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musculoskeletal rehabilitation > Bleeding and inflammation stages > Flashcards

Bleeding and inflammation stages Flashcards

1
Q

is the process different for different tissues?

A

no, process is the same for all types of tissues

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2
Q

what are the three ways tissues are usually damaged due to?

A

excessive ;
- compressive forces
- tensile forces
- shearing/ lacerating forces

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3
Q

what are the four phases of tissue repair?

A
  • bleeding
  • inflammation
  • proliferation
  • remodelling
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4
Q

how long roughly is the bleeding phase?

A
  • short phase
  • 0 to 10 hours
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5
Q

what does the bleeding phase depend on ? (4)

A
  • initial injury type
  • tissues damaged
  • severity of the injury
  • person specific factors e.g., smokers, diabetes, haemophilia
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6
Q

what does bleeding activate and what does this secrete ?

A
  • bleeding activates platelets
  • secretes prothrombin
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7
Q

what does prothrombin convert to? what is this used for?

A
  • prothrombin converted to thrombin
  • thrombin binds to fibrinogen to form fibrin cross- linking that aggregates over the wound
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8
Q

how long is the inflammation stage? how is it described?

A
  • 0-4 days
  • described as an essential component of tissue repair process
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9
Q

what happens at approximately day 1-3?

A
  • rapid onset
  • increases in magnitude
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10
Q

what are inflamed tissues called?

A
  • referred to as ‘itis’
  • no inflammatory markers in tendons
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11
Q

what are the 5 triggers of inflammation?

A
  • bleeding
  • trauma
  • chemical
  • infective
  • immunological
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12
Q

describe a chemical trigger for inflammation

A
  • changes in acid balance
  • changes transfer of liquids
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13
Q

describe a immunological trigger for inflammation

A
  • rheumatoid arthritis ^ inflammation
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14
Q

what are the five cardinal signs?

A
  • pain
  • swelling
  • loss of function
  • heat
  • redness
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15
Q

what is pain?

A
  • unpleasant sensory and emotional experience associated with, or resembling that associated with actual or potential tissue damage
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16
Q

what are the specialised receptors and what do they do?

A
  • nociceptors are activated and send an action potential to the spinal cord, transmitted through fibres which depending on their thickness will transduce information fast or slow
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17
Q

where is the information sent after the spinal cord?

A
  • sent to higher centres
  • spinothalamic or spinoreticular tracts in which the brain recognises if the stimuli is damaging or not
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18
Q

what are the two main fibres? which one is faster?

A
  • A - fibres and C fibres
  • A- fibres conducts the action potential fast (large diameter) whereas C fibres conduct the action potential slower (small diameter)
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19
Q

is there any conscious involvement?

A
  • yes
  • perception and cognition
  • association areas
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20
Q

can you modulate pain?

A
  • modulation via pain gate theory involving a - beta fibres and opioids
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21
Q

what is the primary mechanism?

A
  • markers including macrophage, mast cell, neutrophil accompany the inflammation and cover the damage to activate tissue repair
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22
Q

what are produced as a result of inflammatory pain? where from?

A
  • chemical mediators
  • from the injury itself
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23
Q

what are the chemical mediators?

A
  • serotonin
  • bradykinin
  • histamine
  • nerve growth factors
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24
Q

where are the chemical mediators sent?

A
  • sent to the bloodstream
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25
Q

what is nociception?

A
  • neural process of encoding, transmitting and processing noxious stimuli
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26
Q

is nociception always linked to pain?

A
  • no, nociception doesn’t always result in pain; tissue damage not necessary for pain as peripheral factors also influence pain
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27
Q

what is a noxious stimulus?

A
  • an actually or potentially tissue damaging event transduced and encoded by nociceptors
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28
Q

what are nociceptors?

A
  • sensory receptor that is capable of transducing, encoding and transmitting noxious stimuli
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29
Q

what can stimulation of nociceptors result in?

A
  • nociceptive pain
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30
Q

where do nociceptors transmit info to and why?

A
  • nociceptors in tissues transmit information to CNS to make you aware of the body
31
Q

what are the four main steps of nociception?

A
  1. transduction of stimulus by nociceptors
  2. stimulus conducted to spinal cord
  3. transmitted to higher centres
  4. encoded by action potential travelling from the nerve
32
Q

what is transduction?

A
  • mechanical, thermal or chemical energy is transduced by specialised endings of Ad and C nerve fibres
33
Q

what do some nociceptors respond to ? give an example

A
  • respond to only one stimulus modality
    e.g., mechanoreceptors
34
Q

what are other nociceptors described as?

A
  • polymodal
  • responding to multiple stimuli
35
Q

what are some of the nociceptors doing?

A
  • some are silent/ sleeping
  • woken up by inflammation
36
Q

what is encoding?

A
  • how many action potentials the nociceptor fires to perceive pain
37
Q

why is stimulus intensity proportional to pain intensity?

