Muscle: Background & Degenerative Diseases Flashcards Preview

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Flashcards in Muscle: Background & Degenerative Diseases Deck (39)
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1
Q

What does skeletal muscle do?

A
  1. Posture & movement
  2. Respiration
  3. Glucose metabolism & temperature
  4. Peripheral nervous system
2
Q

Neuropathic changes in muscle

A

Effect or absence of nerve supply

3
Q

Myopathic changes in muscle

A

Primary disease is in the muscle cell

4
Q

Neuromuscular changes in muscle

A

Disease that include muscle cells & neurons

5
Q

Satellite cell

A

Involved in muscle repair

“Resting myoblast”

6
Q

Myocyte

A

Muscle cell

7
Q

Muscle fiber classification

A
  1. Rate of contraction
  2. Rate of fatigue
  3. Type of metabolism
8
Q

Type 1 fibers

A
Lots of mitochondria 
"Light color"
Oxidative metabolism
Slow contraction & slow fatigue
Maintaining posture
9
Q

Type 2 fibers

A
Few mitochondria
"Dark color"
Glycolytic 
2A = oxidative & glycolytic
2B = anaerobic
Fast contracting & fast fatigue 
Sprinting
10
Q

Skeletal muscle metabolism

A

Energy = ATP
Type 1 & 2A = oxidative glycogen & fat
Type 2B = anaerobic

11
Q

What is rigor mortis?

A

Absence of fresh ATP after death prevents the relaxation of muscle
Myosin heads to not release

12
Q

What does necrosis in injured muscle look like?

A

Segmental hypercontraction
Eosinophilia
Pallor of the cytoplasm
Floccular or granular cytoplasm

13
Q

What enzymes are elevated in the plasma when there is muscle damage?

A
Creatine kinase (CK)
Aspartate animotransferase  (AST)
14
Q

How does muscle regenerate after injury?

A

Triggered by increased intra-cellular calcium
Macrophages invade necrotic area
Activation of satellite cells

15
Q

What determines the outcome of muscle regeneration?

A

Whether or not the basal lamina in intact

Keeps nuclei in and fibroblasts out

16
Q

How does muscle regenerate with an in tact basal lamina?

A
  1. Macrophages clean up
  2. Satellite cells enlarge and divide
  3. Damaged cell disappears
  4. Satellite cell moves into vacant area
  5. Differentiation into myoblast
  6. Myoblasts increase in numbers
  7. When myoblasts’ membranes fuse differentiation into mature muscle
17
Q

How does muscle regenerate with an in damaged basal lamina?

A
  1. Satellite cells and damages fiber are NOT contained
  2. Nuclei from damaged ends divide
  3. Ends of fiber bulge
  4. Muscle giant cells form
  5. Large gaps heal by fibrosis
18
Q

What happens when there are no satellite cells to repair damaged muscle?

A

Healing by fibrosis only

19
Q

Atrophy of muscle

A

DECREASE in size of fiber diameter
Causes = denervation, cachexia
Can be seen grossly
NOT hypoplasia = underdevelopment

20
Q

Hypertrophy of muscle

A

INCREASE in muscle fiber diameter

Addition of myofilaments

21
Q

Physiologic hypertrophy

A

Normal process

Exercise conditioning

22
Q

Compensatory hypertrophy

A

Nonspecific process
Secondary to:
1. Decreased number of functional myofibers
2. Problem with normal metabolic processes

23
Q

Downer syndrome

A

Degenerative disease
Cause = muscle ischemia by external pressure
External pressure exceeds venous & arterial pressure
Acute gross = dark & hemorrhagic
Chronic gross = pale

24
Q

Nutritional myopathy

What nutrients are deficient?

A

Selenium

Vitamin E

25
Q

What is the pathologic process in nutritional myopathy?

A
  1. Loss of antioxidant defense mechanisms
  2. Muscle is very sensitive to oxidative injury
  3. Loss of ability to maintain ion gradients
  4. Calcium induced hypercontraction
    Basal lamina is left INTACT
26
Q

Who is most affected by nutritional myopathy?

A

Pigs & herbivores
Young animals = esp in utero
Clinical signs may worsen with physical activity

27
Q

What do lesions look like in nutritional myopathy?

A
Pale muscle = "white muscle disease"
Mineralization of tissue
Thigh & shoulder
Young animals = tongue & neck
Bilaterally symmetrical
May have myoglobinuria
28
Q

Names for Nutritional Myopathy

A

White muscle disease
Stiff lamb disease
Mulberry heart disease (swine)

29
Q

Toxic degenerative diseases of muscle

A

Difficult to distinguish from nutritional
Do NOT act on Vit E or Selenium
MORE lethal than nutritional deficiencies
Mineralization of tissues is common

30
Q

Monensin Toxicity

A
Antibiotic fermentation produce (Streptomyces)
Growth promotion in ruminants
Coccidiostat in birds, etc
Monogastrics (horses) = toxic
Ruminants = toxic at HIGH doses
31
Q

How is Monensin toxic?

A

Distorts membrane transport of Na and K
Calcium overload
Death of skeletal & cardiac muscle

32
Q

Clinical signs of Monesin Toxicity

A
Lethargy
Stiffness
Muscle weakness
Recumbency
Horses = colic symptoms
Pale STREAKS in muscle tissue
NO mineralization!
33
Q

Exertional mypoathy

A
Buildup of lactic acid
Coagulation of contractile proteins
Water is lost to intersitium = pressure & ischemia
Myoglobinurua
Metabolic acidosis
34
Q

Other names for exertional myopathy?

A

Exertional rhabdomyolysis (necrosis)
“Monday morning disease”
“Tying up”

35
Q

Two types of exertional rhabdomyolysis

A
  1. Sporadic

2. Recurrent

36
Q

Sporadic exertional rhabdomyolysis

A

Following exercise with prior good performance
Stiff stride, sweating, elevated RR
Reluctance to move
Myoglobinuria = affects kidneys!
Painful cramps
Muscles = gluteal & lumber regions
Histo = swollen vacuolated disrupted myofibers

37
Q

Why does sporadic exertional rhabdomyolysis occur?

A

Exercise exceeded the horse’s underlying state of training
Need 4-8 weeks of rest to repair muscles!
Maybe affected by viral infections

38
Q

Recurrent exertional rhabdomyolysis (RER)

A

Occurs even with light exercise
Recovery is rapid
NO gross lesions
Autosomal dominant trait

39
Q

Pathogenesis of RER

A

Alteration in muscle Ca regulation
DECREASED threshold for contracture
Disorder in carbohydrate storage and utilization
= Polysaccharide storage myopathy (PSSM)
= Insufficient energy production by fibers