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Skin/Musculoskeletal > SM: Week 4 > Flashcards

SM: Week 4 Flashcards

1
Q

In the Baltimore Classification system, what does group I mean?

A
  • dsDNA viruses

- go through typical cellular steps of transcription and translation

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2
Q

In the Baltimore Classification system, what does group II mean?

A
  • ssDNA viruses

- copied to a dsDNA intermediate through host; only +ssDNA becomes packaged

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3
Q

In the Baltimore Classification system, what does group III mean?

A
  • dsRNA viruses
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4
Q

In the Baltimore Classification system, what does group IV mean?

A
  • (+)ssRNA viruses
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5
Q

In the Baltimore Classification system, what does group V mean?

A
  • (-)ssRNA viruses
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6
Q

In the Baltimore Classification system, what does group VI mean?

A
  • (+)ssRNA viruses
  • replicate through DNA intermediate
  • reverse transcriptase within virion
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7
Q

In the Baltimore Classification system, what does group VII mean?

A
  • dsDNA viruses

- replicate through ssRNA intermediate

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8
Q

Answer the following for Paraymyxoviridae morbillivirus (Measles):

  • Genomic material
  • Baltimore Classification
  • Segmented?
  • Nucleocapsid structure
  • Enveloped?
A
  • (-)ssRNA
  • group V
  • No, it is not segmented
  • Helical
  • Yes, it is enveloped
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9
Q

Answer the following for Picornaviridae Enterovirus (Coxsackievirus A&B, Echovirus):

  • Genomic material
  • Baltimore Classification
  • Segmented?
  • Nucleocapsid structure
  • Enveloped?
A
  • (+)ssRNA
  • group IV
  • No, it is not segmented
  • Icosahedral
  • No, it is not enveloped
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10
Q

Answer the following for Papovaviridae Papillomavirus (HPV):

  • Genomic material
  • Baltimore Classification
  • Segmented?
  • Nucleocapsid structure
  • Enveloped?
A
  • dsDNA
  • group I
  • Circular genome
  • Icosahedral
  • No, it is not enveloped
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11
Q

Answer the following for Poxyviridae Molluscipoxvirus (Poxviruses, such as smallpox):

  • Genomic material
  • Baltimore Classification
  • Segmented?
  • Nucleocapsid structure
  • Enveloped?
A
  • dsDNA
  • group I
  • No, DNA viruses are not segmented
  • Complex (barbell)
  • Yes, it is enveloped
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12
Q

Answer the following for Herpesviridae Simplexvirus/Varicellavirus/Lymphocryptovirus (Herpes Simplex/Chickenpox/Cytomegalovirus):

  • Genomic material
  • Baltimore Classification
  • Segmented?
  • Nucleocapsid structure
  • Enveloped?
A
  • dsDNA
  • group I
  • linear
  • icosahedral
  • yes, it is enveloped
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13
Q

Answer the following for Parvoviridae Erythrovirus (Parvovirus B19):

  • Genomic material
  • Baltimore Classification
  • Segmented?
  • Nucleocapsid structure
  • Enveloped?
A
  • ssDNA
  • group II
  • linear
  • icosahedral
  • no, it is not enveloped
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14
Q

Answer the following for Togaviridae Rubivirus (Rubella):

  • Genomic material
  • Baltimore Classification
  • Segmented?
  • Nucleocapsid structure
  • Enveloped?
A
  • (+)ssRNA
  • group IV
  • No, it is not segmented
  • icosahedral
  • Yes, it is enveloped
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15
Q

Answer the following for Flaviviridae Flavivirus (Dengue Fever, West Nile Virus):

  • Genomic material
  • Baltimore Classification
  • Segmented?
  • Nucleocapsid structure
  • Enveloped?
A
  • (+)ssRNA
  • group IV
  • No, it is not segmented
  • Icosahedral
  • Yes, it is enveloped
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16
Q

Go study the different viruses and learn/review their: clinical presentation, pathology, diagnosis, and treatment.

A
  • HPV
  • Poxviruses (Molluscum Contagiosum, Smallpox)
  • Orf virus
  • VZV
  • HSV 1 & 2
  • EBV
  • Parvovirus B19
  • Picornaviruses (Coxsackievirus A&B, Herpangina)
  • Measles virus
  • Rubella virus
  • Flaviviruses (Dengue Fever, West Nile Virus)
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17
Q

In herpes viruses there are three different classifications used to denote where each virus goes during its latency period. Where do the viruses become latent in alpha, beta, and gamma classifications?

