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130 Cards in this Set
- Front
- Back
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How does arteriole hydrostatic pressure change and contribute to edema?
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Greater blood flow toward area increase arteriole hydrostatic pressure
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How does capillary osmotic pressure change and contribute to edema?
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Decrease in capillary osmotic pressure - less flow away from area (of inflammation)
fewer solutes within capillary, so fluids tend to flow out |
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How does interstitial osmotic pressure change and contribute to edema?
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Interstitial osmotic pressure increases leading to more flow of fluids into the area
more solutes in interstitial space |
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How does venule hydrostatic pressure change and contribute to edema?
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Venule hydrostatic pressure decreases, leading to less flow away from the area of inflammation
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Main reason for swelling/edema during inflammatory response is...
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Increase in interstitial proteins
Leads to osmotic flow of fluid into interstitial tissue |
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What are the purposes of acute inflammation?
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Isolates the injured area
Draws healing agents Rids the area of waste products Prepares for the addition of new tissue |
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How is chronic inflammation different from acute?
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“Inflammation that has outlived its usefulness”
Inflammation events no longer productive to healing creates Secondary Trauma Exacerbation |
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What are the signs of inflammation?
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Redness
Increased temperature Pain / Tenderness to touch Swelling (edema) |
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What are the stages of the healing process?
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Inflammatory Response Phase
(Acute Inflammation) Pain at rest or w/ min movement Fibroblastic Repair Phase (Subacute—Tissue Repair Phase) Pain during movement / activity / tissue resistance Maturation and Remodeling Phase Pain after activity / significant tissue resistance |
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Describe the inflammatory response phase of inflammation
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~ Days 1-4 after injury***
Consists of: Vascular Response - vasoconstriction followed by vasodilation Hemostatic Response -controls blood loss, isolates area (clotting) Cellular Response (phagocytosis) - migration of leukocytes to the area All 3 help prepare tissue for healing and re-growth |
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Vasocontstriction of inflammatory phase
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Constricting of blood vessels in injured tissues
Minimizes blood loss Occurs almost immediately Duration ~ 5-10 minutes Stimulated by chemicals released from endothelial cells and adrenal system Serotonin Norepinephrine |
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Vasodilation of inflammatory phase
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Dilating or “opening” of the blood vessels
Begins within minutes Caused by the release of “chemical mediators” From injured cells From Mast Cells |
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Chemical mediators of vasodilation
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Histamine
Stimulates vasodilation Increases capillary membrane permeability Released by Mast Cells Prostaglandins Stimulate vasodilation React with other substances to cause pain Released from damaged cells BRADYKININS (more info?) |
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What do mast cells release?
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Histamine AND
Substances that attract leukocytes (WBC’s) Leukotrienes Neutrophil chemotaxic factor Heparin Prevents clotting from occurring too early |
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Hemostatic response (of inflammation phase)
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Controls blood loss / Isolates Area
Small blood vessels retract and seal Platelets adhere to collagen fibers in vessel walls exposed by injury Allows additional platelets and leukocytes to adhere and form a “plug” Results in a clot Thromboplastin released from damaged cell Stimulates the conversion of a series of plasma proteins |
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Thromboplastin released from damaged cell
Stimulates the conversion of a series of plasma proteins... what's the process? |
Thromboplastin -> prothrombin → thrombin → fibrinogen → fibrin
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Cellular response of inflammation phase
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Migration of leukocytes to area:
Phagocytic activity Elimination of debris and necrotic tissue by white blood cells “Gobble up” damaged tissue Proteolytic activity Enzymatic degradation of waste & bacteria Release of substances that accelerate healing response (fibroblast recruitment) |
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What are the four forces contributing to fluid flow?
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Capillary osmotic pressure
Pressure due to osmosis Pulls fluid from interstitial area into capillary Interstitial osmotic pressure Pressure due to osmosis Pulls fluid from capillary into interstitial area Arteriole hydrostatic pressure Pressure due to fluid flow thru arteriole Venule hydrostatic pressure Pressure due to fluid flow thru venule |
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Inflammation events leading to edema
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Vasodilation
Causes an increase in blood and plasma flow to injured tissues Increased capillary permeability Allows more leakage of plasma proteins into interstitial tissues Membranes broken during injury Allows membrane proteins to accumulate in interstitial tissues |
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POLICE principle
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Protection
Optimal Loading Ice Compression Elevation |
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Why ice an injury?
