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Gross Anatomy > Quiz 2 Material > Flashcards

Quiz 2 Material Flashcards

1
Q

ATP

A

Energy of the cell
Requires as much ATP to relax muscle as to contract
Addition of ATP allows myosin to interact with actin
Muscle movement = continuous breakdown and reconstitution of ATP

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2
Q

Aerobic Pathway

A

Type I Muscles Prefer
Location: Mitochondria
More Efficient, Slower
Uses Fatty Acids to make ATP

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3
Q

Fatty Acids

A

Stored in fat cells

Must be released into blood stream (triglycerides) during exercise for aerobic pathway

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4
Q

Anaerobic Pathway

A

Creatine Phosphate- used first- allows muscle to immediately contract (always small amount stored)
Glycogen- used second- produces ATP via glycolysis
Lactic Acid- by product of glycolysis
Brain can only produce ATP anaerobically!!!

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5
Q

Exercise (Metabolic View)

A

Phase 1- first few min, creatine phosphate and glycogen primary fuel source
**want to shift to phase 2 quickly
Phase 2- aerobic metabolism & use of fatty acids to produce ATP
**want to stay in phase 2 as long as possible
Phase 3- back to anaerobic (use remaining stored glycogen in muscle fibers and liver cells); lactic acid accumulates

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6
Q

Carb Loading

A

Only for endurance
Goal: Increase storage of glycogen in muscle fibers (Prevent using glycogen from liver during Phase 3- save for NS)
Doesn’t increase strength/run faster
Side effects: hypoglycemia, weight gain (3 grams water:1 gram glycogen)

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7
Q

Caffeine

A

1 hr before event: ingestion may help burn fatty acids more efficiently & increase Ca permeability
Delay glycogen utilization (Phase 1 to Phase 2 faster)
1000mg threshold for competition (only supplement with threshold)

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8
Q

Blood Doping / Induced Erythrocythemia

A

Affects any phase (oxygen always needed)
-increase O2 carrying capacity of RBCs
(Increase concentration of RBCs = increase endurance= exercise longer)

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9
Q

Risks of Blood Doping

A
  1. Rashes/fever
  2. Acute hemolysis (breakdown of RBC’s)
  3. Transmission of viruses
  4. Fluid overload (kidney damage, intravascular clotting)
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10
Q

Erythropoietin (EPO)

A

Natural hormone produced by kidneys

Travels to bone marrow to produce RBC

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11
Q

Synthetic EPO

A

Used to increase RBC concentration

Thickens blood -> cardiac problems and death

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12
Q

Anabolic Steroids

A

Synthetic form of testosterone

“Minimal” androgenic effects and “more” androgenic

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13
Q

Anabolic

A

Stimulation of protein synthesis

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14
Q

Androgenic

A

Development of secondary sexual characteristics

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15
Q

Oil Based

A

Injected

Fewer side effects, detectable longer

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16
Q

Water Based

A

Pill form

More side effect, cleared from body faster

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17
Q

Stacking

A

Take several forms of drug

18
Q

Pyramiding

A

Start with low dosage, raise to a peak, then taper down amount taken

19
Q

Short term side effects of Anabolic Steroids

A 
Acne (esp. back)
Shrinkage of testes
Increased aggressiveness
Gynecomastia
Tendon damage
20
Q

Why is tendon damage a short term side effect of steroids?

A

Tendons respond slowly to strength regimes

Steroids my inhibit formation of collagen (main constituent of tendons and ligaments)

21
Q

Long term side effects

A

CVS
Digestive system
Reproductive System
Endocrine System

22
Q

Adolescent use of steroids

A

Premature closing of growth plates

23
Q

Anabolic steroids work by

A
  1. Increasing secretion of growth hormone

2. Activates protein synthesis and prevents protein breakdown

24
Q

Chemical composition of muscle

A

75% water
20% Protein (mostly myosin)
5% Other

25
Q

Nerve Supply of Skeletal Muscle

A

Motor Nerve Fiber (efferent/motor impulse)

Sensory Nerve Fiber

26
Q

Motor Unit

A

Single motor neuron (nerve fiber) and the group of muscles fibers it supplies

27
Q

Strength of muscle contraction depends on…

A

Number of motor units begin activated/ recruited at same time

28
Q

Size of motor unit (number of fibers in unit) indication of…

A

How much fine control (precision) muscle carries out

29
Q

More Precision a muscle has means…

A

Fewer fibers

30
Q

Neuromuscular Junction

A

Presynaptic portion
Postsynaptic portion
Synaptic cleft

31
Q

Presynaptic portion

A

Nerve ending

32
Q

Postsynaptic portion

A

Sarcolemma of muscle fiber

33
Q

Synaptic cleft

A

Space between pre and post synaptic portions

34
Q

How a nerve impulse makes its way from presynaptic to postsynaptic portion of neuromuscular junction (Steps)

A
  1. Neve impulse reaches presynaptic portion of NMJ
  2. NT ACH is released
  3. ACH will diffuse across synaptic cleft and bind to specific receptor site on sarcolemma of muscle fiber
  4. Binding will result in setting off an action potential down transverse tubule
  5. Actin and myosin interact, causing muscle contraction
  6. Acetylcholinesterase destroys ACH when task is completed
35
Q

Myasthenia Gravis

A 
Most common neuromuscular junction disorder
Autoimmune Disorder (ABS damage/destroy ACH receptor sites on sarcolemma of muscle fibers)
36
Q

Co-morbidities with Myasthenia Gravis

A

Hyperplasia of thymus gland
Thymoma
Gland probably giving incorrect information to immune system about ACH receptor sites

37
Q

Transitional neonatal myasthenia Gravis

A

25% pregnant women will transmit condition to infant

Condition eventually passes once maternal ABS are passed from infant’s system

38
Q

Nicotine

A

Competitive inhibitor with ACH

Action is much more prolonged than ACH (no enzyme to break it down)

39
Q

Snake Venom

A

Competitive Inhibitor
Cytotoxin- destroys tissue
Neurotoxin- makes way to NMJ and competes with ACH to bind at receptor- No action potential produced

40
Q

Organophosphates

A

Inactivate ACHe

Accumulation of ACH at postsynaptic portion of junction- muscles remain contracted

41
Q

Botulin Toxin

A

Blocks release of ACH from presynaptic portion of NMJ

Gross Anatomy (18 decks)

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