A
  • α: nerve cells
  • β: T cells, lymphocytes, monocytes
  • γ: B cells
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18
Q

What are the different types of shoulder dislocations?

A
  • Sternoclavicular
  • Acromioclavicular, “shoulder separation”
  • Scapulothoracic
  • Glenohumeral, “shoulder dislocation”
    • Anterior and posterior dislocations
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19
Q

What are the three main injuries that occur in the shoulder?

A
  • Rotator cuff pathologies
  • Dislocations
  • Fracture
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20
Q

What does it mean when someone has “Tennis elbow?”

A
  • It involves the lateral epicondyle and results in pain due to disease in the extensor tendon origin on the lateral epicondyle, primarily ECRB
  • Resolves with activity modification, gentle PT, and time
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21
Q

What does it mean when someone has “Golfer’s elbow?”

A
  • It involves the medial epicondyle and results from tendon disease of the flexor-pronator origin
  • Resolves with activity modification, gentle PT, and time
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22
Q

What is “nursemaid’s elbow?”

A
  • Occurs when the radius disarticulates with the humerus, but the ulna is still connected to the humerus
  • Caused by a traction (pulling) trauma that is low energy
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23
Q

What are the two main pathologies of the elbow?

A
  • Tendinopathies

- Dislocations

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24
Q

The ___________ is a critical link between the elbow and the _________. One must think about the combined injuries from these locations. What is the most common pathology in the region described above?

A

forearm
wrist

  • fracture of the distal radius is most common (Colles’ and Smith fractures)
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25
Q

What is the most commonly fractured bone in the wrist?

A

Scaphoid bone

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26
Q

What are the intrinsic muscles of the hand and what are the movements of the joints in the hand that they are responsible for?

A
  • Dorsal Interossei, Palmar Interossei, Lumbricals
  • Joints:
    • MP: flex
    • PIP: extend
    • DIP: extend
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27
Q

Go learn/review viruses and their associated diseases.

A
  • HPV - Warts
  • Poxvirus - MOlluscum contagiosum, smallpox
  • Orf virus
  • Herpes virus: Varicella Zoster, Herpes Zoster, Herpes Simplex 1 & 2, 6 & 7 (Roseola), EBV
  • Picornaviruses: Coxsackie A&B, Echovirus
  • Parvovirus B19: Fifth disease (erythema infectiosum)
  • Paramyxovirus: Measles (Rubeola)
  • Togavirus: Rubella
  • Flavivirus: Dengue Fever, West Nile Virus
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28
Q

What are Waddell’s signs for “non-organic back pain?”

A
  1. Sham tenderness: superficial and diffuse tenderness and/or nonanatomic tenderness
  2. Simulation tests: based on movements which produce pain, without actually causing that movement, such as axial loading and pain on simulated rotation
  3. Distraction tests: positive tests are rechecked when the patient’s attention is distracted
  4. Non-anatomic pain distribution
  5. Inappropriate affect
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29
Q

What is the most frequently diagnosed back problem in adults and what are its causes?

A
  • Mechanical LBP
  • Causes: muscle spasm, facet joint inflammation, SI joint dysfunction
  • Frequently followed by an inciting event 1-2 days before pain
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30
Q

What are some treatments for Mechanical LBP?

A
  • Early mobilization, PT, core stability, adjustment/manipulation, massage
  • Pain management: NSAIDs, steroids, narcotics, muscle relaxants, Ice/heat/E stim
  • Change lifestyle and improve fitness to actually improve LBP long term
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31
Q

What is the pathophysiology of Degenerative Disease in the Spine?

A
  • Gradual narrowing of spinal canal and/or neural foramina

- Osteophyte formation, facet hypertrophy, bulging disks, hypertrophy of ligamentum flavum

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32
Q

What is the clinical presentation of Degenerative diseases in the spine?

A
  • may have numbness, tingling, foot drop (esp. when standing)
  • may manifest as hip, knee, ankle or foot pain exclusively
  • imaging will reveal a narrowing of spinal canal
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33
Q

What is the treatment for Degenerative Disease in the Spine?

A
  • PT
  • Medications: corticosteroids, NSAIDs, narcotics
  • Dorsal column stimulators (implanted device)
  • Surgery
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34
Q

What is spondylolithesis?

A

Spondylolithesis is a forward slipping of one vertebrae on another, usually due to bilateral pars interarticularis defect on the vertebral spinous process

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35
Q

What is the clinical presentation of a patient with Spondylolithesis?