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Vasoconstriction
May ↓ arteriole hydrostatic pressure Decrease rate of cellular metabolism |
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Why elevate an injury?
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May ↓ arteriole hydrostatic pressure & ↑ venule hydrostatic pressure
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Why compress an injury?
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May increase venule hydrostatic pressure
May decrease arteriole hydrostatic pressure |
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How is lymphatic drainage achieved?
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Body will rely on respiration, muscle contractions, and gravity for removal of fluid/proteins
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How do we increase lymphatic drainage?
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AROM and Muscle Contraction as tolerated
Stimulate Pumping of smooth muscle in lymph vessels (Knight, 2000; Knight 1995) Compression & Elevation Retrograde Massage? Electrical Stimulation? |
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Proliferation phase
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(fibroblastic)
days 3-21*** Signified by Fibroplasia Synthesis of new connective tissue By fibroblasts |
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Fibroblasts
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Cells that synthesize fibrous, binding, and supportive tissue of the body
Migrate to inflamed area Fibroblast / Macrophage relationship? Synthesize scar tissue Consists mostly of collagen fibers & ground substance (fluid & non-fibrous proteins) |
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Synthesis of collagen
(stages of? process leading to?) |
Revascularization/Epithelialization
Wound contraction Collagen production/Wound Remodeling |
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What is involved in repair phase?
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Also involves capillary budding
Lack of oxygen stimulates growth of capillaries in the area Presence of new capillaries, fibroblasts, & collagen gives area a reddish, granular appearance Granulation tissue |
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Steps of soft tissue repair
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Fibroblast formation
Synthesis of collagen Tissue remodeling Tissue alignment |
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Repair phase - Deposition of collagen fibers
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1st random
Gradually more structured Strength ’s prop. w/collagen synthesis As tissue strength increases, fibroblast action and # decreases Signals start of Maturation phase |
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Fibrosis
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Extended fibroplasia
May affect joint capsules, tendons, ligaments, bursae Can lead to excess scar tissue, ↓ed vascular supply, degenerated tissue state |
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Maturation - Remodeling phase
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day 21 +
More organized structuring of collagen fibers (WHAT MAKES THIS HAPPEN?) Realignment according to tensile F’s to which scar is subjected Realign in position of max effic. Parallel to lines of tension Wolff’s Law Remodeling = collagen turnover Collagen is “taken up” and laid down again in more organized and efficient fashion |
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Wolff's Law
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Both bone and soft tissue will respond to the physical demands placed on them, causing them to remodel or realign along lines of tensile force
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What happens to tissues when stress < maintenance range
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↓ed tissue tolerance to subsequent stresses
Atrophy Tissue degeneration > Tissue production |
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What happens to tissues when stress = maintenance range
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No overall ∆ in tissue quality
Tissue degeneration = Tissue production |
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What happens to tissues when stress level > maintenance range
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↑ed tissue tolerance to subsequent stresses
Hypertrophy Tissue production > Tissue degeneration Increases in: X-sectional area Density Volume Excessive stress = tissue injury |
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Connective Tissue consists of:
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Cells (fibroblasts)
Ground Substance Fibers - Collagen Elastin Reticulum |
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Tropocollagen formation
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Synthesized in Fibroblasts via protein synthesis
In rough ER Amino acids → poly peptide chain 3D chains (3) fit together like puzzle to form procollagen molecule Procollagen = percursor to Tropocollagen, ends trimmed Amino acids → polypeptide →procollagen → tropocollagen |
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Five classifiable types of collagen
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Type I & II most relevant to rehab
Ligaments, tendons, capsules, & cartilage Types III – V Smooth muscle, internal organs, epithelial tissue, placental tissue |
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Type I Collagen
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Type I
Tendon, ligament, scar, jt. capsules Fibroblast Thick, dense fibrils Resist Tension |
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Type II Collagen
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Type II
Hyaline Cartilage Chondroblast Loose fibril network Resist intermittent pressure |
