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477 Cards in this Set
- Front
- Back
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Zygapophyseal (spine) closed pack position |
extension |
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zygapophyseal (spine) open pack |
midway between flexion and extension |
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TMJ closed pack positino |
teeth clenched |
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TMJ open pack position |
mouth slightly open |
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Glenohumeral joint close pack position |
abduction and external rotation |
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Glenohumeral joint open pack positionn |
55° abduction; 30° of horizontal adduction |
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AC joint close pack postion |
arm abducted 90° |
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AC joint open pack position |
arm resting by side |
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SC joint closed pack position |
max shoulder elevation |
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SC joint open pack position |
arm resting by side |
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ulnohumeral joint close pack |
extension |
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ulnohumeral joint open pack |
70° flexion; 10° supination |
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radiohumeral joint close pack |
elbow flexed 90°; forearm supinated 5° |
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radiohumeral open pack position |
full ext.; full supination |
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proximal radioulnar joint close pack |
5° supination |
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proximal radioulnar joint open pack |
70° flexion; 35° supination |
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distal radioulnar joint close pack |
5° supination |
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distal radioulnar joint open pack |
10° supination |
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radiocarpal (wrist) joint close pack |
extension w/ radial deviation |
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radiocarpal (wrist) open pack |
neutral with slight ulnar deviation |
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MCP joint close pack position |
full extension |
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MCP joint open pack position |
slight flexion |
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CMC joint close pack position |
full opposition
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CMC joint open pack position |
midway btwn abduction-adduction and flexion-extension |
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IP joint close pack position |
full extension |
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IP joint open pack position |
slight flexion |
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Hip close pack position |
full extension, internal rotation, abduction |
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hip open pack position |
30° flexion; 30° abduction; slight external rotation |
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tibiofemoral close pack postion |
full ext., external rotation of tibia |
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tibiofemoral open pack position |
25° flexion |
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talocrural (ankle) close pack position |
max dorsiflexion |
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talocrural (ankle) open pack postion |
10° plantarflexion; midway btwn max inversion and eversion |
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subtalar joint close pack position |
supination |
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subtalar joint open pack position |
midway btwn extremes of range of movement |
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midtarsal joint close pack |
supination |
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midtarsal joint open pack |
midway btwn extreme of ROM |
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tarsometatarsal joint close pack |
supination |
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tarsometatarsal joint open pack |
midway btwn extremes of ROM |
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MTP close pack position |
full ext. |
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MTP open pack position |
neutral |
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IP (toe) close pack position |
full ext. |
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IP (toe) open pack position |
slight flexion |
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when does cell injury occur |
when injury/pathology is present |
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what is the purpose of cell injury/tissue healing |
healing starts when waste is removed |
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how does cell injury present |
scar tissue/inflammation |
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what dictates the speed of tissue healing? |
severity length of time of mechanism injury type |
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what is needed for reversible cell injury to take place? |
the nucleus must not be damaged |
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what occurs during a reversible cell injury? |
- increased Na+, Ca+ inside cell causes swelling - nucleus pumps out excess fluid and lactic acid to reverse injury |
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what happens to a cell when stress is increased? |
cell adapts by changing size, #, or function - function improves under prolonged stress increase (CLUTCH PLAYER) |
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what causes irreversible cell injury? |
maintained stress with a high magnitude |
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what happens at the beginning of irreversible cell injury? |
creatine kinase (enzymes) show up to prepare scar tissue |
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What are the mechanisms of injury? |
ischemia physical factors infection immune reaction genetic factors nutritional factors chemical factors |
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why is ischemia a difficult mechanism to work with? |
there are several points during the O2 delivery where this can occur to alter cell metabolism |
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burns are what mechanism of injury? |
physical factor |
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why is nutrition important for tissue healing |
nutrition can impact cell function, protein is needed to rebuild cell |
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what is an indirect chemical factor? |
when a chemical is transformed inside the body (free radical) |
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what are the 4 phases of scar tissue formation |
inflammation granulation fibroplastic maturation |
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what types of tissues does scar tissue heal |
soft tissue - not muscle or liver |
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what is the most vital portion of scar tissue formation |
inflammation - process can't occur without it |
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what is the function of inflammation |
- inactivate injury agent - breakdown/remove dead tissue - initiate healing |
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what are the key components of inflammation |
blood vessels/cells CT cells (fibroblasts) Chem mediators from inflammatory cells collagen |
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what are the adverse effects of inflammation |
healthy cells nearby can be damaged - collateral damage |
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four cardinal signs of inflammation |
redness swelling increase temp pain |
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other indicators of inflammation |
- muscle tone increase or spasm - loss of motion/function - spasm end feel with PROM - pain before resistance in PROM |
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Steps to acute inflammation |
vascular alterations leukocyte accumulation production of chemical mediators |
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what are the vascular alterations after injury
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- capillaries constrict - vasoconstriction reduces blood flow to affected area - platelets produce clot to reduce blood loss |
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what is transudation? |
process that occurs after initial vascular alterations when vasodilation occurs and increased blood flow causes increased hydrostatic pressure pushing fluid to interstitial space |
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what is the byproduct of transudation? |
swelling |
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what is effusion? |
accumulation of transudate/exudate in interstitial space brought about by margination |
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what is margination |
leukocytes adhere to vessel wall to increase BV permeability (allows cells to exit into intersitial space) |
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Transudate |
protein poor cells that accumulate in interstitial space during inflammation |
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Exudate |
protein rich cells - including phagocytes - that accumulate in interstitial space in inflammation |
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what is the purpose of leukocytes and leukocyte accumulation? |
- to fight infection - allow for margination when they adhere to BV wall - increase permeability of BV wall - helps with removing necrotic tissue |
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what happens once an injury is cleaned by leukocytes? |
inflammation decreases, leukocytes leave and macrophages enter to eliminate waste products |
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what happens if leukocytes die? |
pus is created |
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what are the functions of the chemical mediators brought in during acute inflammation? |
- vasodilation/constriction - modulate vascular permeability - activate inflammatory cells - cytotoxicity - degrade injured tissue - pain production/fever |
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what are the chemical mediators? |
histamine platelet activating factor plasma proteins cytokines phagocytes |
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what are the different outcomes of acute inflammation? |
resolution chronic inflammation |
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what are the factors in acute inflammation resolution |
which tissue is involved
amount of tissue effected |
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what are the conditions that favor resolution |
