01a: Muscle Path

Color associated with myoglobin

Rich mahogany

Pigment associated with wear and tear of muscle

Lipofuscin

Dark pigment occasionally present in muscle

Melanin

Color of deposits left by IM tetracycline

Yellow

Color of deposits left by IM PPG

Chalky white/gray/green

Color of deposits left by IM iron dextran

Dark brown

Muscular process that occurs after death

Rigor mortis

Findings associated with rigor mortis

Fixed contraction of all skeletal muscle moving from jaw/head → extremities

How long does it take for rigor mortis to resolve

4 days

Physiology that drives rigor mortis

Lack of ATP

Physiology that leads to the resolution of rigor mortis

Degradation of muscle fibers

Factors that can speed up rigor mortis

• Low glycogen reserve

• Low pH

• High temperature

Where are nuclei located in skeletal muscle

On the outside of the myofibrils

T/F: degeneration = necrosis

False

Degeneration

Muscle cells are not feeling good and organelles are perturbed by “sickness” but the plasma membrane is still intact

Histo finding indicative of skeletal muscle degeneration

Accumulation of cytoplasmic vacuoles

Type of muscle tissue that is most susceptible to degeneration

Myofibrils

Type of muscle tissue that is most resistant to degeneration

Connective tissue

Necrosis

Cell death associated with damage to the plasma membrane

Substances released from dying myofibrils

• Increased CK

• Increased AST

• Ca⁺⁺

How is muscle injury connected to kidney damage

Release of myoglobin → myoglobinuria → myoglobin is nephrotoxic → AKI

When do we see regeneration in response to muscle injury

If the injury is not severe and there is intact basal lamina and viable satellite cells

How long does it take for muscle to regenerate

10-14 days

How is muscle repair altered if the basal lamina is disrupted

The injury is repaired by fibrosis, which results in a loss of function

Features of optimum regeneration

• Intact basal lamina

• Macrophage migration

• Satellite cells fuse to repair scaffolding

• Results in a new myofiber

Features of budding regeneration

• Basal lamina damaged

• Inefficient formation of disorganized myotubes

• Often complete by fibrosis

Muscle atrophy

Decrease in muscle size due to decreased size of myofibers

What happens to the distribution of tissue types in a muscle belly that has atrophied

There is a greater percentage of adipose and connective tissue

Types of atrophy

• Denervation

• Disuse

• Cachexia, malnutrition, senility

• Endocrine

Denervation atrophy

Loss of neural innervation to the muscles, happens quickly

Muscle fibers affected by denervation atrophy

TI and TII fibers

Disuse atrophy

Reduced stimulation or movement, happens more slowly

Muscle fibers affected by disuse atrophy

TII fibers

Atrophy of cachexia/malnutrition/senility

Negative energy balance, the body has depleted source of carbs and fat and is now catabolizing muscle

Muscle fibers affected by atrophy of cachexia/malnutrition/senility

TII

Endocrine atrophy

Various mechanisms: decreased protein synthesis, increased protein degradation, oxidative stress, inflammation

Muscle fibers affected by endocrine atrophy

TII

Examples of endocrine diseases that cause atrophy

• Hypothyroidism

• Hyperadrenocorticism

• Pituitary dwarfism

• PPID

Type of atrophy that is characterized by “fiber type switching”

Atrophy of cachexia; TI fibers are resistant and may hypertrophy