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Ground substance structure and function
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Mixture of H2O & various organic molecules
GAG’s, proteoglycans, glycoproteins Very “hydrophillic” substance Function: Contributes to strength of connective tissues Allows for diffusion of molecules Provides space b/w fibers Strength Organic molecules (GAG’s, proteoglycans, glycoproteins) help form attachments between fibers Diffusion of molecules H2O allows transport of metabolites in & out Space b/w fibers H2O & organic molecules make space b/w fibers Reduces friction Increases elasticity |
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Regions during response to mechanical elongation
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Toe Region - Low stress, hi strain
Linear Region – Hi stress, hi strain, slight tissue failure Progressive Failure – Internal failure with intact structure Major Failure – Shear & Rupture Complete Rupture – Structure breaks |
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Elasticity
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Ability for soft-tissue to return to resting length after passive stretch
Stretch → Elongation → Return to Previous Length Mechanical aspects of elasticity? Straightening of crimp Disruption of bonds between collagen fibers Minor disruption of bonds between collagen fibrils? Elastic changes are reversible !!! Recovery |
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Plasticity
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Tendency for soft tissue to assume and retain greater length after stress is removed
Stretch → Elongation → Retention of Greater Length Mechanical aspects of plastic changes Disruption of collagen fiber infrastructure Subfibrils & tropocollagen |
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Review of inflammation and healing events
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Vascular Response
-Vasoconstriction & Vasodilation Hemostatic Response -Clotting & Isolation Phagocytic Activity -Macrophage activity Fibroplasia -Mass synthesis of collagen Remodeling -Reorganization of collagen |
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Scar Tissue Formation (Days 2-4)**
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Initial fibroblast activity; cont. macrophage activity
Earliest deposition is type III collagen Weaker fibers May act as scaffolding for deposition of type I fibers As approach day 4-5 ↑ in type I fibers Scar tissue “very fragile” |
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Scar Tissue Formation (Days 5-21)
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Significant fibroplasia
w/corresponding ↑ in collagen fibers ↑ in Fibroblasts; ↓ in macrophages Myofibroblasts & Scar shrinkage |
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Scar Tissue Formation
(Days 21-60) |
∆ from mostly cellular → fibrous tissue
~ 4 weeks tissue becomes more organized Greater strength Remodeling !!! Fibroblasts lay down collagen tissue along lines of tension !!! Response to stress |
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Scar Tissue Formation
(Day 60 - 360) |
Further maturation and remodeling
Compact & Large collagen fibers Significantly less fibroplasia Comes to resemble original structure |
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Scar Tissue Formation Summary
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Inflammatory Phase
Vascular, Hemostatic, and Cellular events prepare for new tissue growth Days 2-4 Deposition of fragile scar tissue Days 5-21 Scar laid down in bulk Transition to remodeling Day 21-60 Tissue becomes organized and stronger via remodeling Day 60-360 Maturation of tissue / comes to resemble original state |
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Steps of PT Eval for wound care
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Patient history
Systems review Tests and measures |
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Wound Characteristics: Location
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Can provide information on etiology
Use anatomically correct terminology Document in relation to anatomical landmarks Document side (right or left) Ex: “Wound is located 10 cm superior to the right medial malleolus |
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Wound Characteristics: Size
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Indicator of improvement or decline
Direct measurement Tracings Photography Percent of total body surface area Do NOT document in relation to objects “ The wound is the size of a quarter” |
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Wound Characteristics: Tunneling
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Tunneling
Created by separation or destruction of fascia Measure from top of wound edge Clock terms to identify position Common with surgical and neuropathic wounds |
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Wound Characteristics: Undermining
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Undermining
Tissue under the wound edges become eroded Probe parallel to the wound surface Clock terms to identify position Common with pressure or neuropathic wounds |
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Characteristics of wound bed
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Presence
Color Consistency Amount Adherence Granulation tissue Other structures Necrotic tissue |
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Wound Characteristics: Wound Edge
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Distinctness
Thickness Color Attachment to base of wound Evidence of epithelialization, scarring, pigment changes |
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Wound Characteristics: Drainage
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Type - serous, sanguinous, purulent...
