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MSK: Back/Vertebral Column > Muscle Physiology- Keagan > Flashcards

Muscle Physiology- Keagan Flashcards

1
Q

How is cytosolic calcium removed in skeletal muscles and cardiac muscles

A

Skeletal muscle- SERCA only
Cardiac muscles- SERCA and Na/Ca exchanger

SERCA= sarco-endoplasmic reticulum Calcium ATPase

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2
Q

Magnitude of Calcium release in skeletal muscle vs cardiac muscle

A

Ca induced Ca release from sarcoplasmic reticulum in both
Skeletal muscle- magnitude of SR calcium release can not be altered
Cardiac muscle- magnitude ca be altered

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3
Q

Gap junctions between cells in skeletal vs cardiac muscles

A

Skeletal- absent
Cardiac- present- AP can travel from cell to cell

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4
Q

Skeletal muscle functions

A

Move skeleton
Posture/maintenence
Soft tissue support/internal organ protection
Respiration/voluntary control of digestive and urinary tracks
Body temp regulation

Properties:
Excitability
Contractability
Elasticity

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5
Q

What is a motor unit

A

Alpha motor neuron and all the muscle fibers that supplies it

Postural muscles w tonic contractions= thousands of muscle fibers in motor unit

Smaller muscles/quick response= 1-10 muscle fibers

Lesion of motor unit= paralysis/atrophy

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6
Q

The only adequate stimulus for skeletal muscle is __

A

Nervous impulse

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7
Q

Each muscle fiber is a single ____ cell

A

Multi nucleaated

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8
Q

Three components of actin and what they do

A

Actin- two strands
Tropomyosin- cover myosin binding sites on actin
Troponin- Ca regulator- detects Ca and will tell tropomyosin to leave

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9
Q

Desmin

A

Rod/ column looking thing that holds Z line to sarcolemma

Myofibrillar myopathies

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10
Q

Dystrophin

A

Poly peptide chain/rope looking thing
Holds thick filaments to proteins within sarcolemma

Duchennes muscular dystrophy

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11
Q

Titin
Disease?

A

Thick filament to Z line

stabilize the thick filament, center it between the thin filaments, prevent overstretching of the sarcomere, and to recoil the sarcomere like a spring after it is stretched.

Dilated cardiomyopathy

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12
Q

What enzymes aid in Ach synthesis and degradation

A

CAT (choline acetyltransferase)- synthesizes (choline+ acetyl CoA= Ach)
ACE (acetylcholinesterase)- degrades (Ach= choline + acetate)

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13
Q

Explain what prevents and allows neurotrasmitter exocytosis

A

Before AP- presynaptic vesicle is filled with NT docks- exocytosis impossible
Ca enters= synaptoagmin (regulatory protein/Ca regulator) changes positioning
This change forces the fusion of vesicles to cell membranes= exocytosis

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14
Q

Myasthenia Gravis

A

chronic autoimmune disorder
weakness and rapid fatigue of voluntary muscles.
Immune system creates antibodies that block, destroy or alter Ach receptors= less muscle contraction

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15
Q

Tensilon test

A

Tests for Myasthenia Gravis
- injects Tinsilon (acetylcholinesterase inhibitor) that doesnt break down Ach in NMJ
-this increases Ach in NMJ
If muscle strength improves=positive for myasthenia Gravis

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16
Q

How does botulinum toxicity affect action potentials

A

Botulinum toxicity inhibits the release of Ach from presynaptic nerve

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17
Q

Organic Phosphates poisoning

A

Organophosphate pesticide blocks ACE which prevents Ach breakdown

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18
Q

Myorelaxants

A

Cause myorelaxation by blocking the NMJ

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19
Q

What is a Twitch and its phases

A

Twitch- muscle contraction caused by single AP
1. Latent period- excitation- contraction/no tension
2. Period of contraction- x bridges are forming- tension rises/muscle shortens
3. Period of relaxation- calcium return to SR, tension decrease/ muscle length to normal

20
Q

Stages of excitation contractions coupling

A
  1. AP spreads along sarcolemma and inside T-tubules
  2. Dihydropyridine receptors (voltage sensors) open VG Ca channels (Ryanodine receptors)
  3. Ca released into sarcoplasm from cisterns
  4. Ca binds to C-subunit of troponin
  5. Myosin binding site son actin are uncovered= ready to contract
21
Q

Eaton-lambert myasthenia (ELM)

A

Antibodies destroy VG Ca channels in presynaptic nerve

Decreases Ca influx= decrease Ach release

Failure of neuromuscular transmission and muscle weakness

22
Q

Malignant Hyperthermia

A

Genetic defect of ryanodine receptor (aids in release of Ca into sarcoplasm)

Causes sustained muscle contractions, excessive O2 consumption and CO2 production, acidosis, hyperthermia

