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Physiology (712) > Muscle Tissue Pt 3 > Flashcards

Muscle Tissue Pt 3 Flashcards

1
Q

What are the different phases of tissue repair?

A

Destruction/Degeneration
Inflammation
Regeneration
Remodeling/Fibrosis

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2
Q

What occurs in the destruction/degeneration phase of muscle repair?

A
  • Initial rupture and necrosis of myofibers
  • Influx of Macrophages
  • Pro-inflammatory
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3
Q

What occurs in the Inflammatory phase of muscle repair?

A

-Local macrophages begin tissue clean up

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4
Q

What occurs in the Regeneration phase of muscle repair?

A

Satellite cells migrate to the area and begin reconstruction phase

  • Fibroblast begins producing connective tissue scar
  • Capillary ingrowth occurs
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5
Q

What is the function of Neutrophils in tissue repair?

A

these are WBCs that are the first to arrive on the sight of injury

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6
Q

What is the function of Monocytes in tissue repair?

A

these are the WBCs that arrive later and perform endocytosis, precursors to macrophages

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7
Q

What is the function of Macrophages in tissue repair?

A

M1 cleans the sight of injury, M2 release anti-inflammatory molecules and growth factors

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8
Q

What is meant by the phrase “Coordinated vascular and cellular response of the body to cell injury and cell death” as it relates to inflammation?

A

this is the definition of inflammation and the process of what occurs in this phase of injury

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9
Q

Erythema

A

redness- vasodilation and increase blood flow

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10
Q

Heat

A

if the area is warm- vasodilation and increased blood flow

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11
Q

Edema

A

fluid and cells leaking from local blood vessels into the extravascular spaces

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12
Q

Pain

A

Direct trauma; chemical mediation by bradykinins, histamines, serotonin; internal pressure secondary to edema; swelling of the nerve endings

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13
Q

Loss of function

A

keeps you from “return to play” ex. sprained ankle

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14
Q

Satellite cells

A

small mononuclear progenitor cells or stem cells with no cytoplasm

  • located in the sarcolemma and the BM of muscle fibers
  • quiescent until called upon for injury (chillin until needed)
  • function as a reserve population of the embryonic muscle called that can be recruited and stimulated to mature into adult muscle cells
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15
Q

Clinical significance of satellite cells with aging

A

numbers of satellite cells decline with age so it takes longer for an injury to repair

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16
Q

What is the fate of satellite cells and the path

A
  • after muscle damage occurs, they are activated
  • once activated, they become precursor muscle cells (skeletal myoblasts) and then merge with mature cells in the area of injury
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17
Q

Distinguish between a myoblast, myocyte, a myotube and a myofiber.

A
  • Myocytes are tubular muscle cells or fibers that develop from myoblasts. They are specialized as cardiac, skeletal, or smooth muscle cells.
  • myoblasts are a type of embryonic stem cell that gives rise to muscle cells.
  • Muscle fibers form from the fusion of myoblasts into multi-nucleated fibers called myotubes
  • Myofibers are muscle cells specialized to contract
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18
Q

Damaged muscle repair pathway

A

satellite cells -> proliferate -> myoblasts -> differentiate -> myocytes -> fusion -> myotube -> maturation -> myofibril

19
Q

Some cytokines act to make disease worse ______________, whereas others serve to reduce inflammation and promote healing ______________.

A

pro-inflammatory; anti-inflammatory

20
Q

Why are inflammatory responses important for a chronic disease state?

A

if you do not have pro and anti inflammatory (teeter-totter) balanced; you are more likely to have chronic conditions; chronic states prevents the return to balanced state between Pro and anti.
Tissue repair causes the teeter totter to become imbalance and when in balance (horizontal) it is the optimal state

21
Q

What are cytokines?

A

small proteins that are crucial in controlling the growth and activity of other immune system cells and blood cells. When released, they signal the immune system to do its job

22
Q

What are glucocorticoids?

A

a class of corticosteroid hormones that are prescribed as anti-inflammatory agents

23
Q

What are issues that may come up in the clinic with patients taking glucocorticoids?

A
  • Delayed wound healing (keep a close eye on surgical incisions when treating patients taking glucocorticoids)
  • Cause proximal muscle weakness
  • Linked to skeletal muscle atrophy, protein degradation, and slowed skeletal muscle recovery from injury
24
Q

Define M1 and M2 macrophage and describe their relative role in muscle tissue repair.

A
  • M1 and M2 are phenotypes of Macrophages that aid in cleaning and repair of damaged tissue.
  • M1 is found in greater numbers immediately after injury and they clean the area. A pro-inflammatory phase.
  • M2 is found in greater numbers days (48 or 72 hours) after initial injury, aids in the tissue recovery process and is anti-inflammatory stage.
25
Q

What is angiogenesis and why is it important?