Color - clear, yellow, red, brown, blue-green Consistency - thin/watery, thick Amount - none, minimal or moderate, copious |
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Wound Characteristics: Odor
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Present or absent
Possible indicator of wound infection |
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Wound Characteristics:
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Location
Size Tunneling Edges Drainage Odor |
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Tests of circulation
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Peripheral pulses
Capillary refill Normal: < 3 seconds Graded 0 to 3+ On own, not very sensitive or specific Follow up testing with Doppler ultrasound |
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Circulation: ankle/brachial index
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Ratio of ankle/arm BP measured via Doppler
Dorsalis pedis or posterior tibialis artery Reliable, noninvasive Measures peripheral tissue perfusion < 0.90 is 95% sensitive and 99% specific (very accurate) for PAD < 0.80: intermittent claudication |
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Tests of sensory integrity
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Impaired light touch: risk factor for ulceration/reulceration
Gold standard: Semmes-Weinstein monofilaments 4.17 = 1 g = decreased sensation 5.07 = 10 g = loss of protective sensation 6.1 = 5 g = absent sensation |
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Functions of the epidermis
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Provides a physical and chemical barrier
Regulates fluid Provides light touch sensation Assists with thermoregulation Assists with excretion Critical to endogenous vitamin D production Contributes to cosmesis/appearance |
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Functions of the dermis
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Supports and nourishes the epidermis
Houses the epidermal appendages Assists with infection control Assists with thermoregulation Provides sensation |
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Superficial wound
-tissue involved -Examples |
epithelial tissue
abrasion, 1st degree burn |
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Partial thickness wound
-tissue involved -Examples |
-tissue involved: epidermal, dermis
-Examples: blister, 2nd degree burn, Grade 1 ulcer |
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Full-thickness wound
-tissue involved -Examples |
-tissue involved: epidermal, dermis, subcutaneous tissue, deeper tissue
-Examples: full-thickness burn, stage III pressure ulcer, grade 2-5 ulcer |
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Types of wound closure
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Primary Closure (Primary Intention)
Clean of foreign material and edges are physical approximated Ex. Surgical incision Secondary Closure (Secondary Intention) Follows the 3 phases of wound healing Majority of wounds requiring physical therapy Delayed Primary Closure (Tertiary Intention) Combination of primary and secondary |
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Chronic wounds have
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Chronic Wounds
Senescent cells Higher levels of MMPs Lower levels of tissue inhibitors of matrix metalloproteases (TIMPs) Greater numbers of inflammatory cytokines and chronic wound cells |
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Abnormal wound healing
(possible things) |
Absence of inflammation
Chronic inflammation Hypo- or Hyper-granulation Hypertrophic scarring Keloids Contractures Dehiscence |
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Wound characteristics affecting healing
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Mechanism of onset
Time since onset Wound location Wound dimension Temperature Wound hydration Necrotic tissue or foreign bodies Infection |
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Inappropriate wound management
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Patient compliance
Home remedies Lack of understanding by the patient Limited financial resources or insufficient caregiver support Failure to follow established guidelines Exposure to air or inappropriate dressing Inappropriate use of antiseptics Overuse of whirlpool |
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Issues with devitalized tissue in wound bed
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Medium for bacterial growth
Perpetuates inflammatory response Acts as a physical barrier to wound healing and topical microbials Increases wound odor |
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Contraindications/considerations for wound debridement
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Red, granular wounds
Wounds that require surgical debridement Wound characteristics Status of the patient Clinician characteristics Practice act/laws governing practice Clinician’s knowledge and skill Use of standard precautions |
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Sharp debridement
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Forceps, scissors, scalpel
Most aggressive and fastest form Standard of care for open wound Can be done by PT where allowed by law May require MD order Indications - Large amount of necrosis, advancing cellulitis, sepsis, eschar -Chronic wounds Contraindications: Inadequate visualization Unidentifiable material Infected ischemic ulcers w/ low ABI Hypergranulation |
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Methods of sharp debridement
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Serial debridement
Remove loosely adherent necrotic tissue Occurs over several visits Selective sharp debridement Cut between viable and nonviable tissue May require topical pain medications |
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Autolytic debridement
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Use body’s own enzymes and moisture
Need moisture retentive dressing Least invasive and least painful form Easy to teach Requires minimal time from provider, but long periods often required to complete debridement Use with patients who cannot tolerate other forms Commonly used in home or LTC setting Low cost Contraindications Infected or deep cavity wounds Wounds that require surgical debridement |
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Steps of autolytic debridement
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Procedure:
Crosshatch eschar Protect periwound area Moisture retentive dressing left in place for 72-96 hours |
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Enzymatic debridement
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Also known as “chemical debridement”
MD prescription needed Types of enzymes: Proteolytics Fibrinolytics Collegenases Papain-Urea Contraindications Wounds with exposed deep tissues Facial burns Calluses Exogenous enzymes should not be applied to wounds being autolytically debrided |
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Mechanical debridement
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Use of force to remove devitalized tissue and debris
Nonselective debridement For example: wet to dry dressings, scrubbing, wound cleansing, irrigation, pulsative lavage, whirlpool, hydrogen peroxide Advantages: low cost Disadvantages: painful, time consuming, may traumatize healthy and healing tissue Most should be completed only with 100% necrotic tissue |
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Biologic Debridement
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Maggot therapy: “biosurgeons”
Larvae release enzymes that degrade and liquefy necrotic tissue Larvae ingest debris and bacteria Psychological considerations - people get creeped out! Dressing considerations |
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What components are always present in pain?