- minimal cell death/tissue damage - rapid removal of injurious agent - rapid removal of fluid/debris (why swelling should be decreased quickly) |
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what marks the beginning of the granulation phase? |
- phagocytes come in to debride area |
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what is needed to move onto the granulation phase? why? |
increased blood supply to meet metabolic demands of new tissue |
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what precautions must be made during the granulation phase? |
immobilize injured area to allow for vascular regrowth (vessels start fragile, also prevents injury to neighboring tissue) |
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what is primary occurence during granulation phase? |
angiogenesis - endothelial cells from close BV form new caps to transport oxygen to new tissue |
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what happens to new blood vessels created during angiogenesis |
normally destroyed |
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what marks the beginning of the fibroplastic phase? |
occurs once necrotic tissue removed - synthesis of ECM and collagen occurs |
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what happens during ECM creation? |
- necrotic tissue removed - fibroblasts migrate to site of injury, remove injured cells - remaining cells regenerate thru mitosis (concurrent with collagen synthesis) - scar tissue formed |
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what are the steps of the collagen synthesis? |
- collagen fibrils are synthesized - fibrils released into interstitial spaces - fibrils bond to other fibrils to form collagen fiber |
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what is the importance of collagen in tissue repair? |
- main structural component in healing tissues - provides structural support/tensile strength |
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what are the collagen types that are created? |
initially type 3, mature to type 1 |
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what needs to be known about newly forms collagen fibers? |
- initially made of weak H+ bonds - mature to covalent bonds - initially unorganized and randomly distributed - fibers align once proper stress is applied |
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what happens if proper stress isnt applied after collagen synthesis? |
tissue may not properly function |
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what happens after ECM is formed? |
tissue contracts to decrease area of tissue injury and assist with wound closure. Occurs when fibroblasts turn into myofibroblasts (which have contractile properties) |
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what is purpose of maturation phase? |
- decrease wound size - realign collagen fibers - increase scar tissue strength |
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what happens during maturation phase? |
- collagen formation/cross link continue to increase strength - BF diminishes when new caps close and BF sent to areas of higher demand |
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how long does maturation phase take? |
can take up to 12-18 mos. |
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what is the tensile strength of mature scar tissue? |
70-80% original |
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volume of scar tissue |
normally less than what it replaces - unless there is keloid scarring |
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what are blood flow factors that affect healing? |
anything that decreases it slows the process or if tissue (tendons/fibrocartilage/articular cartilage) has limited BF |
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what are the important nutrients in healing process? |
Vitamin C (Collagen formation) Iron (hGb for oxygen transport) zinc (enzymes that degrade damaged cells) amino acids (collagen production) |
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misc. factors that affect healing? |
smoking COPD CHF heart/lung disfunction immunosuppressants infections neurologic impairments |
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Types of soft tissue injury |
-strain -sprain -rupture |
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causes of strains (muscle/tendon) |
- Overuse/overexertion - some disruption - microtrauma w/ NO lasting deformation - least sever |
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1st degree strains |
Mild - minimal structural damage minimal hemorrhage early resolution |
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2nd degree strains |
moderate - partial tear large spectrum of injury significant early functional loss |
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3rd degree strains |
severe - complete tear may require aspiration may require surgery |
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related factors of 1st degree strains |
- onset at 24-48 hrs. after exercise - sudden overstretch - sudden contraction |
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related factors of 2nd degree strains |
- decelerating limb - insufficient warm up - lack of flexibility |
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related factors of 3rd degree strains |
- increasing severity of strain associated w/ muscle fiber death, more hemorrhage, eventual scarring - steroid use/abuse - previous muscle injury - collagen disease |
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related factors of exercise induced muscle injury |
- increased activity - unaccustomed activity - excessive eccentric work - viral infections - secondary to muscle cell damage |
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related factors of contusion |
direct blow associated with increasing muscle trauma and tearing of fiber proportionate to severity |
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what are the characteristics of a sprain (tendon) |
- severe stress - moderate - may cause some lasting deformation - graded |
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what are the characteristics of a rupture/tear? |
- severe - complete disruption - pain in region of injury during stress if partial tear - no pain during PROM if complete tear |
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what is subluxation? |
paritial dislocation or joint that dislocates and relocates on its own\ |
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what is dislocation |
joint disruption that requires outside force to relocate |
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what normally accompanies dislocation? |
soft tissue damage/inflammation |
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stages of soft tissue healing? |
acute - inflammation subacute - granulation/fibroplastic chronic - maturation |
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general length of acute phase of soft tissue healing?
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10 days |
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signs of subacute phase of soft tissue healing? |
can last up to 6 wks. - stressing tissue causes pain/tightness at end range |
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signs of chronic stage of soft tissue healing |
no inflammation - can last up to a year |
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bone reactions to abnormal condition |
- local death (avascular necrosis)
- alteration of bone deposition - alteration of bone resorption - mechanical failure (fracture) |
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what is a bone fracture? |
defect in continuity of bone, or normal anatomy of bone |
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classifications of bone fractures? |
sudden impact stress/fatigue pathological |
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characteristics of sudden impact bone fractures |
- most common - increased rate of 65 years old - cause mostly by fals - women & caucasians have higher incidence rate |
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how do bone fractures clincally manifest themselves? |
- point tenderness - localized pain - painful mvment/ WB - rapid swelling - anatomical malformations |
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what causes stress fractures? |
muscle fatigue, which limits shock absorption on bone (ultimate overuse injury) |
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risk factors for stress fracture? |
- age - gender - rage - fitness level - menstrual history - physical exam findings |
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what is normally the history of a pt. with a stress fracture? |
- insidious pain onset - pain start with dull ache after exercise - progresses gradually and increases during exercise - eventually always present - more localized as it increases |
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common locations for stress fractures |
- Tibia (50%) - fibula - foot (navicular/5th MT) - Femur (neck or shaft) |
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what are the healing rates of stress frx? |
variable - severity - 12 wks- 2 yrs - need bone scan to assess progress |
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what is primary bone healing? |
- needs rigid compression fixation through surgery - bone grows directly across compressed bone - must have direct, intimate contact btwn frax fragments - slow process for cortical bones |
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what is secondary bone healing? |
- from casting/splinting, stabilization outside body - callus formation covers fracture sight to stabilize frags |
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three phases of bone healing? |
- inflammation - raparative - remodeling |
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what happens during inflammation phase of bone healing? |
- caps torn at frx site, bleed and create hematoma - similar to soft tissue healing - 1 wk later - phagocytes remove hematoma - angiogenesis/initial fibrosis occur |
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when does frx become easier to see on x-ray? |
after about a wk/ when necrotic cells are debrided and inflammation decreases |
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what happens in during callus formation of reparative phase? |
- soft callus forms over frx - hematoma inside invaded by chondroblasts/fibroblasts to synthesize matrix for callus formation - callus is soft bc very few bone cells present |
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what happens at the end of the reparative phase? |
- osteoblasts transform soft callus to hard callus (bone) - this bone weak bc immature/disorganized |
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what two things may happen at end of reparative phase? |
- delayed or non-union - frx line begins to disappear |
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what happens during remodeling phase of bone injury? |