A
  • often asymptomatic unless after deconditioning + new activity
  • may have radicular symptoms with nerve root irritation
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36
Q

What is the treatment of Sponylolithesis?

A
  • Non-operative: pain medication, PT/activity, TENS/stimulator
  • Surgical: for patients with progressive slips, uncontrolled pain
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37
Q

What is the clinical presentation with a patient with an acute herniated disc?

A
  • LBP, radicular symptoms (sciatica), identifiable precipitant, numbness/tingling, motor symptoms (e.g. foot drop)
  • Physical exam findings: splinting, +/- tenderness, positive straight leg raise
38
Q

What is the treatment for acute herniated discs?

A
  • Active rest, oral steroids, pain medication, +/- PT, time (takes 3-6 months to resolve)
  • Surgery
    o Indications: pain, lesion on MRI, radicular symptoms, motor weakness
    o Microdiscectomy
    o Fusion: remove disc, place bone between vertebral bodies – lose motion, sets up for further injury elsewhere
  • 10 year follow up surgery vs non-surgical treatment shows no significant difference, but surgery is helpful in shorter term for many
39
Q

What is the definition and some causes of Sciatica?

A
  • Sciatica involves the general compression or irritation of one the five spinal nerves forming the sciatic nerve
  • Caused by disc disease, spinal stenosis, piriformis or peripheral entrapment, neurogenic claudication, other
40
Q

What are some causes of LBP in children?

A
  • Mechanical (less common than in adults)
  • Spondylolysis/Spondylolithesis (common in gymnasts – hyperextension of back)
  • Disc disease
  • Tumor
  • Infection
  • Rheumatologic
  • Visceral
  • Psychosomatic
41
Q

What does a single leg raise exam test?

A

Tests disc herniation (when positive, a disc is herniated)

42
Q

What does a leg hyperextension exam test?

A

This test puts stress on the pars interarticularis which is fractured in Spondylolysis; positive test would indicate a patient has Spondylolysis

43
Q

What does a bone scan show?

A
  • Shows active areas of growth in bones, esp. growth plates
  • If other areas of bone have intense areas of black that are not growth plates, this indicates the presence of a stress fracture
44
Q

What is Spondylolysis?

A
  • It occurs when the pars interarticularis is fractured which typically results in L5 - Scottie Dog collar
45
Q

What is the treatment for Spondylolysis?

A
  • Activity modification, time, bone stimulator
  • Rarely use bracing anymore
  • Surgery is possible – activity modification is usually sufficient
46
Q

What are some features of skeletal muscle?

A
  • Striated
  • Voluntary
  • Multinucleated with nuclei at cell periphery
  • Well-developed sarcoplasmic reticulum with T-tubule system located at A-I junction
    o Triads = T-tubule + 2 terminal cisternae
47
Q

What are some features of cardiac muscle?

A
  • Striated
  • INvoluntary
  • Sarcoplasmic reticulum less developed and T-tubule system is wider in diameter in comparison to skeletal muscle
    o T-tubules located at Z-disks
    o Diads = T-tubule + 1 terminal portion of sarcoplasmic reticulum
  • single nucleus/cell located in the center of the cell
  • Intercalated disks present; sometimes don’t stain
  • Presence of atrial granules specific to atrial cardiac muscle cells – contain atrial natriuretic peptide
48
Q

What are some features of smooth muscle?

A
  • NO striations
  • NO t-tubules; instead have caveolae that store/release Ca2+
  • INvoluntary
  • fusiform in shape
  • external lamina formed by reticular fibers and are involved in harnessing the force of contraction
  • Dense bodies attach actin and myosin not arranged in any precise order
  • Ca2+ - calmodulin complex activates myosin light chain kinase to phosphorylate the light chains on the myosin heads; this exposes the ‘actin-binding’ sites on myosin head
49
Q

Define myofiber

A

single muscle cell; composed of multiple myofibrils

50
Q

Define myofibril

A

composed of myofilaments; tiny, cylindrical rods within the sarcoplasm of muscle cells

51
Q

Define myofilaments

A

components of myofibrils; actin (thin) and myosin (thick) filaments, associated proteins

52
Q

Define actin

A

G-actin that dimerizes to form F-actin; F-actin becomes helically wound in strands; bound to Z-disk by (α-actinin) and extends to H-band

53
Q

Define myosin

A

composed of 4 light chains and 2 heavy chains and into heavy and light meromyosin; the heavy chains are polarized towards Z-disk