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Sensory AND Emotional
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What are some structures of the limbic system, and what is the system involved in?
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Cingulate cortex, septal area, hypothalamus, hippocampus, and amygdala
Involved in filtering responses to pain based on past experience, culture, present situation, etc. (memory component for sure) |
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Describe pain vs. nociception
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Pain is an unpleasant situation that has been interpreted by higher brain centers
Nociception is the process of encoding/processing noxious stimuli, it's neurophysiological (actual signals through nerves... need interpretation for meaning) |
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Acute vs. Chronic pain
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Acute
Result of recent tissue damage Warning to prevent further damage Chronic Pain that persists beyond usefulness May become disease unto itself Hyperalgesia Hypersensitivity of pain receptors 2ndary to prolonged exposure to painful stimulus Chemical pain |
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Referred Pain
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Pain perceived in an area having little to do with existing pathology
Usually 2ndary to convergence RC referral to deltoid insertion Pain from inflamed structures producing pain elsewhere |
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Radicular Pain
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Result of neural compromise, radiates along dermatome, e.g. sciatica
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What are the three dimensions of pain?
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Sensory-Descriminative
localize the area and type of pain, tell the brain where and what type Cognitive-Evaluative Interpret sensation Affective-Motivational Limbic system, form response |
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Pain Threshold
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How much stimulus is required to be interpreted as pain, alerts to potential threat, signals from A-delta fibers (point when they are recruited = threshold)
Cold application can increase by 89% |
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Pain Tolerance
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How much pain a person can stand
(until withdrawing from stimulus, for instance) Cold application can increase by 76% |
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Types of sensory receptors
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mechanoreceptors
nociceptors proprioceptors thermoreceptors |
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Mechanoreceptors
- stimuli - location |
- stimuli: pressure & touch
- location: skin, hair follicles |
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Nociceptors
- stimuli - location |
- stimuli: painful stimuli (can be pressure, etc.)
- location: various tissues |
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Proprioceptors
- stimuli - location |
- stimuli: change in length, tension, position
- location: tendons, skin, capsules, muscle and ligaments |
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Thermoreceptors
- stimuli - location |
- stimuli: cold and heat
- location: skin, capsules, ligaments |
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First Order Neurons: purpose and types
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Primary Afferents
Transmit impulses from sensory receptors towards CNS Types: Large Diameter Afferents Small Diameter Afferents |
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Characteristics of
Large Diameter Afferents |
Thick myelin sheaths
Wide in diameter Fast conduction velocity Because of above aspects Carry non-noxious (non-painful) stimuli 2 types A-alpha A-beta |
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Characteristics of Small Diameter Afferents
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Less myelinated
Smaller in diameter Slower conduction velocity Carry info about: Mechanical, thermal, chemical ∆’s Includes noxious (painful) stimuli 2 types A-delta fibers (threshold) C fibers (dull pain) |
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Where do first order neurons send their signals?
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1st order neurons synapse in spinal cord
In dorsal horn With 2nd order neurons Substantia Gelatinosa Area in dorsal horn of spinal cord Plays a role in pain control Stimulation of this area may limit transmission of pain messages further on |
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2nd order neurons transmit sensory information from...