A

Angiogenesis is the development of new blood vessels that allows for the exchange of materials in new forming tissue in order to function.

26
Q

What occurs in the Fibrosis/Remodeling phase of muscle repaid?

A
  • Myofibers form branches and try to penetrate the scar and form min-MTJ
  • Proinflammatory state transitions to anti-inflammatory state
  • In migration of fibroblast.
27
Q

What are fibroblasts? When are they helpful in the repair process? When are helpful? When are they damaging?

A
  • Fibroblasts replace ct and provide a scaffold for new tissue to grow into
  • They synthesize a new ECM and collagen.
  • They are helpful in the fibrosis/remodeling phase
  • Fibroblasts help to stabilize the tissue and create pathways for repair cells to follow
  • Fibroblast can delay or limit full functional recovery due to Fibrotic tissue deposition.
28
Q

What is Fibrosis of the muscle tissue?

A

an excessive accumulation of ECM components and collagen that can occur after muscle injury

29
Q

What are the PT implications of Fibrosis?

A
  • Occurs in muscular dystrophies, diabetes, immobilization, and aging
  • Is relevant because the connective tissue has a strong influence on the mechanical properties of muscle
  • Alters ROM
  • Goal of PT is to limit excessive fibrosis
30
Q

What is sarcopenia? How does it affect fiber type distribution? How might these changes impact basic muscle function?

A
  • sarcopenia is the loss of muscle associated with aging
  • there are less type II muscle fibers (fast-twitch) and more type I (slow twitch) muscle fibers
  • All of the muscle fibers are also smaller in size
  • Limit strength and power
  • As a PT we want to measure strength and write them an exercise program if patients are over 60
  • Can not completely stop sarcopenia but can try to change the rate at which it occurs
31
Q

What is myostatin?

A

Myostatin limits the growth of skeletal muscle and strength gain that can be achieved through wt training (really strong cow example)

32
Q

Explain muscle plasticity.

A

-ability of a given muscle to alter its structural and functional properties in accordance with the environmental conditions imposed on it

33
Q

What is a signal that drives muscle plasticity?

A

Stimulation

  • The more we get our pts to use their muscles, the better off they’ll be
  • We have to make use of the plasticity
34
Q

What tests and interventions might you use with a patient you suspect of being frail?

A
  • Injury and Fall prevention exercises (balance training)
  • Grip strength test
  • Gait speed
35
Q

“The bed is not your patient’s best friend”. Explain this phrase in terms of physiology

A

Laying in bed will detrain your muscles

36
Q

How active are healthy American adults. What does this mean for the practice of physical therapy?

A
  • 2/3 of pts that come into clinic don’t meet exercise guidelines
  • You can treat them beyond the specific problem they come in for
37
Q

Define Frailty

A

impaired mobility loss, loss of strength, slow gait speed, nutritional problems, reduced physical activity

38
Q

Define Prefailty

A

having 1-2 criteria that define frailty

-opportunity to practice PT to prevent the patient from completely becoming frail

39
Q

What is a phenotype?

A

Phenotype: set of observable characteristics of an individual resulting from the interaction of its genotype with the environment
Ex: gene responsible for eye color

40
Q

Explain the disability threshold.

A

-Go below threshold and are truly disabled
–Loss of many functions
–ADLs are impacted
-As we get older, we move towards the threshold
Perseverance of strength and maintaining exercise delays reaching threshold
–Goal as a PT

41
Q

Symptom Burden

A 
Deficiencies that the pt is experiencing for whatever reasons but they add up 
-How frequent your symptoms are
-Physiologic burden
-Can be physical or emotional
EX: 45 y/o who doesn't exercise
Enjoy steaks
Butter on the baked potato or in his coffee (aka JC)
Symptom burdens:
-SOB after physical activity 
-Trouble doing daily activities because they’re out of shape 
-High BP
-Type 2 diabetes 
-Geriatric pt carry significant burden
42
Q

Cachexia

A

“wasting” disorder that causes extreme weight loss and muscle wasting, and can include loss of body fat

  • associated with increased levels of cytokines, inflammatory markers and tumor products
  • upregulation of hypermetabolic activity
  • -constantly in a hypocaloric state and losing weight
  • autonomic dysfunction
43
Q

What are possible causes of cachexia?

A

cancer, CHF, kidney disease, AIDS

44
Q

Important differences between striated and smooth muscle

A 
Striated = located in heart, voluntary, multi nuclei, sarcomeres, all-or-none contractions
Smooth = located in visceral organs besides heart, involuntary, no sarcomeres, single nuclei, graded contractions, can contract individually, resistant to fatigue, found lining of hollow organs used to restrict flow

Physiology (712) (9 decks)

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