PS 1001:03 Lecture Notes - Lecture 4: Antihemorrhagic, Manual Therapy, Exudate
Interchangeable
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Solid understanding needed to devise treatment techniques of ice, heat, electrical physical
agents and manual therapy
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Pain, inflammation and tissue repair
Identify the sources and causes of injury
Bleeding/haemorrhage - damage to capillary walls
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Cell damage
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Exposure of tissues to foreign material/microorganisms
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Trauma e.g. burns, laceration, sprain, contusion, disrupts microvasculature and may produce
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When tissue is damaged
Identify the body's natural physical and physiological defences
Inflammation - good or bad?
Vascular, haemostatic, cellular and immune effects
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Protection from movement
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Vascular response intitially (vasoconstriction)
1.
Prolonged vasodilation at the capillary - triggered by chemical mediators which can also cause
pain e.g. histamine
2.
Clotting
3.
Pain
4.
Migration of leukocytes to area and fluid to interstitial area
5.
Necessary for healing in acute phase
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Oedema limits ROM, continued pain
Inflammatory exudate becomes more protein rich, chemicals are destructive to tissue
Secondary changes - scarring, contracture
HOWEVER prolonger inflammation (chronic)
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Describe the inflammatory response. Describe the different types,
causes, signs and symptoms of inflammation
Causes: microbial infections (viral, bacterial, parasitic), hypersensitivity, physical agents,
irritant and corrosive chemicals, tissue necrosis, thermal (heat)
Signs and symptoms
Screen clipping taken: 27/02/2018 10:37 AM
Changes in vessel calibre and thus flow
1.
Increased vascular permeability and formation of the fluid exudate (ie. Let ions nutrients
2.
Stages
Acute
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L2 - inflammation, healing, repair
Tuesday, 27 February 2018
10:29 AM
Week 2 Page 1
Increased vascular permeability and formation of the fluid exudate (ie. Let ions nutrients
flow more easily across membrane)
2.
Formation of the cellular exudate by emigration of the neutrophil polymorphs into the
extravascular space
3.
0-14 days
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Could be longer due to irritation, fracture, infection, glass, bruising, joint damage
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Damaged vessels respond with immediate vasoconstriction usually 5-10 mins
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Acute phase lasts 24-48 hours
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Sub-acute phase - 10-14 days
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Length of inflammatory phase
Retraction and sealing off of blood vessels
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Platelets form clots and assist in building lattice
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Haemostatic response
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Activation of systems result in increased vascular permeability, stimulation of
phagocytosis and act as stimuli for leukocytes (WBCs)
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Immune response
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Leukocytes move to area of injury to rid are of bacteria and debris by phagocytosis
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Monocytes converted into macrophages which produce essential products for
healing
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Cellular response
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Summary of events
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Inflammation cascade
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Chronic
Lasts for longer, usually more than 3 months
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An inflammatory response of prolonged duration, weeks, months or longer
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Possibly failure of extradate removal
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Persistent injury or irritation
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Progression from acute inflammation
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After repeated episodes of acute inflammation
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Due to
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Prolonged inflammation -> excessive scar tissue -> reduction in function
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Essential component of tissue repair
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Rapid onset - few hours
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Inflammatory phase
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Week 2 Page 2
Document Summary
Solid understanding needed to devise treatment techniques of ice, heat, electrical physical agents and manual therapy. Trauma e. g. burns, laceration, sprain, contusion, disrupts microvasculature and may produce. Identify the body"s natural physical and physiological defences. Prolonged vasodilation at the capillary - triggered by chemical mediators which can also cause pain e. g. histamine. Migration of leukocytes to area and fluid to interstitial area. Inflammatory exudate becomes more protein rich, chemicals are destructive to tissue. Describe the different types, causes, signs and symptoms of inflammation. Causes: microbial infections (viral, bacterial, parasitic), hypersensitivity, physical agents, irritant and corrosive chemicals, tissue necrosis, thermal (heat) Increased vascular permeability and formation of the fluid exudate (ie. let ions nutrients. Increased vascular permeability and formation of the fluid exudate (ie. let ions nutrients flow more easily across membrane) Formation of the cellular exudate by emigration of the neutrophil polymorphs into the extravascular space. Could be longer due to irritation, fracture, infection, glass, bruising, joint damage.