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Transmit sensory information from dorsal horn of spinal cord to brain
Wide dynamic range 2nd order neurons Input from large areas of receptor fields Input from A-beta, A-delta, C fibers Nociceptive specific 2nd order neurons Only noxious stimuli Input from A-delta & C fibers |
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3rd order neurons
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2nd order neurons synapse on 3rd order neurons in brain
Connect various regions of the brain “Higher centers” From thalamus to cortex often |
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Excitatory and Inhibitory Transmitter Substances
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Neurotransmitters
Some excititory -Acetylcholine -Substance P (released by nociceptor to stimulate 1st neuron --Transmission of noxious input Some inhibitory -Enkephalin *** (inhibits pain perception) -Many others |
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Nociceptors often “hypersensitized” by
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release of prostaglandins & bradykinin
From injured cells |
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Stimulation of nociceptor causes release of
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Substance P
Initiates impulse along 1st order neuron Small diameter afferent (A-delta or C) Also released at synapse b/w 1st & 2nd order neurons in Dorsal Horn of Spinal Cord |
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Transmission of pain and temperature stimuli through CNS follow similar pathways
Pathways are named |
Spinothalamic tract***
Spinoreticular tract Spinoencephalic tract |
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Gate Theory of Pain Control
A-beta fibers (non-noxious input) stimulate |
substantia gelatinosa in SC
Substantia gelatinosa inhibits transmission of impulses from A-delta & C fibers (noxious input) onto 2nd order neurons Inhibition of A-delta & C fiber transmission “closes the gate” |
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Alternate Theory of Pain control through ascending mechanisms
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Ascending control mechanism
Initial stimulus is similar to Gate theory Non-noxious input Blocks transmission of pain thru “interneuron” A-beta neurons are stimulated Stimulate an “interneuron” Connects 2 neurons Interneuron releases enkephalin Inhibits small diameter (A-delta & C fibers) by blocking substance P The release of spinal opioids has been liked to the closing of the gait. The large diameter afferents synapse with spinal enkephalin interneurons, which release enkephalin at the spinal level, having an inhibitory effect of small diameter afferents |
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Central Biasing Model
(Descending Control Mechanism) |
1. Brief intense pain stimulus to higher centers of brain
2. Impulse carried thru higher centers (PAG -> Raphe Nucleus) (periaquaductal gray region of midbrain to raphe nucleus in the pons) 3. These relay impulses that descend thru the spinal chord 4. Serotonin is released at spinal level to inhibit the SON 5. Synapse on enkephalin interneuron 6. Blocks substance P (Signal goes up to brain then back to spinal cord where enkephalin interneuron is stimulated and inhibits more substance P and ascending pain signals) |
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In what treatment settings could the central biasing model be acting?
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Analgesia via a brief intense stimulus
Accupressure Accupuncture? Some TENS settings |
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Descending pain control mechanism involving Beta Endorphin release
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Descending Mechanism of Control
Prolonged intense stimulus to higher centers of brain Passes thru higher centers (Reticular formation, Hypothalamus) Beta endorphin released at Hypothalamus Stimulates other higher centers (PAG, Raphe Nucleus) These relay impulses that descend thru the spinal chord Synapse on enkephalin interneuron Blocks substance P Analgesia via prolonged intense stimulus TENS Low pulse rate, long pulse width These parameters perceived as uncomfortable or painful Electroacupuncture |
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What's important to know about the methods of pain control?
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General differences between mechanisms of control
What is the initial stimulus for each mechanism? What types of fibers carry the initial stimulus? Ascending vs. Descending pathways? Does the pathway include Higher Brain centers? Enkephalin Interneuron? Beta-Endorphins? Substantia Gelatinosa |
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What three ways do medications affect pain?
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Decrease the inflammatory response
Block transmission of noxious stimuli Altering the perception of pain |
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Analygesics and Anti-inflammatory medications
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NSAID
Prescription Naproxen Over-the-counter Aspirin, acetaminophen Primary function is to inhibit the cyclooxygenase enzymes COX-1 and COX-2. COX-2 inhibited prostaglandin production is blocked |
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How do local anesthetics affect pain?