A
  • stimulus intensity is encoded to be proportional to nociceptor firing frequency
  • nociceptor firing frequency is decoded to be proportional to pain intensity
38
Q

what happens if the nociceptor is stimulated more?

A
  • it produces a larger, more painful response
39
Q

what does repetitive stimulation of nociceptors by chemical mediators and noxious stimuli cause?

A
  • causes nociceptors to lower their activation threshold
  • lower stimuli ^ pain experienced
40
Q

what can threshold reduction lead to?

A
  • peripheral sensitisation
41
Q

what does peripheral sensitisation lead to?

A
  • increased responsiveness
  • reduced threshold of nociceptive neurons in periphery to stimulation of receptive fields
42
Q

what can nociception cause?

A
  • causes local and remote sensitivity
43
Q

what can peripheral sensitisation transfer to?

A
  • central sensitisation
  • CNS more responsive to pain
44
Q

what are the two central sensitisations? what does this cause?

A
  • hyperalgesia
  • allodynia
  • pain becomes widespread
45
Q

what is hyperalgesia?

A
  • increased pain to a noxious stimulus
    e.g., touched with lower pressure ^ pain
46
Q

what is allodynia?

A
  • pain response to innocuous (non- noxious) stimuli
    e.g., touched in different place and pain felt
47
Q

what is referred pain?

A
  • intensity and size correlates with CNS excitability
48
Q

what is chronic pain?

A
  • more sensitised
  • more pain travels to brain
49
Q

what is conduction?

A
  • axons transmit information via action potentials conducted along nerve fibre axon
50
Q

describe Ad fibres

A
  • greater diameter
  • fast
  • 5 to 35 ms- 1
  • faster than vision
51
Q

describe C fibres

A
  • smaller diameter
  • slow
  • 0.5 to 2 ms-q
  • unmyelinated
52
Q

what are other important afferent fibres ?

A
  • beta fibres, gamma fibres
  • sensed in muscle, etc and sent back to spinal cord/ brain
53
Q

what is transmission?

A
  • action potential transmitted to neurons in dorsal horn of spinal cord
54
Q

what are dorsal horns?

A
  • sensory sites in which dynamic activities occur
55
Q

where are Ad fibres transmitted?

A
  • Ad fibres to Lamina I
  • Laminae marginalis
56
Q

where are C fibres transmitted?

A
  • C fibres to Lamina II
  • Substantia gelatinosa
57
Q

where is the action potential transmitted after the dorsal horn?

A
  • transmitted to higher centres
    such as primary somatosensory cortex, sensory homunculus
58
Q

what is the gate theory?

A
  • afferent impulses ‘gated’ (modulated) within the spinal cord
59
Q

what closes the gate?

A
  • impulses from large, myelinated fibres tend to block nociception
60
Q

what opens the gate?

A
  • impulses in nociceptors facilitate transmission
61
Q

what is descending inhibition?

A
  • inhibitory affect from brain down to spinal cord to inhibit pain pathways, excite inhibitory interneurons which inhibit pain
62
Q

what are the two main reasons for redness and heat production?

A
  • chemical mediators trigger vasodilation
  • release of nitric acid
63
Q

what three substances impact redness and heat?

A
  • substance P > short acting vasodilator
  • serotonin (5HT) and Bradykinin
64
Q

how does blood flow cause redness?

A
  • blood flow increases
  • hyperaemia
  • generates localised heat
65
Q

does swelling occur immediately? does this change meaning?

A
  • may not occur immediately and may take serval hours to develop
  • when swelling is immediate it indicates substanial injury
66
Q

what indicates inflammatory injury? why does this occur?

A
  • inflammatory exudate
  • occurs due to alteration of hydrostatic an osmotic pressures in capillaries
  • if pressure is higher than oedema and swelling produced as fluid forced out
67
Q

how does functional loss of mobility occur?

A
  • due to pain, fear of movement, swelling and tissue damage
  • should assess limping
68
Q

what alters permeability of capillary walls? what does this allow?

A
  • chemical mediators
  • bradykinin and histamine
  • alteration allows plasma proteins to move from capillaries to interstitial space
69
Q

what gradient is altered and what does this cause?

A
  • osmotic gradient altered
  • net flow of fluids is greater into interstitial space
70
Q

what happens as blood flow slows down?

A
  • white blood cells move towards margin of blood vessels
  • via process of margination
71
Q

where do white blood cells emigrate to and how? what are they guided by?

A
  • emigrate into interstitial spaces by pseudoposis
  • guided by chemical mediators via chemotaxis
72
Q

what does inflammatory exudate dilute and allow?

A
  • dilutes toxins
  • allows passage of antibodies and plasma proteins
73
Q

what happens in inflammatory exudate?

A
  • neutrophils and macrophages engulf debris and bacteria via phagocytosis

musculoskeletal rehabilitation (13 decks)

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