54
Q

Define troponin

A

Troponin is a complex with three different subunits: TnT, TnC, TnI
o TnT: binds troponin complex to tropomyosin
o TnC: has great affinity for Ca2+
o TnI: binds troponin complex to actin; prevents actin-myosin interactions

55
Q

Define α-actinin

A

anchors actin filaments to Z-disk and holds the actin filaments in parallel array

56
Q

Define t-tubule

A

part of sarcoplasmic reticulum and is responsible for storage/release of Ca2+
o Skeletal muscle – located at A-I junction
o Cardiac muscle – located at Z-disk

57
Q

Define nebulin

A

long, non-elastic protein that wraps around actin filaments and helps anchor them to the Z-disk; regulates the length the actin filaments achieve

58
Q

Define titin

A

large, elastic protein that position myosin filaments precisely within the sarcomere; acts like a spring

59
Q

Define caveolae

A

small vesicles that store/release Ca2+ in smooth muscle; equivalent to T-tubules in skeletal/cardiac muscle

60
Q

Define dense bodies

A

found in smooth muscle scattered throughout the sarcoplasm and underneath the sarcolemma; serve as Z-disks in smooth muscles and anchor actin filaments and intermediate filaments

61
Q

Define motor unit

A

ONE motor neuron and ALL the muscle fibers it innervates
o smaller the ratio of motor neurons to number of muscle fibers results in finer muscle control
- i.e. 1:1 = very fine control; 1:1600 = very coarse control

62
Q

What happens to the different bands within a sarcomere upon muscle contraction?

A

o A band remains constant
o I-band becomes smaller; may disappear as muscle shortens
o Z-disks come closer together (sarcomere shortens!)
o H-band narrows and eventually is not seen

63
Q

What is the structure of neuromuscular spindles?

A
  • consist of small specialized muscle fibers enclosed in two CT capsules: internal and external
  • central intrafusal cells contain nuclei with different arrangements:
    • nuclear bag fibers = nuclei mixed around
    • nuclear chain fibers = nuclei in a straight line
  • fusiform shaped (bigger in the middle, tapered towards ends)
64
Q

What is the function of neuromuscular spindles?

A
  • Act as miniature strain gauges
  • Sensory:
    • annulospiral/primary endings – located around mid-portions of nuclear bag and chain fibers; large diameter
    • flower spray/secondary endings – around the distant regions from the mid-region; smaller diameter
  • Motor:
    • efferent fibers form motor end plates on either side of mid-region of intrafusal fibers
65
Q

What is the structure and function of golgi tendon organs?

A

o Structure: spindle shaped bodies, enclosed by a thin capsule
o Function: have afferent fibers (Ib) that penetrate between collagen fibers and are sensitive to stretching forces on muscle tendons
• prevents over-contraction of muscle

66
Q

What is the structure and function of motor end plates?

A
  • Structure:
    • non-myelinated axon terminal branches occupy recesses in surface of muscle fiber; these recesses are called synaptic troughs/primary synaptic clefts
    • In the muscle, the subneural apparati/secondary synaptic clefts are made by infolding of the sarcolemma and have ACh receptors (aka nicotinic receptors) that react to ACh from the axon terminal
    • ACh was released via synaptic vesicle fusion with the axon terminus
  • Function: nerve impulse conduction to muscle to elicit an action
67
Q

What are the three types of channels in neurons?

A
  • “Leak” channels
  • Voltage gated channels:
    o Na+: activation voltage must be ~ -40mV; activating
    o K+: activation voltage ~ -20 to 0 mV; NOT inactivating
  • Selective/non-selective channels
68
Q

What are the three different types of potentials in neurons?

A
  • RMP = -70mV to relative to outside
  • Graded potentials: vary in amplitudes due to strength of stimulus (may be depolarizing (EPSP) or hyperpolarizing (IPSP)); bidirectional
  • Action potentials: “all or none” - amplitude independent of initiating event; starts with depolarization and ends with repolarization/hyperpolarization
69
Q

What is a length constant?

A
  • Length constants are determined by membrane resistance and axial resistance
    o membrane resistance: amount of channels open/closed – closed channels = greater resistance, greater length constant
    o axial resistance: > diameter of axon results in decreased resistance, ions flow further, increased length constant
  • It can transmits potential changes over long distances
  • when the amplitude has decayed away to a particular height - 37% of original amplitude
70
Q

What are the different stages of an AP and what are the actions of the channels involved at each stage?