- disorganized bone replaced by mature lamellar bone
- medullary canal becomes the final thing to reform |
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what should be happening/evident at end of remodeling phase? |
- frx line should be gone - callus formation still evident - lamellar bone continues to form for about a yr |
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what can delay bone healing? why? |
intermedullary rodding, the procedure for the placement of rodding disrupts blood supply to healing bone |
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how long does hematoma formation take in bone healing? |
1-2 days |
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how long does it take for inflammation phase of bone healing to end? |
2-5 days |
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how long does it take for soft callus formation to take place in bone healing? |
4-12 days |
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how long does it take for hard callus formation to take place in bone healing? |
17-40 days |
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how long does it take for maturation of callus to take place in bone healing? |
3 wks - 4 mos. |
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how long does it take for bone to restore to normal post injury? |
6 wks - 1/2 yrs. |
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two main types of cartilage injuries |
Fibrocartilage articular cartilage |
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where do fibrocartilage injuries mostly take place? |
knee spine (IV disc) |
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types of forces that cause knee fibrocartilage injuries |
torsional forces |
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what type of forces normally cause IV disc injuries |
bending |
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what is the vascularity of the knee fibrocartilage? |
outer 1/3 to 1/2 with a direct blood supply |
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what is the vascularity of the IVD? |
- highly vascular neurovascular capsule - less vascular outer annulus - no direct blood supply to inner annulus |
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what is a type 1 articular cartilage injury? |
superficial injury - microscopic damage to chrondrocytes & ECM |
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what is a type 2 articular cartilage injury |
partial thickness injury - chondral frx |
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what is a type 3 articular cartilage injury? |
full thickness injury that penetrattes subchondral bone |
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which articular cartilage injury has the worst prognosis- why? |
type 2, there is no Blood flow, so no ability for standard healing |
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which type of articular cartilage injury goes through standard healing? |
type 3, depth allows for inflammation from BF of subchondral bone |
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what is long term effects of articular cartilage injury? |
only replaced by fibrocartilage |
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techniques for fixing larger defects |
- autologous chondrocyte implantation - osteochondral grafting/mosiacplasty - microfracture - arthroscopic lavage and debridemnet |
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steps to cartilage healing without surgical intervention |
2 wks- mesenchymal cells transform to chondrocytes and replicate 6 mos- subchondral bone healed, but chondral defect does not completely fill in entire injured tissue |
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what is issue with cartilage healing without surgical intervention? |
insufficient proteoglycan - new tissue not as functional as original |
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what is important about myotendinous junction? |
- where forces from muscle contraction are transferred to tendon - collagen inserts to finger like processes - weakest part of muscle/tendon unit - most susceptible to injury |
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why are there finger like projections on myotendinous junciton |
the increase in contact area decreases the amt of force applied to the area |
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which muscle fiber has the highest amount of contact surface at MTJ? why? |
type 2- they can produce large contraction force |
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similarities of tendon and ligaments? |
- both made of type 1 collagen (parallel fibers) - similar elastin components (w/ some exceptions) |
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what are the two scenarios of tendon injury? |
- Full tear - typically require surgery - adhesions are common - partial tear - can heal on own - 4 phases |
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what are the four phases of tendon healing? |
- hemorrhagic/hemostasis - inflammatory/granulation - proliferation/fibroplastic - remodeling/maturation |
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what happens during the hemorrhagic/hemostasis phase of tendon healing?
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- platelets cause quick clot
- leukocytes/monocytes recruited to progress inflammation - histamine/bradykinin increase vascular permeability |
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When does inflammatory/granulation phase start in tendon healing? |
typically 2-3 wks after injury, as early as 48 hrs. |
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what happens during inflammatory/granulation phase of tendon healing? |
- macrophages remove dead tissue - prepare for angiogenesis -chem mediators (GF) released which signal fibroblasts |
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what happens during proliferation/fibroplastic phase of tendon healing? |
- fibroblasts begin to produce collagen/ECM - replaces clot/scaffolding built during inflammatory phase |
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what type of collagen/ECM is built during proliferation/fibroplastic phase? |
type III - randomly distributed and disorganized |
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what happens to the type III collagen built during proliferation/fibroplastic phase? |
form fibrils
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what is done to the injury area during proliferation/fibroplastic phase? |
typically immobilization |
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when does remodeling/maturation phase begin? |
wk 3 |
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what happens during the remodeling/maturation phase of tendon healing? |
- type III turns to type I collagen - controlled stress aligns the collagen fibers |
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how long before an injured tendon can be significantly stressed? |
3-4 mos. |
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when can max muscle contraction begin? |
8 wks |
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what contractions should be done before the tendon can be significantly stressed? |
- controlled submax isometric - low force concentric |
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what is the timeline of healing for an injured tendon |
6 mos - 50% tensile strength 1 yr - 80% 1-3 yrs. - 100% |
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what are symptoms of ligament injuries? |
- point tenderness - joint effusion - history of trauma |
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how are ligament injuries graded? |
same as soft tissue |
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what are the differences between intra-articular ligament injuries vs. extra-articular? |
- intra-articular require surgery bc lack of blood supply inhibits inflammation/healing - extra-articular heal via 4 phases - similar to tendons (there is a blood supply) |
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what are the 4 processes of healing for a muscle injury? (degeneration-regeneration cycle) |
1. damaged cellular components digested 2. satellite cells proliferate to form muscle fiber building materials 3. satellite cells fuse to form new mytubes/muscle fibers 4. regeneration of NM junction |
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what are the major differences in muscle injury repair from other repair processes? |
- satellite cells fuse to form myotubes and muscle fibers - regeneration of NM junction |
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what happens during the damaged cellular components digested phase of muscle regeneration? |
- happens via protease enzymes (lysosomes) and exogenous proteases (macrophages) - affects cellular components and fibers itself |
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how does the proliferation of satellite cells occur in muscle regeneration? |
- satellite cells btwn basal lamina and sarcolemma represent precursor cells to myoblasts - cells are signaled via charge (+ or -) |
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what is the signal when muscle cells are injured? |
send out a positive charge, negative charge means no injury |
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when does proliferation of satellite cells occur? |
3-4 days of injury
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how do satellite cells produce myoblasts and fuse/develop new myotubes and muscle fibers |
- align along basal lamina, begin to fuse into myotubes - similar to normal development process - synthesis of contractile proteins |
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why is basal lamina important? |
bc of collagen content |
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what are the factors important in proper regeneration during satellitte cells producing myoblasts? |
proper stress - assists with alignment |
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how does regeneration of NM junction occur? |
in new tissue - the receptors in sarcolemma congregate underneath nerve were ACh (NT) is released that becomes new neural contact |
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how long does it take to regenerated new muscle? |
6 mos. |
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why does it become more difficult regenerate muscle tissue? |
impaired development of the NM junction |
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what are the intrinsic factors that impact healing? |
- extent of injury - edema - hemorrhage - poor vascular supply - separation of tissue - muscle spasm - atrophy - degree of scarring |
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how does edema/hemorrhage negatively impact healing? |
can increase pressure that can impede needed nutrition to injury, inhibit NM control, and delay process |
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how does the separation of tissue impact healing? |