23
Q

Huxley-Hanson theory

A

Myofibrils contracted due to contraction of a lot of sarcomeres
Length of actin and myosin don’t change
Contraction is due to actin filamanets sliding along myosin filaments
Proces requires ATP

24
Q

What is rigor mortis

A

The state of muscle rigidity that develops after death
Muscle fibers depleted of ATP= no relaxation
Almost all myosin heads fixed to actin

25
Q

Metabolic myopathies are a group of genetic disorders that compromise ____

A

ATP production

26
Q

Total Tension= __ + __

A

Passive Tension + Active Tension

Passive- force generated due to stretch without contraction

Active- force generated by sliding of microfilaments proportional to number of active cross-bridges

27
Q

What creates a plateau in the level of force from a muscle

A

Max number of cross bridges

28
Q

What is Tetanus- complete and incomplete

A

Tetanus- result of summation of many contractions occurring in rapid succession- effects of previous contractions are still remaining before next occurs

Incomplete- stimulation is reduced- results in jerky contraction-relaxation of cycles (wavy)

Complete- sustained muscle contraction (straight)

29
Q

Clostridium tetanus

A

Toxin clostridium tetanus blocks release of inhibitory NTs (GABA/glycine) by Renshaw Cells
Results in repetitive stimulation of motor neurons= increased intracellular calcium= sustained muscle contraction= TETANUS

Ex. Lock jaw

30
Q

Isometric muscle contraction

A

No change in length/ no movement

31
Q

Isotonic

A

Movement of muscle and joint- change in length of muscle

32
Q

Structural peculiarities of smooth muscle

A

No sarcomeres
No T-tubules- but small caveoli
Not well developed SR (high dependence of ECF calcium
1/5 myosin of skeletal muscle
Longer myosin

33
Q

Single unit v multi unit

A

Applies to smooth muscle

Single unit- cells connected by gap jxns- muscle contracts as one whole unit (Uterus, bladder)

Multi unit- each muscle cells behaves as separate cell- fast response to stimuli (muscles of iris)

34
Q

Cholecytokinin stimulates contraction of __

A

Gall bladder

35
Q

Vasopressin and Angiotensin II stimulate contraction of __

A

Blood vessels

36
Q

Sildenafil enhances effect of ___ in ___

A

Enhances effect of nitric oxide (NO) in corpus cavernosum

37
Q

Nervous supply to smooth muscles
-supplied by __
- nervous endings form, __
-NT released into __

A
  • supplied by PNS/SNS
    -no synapses-nerve endings form varicosities
    -NTs released into extracellular fluid
    AP spreads to other cells along gap jxns
38
Q

Smooth muscle differences in excitability

A

Threshold is lower
AP amplitude is lower/longer
Depolarization opens up VG calcium channels, Ca influx slows repolarization

39
Q

Automaticity

A

The ability of cell to generate AP without any external stimuli

Smooth muscle slowly permeable to Na= depolarization w/o AP

40
Q

Smooth muscle Actin and myosin differences

A

-thin filament doesn’t have troponin
-myosin binding sites are always ready
-myosin heads are inactive at rest

41
Q

Excitation-contraction coupling in smooth muscle- how do differences Ca channels open

A

From extracellular space:
-VG Ca channel- open change in membrane potential
-ligand-gated- NT binding opens
-mechanical sensitive Ca channel- open in response to stretch stimulus

From SR
- chemical stimuli (NT, hormone,drug) bind to receptor on cell membrane—> cause intracellular formation of IP3–> IP3 bind to sarcoplasmic receptors to stimulate Ca release
-Ca-induced calcium release- Ca from outside comes in and opens intracellular Ca channel

42
Q

Cross-bridge cycling- smooth muscle

A

thick filament regulation
Cytoplasmic Ca bind to calmodulin (CaM)-
Ca-calmodulin complex binds to myosin light chain kinase (MLCK) and activates it
Active MLCK catalyzes phosphorylation of myosin light chain on myosin head
This causes conformational change that enables myosin to bind to actin

43
Q

Limiting factor that causes SM X-bridge to be slow

A

ATPase is slow

To stop cycle, the head must be dephosphorylated

44
Q

The latch phenomenon

A

If myosin head is inactive (dephosphorylated) while attached- cycle is finished VERY SLOWLY
-keeps smooth muscle partially contracted for low ATP cost

Allow smooth muscle to stay contracted for long time

45
Q

Why is the range length greater in smooth muscle?

A

Thick filaments are longer that skeletal muscle and force can be developed over greater range of stretched lengths

46
Q

Why is maximum force greater at optimum length in smooth muscle?

A

Because passive tension is much greater at optimal length
Smooth muscle forms hollow structures with a lot of connective tissue which gives it higher passive force

MSK: Back/Vertebral Column (12 decks)

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