LM Flashcards

look ossification/formation

1
Q

What is a motor unit?

A
  • group of fibres activated by a single motor neurone
  • fine motor control will have smaller number of motor units
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2
Q

How is force generated in the NMJ?

A
  • recruiting motor units
  • recruited in size order until force is generated
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3
Q

What is the motor endplate?

A
  • large/specialised synapse on muscle fibre.
  • offers direct access to pre-synaptic nerve terminals
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4
Q

Describe the structure of presynaptic NMJ

A
  • complex branching of axon terminal
  • multiple terminal boutons: capable of releasing neurotransmitter. total always enough to cause contraction
  • uses ach
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5
Q

What happens during signal transduction in NMJ?

A
  • Ach binds to receptors, causing depolarisation around folds. always sufficient to cause voltage-gated sodium channels to open
  • causes depolarisation
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6
Q

How is the force of the NMJ contraction controlled?

A
  • frequency of action potentials
  • temporal/spatial summation
  • recruitment of additional motor units, more power required, more motor units to be added
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7
Q

What are proprioceptors?

A
  • specialised sensory receptors which provide information about body position, movement and muscle tension
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8
Q

What is mechanoreceptor adaptation?

A
  • reduction in sensitivity to a stimulus when exposure to stimulus remains constant.
  • fast adapting sensory organs are more responsive to higher frequency stimulation
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9
Q

What do mechanoreceptors sense?

A
  • steady pressure
  • changes in pressure
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10
Q

What type of axons do mechanoreceptors give rise to?

A
  • A beta axons
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11
Q

Generally, fast adapting sensory organs are more responsive to?

A
  • higher frequency stimulation
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12
Q

Characteristics of an intact Pacinian corpuscle?

A
  • rapid adaptation
  • no response to sustained pressure
  • dermis and hypodermis
  • responsible for detecting vibration and deep pressure stimuli
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13
Q

Characteristics of a stripped pacinian corpuscle?

A
  • little adaptation
  • response to sustained pressure
  • more sensitive to lower-frequency stimuli
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14
Q

What do nociceptors detect?

A
  • pain
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15
Q

What do A delta fibres usually detect?

A
  • cooling and prickling pain
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16
Q

What do C fibres usually detect?

A
  • warming
  • burning pain
  • itch
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17
Q

Explain how nociception is biphasic?

A
  • A3 fibres detect initial perception of sharp pain
  • C fibres detect perception of prolonged dull pain and itching
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18
Q

How are nociceptors activated?

A
  • directly by physical or chemical stimuli
  • indirectly by mediators of tissue damage
  • > 45C, <5C
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19
Q

Describe spinal reflexes

A
  • unconscious reaction to a stimulus
  • predominantly to ensure muscle length and tension are maintained
  • react to pain/danger
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20
Q

Outline the stretch reflex

A
  • hitting tendon, detects stretches in quadriceps, send information through sensory afferent (1A)
  • to dorsal horn, ventral horn, synapse with alpha motor neurone, innervate muscle, muscle contracts
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21
Q

Explain UMN

A
  • motor pathways from brain send long axons down the spinal cord
  • synapse with motor and sensory neurons in the spinal cord
  • reduce strength of the reflex
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22
Q

What do UMN lesions result in?

A
  • muscle spasticity and are usually associated with hyperreflexia
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23
Q

In what direction do spindle fibres run?

A
  • in parallel with muscle fibre (intrafusal)
  • in order to detect stretch
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24
Q

What are present in the contractile/non-contractile area of the muscle fibre?

