Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Unit 3 > Tevald > Flashcards

Tevald Flashcards

1
Q

Place in order from largest to smallest the parts of the muscle.

A

Epimysium -> contains fascicles the lining of which is perimysium (contains blood vessels), -> contain myofibrils or myofibers encased by the endomysium -> myofibrils are made of sarcomeres which are made of myofilaments (actin and myosin).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name all of the bands/structures in a sarcomere.

A

From z-disc to z-disc is a sarcomere. The M-line is in the middle. The H zone is ONLY myosin (tails, specifically). The A bands are where the myosin and actin are actively overlapping. The I zones are where the actin is alone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tell me bout the triad in the sarcolemma.

A

It’s two Ryanodine receptors surrounding a t-tubule. The ryanodine receptors mediate the release of the Ca+ from the SR. The T-tubule receives the depol signal through DHP receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Distinguish troponin from tropomyosin.

A

Troponin is where the myosin heads bind (also Ca+). Tropomyosin blocks the myosin from bonding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are Titin and nebulin chiefly responsible for?

A

Stabilizing actin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is desmin responsible for?

A

Attaching myofibrils to each other and to the sarcolemma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is dystrophin responsible for and what happens if it is inactive?

A

It’s responsible for stabilizing the sarcolemma during contraction. When we don’t have this we can get a lot trauma in the muscle that doesn’t heal properly. In men (males only!) a mutation in dystrophin causes failed muscle regeneration, atrophy, weakness, and intramuscular fat and scar tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do the golgi tendon organs detect?

A

Stretch in tendons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the two ways that a muscle can “grow”?

A

In number of cells = hyperplasia. Only happens in prenatal and post natal env.

In size = hypertrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do muscles do?

A

Produce force, passively and actively.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do muscles produce force?

A
  1. NM transmission
  2. Excitation-contraction coupling
  3. Cross-bridge cycling
  4. Calcium re-uptake and relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where does the NM transmission occur?

A

From the brain to depolarization in the sarcolemma, then into the SR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the process of Excitation Contraction Coupling.

A

The action potential from the Ryanodine receptors in the SR pass a depol signal to the DHP receptors on the t-tubule. The t-tubule then releases Ca+ that starts Cross Bridge Cycling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the process of cross-bridge cycling.

A

Troponin causes tropomyosin to swing out of the way which then exposes the active site on actin for the myosin head to latch. Z-lines move closer together / the muscle contracts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the relationship of ATP to Crossbridge Cycling.

A

Actin + myosin happens when ATP comes along and is used to bind myosin to actin. When this happens we have an extra phosphate and ADP. Rigor Mortis happens because there is no ATP present in the body upon death. Myosin heads stay latched.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the process of Ca+ re-uptake and relaxation.

A

Ca+ leaves the troponin which then hides the site of the attachment again (tropomyosin covers again).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why is muscle force devpt slower than action potentials?

A

Ca+ peaks in 5-6ms, and then is resequestered in SR in 40-60 sec - SO… this takes so long because the tendon has an elastic component that pulls on the bone and requires time. The mechanical response to an action potential is much slower than Ca++ dynamics because of the “series elastic component”.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What determines how much force a muscle can produce? From an architectural perspective?

A

Sarcomere arrangement, yo.
In series, will determine muscle length / how much shortening we can do.
In parallel, will determine CSA and therefore strength.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How are the soleus and sartorius an example of how form follows function?

A

The soleus’s fiber length is short, but the PCSA is large - this is because it propels the whole body forward, but experiences very little excursion.

Compare this to the sartorius, the fiber length is long, but the PCSA is small - this experiences long excursion, but produces little force.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are some of the key mechanical relationships that dictate muscle performance?

A
  1. Resting muscle is elastic. Can cause passive insufficiency - think of where you test ham length. You can also get active insufficiency (grip, when the wrist is flexed is weaker). Passive tension can also compensate for muscle weakness as in a tenodesis grip.
  2. Muscle length determines force generating capacity. Length determines how much overlap you’ve got. If you have more crossbridges, you have more force.
  3. The highest force is a result of active and passive forces.
  4. The velocity of a contraction impacts crossbridge formation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is muscle force graded (4 thangs)?

A
  1. Physiological CSA - # of sarcomeres in parallel
  2. Muscle Length - determines degree of myofilament overlap
  3. Velocity of contraction - impacts cross-bridge kinetics.
  4. Degree of activation of the muscle - recruitment and rate of firing
22
Q

What role do motor units play in the grading of muscle force?

A

The more motor units that fire, the more force you get. These are recruited from smallest to largest.

Also, the rate of firing motor units effects this too.

23
Q

Why adapt?

A

Because muscle is highly plastic.

24
Q

What is increased use?

A

Metabolic Stress - low load, long duration

Mechanical Stress - high load, short duration

25
Q

How does a muscle adapt to endurance training?

A

PGC -1 alpha, is a key regulator of a muscle’s response to mechanical stress.

Basically this regulates the mitochondrial biogenesis.

26
Q

What happens to a muscle’s CSA as it gets stronger and how long does it take?

A

The CSA increases but this is because there are more sarcomeres in parallel (not in series - that would effect length).

This typically takes about 6-8 weeks.

27
Q

What drives hypertrophy in the muscle and what activates this?

A

MTORC1, drives protein synthesis, activated by mechanical stress, growth factors, and amino acids.

Satellite cell activation -» adds new nuclei.

28
Q

In the creepy picture of a jacked bull what is the bull missing?

A

Myostatin, which is a muscle synthesis inhibitor.

29
Q

What influences the magnitude of hypertrophy?