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Temporarily block nerve conduction
Result in loss of sensation in area lidocaine |
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How do opioid analgesics affect pain?
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Interact with neurotransmitter receptors on cells in the nervous system
Morphine, hydrocodone, tramadol, codeine |
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Psychological reactions to pain
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Past experiences, pain expectations, and sociocultural experiences influences a person’s pain response. Personality, age, and gender can also influence pain perceptions. Extroverts express pain, but introverts are more sensitive to pain. As a person ages they can handle more pain
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An increase in non-nociceptive stimuli from the periphery characterizes the
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ascending mechanism for pain relief.
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Gate Control Theory Summary
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An increase in non-nociceptive stimuli from the periphery characterizes the ascending mechanism for pain relief. A-beta fiber receptors can decrease the possibility of nociceptive stimuli input travelling to SON. The mechanism occurs in the lamina II (substantia gelatinosa). Stimuli from the larger, myelinated A-beta fibers entering the dorsal horn synapse with SON and spinal interneurons, closing the gate causing an inhibitory effect on smaller diameter afferent C and A-delta fibers. The interneurons’ role is to open and close the gate, depending on the type of input from peripheral receptors. The descending mechanism of pain relief maintains that structures within the brain can assist in closing the gait or inhibiting the smaller diameter afferent traffic through descending connections in the dorsal horn.
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Descending mechanism for pain relief - summary
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Within cerebral cortex, PAG activates raphe nuclei to initiate this mechanism. Serotonin is released at the spinal level to inhibit the SON and activate the spinal enkephalin interneuron. In addition, norepinepherine is released and inhibits pain transmission at the spinal level.
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Endogenous Opiates Theory
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Uses higher centers of the brain. Theory focuses on the hypothalamus, because it controls pain caused by prolonged intense stimulation. Beta-endorphins, powerful endogenous opiates, are released from the pituitary gland, which is controlled by the hypothalamus. The beta-endorphins circulate through the bloodstream, inhibiting pain perception. Another endogenous opiate that assists with reducing pain is enkephalin, which is triggered by the descending mechanism of pain relief.
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Thermal Agents (pain): Cold
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Cold: triggers descending pain control via release of enkephalin. Slowing sodium-potassium pump, rate of nerve depolarization is decreased and nerve depolarization threshold is increased. Small-diameter, myelinated nerves are the first to exhibit this change.
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Thermal Agents (pain): Heat
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Heat: also counterirritant to reduce pain via the gate mechanism. The stimulation of sensory nerve fibers, including polymodal thermoreceptors, increases depolarization threshold of peripheral nerves, and acts centrally in the thalamus.
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Thermal Agents (pain): UltraSound
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Alter cell membrane permeability that slows the nerves’ rate of depolarization. Increasing cell membrane permeability opens the sodium channels and congests the area with sodium. Thereby inhibiting the sodium-potassium pump.
Also as it increases blood flow, it can reduce pain caused by ischemia and hypoxia |
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Thermal Agents (pain): Electric Stimulation
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sensory, motor, and noxious level.
Sensory: submotor intensity & high pps to activate A-beta fibers, inhibiting pain at the spinal level via the ascending mechanism of the Gate Control theory. Motor: low # pps to evoke moderate to strong contractions that, in addition the ascending gate control theory, activate the release of endogenous opiates via the gate’s descending component. Noxious: activate C-fibers results in pain control via the central biasing mechanism |
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Drugs decreasing inflammatory response
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NSAIDS nonsteroidal anti-inflammatory drugs
Inhibit enzymes COX-1 and COX-2 COX-2 inhibition – prostaglandin production is blocked, decreasing the sensitization of peripheral nerves Primary action block prostaglandin Aspirin counteracts prostaglandin effect |
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Drugs that block the transmission of noxious stimuli
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Local Anesthetics
Temporary block nerve conduction results in loss of sensation in the area Lidocaine block the action of voltage-gated sodium channels and very effectively shut down potential production in nerve fibers |
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Drugs that alter the perception of pain
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Opioid analgesics
Opioids block the affective component of pain-the unpleasantness-with little effect on touch or proprioception Act by interacting with neurotransmitter receptors on cells in the nervous system to altar pain perception These cells are normally regulated by endorphins |