A
  • non-contractile: 1A sensory afferents wind around
  • contractile: small diameter motor neurons innervate. have own GMN providing stimulus
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25
Role of GMN in the control of movement
- cell bodies located within ventral horn alongside alpha motor neurons which cause contraction of main muscle - influence length of spindle - simultaneous activity of AMN and GMN ensure length of spindle relative to length is maintained
26
What allows for fast compensation for unexpected changes in muscle length?
- co-activation of AMN and GMN, resulting in spindle shortening simultaneously with muscle fibres ensuring it remains active
27
Outline pain reception
- nociceptors detect which synapse in spinal cord with excitatory interneuron - interneuron synapse with LMN for flexor muscles - flexion causes limb to move away from source of pain
28
Pain reception in lower limb?
- flexion reflex will cause loss of balance - need to extend opposite limb at same time, leads to complex interneuron interaction on ipsilateral and contralateral sides of the spinal cord - flexion crossed-extension reflex
29
Describe Renshaw cells
- get input from axon collateral from LMN - inhibitory: glycine as a neurotransmitter - acts as a feedback mechanism to prevent muscle damage during tetanic stimulation - always modulated by descending motor pathway
30
Describe Golgi tendon organs
- located between termination of muscle fibres and tendon - in series with muscle, detect changes in tension
31
What is meant by isometric contraction?
- tension increases, length remains the same. - no activation of muscle spindles, feedback on tension provided solely by Golgi tendon organs
32
Describe arrangement of myosin to actin?
- each myosin filament is surrounded by 6 actin filaments in a hexagonal arrangement
33
Describe structure of actin filament
- actin subunits polymerise to form chains, molecules extend in opposite directions from Z line
34
Tropomyosin
- fibrous protein which extends along groove of actin polymers and stabilises them - in absence of calcium, tropomyosin blocks myosin binding site on actin
35
Troponin
- protein complex critical for function bound to tropomyosin
36
Describe muscle structure at resting state
- muscle-calcium conc. is low and head group of myosin filament is bound to ADP and Pi - binding blocked by tropomyosin despite high affinity
37
What does the troponin complex contain?
- Tn T: tropomyosin binding - Tn C: calcium binding - Tn I: inhibitory subunit
38
Describe cross-bridge formation
- TnC induces changes in TnI which is transducer through TnT to tropomyosin, moving out of myosin binding site permitting the formation
39
What occurs once cross bridge formation is formed?
- conformational changes in troponin cause it to shift, dragging tropomyosin along and exposing myosin binding site - triggers release of Pi, resulting in muscle contraction causing myosin heads to bend and actin filaments to be pulled past myosin fibres
40
What does ATP binding do in the muscle structure?
- causes actin and myosin to dissociate - ATP hydrolysed - energy released by hydrolysis moves myosin heads for another cycle
41
Reduction in calcium has what effect in muscle structure?
- cause troponin to release bound calcium and myosin binding sites are hidden by tropomyosin - actin and myosin filaments relax back to original positions
42
Role of sarcoplasmic reticulum in regulation and control of muscle contraction
- endoplasmic reticulum of striated muscle specialised for sequestration of calcium ions that are released upon receipt of signal relayed by T tubules from NMJ
43
What are T tubules?
- tubule that passes in a transverse manner from sarcolemma across a myofibril of striated muscle
44
Give three sources of high energy phosphate to keep ATP pool filled
- creatine phosphate: for short bursts of energy (muscle, brain and cardiac tissue form) - muscle glycogen - cellular respiration
45
What is cortical bone?
- compact - dense/stiff structure - low porosity
46
What is trabecular bone?
- spongey light structure - high porosity
47
Describe woven bone
- produced rapidly - immature bone - disorganised structure
48
Describe lamellar bone
- mature - produced by remodelling - organised into layers
49
Describe role of osteoblasts
- produce osteoid - initiate mineralisation with ALP - become bone lining cells or osteocytes