  • draw out an action potential
A
  • Different stages:
    • #0: RMP
    • #1: EPSP sufficient to reach #2
    • #2: Action potential threshold: change from graded potential to AP
    • #3: “Rising phase”
    • #4: Peak (usually between 0 and +40mV)
    • #5: Falling phase - rapid repolarization (Vm > RMP)
    • #6: Afterhyperpolarization (Vm < RMP)
    • #7 Repolarization to RMP
  • Actions of channels during stages:
    • #0: primarily K+ leak channels are open; some Na+ leak open
    • #1: ligand gated and non-selective cation channels open
    • #2: VG Na+ activated and open
    • #3: VG Na+ channels open, some K+ channels open around 0mV
    • #4/5: DR K+ channels open, VG Na+ become deinactivated (closed) below -40mV
    • #6: DR K+ channels overshoot
    • #7: VG K+ channels close
71
Q

What is hyperkalemia and what is it caused by?

A
  • Hyperkalemia is a condition where there is persistent depolarization of a neuronal membrane
  • Caused by increased extracellular [K+] which causes depolarization of Vm. Thus VG Na+ channels cannot become deinactivated (closed) and are unable to generate APs resulting in no heart beat.
72
Q

What is the relationship between conduction velocity and axon diameter?

A

increase conduction velocity = increase in axon diameter

Conduction velocity depends on spacing of VG channels - myelinated fibers > unmyelinated fibers

73
Q

What type of neurons are associated with myelinated and unmyelinated fibers?

A
  • Myelinated fibers = motor neurons

- Unmyelinated fibers = sensory neurons (esp. pain)

74
Q

What are the two types of synapses in neurotransmission?

A
  • Electrial - passage of graded potential from one cell to another; passive
  • Chemical - active process, involves diffusion
75
Q

What are the three fundamental steps in chemical neurotransmission?

A
  • NT release
  • Receptor activation
  • NT inactivation
76
Q

What are the five steps of NT release?

A
  • Depolarize terminal membrane
  • Activation of VG Ca++ channels
  • Ca2+ entry
  • Change in conformation of docking proteins
  • Fusion of vesicles to plasma membrane
77
Q

What is Lambert-Eton syndrome?

A
  • It is an autoimmune disease in which peripheral VG Ca2+ channels are attacked which causes a decrease in Ca2+ triggered by NT release.
  • Manifests as muscle weakness that goes away with repeated contraction.
  • Treated with Diaminopyridine (DAP), a K+ channel blocker which prolongs APs in the presynaptic nerve by increasing the amount of Ca2+ that enters the cell
78
Q

What are the consequences of Botox toxin and Tetanus toxin?

  • Hint: both are involved in the docking/fusion steps in NT release
A
  • Botox toxin: destroys docking proteins in cholinergic nerves which results in decreased muscle contraction
  • Tetanus toxin: is transported across the synapse in a retrograde manner and results in decreased transmission and increased muscle contraction
79
Q

What is Dale’s Principle and what are the added stipulations to this principle?

A

In general, all axonal branches of a neuron release the same neurotransmitter substance or substances from each nerve terminal .

  • Applies only to axons, as dendrites can release different NTs than their associated axon terminal
  • Primary NTs have associated neuromodulator peptides that influence the action of the primary NT
80
Q

What are some different ionotropic receptors (7)?

A
  • nAChR
  • AMPA
  • NMDA
  • 5HT3
  • P2X (NT = ATP, involved in fast nociception)
  • GABA (IPSP)
  • Glycine (IPSP)
81
Q

What are some features of the nAChR?

  • Agonist
  • Number of subunits, binding sites
  • Type of receptor
A
  • Agonist = ACh
  • 5 subunits with 2 binding sites for ACh, which cause the channel to open
  • Non-selective cation channel - permits K+, Na+, and Ca2+ to enter
    o Na+ has the largest driving force at RMP (furthest from Erev of Na+)
    o As depolarization continues, the driving force for Na+ decreases and the driving force for K+ increases (causes K+ to leave the cell)
82
Q

What is Myasthenia Gravis?

A

Myasthenia Gravis is an autoimmune disease in which antibodies attack the nicotinic ACh receptor (nAChR) which causes rapid muscle fatigue and muscles that cannot sustain a muscle contraction.

  • Treatment involves preventing ACh degradation (aka AChE inhibitors) – allows the amount of ACh that is available to work on the rest of the available receptors
83
Q

What are the two types of glutaminergic receptors and what are they mainly involved in?

