Muscle biochemistry Flashcards

1
Q

5 functions of muscle

A
  1. locomotion
  2. autonomic response - dilation
  3. homeostatis - BP, temp
  4. thermal generation
  5. metabolic regulation
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2
Q

2 things that create strength in mucles

A
  1. four fascia

2. many small compartments

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3
Q

descending order of muscle

A

body>fascicle>fiber>fibril>filament

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4
Q

4 ways muscles maintain coordination

A
  1. nerve transmission
  2. multinucleated cells
  3. SR
  4. T-tubules
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5
Q

define z-line

A

alpha actinin - where actin attaches

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6
Q

define z-line to z-line

A

sarcomere

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7
Q

define A-band

A

where think filaments exist

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8
Q

define H-band

A

space between myosin and actin - zone of functional reserve - that filaments can move against each other

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9
Q

define I-band

A

distance between mysoin and z-line - also zone of functional reserve

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10
Q

4 basic components to thin filament

A
  1. G-actin - monomers
  2. F-actin - double helix of g-actin
  3. tropomyosin - string that associated with actin
  4. troponin - complex of Ca regulated contraction
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11
Q

3 types of troponin and what they bind

A
  1. T- binds tropomyosin
  2. I - binds f-actin
  3. C - binds Ca
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12
Q

what happens to troponins in MI

A

releases

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13
Q

3 requirements of WHO def of MI

A
  1. EKG changes
  2. elevated cardiac enzymes
  3. typical physical symptoms
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14
Q

how many Ca can a trop. C bind?

A

4, but usually has 2 bound already

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15
Q

what happens when trop C binds Ca?

A

conformation change>allows myosin to bind actin>contraction

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16
Q

what is required for myosin to move forward to bind actin?

A

ATP

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17
Q

why is dose response of drug not linear

A

cooperativity of binding of Ca

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18
Q

first step in contraction

A

release ACh

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19
Q

what does ACh receptor release

A

small volume of Ca into T-tubule

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20
Q

what allows Ca into sarcolemma

A

L-type channel

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21
Q

what does Ca stimulate inside fiber

A

ryanodine receptor on SR

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22
Q

what does ryanodine receptor do?

A

releases large amount of Ca from SR

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23
Q

what does Ca do inside fiber

A

enters filament and bind to troponin

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24
Q

3 small ways to remove some Ca from fiber

A
  1. pump out for cost of ATP
  2. Na/Ca pump, then need to pump out Na/K pump for cost of ATP
  3. mitochondria can absorb some
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25
biggest way to get Ca back into SR
SERCA2a - ATP dependent
26
what is major inhibitor of SERCA
phospholambin (PLB) - prevents quick contractions
27
how to inhibit PLB
phosphorylate via PKA - allows contraction
28
what can be given to stimulate PKA
epinephrine via cAMP
29
what happens if L-type channel is dysregulated
arrythmias
30
what happens if mitochondria absorbs too much Ca
apoptosis
31
what happens if no reuptake
can't release any > no contraction
32
2 drugs that increase heart contraction
1. milronone - inhibits phosphodiesterase>so doesn't break down cAMP>more PKA>PLB is phosphyslated>allows SERCA to pump 2. dobutamine - via Beta-1 andronergic receptor>activates adenylate cyclase>more cAMP
33
what do catecholamines (epinephrin) do
also stims Beta-1 receptors, less specific and lead to blood vessel dilation, which can drop BP
34
what is malignant hyperthermia
mutation of ryanadine receptor that make it super reactive>pumps out Ca like crazy and overwhelms ATP use in SERCA > muscle breakdown and acidosis
35
5 things that happen in hyperthermia
1. cells contract but don't release 2. ATP hydrolysis - overheat 3. lose membrane potential - myoglobin in kidney 4. leads to apoptosis 5. releases H into blood - acidosis
36
2 types of muscle relaxants, what and how they work
1. depolarizing - succinylcholine - bind to Ach receptor when open - get inital contraction and then can't bind again 2. non-depolarizing - vecuronium - bind to closed receptor and don't allow reactivation
37
how to reverse muscle relaxants
neostigmine - stimulates release of Ach to outcompete neuromuscular blockade
38
L channel diffs. between cardiac and skeletal muscle
cardiac - L-channel v. important and triggers RYR, t-tubules better developed
39
communication diffs. between cardiac and skeletal muscle
cardiac - electrochemical | skeletal- multinulear
40
t-tubule diffs. between cardiac and skeletal muscle
cardiac - large | skeletal- small
41
receptor diffs. between cardiac and skeletal muscle
cardiac - many hormones | skeletal- Ach
42
cross bridge cycling diffs. between cardiac and skeletal muscle
cardiac - rapid strong contractions | skeletal- slower consistent contractiosn that don't tire
43
need for ECF Ca diffs. between cardiac and skeletal muscle
cardiac - Ca essential | skeletal- Ca not essential
44
**what is frank-starling law comparison of
stroke volume vs. ventricular end-diastolic volume
45
2 things that increase stroke volume
1. muscle contraction | 2. cardiac output
46
what determines ventricular diastolic volume
functional reserve of sarcomere
47
3 ways of increasing contractility
1. sympathetic stimulation (epinephrine) 2. inotrpoes - milrinone or dopamine 3. luisotropes - relaxes heart of over stimed
48
protein missing in smooth muscle
troponin
49
what does Ca bind to in smooth muscle
calmodulin
50
what does calmodulin do?
upregulates MLCK > phosphrylates MLC > contract
51
what does cAMP do in smooth muscle
inhibits MLCK > no contractions
52
what controls smooth muscles (2)
1. autonomic system | 2. hormones
53
how does B-andronergic control of smooth muscle happen
epinephrine>Beta2 receptor>incr. cAMP>activates PKA>phosphorylates MLCK which inhibits its action>relaxation
54
how is NO released
pressure or bradykinins (inflammation) in endothelial cell produce NO
55
how does NO dilate smooth muscle
NO moves into muscle cell and increases cAMP> inhibits contractions
56
3 ways to treat pathologic lung vasoconstriction
1. direct vasodilation via inhaled NO 2. increase smooth muscle cAMP : viagra 3. block vasocontriction - bosetan - antagonist of endothelin receptor
57
how to change blood flow up and down
dilate: nitroglyrcerine or nitrates contract: beta-1 andrenergic blockers
58
What happens in myasthenia gravis
antibodies to ACh receptors - chews them up>no contraction
59
treatment of myasthenia gravis
incr ACh at NMJ - remove thymus or give pyridostigmine
60
what causes lambert eaton syndrome
anitbodies against presynaptic voltage-gated Ca channels
61
what does botulism toxin do?
prevetns Ach release by digesting SNARE, a protein responsible for exocytosis
62
6 possible causes of loss of muscle stim.
1. upper motor neuron damage 2. lower motor neuron damage 3. congential metabolic disease 4. chonic illness - atrophy 5. immune reactions 6. autoimmune disease
63
what happens in muscular dystrophy
loss of anchor protein means muscle can't pull agains anything when it contracts
64
muscle energy source at rest
lipids
65
muscle energy source in low excercise
glucose and glycogen
66
muscle E source in high excrecise (2)
1. anaerobic glycolysis | 2. creatine phosphate conversion to ATP