Pathology of Skeletal Muscle Flashcards
What are the 3 major connective tissue coverings of skeletal muscle?
- epimysium (covers everything)
- perimysium (covers fascicle)
- endomysium (covers individual fibers)
What is a sarcomere?
structural/functional unit of skeletal muscle
- actin = thin
- myosin = thick
What is the most common artifact when processing skeletal muscle tissue? How can this be avoided?
contraction of the muscle following contact with the fixative (forms contraction bands)
- use special clumps
- stretch the muscle on a tongue depressor and stabilize with needles
What are the 2 types of muscle fibers? How do each of them create energy?
TYPE I: red, slow twitch and slow fatiguing; oxidative phosphorylation using fats
TYPE II: white, fast twitch; anaerobic glycolysis
How do the 2 types of muscle fibers stain?
TYPE I: rich in mitochondria; stains strongly with SDH and NADH stains
TYPE II: scarce in mitochondria; stains strongly with the myosin-ATPase reaction
NADH stain:
Type I = dark
ATPase stain:
Type II = dark
What are the main 2 causes of post-mortem change in muscle into a pallor color? Dark-red?
- secondary to anemia
- normal in neonates
- rhabdomyolysis
- putrefaction
What is rigor mortis? How does it develop?
contraction of muscles that occurs after death, resulting in the stiffening of the muscles and immobilization of the joints
starts at the jaws and trunk and progresses to the limbs; commonly begins 2-4 hrs after death and reaches a maximum at 24 hrs before disappearing gradually in the oppositeorder
What are 4 possible factors that affect the rapidity of the onset of rigor mortis?
- environmental temperature
- internal temperature
- muscle pH
- glycogen reserves in muscle at the time of death
How does rigor mortis change in emaciated individuals?
emaciated bodies may not develop rigor mortis, since they will typically have weaker muscles and not enough energy
What is atrophy? Is it reversible?
reduction in muscle size
YES
What are the 3 types of atrophy?
- denervation atrophy - rapid atrophy due to damage to nerves supplying the muscle
- disuse atrophy - atrophy associated with immobilization of the limb or body part because of pain (fracture, tenotomy, ankylosis)
- cachexia/malnutrition - slow atrophy typically due to a lack in proper energy input
What can long-standing denervation cause in the affected muscle?
fibrosis and fat infiltration (steatosis)
What muscle fibers are most affected by cachexia/malnutrition?
Type II (white, fast twitch)
What atrophy is associated with Roarers?
denervation of the left recurrent laryngeal nerve, causing laryngeal hemiplegia and the atrophy of the left crico-arytenoideus dorsalis
What is hypertrophy?
muscle response to increased work where there is an increase in the size, but not the number of muscle fibers
- can be enhanced by steroids
What is hyperplasia?
increase in the number of muscle fibers that are of normal size and structure
Why is hyperplasia common in some beef cattle (Charolais, Santa Gertrudis, Angus, Belgian Blue)?
inherited defect in the myostatin gene that is usually responsible for limiting muscle growth
(“double muscling”)
What muscles are most affected by the myostatin gene defect? What is a common secondary defect caused by this mutation?
those of the thigh, rump, loin, and shoulder
dystocia
What is the common name of the myostatin gene defect in Whippets?
Bully Whippet Syndrome
What is the most common sequel to myofiber injury regardless of its cause? How can it present?
degeneration/necrosis
segmentally along the length of the myofiber
When is degeneration/necrosis reversible?
if the basement membrane and satellite cells are intact
- satellite cells will become myoblasts and repair damage
Degeneration/necrosis can be detected grossly in severe cases. What are the main 2 possibilities?
- pale and calcified
- red, caused by hemorrhage or rhabdomyolysis (release of myoglobin into the interstitium)
How does early degeneration/necrosis appear microscopically?
swollen, eosinophilic fibers
hyalinization, loss of striations and fragmentation
Loss of striations and fragmentation:
degeneration/necrosis
Segmental necrosis, skeletal muscle
When is it common for calcification to be observed grossly?
severe cases of mitochondrial calcium overload —> white chalky gritty foci scattered throughout the affected muscle
What happens when muscle injury disrupts the basal lamina (BM)?
repair will not be as efficient and scarring will occur (part of the damaged muscle is replaced by fibrous connective tissue)
- common in lacerations and tearing
What happens during a non-disruptive muscle injury? What is indicative of this having happened?
satellite cells proliferate and migrate to the damaged myofiber, where they become myoblasts that are able to form multinucleated bands and regenerate the myofiber
nuclear rowing of myoblasts
Nuclear rowing:
regenerated muscle will be more blue, since it will be producing more protein and mRNA
(myofiber regeneration)
Why is the presence of segmental necrosis and regeneration not helpful in determining their cause? What is useful?
this is a generalized response to muscle injury
assessing the distribution (focal, multifocal, etc.) and duration (acute, chronic, etc.) of the lesions
What are monophasic lesions? Polyphasic lesions? What are examples of each?
same duration, indicative of a single insult; leaving the myofibers and the same level of regeneration at the same time; injection site reaction (FOCAL)
different stages of development, indicative of an ongoing degenerative process; myofibers at different levels of regeneration; vitamin E and selenium deficiency, strenuous exercise, single exposure to muscle toxin monensin (MULTIFOCAL)
Polyphasic lesion from nutritional myopathy - vitamin E and selenium deficiency
muscular dystrophy —> muscle at different points of regeneration
- normal
- swollen, fragmented
- regeneration
