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Undeleted > Muscle biochemistry > Flashcards

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
Q

biggest way to get Ca back into SR

A

SERCA2a - ATP dependent

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26
Q

what is major inhibitor of SERCA

A

phospholambin (PLB) - prevents quick contractions

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27
Q

how to inhibit PLB

A

phosphorylate via PKA - allows contraction

28
Q

what can be given to stimulate PKA

A

epinephrine via cAMP

29
Q

what happens if L-type channel is dysregulated

A

arrythmias

30
Q

what happens if mitochondria absorbs too much Ca

A

apoptosis

31
Q

what happens if no reuptake

A

can’t release any > no contraction

32
Q

2 drugs that increase heart contraction

A
  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
Q

what do catecholamines (epinephrin) do

A

also stims Beta-1 receptors, less specific and lead to blood vessel dilation, which can drop BP

34
Q

what is malignant hyperthermia

A

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
Q

5 things that happen in hyperthermia

A
  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
Q

2 types of muscle relaxants, what and how they work

A
  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
Q

how to reverse muscle relaxants

A

neostigmine - stimulates release of Ach to outcompete neuromuscular blockade

38
Q

L channel diffs. between cardiac and skeletal muscle

A

cardiac - L-channel v. important and triggers RYR, t-tubules better developed

39
Q

communication diffs. between cardiac and skeletal muscle

A

cardiac - electrochemical

skeletal- multinulear

40
Q

t-tubule diffs. between cardiac and skeletal muscle

A

cardiac - large

skeletal- small

41
Q

receptor diffs. between cardiac and skeletal muscle

A

cardiac - many hormones

skeletal- Ach

42
Q

cross bridge cycling diffs. between cardiac and skeletal muscle

A

cardiac - rapid strong contractions

skeletal- slower consistent contractiosn that don’t tire

43
Q

need for ECF Ca diffs. between cardiac and skeletal muscle

A

cardiac - Ca essential

skeletal- Ca not essential

44
Q

**what is frank-starling law comparison of

A

stroke volume vs. ventricular end-diastolic volume

45
Q

2 things that increase stroke volume

A
  1. muscle contraction

2. cardiac output

46
Q

what determines ventricular diastolic volume

A

functional reserve of sarcomere

47
Q

3 ways of increasing contractility

A
  1. sympathetic stimulation (epinephrine)
  2. inotrpoes - milrinone or dopamine
  3. luisotropes - relaxes heart of over stimed
48
Q

protein missing in smooth muscle

A

troponin

49
Q

what does Ca bind to in smooth muscle

A

calmodulin

50
Q

what does calmodulin do?

A

upregulates MLCK > phosphrylates MLC > contract

51
Q

what does cAMP do in smooth muscle

A

inhibits MLCK > no contractions

52
Q

what controls smooth muscles (2)

A
  1. autonomic system

2. hormones

53
Q

how does B-andronergic control of smooth muscle happen

A

epinephrine>Beta2 receptor>incr. cAMP>activates PKA>phosphorylates MLCK which inhibits its action>relaxation

54
Q

how is NO released

A

pressure or bradykinins (inflammation) in endothelial cell produce NO

55
Q

how does NO dilate smooth muscle

A

NO moves into muscle cell and increases cAMP> inhibits contractions

56
Q

3 ways to treat pathologic lung vasoconstriction

A
  1. direct vasodilation via inhaled NO
  2. increase smooth muscle cAMP : viagra
  3. block vasocontriction - bosetan - antagonist of endothelin receptor
57
Q

how to change blood flow up and down

A

dilate: nitroglyrcerine or nitrates
contract: beta-1 andrenergic blockers

58
Q

What happens in myasthenia gravis

A

antibodies to ACh receptors - chews them up>no contraction

59
Q

treatment of myasthenia gravis

A

incr ACh at NMJ - remove thymus or give pyridostigmine

60
Q

what causes lambert eaton syndrome

A

anitbodies against presynaptic voltage-gated Ca channels

61
Q

what does botulism toxin do?

A

prevetns Ach release by digesting SNARE, a protein responsible for exocytosis

62
Q

6 possible causes of loss of muscle stim.

A
  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
Q

what happens in muscular dystrophy

A

loss of anchor protein means muscle can’t pull agains anything when it contracts

64
Q

muscle energy source at rest

A

lipids

65
Q

muscle energy source in low excercise

A

glucose and glycogen

66
Q

muscle E source in high excrecise (2)

A
  1. anaerobic glycolysis

2. creatine phosphate conversion to ATP

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