a wound with smooth edges tends to heal by primary intention w/ minimal scarring |
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how does a muscle spasm impact healing? |
causes traction on injured tissue |
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what are the systemic factors that impact healing? |
- age - obesity - malnutrition - hormone levels - infection - general health |
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how does obesity impact healing? |
oxygen pressure in tissue is lower |
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what are the extrinsic factors that impact healing? |
- drugs - absorbent dressings - temp and oxygen tension - physical modalities - exercise |
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how does absorbent dressings impact healing? |
humidity increases the rate of epithelium regeneration |
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what is pain? |
sensation that alerts a person that a tissue has been injured or damaged - warns body of potential or actual injury |
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types of pain |
- acute - chronic - recurrent |
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what is the focus of old medical models of pain? |
try to explain pain as a direct correlate of physical disease or injury |
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what is the focus of the gate control theory of pain? |
neurophysical mechanisms of pain transmission/modulation centered on the dorsal horn of spinal cord |
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what was unique about the gate control theory of pain? |
- degree of specificity for peripheral nerve function - degree of pattern recognition that was responsible for underlying peripheral and central processig of noxious information |
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what has been changed in modern models of pain? |
- acknowledge usefulness of earlier models - they try to explain the variable/inconsistent relationship btwn pathology and pain |
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what is the biopsychosocial model of pain |
tries to take biological processes, psychological emotions, and social implications and how pain impacts a person's life into account |
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what is the mature organism model? |
- expands on the mechanisms based approach - integrates neurophysical mechanisms with stress biology and biophyschosocial model of pain |
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what does the mature organism model describe? |
numerous and interrelated biological systems/processes involved in the initiation, maintenance and perception of pain together w/ the physiological and behavioral reactions to it |
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why is the mature organism model of pain important? |
broad understanding is required so that clinical presentations of pain might be better managed |
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what is important to remember about the experience of pain? |
everyone's pain experience is different and it must be put into context. |
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what is the general reason pain experience is varied? |
The stimulus is not the only thing that creates the response |
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what are nociceptors? |
- specialized sensory receptors responsible for detection of noxious stimuli - free nerve endings of primary a(delta) and C fibers |
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what do nociceptors do? |
transform stimuli into electrical signals that are sent to the CNS |
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where are nociceptors found? |
all over body (skin, viscera, muscles, joints, meninges) |
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what can stimulate nociceptors? |
mechanical thermal chemical stimuli |
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how do inflammatory mediators affect pain?
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- can stim nociceptors directly when they are released from damaged tissue - can reduce the activation threshold so the stim required to cause activation is less |
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causes of musculoskeletal pain
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- ischemia - muscle spasm |
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what affects the level of pain with ischemia? |
the greater the rate of metabolism of the tissue - the more rapidly the pain appears |
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what causes pain during ischemia |
- large amount of lactic acid - chem agents (bradykinin and proteolytic enzymes) stim pain nerve endings |
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what causes pain from muscle spasm? |
- effect of spasm stimulating mechanosensitive pain receptors - spasm compressing blood vessels resulting in some ischemia |
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how does spasm modulate pain? |
spasm increases metabolism rate in tissue making relative ischemia increase pain inducing substances |
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process/pathway of ischemia pain |
- blockade of blood flow - accumulation of lactic acid and release of chem responses - excite nociceptors - pain |
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adaptation of pain receptors? |
very little |
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hyperalgesia |
when excitation of pain fibers becomes progressively greater with increased sensitivity of pain receptors |
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why do pain receptors not adapt when consistently excited |
allows pain to keep person apprised of tissue damaging stimulus
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nerve transmission of pain |
Nerves in PNS send signals to dorsal horn of CNS - which transmits signals to brain through spinothalamic tract |
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where is pain interpreted and perceived as sensation of pain? |
CNS |
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how are the three types of fibers split up into classifications? |
- axonal diameter - conduction velocity |
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what are the smallest among the types of fibers? |
C fibers |
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what are the most common types of A fibers |
A-gamma A-delta (smallest) |
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what fibers carry pain to the CNS? |
C fibers A-delta |
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A-delta signals |
- travel faster than C fibers - sharp pain - more localized |
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C fiber signals |
- slower - diffuse/dull pain signals - less localized |
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A-beta fiber signals |
carry non-noxious stimuli |
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Speed of different fiber types |
A-alpha higher conduction velocity than A-delta which are faster than C fibers |
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Order of pain signal activation |
A-delta fibers activated first, followed by C fibers |
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what role does the SC have have in pain (besides transmission)? |
process nociceptive information at the dorsal horn |
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what are the two main pathways for pain signals? |
- spinothalamic tract - spinoreticular tract (mostly collateral branches of spinothalamic tract) |
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what are interneuronal networks in posterior horn responsible for? |
transmission of nociceptive info to neurons that project to brain |
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what is the pain pathway from nociceptor to brain? |
- enter SC at dorsal horn - stim lateral spinothalamic tract - sends collaterals into brainstem reticular formation - reticular formation proects to thalamus - these signals are poorly localized |
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what role may the thalamus/hypothalamus play in pain? |
emotional component |
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what muscles refer pain to the chest |
- pec major/minor - scalenes - SCM (sternal) - sternalis - iliocostalis cervicis - subclavius - external ab oblique |
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What muscles refer pain to side of chest? |
serratus anterior latissimus |
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what muscles refer pain to abdominal area? |
- rectus abdominis - ext. ab. oblique - transversus abdominis - iliocostalis thoracis - multifidi - quadratus lumborum - pyramidalis |
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which muscles refer pain to low thoracic back? |
- iliocostalis thoracis - multifidi - serratus post. inf. - rectus ab. - latissimus |
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which muscles refer pain to lumbar region?
|
- glute med. - mulitifidi - iliopsoas - longissimus thoracis - iliocostalis lumborum/thoracis - rectus ab. |
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which muscles refer pain to pelvic region? |
- coccygeus - levator ani - obturator internus - adductor magnus - piriformis - obliquus internus abdominis |
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which muscles refer pain to buttocks? |
- glute med - quad. lumborum - glute. max - iliocostalis lumborum - longissimus thoracis - semitendinosus - semimembranosus - piriformis - glute min - rectus ab. |
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what is mechanotransduction? |
process by which body converts mechanical loading to cellular responses that promote structural change |
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3 steps of mechanotransduction |
- mechanocoupling - cell cell communication - effector response |
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what is mechanocoupling? |
physical load causing a physical perturbation to cells that make up tissue |
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what is cell-cell communication? |
stimulus in one location leads to distant cell registering a new signal even though distant cell does not receive mechanical stim |
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what is the effector cell response? |
when there are loads above tissues set body - mechanotransduction causes the body to adapt (it is an on going proocess) |
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NE role in pain management? |
modulates gain of nociceptive info as it is relayed for processing in brain from thalamus |
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Opoid role in pain management? |
inhibit pain processing when stimulate, natural or synthesized |
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GABA role in pain management?
|
augments descending inhibition of spinal nociceptive neurons |
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how does attention to pain change the perception of pain? |
the more focus that is put into pain, the more intense the pain will feel |
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how does cognition affect the perception of pain? |
- if a painful stimuli is a known stimuli, it will feel less intense and easier to "ignore" - intensity is reduced when pain is perceived to be controllable |
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what affect does pain have on autonomic NS? |
elevates sympathetic NS activity - increased anxiety, HR, glavanic skin response |
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what are long term affects of autonomic NS response to pain? |
- muscle tension |
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how do negative emotions affect pain perception? |
place attention towards pain - which increases the unpleasantness |
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how does behavioral reactions to pain affect daily life? |
pt. that communicates pain through non-verbal cues generally avoid pain most - which can lead to disability - some pain should be worked through |
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when does the spinothalamic tract decussate? |
within a few segments of entry from the PNS |
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what part of the brain is important for localizing pain? |
somatosensory cortex |
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where is the pain matrix? |
primary/secondary somatosensory cortex insular anterior cingulate cortex prefrontal cortex thalamus |
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what parts of the brain are important in descending inhibition? |
periaqueductal grey rostral ventromedial medulla |
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why can visceral pain present in an area away from the pain site? |
convergence of different afferents onto the same dorsal horn neurons in SC |
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how is neuropathic pain described? |
- spontaneous - burning, shooting, stabbing |
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how can pain transmission be modulated? |
dorsal horn of SC descending inhibitory pathways |
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what are red flag findings? |
symptoms/conditions that require immediate attention and supercede PT -- normally of visceral origin |
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what are yellow flag findings? |
potential confounding variables that may be cautionary warnings/ require further investigation |
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|
what are common red flags? |
- fevers, chills, night sweats - recent unexplained wt. changes - malaise/fatigue - unexplained nausea/vomiting - unilateral, bilateral, quadrilateral paresthesias - shortness of breath - dizziness - nystagmus - bowel/bladder dysfunction - severe pain (insidious onset - no mechanism) - Radiculopathy |
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What is malingering? |
intentional production of false symptoms or exagerration of symptoms that do exist
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what can alert a practitioner to malingering? |
- subjective complaints of paresthesia consistent w/ diabetes and T4 syndrome (but those two have been ruled out - inappropriate score on Oswestry Low Back Disability questionnaire - stretch reflexes inconsistent w/ presenting problem - cogwheel motion of muscles during strength testing - inconsistent ability to do movements |
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what do fever, chills, night sweats normally signify? |
systemic disorder (infection) |
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why is paresthesia considered a red flag? |
indicates a CNS issue |
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what is nystagmus? |
rhythmic movement of eyes w/ abnormal shifting away from fixation and rapid return |
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|
what characterized fibromyalgia (FM) |
- widespread, generalized body aches of at least 3 mos. duration - can cause pain or paresthesia in nonradicular pattern |
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what happens in pain pathways during FM? |
C fibers are constantly bombarded - leading to central sensitization, and A-delta fibers begin carrying signals normally carried by C fibers |
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who is more at risk for FM? |
women |
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FM intervention |
drugs that influence chemicals in ascending/descending tracts |
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|
FM PT intervention |
- cardio fitness training - spreay and stretch - strength and endurance - massage - modalities |
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what is the process of differential diagnosis? |
- rule out sinister problems - identify appropriate location - ID other contributors/modifiers to condition |
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|
what are the different types of symptoms? (-ogenics) |
viscerogenic vasculogenic spondylogenic neurogenic psychogenic |
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|
what are the systemic pain descriptors? |
- disturbs sleep - deep ache/throb - reduced by pressure - constant waves of pain/spasm - not aggravated by mechanical stress |
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|
what are non pain symptoms associated with systemic pain descriptors? |
- jaundice, migratory arthralgia, skin rash - fatigue, weight loss, low grade fever - generalized weakness, cyclic and progressive symptoms - tumors, history of infection |
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what are musculoskeletal pain descriptors? |
- generally lessens at night - sharp, superficial ache - usually decreases w/ cessation of activity - usuallly continuous or intermittent - aggravated by mechanical stress |
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|
what cause viscerogenic symptoms? |
- symptoms referred from any viscera in trunk/abdomen - normally produced by chem damage, ischemia, spasm of smooth muscles |
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|
what type of pain does viscerogenic symptoms cause? |
- diffuse and poorly localized
- related to nausea/vomiting - not altered w/ movement/positional change |
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|
what are symptoms of gastrointestinal/genitourinary problems? |
- frequent/severe ab pain - frequent heartburn/indigestion - frequent nausea/vomiting - change in/problems with bowel and bladder function - unusual menstrual irregularities |
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what causes vasculogenic symptoms? |
venous congestion or arterial deprivation to musculoskeletal areas |
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what happens to vasculogenic symptoms during activity? |
pain worsens |
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|
why are vasculogenic symptoms difficult to recognize? |
they may mimic musculoskeletal, neurological, and arthritic disorders |
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|
how can vasculogenic symptoms be uncovered? |
cardiopulmonary/hematologic, and neurologic systems questions and screening during exam |
|
|
what are cardiovascular/vasculogenic symptoms? |
- SOB - dizziness - pain or heaviness in chest - pulsating pain - constant/severe pain in lower leg or arm - discolored or painful feet - swelling w/ no history of injury |
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|
what causes neurogenic symptoms? |
- tumor compressing/irritating a neural structure of spinal cord or meninges - spinal nerve root irritation - peripheral nerve entrapment - neuritis |
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|
what are neurological symptoms? |
- changes in hearing - frequent/severe headaches w/ no history of injury - problems w/ swallowing, changes in speech - changes in vision - balance, coordination problems/ falling - faint spells - sudden weakness |
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|
what causes spondylogenic symptoms? |
- infections - inflammatory disorders - neoplasms - metabolic disorder (Paget's and osteopenia) |
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|
what are spondylogenic Symptoms? |
- SEVERE, UNRELENTING PAIN
- Fever - Bone tenderness - Wt. loss |
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|
what disorders would cause spondylogenic symptoms? |
- RA - Osteomyelitis - JRA - Gout - Ankylosing Spondylitis - Psoriatic arthritis |
|
|
what are some symptoms of cancer? |
- persistent pain at night - constant pain anywhere - unexplained wt. loss (10-15 lbs in 2 wks) - Loss of appetite - unusual lumps/growths - unwarranted fatigue |
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|
Miscellaneous Red Flags |
- fever or night sweats - Recent severe emotional disturbances - swellling/redness in any joint - pregnancy |
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|
what causes psychogenic symptoms |
- affective, cognitive, behavioral sources |
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|
what should be used to assess psychogenic symptoms? |
outcome measures (NDI, ODI, PBSI, MSP) |
|
|
what are psychogenic symptoms? |
- Emotional overtones (low back and neck pain) - Somatosensory amplification (anxiety leads to increase in pain perception) - abnormal illness behaviors exhibited (depression, emotional disturbances, etc.) |
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|
what is a red flag? |
signs and symptoms found in pt. history and clinical exam that may tie a disorder to serious pathology |
|
|
what is a prognostic red flag? |
identified as a finding that is reflective of a delayed or poor outcome |
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|
General Red Flags? |
- Abnormal signs and symptoms - Bilateral symptoms - symptoms perifpheralizing - Abnormal sensation patterns |
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|
Neurological red flags |
- nerve root/peripheral nerve symptoms - multiple nerve root involvement - saddle anesthesia - vertigo - ANS symptoms - progressive weakness/gait disturbances |
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|
MSK red flags
|
- multiple inflamed joints - progressive |
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|
vasculogenic red flags |
- circulatory/skin changes - fainting - drop attacks |
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|
psychogenic red flags |
psychosocial stresses |
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|
red flags associated with cauda equine syndrome |
- fecal incontinence - saddle anesthesia - urinary retention |
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|
red flags associated with infection |
- immunosuppression - IV drug use - Unexplained fever |
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|
red flags associated with Fracture or infection
|
chronic steroid use |
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|
red flags associated with fracture
|
- osteoporosis - significant trauma at any age |
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|
Red flags associated with neoplasm or fracture |
older than 50 yrs. and mild trauma |
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|
red flags associated with neoplasm |
- history of cancer - unexplained wt loss |
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|
red flags associated with any spinal disorder |
- focal neurologic deficit progressive or disabling symptoms - no improvement after SIX WKS of conservative management |
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|
what is a category I Red Flag? |
requires immediate medical attention |
|
|
what is a category II Red Flag? |
require more questions and precautionary exam and treatment procedures |
|
|
what is a category III Red flag? |
requires further physical testing and differential diagnosis/analysis |
|
|
what are some examples of Category I red flag? |
- blood in sputum - elevated sedimentation rate - loss of consciousness/altered mental state - bowel/bladder dysfunction - Severe non-mechanical pain - progressive neurological deficit - Heart-related symptoms |
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|
what are category II red flags? |
- >50 yrs. old - clonus - fever - gait deficits - history of metabolic bone disorder/cancer - long term steroid use/ worker's comp - non healing wounds/sores - unexplained wt. loss - writhing pain - impairment from recent trauma |
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|
what are category III red flags? |
- Myelopathic symptoms - abnormal reflexes - bilateral/unilateral radiculopathy - paresthesia - unexplained referred pain - unexplained significant upper or lower limb weakness |
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|
Red flag questions |
- How old are you? - Do you have any previous history of cancer or family cancers? - Have you had any recent and/or unexplained weight loss - How long have you had your symptoms/pain? - Have you responded to any previous therapy OR treatment for this condition |
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|
Age red flag? |
- above 55 yrs old (specifically over 65) |
|
|
what are the most common warning signs of cancer? |
- change in bowel/bladder habits - sores that don't heal - unusual bleeding/discharge - thickening/lump (breast) - Indigestion or difficulty swallowing - Obvious change in wart or mole - nagging cough or hoarseness |
|
|
what is the threshold for wt. loss cause for alarm? |
5% or more within 4 wks |
|
|
most common place for metastases? |
thoracic |
|
|
what are red herrings? |
any misleading biomedical or psychosocial factors that will deflect the course of accurate clinical reasoning |
|
|
what are the common red herrings for serious spinal pathology? |
- upper motor neuron disease - MS - Diabetes - Alcoholism - Cervical myopathy - peripheral neuropathy - lower limb edema - spinal stenosis - Nerve root compression |
|
|
what are yellow flags? |
risk factors or findings that are potential confounding variables which are cautionary warnings regarding the pt's condition and that could have impact of pt. prognosis/outcome |
|
|
What should Yellow flags tell PT?? |
slow down or monitor influence of finding |
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|
psychosocial factors of yellow flags? |
psychosocial indicators suggesting increased risk of progression to long term distress, disability, pain - designed for use in acute low back pain |
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|
how may yellow flags be used? |
assess likelihood of development of persistent problems from any acute pain presentations |
|
|
what can yellow flags relate to? |
- beliefs - emotions/behaviors - family - workplace - behavior of health professionals (have an influence) |
|
|
Key factors in low back pain? |
- belief that pain is harmful/disabling - fear-avoidance behavior - low mood and social withdrawal - expectation that passive treatment will help |
|
|
what are sources that refer pain to shoulder?
|
- heart - pleura - lung tissue - diaphragmatic pain - neck lymph nodes - shoulder, chest, breast |
|
|
what should be suspected if shoulder pain with normal physical exam of shoulder and c-spine? why? |
malignancy, humerus and scapula are frequent locations of metastases |
|
|
what are the shared clinical signs and symptoms of both inflammatory and non inflammatory arthritis? |
- impaired mobility - impaired muscle performance - impaired balance - functional limitations |
|
|
what is osteoarthritis? |
chronic, degenerative disease affecting articular cartilage of synovial joints |
|
|
what is thought to be the cause of OA? |
- low level trauma that causes wear and tear - absence of movement of synovial fluid w/ immobilization |
|
|
what is primary OA? |
no underlying cause of joint disease apparent -related to age/hereditary |
|
|
what is secondary OA? |
onset of OA from disease or injury |
|
|
Characteristics of OA? |
- hypermobility/instability - contractures and limited mobility - cartilage splitting/thinning, crepitus, loose bodies - subchondral bone exposure (LATE STAGES) - asymptomatic early |
|
|
what impacts prevalence of OA? |
- genetics - obesity - muscle weakness - joint impact - occupational activities - sports |
|
|
why is OA typically asymptomatic early? |
cartilage is aneural |
|
|
what joints are generally affected by OA? |
- WB joints - spine - DIP of fingers - CMC of thumb |
|
|
initial degenerative changes of OA? |
joint space narrows |
|
|
severe progressive changes of OA |
- Osteophytes from increased bone force - erosion of cartilage and bone - bone cysts |
|
|
what are the early signs and symptoms of OA? |
stiffness/aching pain in joint and common referred pain sites |
|
|
Later signs and symptoms of OA? |
- typically one or more joints on same extremity (not bilateral) - pain increases after prolonged activity - pain relieved by heat, rest, NSAIDs - pain is worse in cold, wet weather - crepitus in joint during ROM - nodules |
|
|
what are the nodules in OA called? |
Heberden's (DIP) Bouchard's (PIP) |
|
|
what is rheumatoid arthritis? |
chronic, progressive, systemic inflammatory disease of connective tissue characterized by spontaneous remissions and exacerbations and is 2nd most common rheumatic disease |
|
|
what kind of disease is RA? |
autoimmune, chronic, inflammatory, systemic |
|
|
what does RA affect? |
synovial lining of joints and other CT |
|
|
what is criteria for RA diagnosis? |
- morning stiffness - 3 or more joint areas with swelling - swelling in MCP, PIP, or wrist - bilateral or symmetrical - Rheumatoid nodules - serum rheumatoid factor - radiographic changes (destructive) |
|
|
what are affects of RA outside of musculoskeletal system? |
cardiopulmonary system GI system MS |
|
|
etiology of RA? |
unknown (slight genetic predisposition |
|
|
what are the characteristics of RA? |
- period of flare up and remission - Tenosynovitis w/ potential for rupture - extra-articular pathological changes - progressive functional deterioration - Variety of degree of involvment |
|
|
what happens during RA flare ups |
inflammatory changes to synovial membrane, articular cartilage, subchondral bone marrow |
|
|
what are the after effects of RA flare ups? |
- formation of granulation tissue - adhesions - exposure of cancellous bone - ankylosis - deposits of crystals in tendon sheaths |
|
|
what are the extra-articular pathological changes that happen during RA? |
- Rheumatoid nodules - weakness and fatigue - muscle atrophy |
|
|
what should be done during remission of RA? |
restorative care bc pt. normally unable to move well during flare ups |
|
|
what are signs and symptoms of RA flare- ups? |
- effusion/swelling of joints - pain/ache limited motion (in AM & after strenuous activity) - increase in skin temp over joints[ - symmetrical, bilateral onset in smaller joints - joint deformation/ ankylosis - muscle pain atrophy, wkness |
|
|
what are the systemic S&S of RA flareup |
- low- grade fever - loss of appetite and wt. - malaise - fatigue |
|
|
differential diagnosis of OA/RA |
OA - local disease, common in WB joints, DIP joint more common, bony ankyloses uncommon RA - systemic diesease (pt sick), acute inflammation, PIP joint more common |
|
|
What is gout? |
metaboloic disorder where uric acid isn't filtered by kidneys and forms crystals which collect in joints and periarticular tissues |
|
|
who is normally affected by gout? |
men over the age of 40 |
|
|
predispositions to gout? |
- obesity - high purine diet - habitual alcohol ingestion |
|
|
What joints are normally affected by gout |
joints of hand and feet - mostly 1st MTP joint |
|
|
what are S&S of gout? |
- acute inflammation, exquisite tenderness
- unable to tolerate any pressure to joint- acute - pain is sudden and inflammation rapid - systemic signs |
|
|
what are systemic signs of gout? |
- fever - chills - malaise |
|
|
how long does gout typically last? |
1-2 wks unless treated with oral steriods |
|
|
what is ankylosing spondylitis classified as? |
inflammatory arthritis |
|
|
who is affected most by ankylosing spondylitis? |
- 15-40 yrs old - thoracic involvement - males more than females - hereditary |
|
|
where does ankylosing spondylitis involve? |
- ant. long. ligament - ossification of IVD, zygapophyseal joints, costovertebral joints, manubrio-sternal joint |
|
|
what does ankylosing spondylitis affect? |
chest expansion |
|
|
what are the presenting signs/symptoms of AS? |
pain at night stiffness |
|
|
what are the 5 screening questions for ankylosing spondylitis? |
- is there morining stiffness? - does discomfort improve w/ exercise? - onset of back pain before 40? - did problem begin slowly? - has pain persisted for at least 3 mos? |
|
|
what are the S&S of ankylosing spondylitis |
- postural abnormalities - flexion contractures of hips/knees - limited side-bending - radiographic signs |
|
|
what are the postural abnormalities associated with ankylosing spondylitis? |
- flattened lumbar spine - thoracic kyphosis - cervical hyperextension |
|
|
what radiographic sign is associated with ankylosing spondylitis? |
bamboo spine |
|
|
what is the definition of osteoporosis |
disease that leads to decreased bone mineral content and weakening of the bone |
|
|
what causes osteoporosis? |
alteration in balance btwn bone formation and resorption |
|
|
who is most at risk for osteoporosis? |
80% women |
|
|
how is osteoporosis diagnosed?
|
T-score of bone mineral density scan: >-1 = normal -1.1 to -2.4 = osteopenia <-2.5 = osteoporosis |
|
|
what is type 1 osteoporosis? |
post menopausal - estrogen deficiency |
|
|
what is type 2 osteoporosis? |
secondary - associated with other medical conditions/medications (heparin) that decrease Ca2+ and vitamin D |
|
|
how can a compression frx in spine be found on a radiograph? |
collapsing of ht. in vertebral body? |
|
|
what is Charcot-Marie-Tooth (CMT) disease? |
a group of inherited disorders that affecct the peripheral nerves (There are more than 70 types) |
|
|
what are some of the types of damage from CMT? |
- myelin sheath damage - nerve fibers (results in neuropathy) |
|
|
which nerves are generally affected first in CMT? |
nerves to arms and legs (longest) |
|
|
what types of nerve fibers are affected by CMT? |
motor and sensory fibers |
|
|
what does CMT cause from nerve damage? |
weakness and numbness, starting in feet |
|
|
when do symptoms of CMT usually begin? |
before age of 20 |
|
|
what are the S&S of CMT? |
- high arched feet - foot drop - slapping gait - loss of muscle in lower leg (skinny calves) - numbness in feet - difficulty with balance - later on - similar S&S in arms and hands |
|
|
what is normally untouched by CMT? |
brain function |
|
|
what is known as a "silent disease" |
systemic lupus erythematosus |
|
|
what is systemic lupus erythematosus? |
chronic inflammatory autoimmune disorder where the body produces antibodies against its own cells |
|
|
what does Lupus affect and what are the symptoms? |
- can affect any organs - symptoms are never identical |
|
|
Who is most at risk for lupus? |
women btwn 15-40 |
|
|
what is the cause of lupus? |
unknown - but believed to be btwn immunologic, environmental, hormonal and genetic factors |
|
|
what are common cutaneous and membranous lesions of lupus? |
- butterfly skin rash - skin sensitive to sunlight |
|
|
why do skin lesions appear with lupus? |
inflammation of blood vessels
|
|
|
what is typically the MSK involvement of lupus? |
arthralgia arthritis |
|
|
what are the characteristics of arthralgia/arthritis from lupus? |
- involved joints symmetrical - no erosive to cartilage or destructive to bone - joint deformities in wrist/hang are common - tenosyovitis/tendon ruptures not uncommon |
|
|
common brain symptoms of lupus? |
- persistent/unusual headaches - memory loss - confusion |
|
|
common eye symptoms of lupus |
-dry/puffy eyes - increased sensitivity to light |
|
|
common mouth/nose symptoms of lupus |
- sores inside mouth/nose |
|
|
common lung/heart symptoms of lupus |
- SOB - chest pain |
|
|
common symptoms of lupus in fingers, toes, tip of nose |
turn white or blue with exposure to cold or under stress |
|
|
what are the common skin symptoms of lupus? |
butterfly rash on face that worsens with exposure |
|
|
common stomach symptoms of lupus |
- nausea - vomitting - recurring persistent ab pain - bladder infections - blood in urine |
|
|
joint symptoms in lupus? |
pain/swelling of legs, joints and feet |
|
|
what is similar about fibromyalgia and myofascial pain syndrome? |
- pain in muscles - decreased ROM - postural stresses |
|
|
what are S&S of FM not shared with myofascial pain syndrome? |
- tender/painful points - poor sleep - no referred patterns of pain - fatigue - 11 off 18 trigger points at specific spots in body - non-restorative sleep - morning stiffness - fatigue/decreased exercise tolerance |
|
|
what are S&S of MFPS not shared with FM? |
- trigger points in muscle - referred patterns of pain - tight bands of muscle |
|
|
what is FM? |
chronic condition characterized by pain that covers 1/2 the body ( R/L, Upper/Lower) and has lasted more than 3 mos. |
|
|
what exacerbates FM? |
- Environmental stresses (weather changes, lights) - physical stresses (repetitive activities - emotional stresses |
|
|
what is a common comorbidity of FM? |
psychological problems |
|
|
What are the tender points of FM (bilateral) |
- Low cervical (C5-7) - second rib - greater trochanter - knees (medial fat pad proximal to joint) - occiput (@ muscle insertions) - Trapezius (midpt of upper border) - supraspinatus - lateral epicondyle - gluteal region |
|
|
what are the steps of the pain/fatigue cyce |
1. disease 2. tense muscles 3. poor sleep 4. stress/anxiety 5. difficult emotions 6. depression 7. medication problems (back to 1) |
|
|
when does FM normally appear/develop? |
during early/middle adulthood after a physical trauma or infection |
|
|
what are the hallmark complaints of FM? |
- pain muscular in origin - prodominantly in scapula, head, neck, chest, low back |
|
|
what are common comorbidities of FM? |
- tendonitis - HA - IBS - TMD - Anxiety/depression |
|
|
what is MFPS? |
chronic regional pain syndrome |
|
|
hallmark classifications of MFPS |
- myofascial trigger points w/ referred pattern of pain - pain from trigger point is dull, aching, deep - decreased ROM, strength - increased pain with stretching |
|
|
what are trigger points? |
- area of hyperactivity in tight band of muscle that refers out - may be active or latent |
|
|
what happens in an active trigger poitn |
produces classic pain pattern w/ or w/out palpation |
|
|
what happens in a latent trigger point |
asymptomatic unless palpated |
|
|
what causes trigger points? |
- chronic overload - acute overload - poorly conditioned muscles - postural stresses - poor body mechanics |
|
|
what is complex regional pain syndrome (CPRS) |
uncommon form of chronic pain that affect arm or leg, where pain is out of proportion to severity of injury |
|
|
when does CPRS normally develop? |
after injury, surgery, stroke, heart attack |
|
|
what causes CPRS? |
not well understood, possible dysfunctional interactionn btwn CNS and PNS and inappropriate inflammatory responses |
|
|
mechanisms of CPRS? |
1. original injury impulse to brain 2. triggers an impulse in sympathetic NS which returns to injury site 3. impulse triggers inflammatory response that causes pain 4. restart process |
|
|
what is the resulting condition of CPRS mechanism? |
burning extremity pain, red mottling of skin - correlates w/ pt. verbal/nonverbal pain behaviors |
|
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what is type 1 CRPS? |
reflex sympathetic dystrophy - occurs after injury/illness that didn't directly damage nerves in affected limb. (90% of cases) |
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what is type 2 CRPS? |
this follows a distinct nerve injury |
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Precipitating event in CRPS? t1 vs. t2 |
type 1 - sometimes
type 2 - yes |
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single PN involvement in CRPS? t1 vs. t2 |
type 1- sometimes type 2 - yes |
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physiologic changes in affected limb CRPS t1 vs. t2 |
type 1- yes type 2 - no |
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cardinal signs of t1 CRPS? |
- spontaneous pain - swelling - different skin temps |
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cardinal signs of t2 CRPS? |
- burning pain - allodynia - hyperalgesia |
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progressive? CRPS t1 vs. t2 |
type 1 - yes type 2 - sometimes |
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bone atrophy in CRPS? t1 vs. t2 |
type 1 - yes type 2 - no |
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what are most common initial symptoms of CRPS? |
- pain
- swelling - redness - noticabel changes in temp and hypersensitivity |
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what happens to affected limb over time in CRPS? significance? |
- becomes cold and pale, skin and nail changes take place, muscles spasm and tighten
- irreversible after these changes |
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what may make pain in CRPS worse? |
emtional stress - may even cause spread |
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what are S&S of CRPS? |
- continuous burning/throbbing - sensitivity to touch/cold - swelling in painful area - changes in skin temp/color/texture - changes in hair/nail growth - joint stiffness - muscle spasms - decreased ability to move body part |
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what is diabetes? |
life long disease that affects the way your body handles glucose in blood |
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what happens in type 1 diabetes |
chronic condition where pancreas produces little to no insulin to allow glucose into cells for NRG |
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what happens in type 2 diabetes? |
body becomes resistant to insulin or does not make enough insulin |
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differences btwn type 1 and type 2 diabetes? |
type 1 - no insulin to let glucose into cells, so sugar builds up in bloodstream type 2 - islet cells still function but body is resistant to insulin or pancreas does not produce enough |
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risk factors for type 2 diabetes? |
- genetics - obesity - metabolic syndrome (HTN, High cholesterol/TG's) - too much glucose - bad communication btwn cells - broken beta cells |
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how do broken beta cells create a risk for type 2 diabetes? |
cells make insulin send out wrong amount of insulin at wrong time, blood sugar is thrown off and high blood glucose can damage these cells |
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what is obesity |
excessive accumulation of body fat |
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what systems are involved in obesity? |
- hypothalamic - endocrine - genetic - environmental - behavioral |
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what is the primary cause of obesity? |
energy imbalance from consuming excess calories and a sedentary lifestyle |
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what physiological responses are increased from obesity? |
- fasting insulin - insulin response to glucose - adrenocortical hormones - cholesterol synthesis and excretion |
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what physiological responses are decreased from obesity? |
- insulin sensitivity
- growth hormone - growth hormone response to insulin stim - hormone sensitive lipase |
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what are the factors that should be considered when assessing obesity health risk? |
- location of fat deposits, distribution - other comorbidities - body comp (BP and cholesterol), % body fat, waist to hip ratio |
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what is android obesity? |
upper body fat distribution |
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what is gynoid obesity? |
lower body fat distribution |
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what does obesity increase the risk of? |
- CAD disease - HTN - hyperlipidemia - diabetes - hormone/menstrual dysfunction |
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what is the waist to hip ratio? |
- body fat distribution technique - corrolates w/ CAD Disease risk |
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how is waist to hip ratio found? |
minimal waist (umbilicus) and divide by circumference of hips at widest level |
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what is the number of a lower body distribution ratio? |
< 0.776 |
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fat upper body distribution? |
men - >0.913
women - >0.861 |
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how does exercise impact obese patient
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- effective in altering body wt. and composition - promotes loss of ab fat (dangerous area) - positive effect on fasting glucose/insulin and insulin resistance - improved glucose tolerance |
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what are changes in obese pt. immediately post exercise? |
- elevated energy expenditure - no changes in RMR but caloric restriction can detrimentally affect RMR |