A

Dose
Training status
Muscle type (UE vs. LE, a single muscle, fiber type)
Individual factors (age, health status)

30
Q

Type II fibers experience _______ hypertrophy than type I fibers.

A

MORE

31
Q

Which muscles have the most potential for hypertrophy: Proximal / Middle / or Distal?

A

Distal

32
Q

What are “neural factors”?

A

Motor learning
-improved coordination of synergistic vs. stabilizers vs. antagonists.

Increased agonist activation.

*think of that monkey, yo.

33
Q

What is some indirect evidence for increased agonist activation?

A

Bilateral deficit - the sum of 2 legs does not equal legs added.
Cross-over effect
Imagined contractions increase strength

34
Q

What are some potential mechanisms of increased neural activation?

A

Your max motor unit firing rate.

The pattern of your firing - so, you might get better synchronicity or more firing at the same time.

35
Q

What causes muscle damage?

A
  1. External trauma
  2. Ischemia
  3. Diseases - inflammation, muscular dystrophy, muscle tears
  4. Contraction-induced exercise
36
Q

What are the signs/symptoms/markers of muscle damage?

A

Damage to structure: z-line streaming, usually more in the type II fibers, usually for 24-48 hrs (DOMS, from pressure in fibers)

In an MRI - t2 weighted images show damage bc they show swelling of the fibers.

Creatine Kinase in the blood

Force Loss

37
Q

What are the three hypotheses for force loss?

A 
#1 - popping sarcomeres
#2 - calpain induction (calpain is a protease which might be digesting desmin which holds z-discs together). 
#3 - an EC-coupling dysfunction
38
Q

How does the muscle respond to damage?

A

It repairs by regeneration:

  1. Digestion of damaged components.
  2. Proliferation of satellite cells.
  3. Fusion of satellite cells into myotubes
  4. Synthesis of contractile proteins.

It can also repair by fibrosis (in disease states and with repeated trauma).

39
Q

What is the repeated bout effect?

A

Pain/damage/force loss are significantly less following a second bout of ecc exercise 1-2 weeks following the initial bout.

40
Q

How do NSAIDS affect the response to damage?

A

NSAIDS inhibit COX 1 & 2 which decreases satellite cell differentiation, proliferation, and fusion.

BUT NSAIDS following muscle damage are associated with an increase in force in the short term but a decrease in force in the long term.

41
Q

What are the clinical implications of muscle damage?

A

Muscle damage occurs with unaccustomed exercise - pt. education is super important.

42
Q

What is the purpose of the immune system and how is it organized towards this goal?

A

To defend the body against pathogens or abnormal cells.

It is organized by the 3Rs

  1. Recognize self and non-self (an antigen)
  2. Responds
  3. Remembers
43
Q

How do the innate and adaptive parts of the immune system differ?

A

The innate system is rapid, non-specific (so might damage healthy tissue), has no memory

The adaptive system is slow, specific, and remembers.

44
Q

What are the components of the innate immune system?

A

Physical and chemical barriers

Inflammation

45
Q

What are the 4 components of inflammation that contribute to a non-specific response?

A

Mast and Dendritic Cells - sound the alarm
Phagocytic leukocytes - become antigen presenting cells (after eating the cells they are after)
Complement System - proteins that enhance inflammation
Natural Killer Cells - don’t recognize self or non-self, just stressed cells

46
Q

What are the major components of the adaptive immune system?

A

Lymphocytes!!!

B cells mediate the humoral response against free-floating pathogens. This is 10-20% of lymphocytes. These respond to only 1 antigen.

T cells mediate the cell-mediated response (for pathogens in cells). This is 60-70% of lymphocytes. These recognize MHC 1 on cells.

47
Q

How does the immune response work?

A

Physical Barriers -> Inflammation -> Recognition (basically everything goes to the lymph nodes to be taken care of) -> Response (see below)

B cells become plasma (most of these eventually die) and memory cells (which stay in the bone marrow).

T cells become helper T cells and Cytotoxic cells that kill infected cells.

48
Q

How do we obtain adaptive immunity?

A

Active: Infection (naturally acquired) or vaccine (artificially acquired)

Passive: antibodies from mother to fetus (naturally acquired) or injection of immune serum (artificially).

In the passive cases the immunity is temporary.

49
Q

What is are the four types of hypersensitivity? What are examples of disorders of each?

A

Type I - Immediate, ex: allergies, asthma, anaphylaxis
Type II - Antibody-mediated, ex: rheumatic heart disease, type II diabetes
Type III - Immune Complex Mediated(these are actually in the tissues) ex: RA, vasculitis
Type IV - Cell-mediated (mediated by T cells - deadly cells), delayed hypersensitivity (bc this route takes longer, I think) - > poison ivy, or Type I diabetes, Crohn’s, MS.

Autoimmune Diseases - genetics, thought to be triggered by an infection - inflammation often a sign, and characterized by flare ups and remissions.

50
Q

What is immunodeficiency and what are some examples of problems with immunodeficiency?

A

Primary disorders are due to a genetic mutation. Ex: DiGeorge syndrome is the absence of a thymus, T and B cell disorders.

Secondary disorders are from other medical issues. Ex: HIV/AIDS (loss of T helper cells), DM, Cancer, OR, they can come from medical treatment - corticosteroids, cytotoxic drugs, or cyclosporine which is a drug that is given upon organ transplant.

51
Q

How does the immune system affect organ transplantation? What types of grafts are possible?

A

Success depends on MHC match OR lifelong immunosuppression.

Autograft - from yourself
Isograft - from a twin
Homograft/Allograft - from the same species
Xenografts - from another species

Unit 3 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions