- toxic for monogastrics or at high doses for ruminants (horses > dogs/pigs > sheep/goats > cattle > poultry)
- monensin in an ionophore that distorts membrane transport of Na/K
- results in Ca overload --> death of skeletal and cardiac muscle
27
clinical signs and lesions of monensin toxicity
- lethargy, stiffness, muscular weakness, recumbency, colic
| - pale streaks in muscle, atrophy in chronic cases
28
what are exertional myopathies
- degenerative muscle disease
- intensive or exhaustive activity of major muscle masses
- coagulation of contractile proteins, diffusion of lactate and heat, water loss, increased pressure, myoglobinemia, myoglobinuria, acidosis
29
exertional myopathy in horses (general)
- extertional rhabdomyolysis ("tying up")
| - sporadic or recurrent
30
clinical signs of sporadic exertional rhabdomyolysis
- occurs following exercise in horses with previous history of satisfactory performance
- mild stiffness to recumbency
- during exercise: short stride, sweating, elevated respiratory rate
- upon stopping: reluctant to move
- myoglobinuria in severe cases
- muscle cramps and pain for several hours, elevations in serum myoglobin
31
lesions in sporadic exertional rhabdomyolysis
- gross lesions most obvious in gluteal and lumbar regions but often widespread
- muscles moist, swollen, dark, streaks of pallor
- kidneys swollen, damaged
- oliguria, anuria, renal failure, death
32
etiology of sporadic exertional rhabdomyolysis
-viral infection (EHV-1, EIV)
33
recurrent exertional rhabdomyolysis indo
- recurrent episodes even with light exercise
- recovery rapid and complete
- no gross lesions
- inherited as an autosomal dominant trait
34
pathogenesis of recurrent exertional rhabdomyolysis
- alteration in muscle cell Ca regulation
| - disorder of carbohydrate storage and utilization (PSSM)
35
bacterial myositis - gas gangrene
- clostridium bacteria contaminate wound --> necrosis, gas formation
- death from systemic intoxication
- ruminants, horses, swine mostly
- local infections: edema, gas bubbles (crepitation), discoloration, toxemia, death
- lesions: dark muscles, pulmonary congestion, toxic degeneration
36
myositis - blackleg
- gangrenous myositis of ruminants from c. chauvoei
- latent spores germinate when local event creates muscle damage or low O2 tension
- signs: lameness, swelling, crepitation, fever, depression, death
- lesions: bloat, blood-stained froth, yellow gelatinous fluid, gas bubbles, dark muscle
37
masticatory myositis of dogs
- eosinophilia of blood and muscle tissue
- progressive course with acute episodes
- initiated by Ab formation to unique myosin isotypes found in muscles of mastication
- pain, swelling, atrophy of mandibular muscles
- manage with corticosteroids
38
trichinellosis
- muscle is habitat for encysted larvae of nematode trichinella spiralis
- animal to animal transmission by consumption of infected muscle (zoonotic)
- if infected muscle degenerates, larva exposed, dies, becomes center of acute inflammatory reaction
- respiratory and masticatory muscles preferentially infected
39
congenital muscular hyperplasia
- increased number of fibers in affected muscles ("double muscling")
- individual fibers are of normal size and structure
- inactivation of myostatin gene by various mutations in DNA coding sequence increases proliferation of muscle fiber numbers
- increased muscle mass with equal reduction in carcass fat
- increased incidence of dystocia, decreased fertility
40
polysaccharide storage myopathy (PSSM)
- stiff gait, muscle atrophy, muscle weakness, recumbency
- signs due to insufficient energy production by affected muscle fibers
- GSYI mutation --> alteration of glycogen formation, increased insulin sensitivity and cellular glucose uptake
41
hyperkalemic periodic paralysis (HYPP)
- mutation in gene encoding the a subunit of the skeletal muscle Na channel
- abnormal (delayed) inactivation of Na channel activity --> membrane instability, continuous muscle fiber electrical activity
- transient myotonia (mm spasm), protrusion of 3rd eyelid, flaccid paralysis/collapse
- no gross lesions other than prominent muscling
42
malignant hyperthermia
- humans, dogs, swine
- inherited defect in intracellular mechanism for uptake, storage, release of Ca ions (SR Ca channel release mutation)
- anesthetic drugs induce metabolic acidosis, increased body temp, tachycardia, mortality
43
porcine stress syndrome (PSS)
- naturally occurring condition that affects malignant hyperthermia-susceptible swine under stress
- meat is pale, soft, exudative
- heavily muscled pigs most susceptible
- acute heart failure, rapid rigor mortis
44
muscular dystrophy
- X-linked duchene-like dystrophy
- several dog breeds, cats
- dystrophin gene missing
- cats develop marked muscular hypertrophy
45
exercise-induced collapse in labs/labrador retriever myopathy
- signs become apparent with heavy training
- quickly return to normal
- muscle biopsies structurally normal
- dynamin I gene issue
46
myasthenia gravis
- transmission of nerve impulse across neuromuscular junction is inadequate, hampered, or blocked
- weakness, fatigue
- congenital --> 10% of cases, autosomal recessive, decreased number of acetylcholine end-plate receptors
- acquired --> autoimmune disease, target is AChR of postsynaptic membrane of NMJ (ACh receptors blocked)
47
neoplastic disease of muscle
- primary tumors of striated muscle are rare
- malignant more common (2x) than benign
- ABOUT HALF ARISE FROM SITES OTHER THAN SKELETAL MUSCLE
48
tumors of striated muscle
- rhabdomyoma (benign): congenital tumor of heart, larynx in adult dogs
- rhabdomyosarcoma (malignant): most common in young animals
49
secondary tumors
- direct invasion by neoplasm into adjacent tissue is common
| - metastatis from a distant site is uncommon
