Pathology of Skeletal Muscle

Question 1

What are the 3 major connective tissue coverings of skeletal muscle?

Answer 1

1. epimysium (covers everything)
2. perimysium (covers fascicle)
3. endomysium (covers individual fibers)

Question 2

What is a sarcomere?

Answer 2

structural/functional unit of skeletal muscle
- actin = thin
- myosin = thick

Question 3

What is the most common artifact when processing skeletal muscle tissue? How can this be avoided?

Answer 3

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

Question 4

What are the 2 types of muscle fibers? How do each of them create energy?

Answer 4

TYPE I: red, slow twitch and slow fatiguing; oxidative phosphorylation using fats

TYPE II: white, fast twitch; anaerobic glycolysis

Question 5

How do the 2 types of muscle fibers stain?

Answer 5

TYPE I: rich in mitochondria; stains strongly with SDH and NADH stains

TYPE II: scarce in mitochondria; stains strongly with the myosin-ATPase reaction

Question 6

NADH stain:

Answer 6

Type I = dark

Question 7

ATPase stain:

Answer 7

Type II = dark

Question 8

What are the main 2 causes of post-mortem change in muscle into a pallor color? Dark-red?

Answer 8

1. secondary to anemia
2. normal in neonates
3. rhabdomyolysis
4. putrefaction

Question 9

What is rigor mortis? How does it develop?

Answer 9

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

Question 10

What are 4 possible factors that affect the rapidity of the onset of rigor mortis?

Answer 10

1. environmental temperature
2. internal temperature
3. muscle pH
4. glycogen reserves in muscle at the time of death

Question 11

How does rigor mortis change in emaciated individuals?

Answer 11

emaciated bodies may not develop rigor mortis, since they will typically have weaker muscles and not enough energy

Question 12

What is atrophy? Is it reversible?

Answer 12

reduction in muscle size

YES

Question 13

What are the 3 types of atrophy?

Answer 13

1. denervation atrophy - rapid atrophy due to damage to nerves supplying the muscle
2. disuse atrophy - atrophy associated with immobilization of the limb or body part because of pain (fracture, tenotomy, ankylosis)
3. cachexia/malnutrition - slow atrophy typically due to a lack in proper energy input

Question 14

What can long-standing denervation cause in the affected muscle?

Answer 14

fibrosis and fat infiltration (steatosis)

Question 15

What muscle fibers are most affected by cachexia/malnutrition?

Answer 15

Type II (white, fast twitch)

Question 16

What atrophy is associated with Roarers?

Answer 16

denervation of the left recurrent laryngeal nerve, causing laryngeal hemiplegia and the atrophy of the left crico-arytenoideus dorsalis

Question 17

What is hypertrophy?

Answer 17

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

Question 18

What is hyperplasia?

Answer 18

increase in the number of muscle fibers that are of normal size and structure

Question 19

Why is hyperplasia common in some beef cattle (Charolais, Santa Gertrudis, Angus, Belgian Blue)?

Answer 19

inherited defect in the myostatin gene that is usually responsible for limiting muscle growth
(“double muscling”)

Question 20

What muscles are most affected by the myostatin gene defect? What is a common secondary defect caused by this mutation?

Answer 20

those of the thigh, rump, loin, and shoulder

dystocia

Question 21

What is the common name of the myostatin gene defect in Whippets?

Answer 21

Bully Whippet Syndrome

Question 22

What is the most common sequel to myofiber injury regardless of its cause? How can it present?

Answer 22

degeneration/necrosis

segmentally along the length of the myofiber

Question 23

When is degeneration/necrosis reversible?

Answer 23

if the basement membrane and satellite cells are intact
- satellite cells will become myoblasts and repair damage

Question 24

Degeneration/necrosis can be detected grossly in severe cases. What are the main 2 possibilities?

Answer 24

1. pale and calcified
2. red, caused by hemorrhage or rhabdomyolysis (release of myoglobin into the interstitium)

Question 25

How does early degeneration/necrosis appear microscopically?

Answer 25

swollen, eosinophilic fibers

hyalinization, loss of striations and fragmentation

Question 26

Loss of striations and fragmentation:

Answer 26

degeneration/necrosis

Question 27

Segmental necrosis, skeletal muscle

Answer 27

Question 28

When is it common for calcification to be observed grossly?

Answer 28

severe cases of mitochondrial calcium overload —> white chalky gritty foci scattered throughout the affected muscle

Question 29

What happens when muscle injury disrupts the basal lamina (BM)?

Answer 29

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

Question 30

What happens during a non-disruptive muscle injury? What is indicative of this having happened?

Answer 30

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

Question 31

Nuclear rowing:

Answer 31

regenerated muscle will be more blue, since it will be producing more protein and mRNA
(myofiber regeneration)

Question 32

Why is the presence of segmental necrosis and regeneration not helpful in determining their cause? What is useful?

Answer 32

this is a generalized response to muscle injury

assessing the distribution (focal, multifocal, etc.) and duration (acute, chronic, etc.) of the lesions

Question 33

What are monophasic lesions? Polyphasic lesions? What are examples of each?

Answer 33

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)

Question 34

Polyphasic lesion from nutritional myopathy - vitamin E and selenium deficiency

Answer 34

muscular dystrophy —> muscle at different points of regeneration

• normal
• swollen, fragmented
• regeneration