A
  • AMPA: excitatory neurotransmitter in brain

- NMDA: receptor for learning and memory

84
Q

What are some unique features of AMPA receptors?

A
  • It is a non-selective cation channel
  • Once glutamate binds, the channel opens; thus it is ligand gated
  • Opens/closes quickly due to desensitzation
85
Q

What are some features of the NMDA receptor and the mechanism by which it opens?

A
  • Both voltage regulated and ligand gated!!!!! – very unique to these receptors!! involved in memory and learning
  • Structure: binding sites for glutamate and an Mg2+ block within channel
  • Upon depolarization, the Mg2+ block is pushed away, glutamate is able to bind (released previously from presynaptic cell upon depolarization), the NMDA channel opens
    o Na+ keeps the NMDA channel open (positive feedback loop)
    o Ca2+ induces Ca2+ release which changes the function of the channel and leads to long-term potentiation and long-term changes in gene expression
86
Q

What are some features of GABA receptors?

  • Action and location of action
  • Function of receptor
A
  • Ligand gated
  • Predominant inhibitory receptor in the brain (spinal cord uses glycine)
  • It is a Cl- channel that elicits an IPSP upon influx of Cl-
  • IPSP occurs only if cell is depolarized above Erev of Cl- (-61mV)
  • If cell is hyperpolarized, then Cl- leaves the cell and causes the membrane to become depolarized
    o Net effect: stabilizes membrane potential around -61mV
  • Many drugs take action on the GABA receptor: barbituates, benzodiazapenes, ethanol (general anesthetics), etc.
87
Q

How is NT release terminated? There are three different mechanisms…

A
  • Diffusion (NTs diffuse out of synaptic cleft)
  • Enzymatic degradation (i.e. AChE action on ACh)
  • Reuptake (i.e. Monoamines, such as serotonin, are taken back up in the presynaptic cell terminus)
88
Q

What are examples of monoamines and how are they terminated?

A
  • Monoamines: dopamine, norepinephrine, serotonin
  • Terminated by reuptake

o Drug targets:
• tricyclic antidepressants: block reuptake of NE and serotonin
• cocaine and amphetamine: block all three monoamines from reuptake
• Specific Serotonin Reuptake Inhibitors (SSRIs): block serotonin (5HT) reuptake; used to treat depression

89
Q

What is the mechanism of muscle contraction starting with innervation, NT release, receptor interaction, signal transduction, Ca2+ release, and finishing with Ca2+ binding to troponin (TnC)?

  • Draw this out!
A
  • Motor neuron axon terminal, at NMJ, becomes depolarized due to saltatory conduction vis VG Na+ channels along axon
  • VG Ca2+ channels open upon depolarization reaching the axon terminus and cause an influx of Ca2+
  • The influx of Ca2+ in the presynaptic cell causes the synaptic vesicles to bind to the presynaptic end plate and exocytose their contents (ACh) into the synaptic cleft
  • ACh diffuses passively across the synaptic cleft and binds to the nAChR on the muscle end plate, resulting in the opening of the nAChR as a Na+ channel (lidocaine blocks these Na+ channels)
  • Na+ entry causes depolarization of the muscle endplate to occur; if depolarization is great enough this will propagate an AP throughout the muscle
  • The AP in skeletal muscle results in opening of VG Ca2+ channels (aka L channels) which are physically coupled to Ca2+ release channels (aka ryanodine receptors)
  • Ryanodine (and caffeine) bind to these ryanodine receptors and cause the release of Ca2+ intracellularly within the muscle
    o Note: intracellular [Ca2+] > 10^-6 induce muscle contraction
  • Ca2+ binds to troponin C (TnC) - this initiates muscle contraction
90
Q

What is a summary of excitation contraction signaling in skeletal muscle?

A

i. Motor neurons releasing acetylcholine
ii. Acetylcholine interactions with skeletal muscle nicotinic receptors to:
• Increase sodium permeability and depolarize skeletal muscle
• Skeletal muscle depolarization causes activation of L calcium channels (dihydropyridine receptors)
iii. Calcium entry into muscle releases calcium from intracellular storage sites (sarcoplasmic reticulum) via calcium-induced calcium release (ryanodine receptors – Ry1)
iv. Elevated intracellular calcium concentrations result in calcium binding to troponin C
v. Calcium binding to troponin C releases inhibition of actin-myosin interactions
vi. Myosin heads then contact actin to create muscle shortening and force generation, provided energy in the form of ATP is present

Skin/Musculoskeletal (5 decks)

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