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My MSK > Physiology > Flashcards

Physiology Flashcards

1
Q

What are the functions of skeletal muscle?

A
  • posture
  • purposeful movement
  • respiratory movement
  • heat production
  • whole body metabolism
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2
Q

Which muscle types are striated?

A

skeletal and cardiac are striated

smooth isn’t

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3
Q

Which muscle types are voluntary?

A

skeletal muscle is voluntary (somatic)

smooth and cardiac muscle are involuntary (autonomic)

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4
Q

What initiates skeletal muscle contraction?

A

neurogenic initiation

  • no continuity of cytoplasm between nerve and skeletal cells
  • ACh is used as a transmitter at NMJ
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5
Q

What is a motor unit in a skeletal muscle fibre?

A

a single alpha motor neurone and all the skeletal fibres that it supplies

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6
Q

Why does the number of muscle fibres per motor unit vary?

A

the number of fibres per motor unit depends on function

  • fine movements: less fibres
  • powerful movements: more fibres
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7
Q

How are skeletal muscles attached to skeleton?

A

by tendons

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8
Q

What are ATP and calcium ions needed for in contraction?

A
  • ATP is needed for contraction to power cross bridges and relaxation release and to pump Ca2+ back into SR
  • Ca2+ is needed to switch on cross bridge formation, this is link between excitation and contraction, it is derived from SR in skeletal muscle
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9
Q

What is excitation contraction coupling?

A

where the surface potential results in activation of contractile structure of the muscle fibre

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10
Q

What is the process of contraction?

A
  • AP spreads down T tubules
  • Ca2+ is released from lateral sacs of SR
  • Ca2+ causes movement when it binds to troponin so tropnin-tropomysoin complex moves so actin has a free myosin binding site
  • power stroke so actin is dragged
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11
Q

What does the amount of skeletal muscle tension depend on?

A
  • no. of muscle fibres contracting (motor unit stimulation)

- tensions developed by each muscle fibre (frequency of stimulation, summation and length of fibre at onset)

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12
Q

What can prevent muscle fatigue?

A

asynchronous motor unit recruitment during sub maximal contractions

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13
Q

When is skeletal muscle at optimal length?

A

under resting conditions and this is when there is optimum overlap of thick and thin filaments

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14
Q

What can twitches help to do?

A

twitches can be summated so there is a stronger contraction as the duration of an AP is shorter than a twitch

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15
Q

What is tetanus of muscle?

A

the muscle can be stimulated so rapidly that it can’t relax between stimuli (not possible in cardiac tissue due to long refractory period)

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16
Q

How is skeletal muscle tension is transmitted to bone?

A

via stretching and tightening of muscle, connective tissue and tendon

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17
Q

What are the two types of skeletal muscle contraction?

A
  • isotonic contraction: eg body movements, muscle tension remains constant but muscle length changes
  • isometric contraction: eg posture, muscle tension develops at constant muscle length
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18
Q

What are the differences in skeletal muscle fibres?

A
  • enzymatic pathways for ATP synthesis
  • resistance to fatigue (greater ATP making capacity means less fatigue)
  • activity of myosin ATPase (speed of contraction)
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19
Q

How is ATP made?

A
  • with ADP and creatine phosphate which is immediate (not high amounts)
  • through oxidative phosphorylation (main source when there is O2)
  • through glycolysis (when O2 is low)
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20
Q

What are the characteristics of Type 1 fibres?

A
  • slow twitch
  • resistant to fatigue
  • myoglobin
  • red
  • good for low work
  • aerobic activities
    aka slow oxidative
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21
Q

What are the characteristics of Type 2a fibres?

A
  • aka fast oxidative, intermediated twitch
  • use both aerobic and anaerobic so useful in moderate work
  • myoglobin
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22
Q

What are the characteristics of Type 2x fibres?

A
  • aka fast twitch or fast glycolytic
  • use aerobic metabolism
  • white
  • short-term high intensity activities
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23
Q

What are the features of the stretch reflex?

A
  • simplest monosynaptic spinal reflex
  • negative feedback that resists passive change in muscle length
  • tap tendon with hammer
  • rapid stretch of muscle so contraction
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24
Q

What is the process in a stretch reflex?

A
  • sensory receptor is muscle spindle
  • stretch of spindle leads to increased firing in afferent neurone
  • synapse to alpha motor neurons which innervate stretched muscle
  • coordinated by relaxation of antagonists muscle
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25
Q

Where are the sensory receptors of the stretch reflex?

A

in the muscle spindles in the belly of muscles and they run parallel to ordinary fibres
they have sensory nerve endings called annulospiral fibres

26
Q

What are the features of muscle spindles?

A
  • discharge increases as muscle is stretched
  • have own efferent supply by gamma motor neurones which adjust tension level to maintain sensitivity when muscle shortens
  • do not contribute to strength
27
Q

What can impairment of skeletal muscle function be caused by?

A
  • intrinsic disease of muscle
  • disease of NMJ
  • disease of lower motor neurone which supply muscle
  • disruption of input to motor neurones
28
Q

What are general symptoms of muscle disease?

A
  • muscle weakness
  • delayed relaxation
  • muscle pain
  • stiffness
29
Q

What are the investigations of neuromuscular disease?