50
Examples of diseases arising from faulty osteoblasts
- scurvy - osteogenesis imperfecta: abnormal collagen formation reducing bone density and increasing fragility
51
Describe role of osteoclasts
- attracted to and resorb mineralised bone - create absorption pits - form actin ring around base
52
How do osteoclasts form?
- require RANKL factor from osteoblasts which react with CD4 and monocytes
53
Outline the stages of bone remodelling cycle
- resting stage - bone resorption - transition stage/reversal stage - bone formation
54
What are the stages in the bone remodelling cycle?
- activation - resorption - reversal - formation
55
Give advantages to bone remodelling
- enables adaptation to mechanical loading - enables fracture healing - prevents bone fatigue
56
Describe osteoporosis
- systemic skeletal disease characterised by low bone mass and micro architectural deterioration of bone tissue, fragility and susceptibility to fracture - osteoclasts lower pH dissolving bone mineral, produce proteolytic enzymes - osteoclasts:osteoblasts balance
57
What are the typical sites of fracture in osteoporosis?
- neck of femur, wrist and vertebrae
58
Examples of treatments for osteoporosis
- biphosphonates: bind hydroxyapatite, N-containing R chains adapted cause osteoclasts cell death. cheap and widely used - denosumab: anti-RANKL antibody. stops fusion of osteoclast precursors into osteoclasts
59
Components of cartilage
- chondrocytes, collagens, proteoglycans, water
60
What occurs when cartilage aggrecan is degraded?
- loss of shock absorbing capacity - painful movement - inflammation
61
What is meant by anlage?
- long bones formed as cartilage - early structural basis of a particular organ - can expand from within
62
What is the recommended amount of vitamin D per day?
- 10 micrograms
63
Where does PTH come from?
- parathyroid glands - regulates plasma Ca levels - cells of parathyroid glands continuously sense extracellular Ca via G protein-linked transmembrane Ca-sensing receptors
64
Role of PTH in low plasma Ca
- promotes bone resorption/action of osteoclasts - mobilises bone stores of calcium and phosphate of plasma - hydroxyapatite broken into constituent parts
65
Role of PTH in kidneys
- reduce renal excretion of calcium and increase renal excretion of phosphate - promotes conversion of VD3 to calcitriol
66
Role of PTH in high plasma Ca
- secretion ceases - renal excretion of Ca increases
67
Role of calcitriol in regulation of plasma Ca
- increases intestinal absorption of dietary Ca to be added to plasma
68
Importance of calcium
- transmission of nerve impulses - regulation of muscle contraction - hydroxyapatite provides strength for skeletal system - cell signalling: intracellular messenger for hormone action - blood clotting - maintenance of healthy teeth
69
What serves as a large reservoir of Ca in the body?
- bone
70
What is the normal range of total plasma calcium?
- 2.25-2.5 mmol/L
71
What composes the diffusible pool Ca?
- free/unbound ionic calcium - 50%
72
What composes the non-diffusible pool of Ca?
- 40% of plasma Ca - bound to Ca-binding proteins and plasma proteins (albumin) - sensitive to pH
73
Describe alkalosis/alkalaemia
- high pH, low H+ conc - fewer H+ bound to albumin - favours binding of albumin to calcium - conc. of albumin bound calcium in non-diffusible pool increases - conc. of ionic Ca in diffusible pool decreases - results in hypocalcaemia
74
Describe acidosis
- low pH/high H+ conc. - more H+ bound to albumin - favours binding of albumin to H+ over Ca - conc. of albumin-bound calcium in non-diffusible pool decreases - conc. of ionic Ca in diffusible pool increases - results in hypercalcaemia
75
What is the physiologically/functionally important form of Ca?
- free/unbound ionic calcium
76
Clinical importance of hypocalcaemia
- increased excitability - neuronal membrane becomes increasingly permeable to Na ions which allow easy initiation of action potentials
77
Clinical relevance of hypercalcaemia
- decreased interaction between Ca and Na channels - Ca ions block sodium channels, threshold for depolarisation of nerve and muscle fibres raised
78
What are the consequences of vitamin D deficiency?
- rickets (children) - osteomalacia (adults) - impaired mineralisation of osteoid, poorly mineralised bones are structurally weak
79