A
  • EMG- electrical activity of muscle
  • nerve conduction studies
  • muscle enzymes
  • inflammatory markers
  • muscle biopsy
30
Q

What are the three types of joint?

A
  • synovial
  • fibrous: bones united by fibrous tissue, no movement eg skull
  • cartilaginous: bones united by cartilage, limited movement eg symphysis
31
Q

What are the features of synovial joints?

A
  • cavity with synovial fluid
  • united by fibrous capsule
  • lined by synovial membrane of vascular connective tissue
  • membrane contains synovial cells which make synovial fluid
32
Q

What are the functions of synovial fluid?

A
  • lubrication
  • joint movement
  • minimised wear and tear
  • cartilage nutrition
  • supplies chondrocytes with O2, nutrients and removes CO2 and waste
33
Q

What is in synovial fluid?

A
  • mucin gives it a high viscosity (this can vary with movement)
  • other constituents are from dialysis of blood plasm
  • only a few cells (increase in inflammation and septic arthritis)
34
Q

What is needed for rapid movement in terms of synovial fluid?

A
  • low viscosity

- high elasticity

35
Q

What are the features of articular cartilage?

A
  • hyaline
  • elastic
  • sponge-like
  • covers articular surfaces
  • has ECM
36
Q

What is in the ECM?

A
  • water: maintains resiliency, contributes to nutrition and lubrication
  • collagen: maintains stiffness
  • proteoglycans: compressive properties and is weight bearing
37
Q

How is ECM controlled and supplied?

A
  • made and degraded by chondrocytes

- it is avascular so cells receive sustenance by synovial fluid

38
Q

What are the markers of cartilage degradation?

A
  • serum and synovial keratin sulphate

- type 2 collagen in synovial fluid

39
Q

What are the crystals in pseudo-gout?

A

rhomboid shaped crystals of calcium pyrophosphate which are positively birefringent

40
Q

What is transduction of a pain signal?

A

translation of noxious stimulus so there is electrical activity at peripheral nociceptor

41
Q

What is transmission of pain signal?

A

propagation of pain signal as nerve impulses through the nervous system

42
Q

What is modulation of pain signal?

A

hindering of pain transmission in nervous system

43
Q

What is perception of pain signal?

A

conscious experience of pain leading to response

44
Q

What is the role of nociceptors?

A

have free nerve endings for transduction and relay information to second order neurons in CNS

45
Q

What is the process of pain signalling?

A
  • neuron enters posterior/dorsal horn of spinal cord
  • synapses with second order neurone using glutamate
  • crosses spinal cord and ascends causing pain
46
Q

What is the spinothalamic tract?

A

involved in pain response so location and intensity

47
Q

What is the spinoreticular tract?

A

autonomic responses so arousal, emotion and fear

48
Q

What are the different types of nociceptors?

A
  • Adelta is fast pain, mechanic and thermal, myelinated

- C fibres is slow and lasting pain, unmyelinated

49
Q

What is nociceptive pain?

A
  • response to injury
  • intense stimulation of pain receptors
  • adaptive pain
  • warning to avoid harm
50
Q

What is inflammatory pain?

A
  • activation of immune system
  • variety of mediators
  • heightened due to painful stimuli
  • stops movement of harmed area
51
Q

What is pathological pain?

A
  • neuropathic: damage to neural tissue causing burning, shooting or numbness
  • dysfunctional: no identifiable damage, try anti-depressants as pain meds don’t work
52
Q

What is referred pain caused by?

A

convergence of nociceptive visceral and skin afferents upon same spinothalamic neurone

53
Q

What is skeletal muscle innervated by?

A
  • alpha motor neurones with myelinated axons
  • these branch into unmyelinated axons that innervate individual fibres
  • the terminal bouton is the synapse with ACh as transmitter
54
Q

What happens presynaptically?

A
  • choline symport with Na+

- choline is combined with acetyl from acetyl CoA by CAT enzyme

55
Q

What is needed to open the nicotinic ion channels?

A

two ACh per channel as these are pentameric ligand-gated channels

56
Q

What is an e.p.p?

A

this is an end plate potential and is due to the influx of Na+ being greater than the efflux of K+ and many channels are opened

57
Q

What happens when a vesicle relates ACh?

A

there is a quantum released every time
there is a m.e.p.p
many mepps make an epp

58
Q

What happens to the ACh after?

A
  • AChE hydrolyses it
  • choline is taken up by choline transporter
  • acetate diffuses from synaptic cleft
59
Q

What is neuromyotonia?

A
  • antibodies against voltage-activated K+ channels
  • the AP is longer so cramps, stiffness
  • treat with Na+ channel blockers
60
Q

What is Lambert-eaton myasthenic syndrome?

A
  • antibodies against Ca2+ voltage-activated channels sp less ACh release
  • muscle weakness
  • drug therapy targets AChE
  • this is associated with small cell carcinoma
61
Q

What does the Botulinum toxin do?

A

causes irreversible inhibition of ACh release at the junction so no AP and there is no treatment

62
Q

What do curare-like compounds do?

A
  • competitive antagonisms of nAChRs
  • this reduces the epps so they are below threshold
  • use din surgery fro reversible paralysis

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