Clinical Procedures I Flashcards
test 1
Pain
Unpleasant sensation with actual or potential tissue injury
- v subjective & depends on factors like anxiety, fatigue, previous experiences, cultural norms
- human nature to try to move away from pain & body tries to prevent more damage
- v hard for pt to quantify pain
muscle guarding
protective response in a mm that results from pain or fear of mvmt
- occurs to protect area from further trauma by contracting surrounding mm & providing “exoskeleton”
What factors of mm guarding contribute to continued dysfunction?
- pain may increase mm guarding
- mm guarding decreases circulation
- decreased circulation reduces healing
- pain-spasm cycle: pain- guarding-dysfunction triangle
What is very important to help decrease pain in pt?
Education!! Educate on what you’re doing & why you’re doing it - this increases trust and helps them relax their mm, increasing pain threshold
Types of pain producing substances
potassium, serotonin, bradykinin, histamine, prostaglandins, leukotrienes, substance p, ACH, ATP, calcitonin gene-related peptide (CGRP), nerve growth factor (NGF), thromboxane, acid environment
What triggers pain producing substances to infiltrate that specific area?
injury
Function of pain producing substances
- can directly activate nociceptors to send pain message to CNS
- sensitize nerve endings
- lower pain threshold after tissue injury & inflammation
types of pain
acute, chronic, referred
Acute pain
< 3 months
due to injury/trauma
easiest to understand, dx & rx
How do vitals relate to acute pain?
Acute pain often results in changes in HR, BP, RR
take vitals! - they may help know if acute pain present
Function of acute pain
Protect against further tissue damage & maintained to allow for proper time of tissue healing
Chronic pain
> 3-6 months (can last years)
doesn’t appear correctable or rx-able
could be referred pain
may need lots of modalities to relieve it
associated with physical, emotional, social & financial disability
difference between chronic & acute pain
chronic pain is pain that used to be acute but is past expected healing time for injury/insult chronic pain no longer protective mechanism & may be considered a disease itself
what is a characteristic of chronic pain?
central sensitization…amplification of neural signaling w/in CNS that underlies pain hypersensitivity
referred pain
comes form deep structures but felt at remote site radiating (continues to move) pain is type of referred pain
has patterns to help determine source of pain
Ex. “brain freeze” when you eat something cold, heart attack causing pain in left arm
believed etiology of referred pain
convergence of cutaneous, visceral, & skeletal mm nociceptors on common nerve root of SC -> brain interprets afferent input as coming from cutaneous structures bc higher proportion of cutaneous afferents
examples of referred pain
MI - pain in jaw, L shoulder/arm, stomach CSP nerve root compression - pain in arm/hand
referred patters for determining source of pain
dermatomes - areas of skin innervated by specific nerve root
myotomes - areas of mm innervated by specific nerve root
sclerotomes - areas of bone innervated by specific nerve root
nociceptors
“pain receptors”
nerve endings that conduct nerve impulse to CNS
- found in skin, mm, joints, bone & viscera
- high threshold for activation
- types: A-delta & C fibers
A-delta pain fibers
small & MYELINATED nociceptors
- respond to high-intensity mechanical (MSK) & thermal (heat) stimuli (immediate response)
- conduct peripheral pain signals very quickly (5-30 m/s)
- FIRST pain sensation & precise localized pain
- generation w/drawl reflexes
How are A-delta pain fibers described?
Sharp, stabbing or pricking pain
C pain fibers
thin & UNMYELINATED nociceptors
- respond to broad range of painful stimuli (including mechanical, thermal or chemical - polymodal)
- longer lasting & slow conduction (0.5-2 m/s)
- poorly localized pain
-help prevent further tissue damage
How are C pain fibers described?
They are the “second pain” - dull, burning, throbbing, and aching
Ascending pain pathways
nociceptors enter the dorsal horn of the SC for processing
–> send to brain (to thalamus) via tracts where pain is actually perceived
ascending pain tracts
spinothalamic tract (STT) - sharp & localized pain (A-delta)
spinoreticulothalamic - diffuse & poorly localized pain, visceral pain (C fibers)
descending pain
endogenous opiates released through pain, exercise, laughter, relaxation, meditation, acupuncture, and EStim
*not completely understood
What are endogenous opiates?
naturally occurring substances that inhibit perception of pain
Pain theories
began in 1965 and constantly evolving - gate control theory & endogenous theory
gate control theory
injury activates A-delta & C fibers –> dorsal horn decides whether or not to send signal to brain, depending on noxious stimuli
- dorsal horn contains central transmission cells
- summation of excitatory & inhibitory influences determine if signal moves up the chain
How to close gate, according to gate theory?
If you have non-noxious stimuli (modalities) greater than noxious stimuli, gate is closed & pain signal doesn’t go to brain
endogenous opiate theory
- neurotransmitters that are considered descending control mechanisms
- operate on spinal cord level
- “block the gate” by interfering w/ A-delta & C fiber signal transmission to T cells
Types of endogenous opiates?
enkephalins - activated by rubbing
endorphins - exercise, laughter, unnerving/shaky
serotonin - link to analggesia (lack of feeling pain)
dopamine - pleasure
factors making it hard to close the gate
extreme emotions, same previous injury, attention to pain
counter irritation theory
counter the noxious stimuli w/ non-noxious stimuli
Ex. other hand squeezes finger that was just smashed in door
use of biophysical agents for pain
pain modulation - blocking transmission of pain at the gate or dorsal horn of spinal cord
types of modalities to close gate
ice/heat, compression, Estim, massage - get pain assessment to see if effective
What are different pain assessment tools?
McGill pain questionnaire - body drawing & pt circles, Xs, etc on body part for type of pain
Visual analogue scale (VAS) 0—-I—-10
Numeric pain rating - “pain on a scale of 0-10?” “4/10”
Baker-Wong scale - smiley faces & numbers 1-10 (peds, HOH, language barrier)
Why and when do we check sensation?
Why - looking for gross sensory abnormalities
When - BEFORE rx - always before modality - if pt doesn’t have sensation, modality can injure them
How do you check sensation?
- pain: top of reflex hammer (pointy)
- light touch: cotton ball, little brush
- temperature: test tube w/ cold or
warm water (dif stages of
cold/heat) - vibration: tuning fork (rarely done)
- proprioception: position of limb or jt in space (eyes closed, able to point out where sensation is)
- deep tendon reflexes: reflex hammer (patellar tendon, tendoncalcaneus, biceps tendon, triceps tendon)
Other ways to gauge if pt is in pain/if pain increasing?
body language, facial expressions, discoloration, not breathing, mm guarding, goni and/or MMT greatly decreased over short period, increased swelling
APTA recommendation of use of modalities
passive physical agents should only be used as complimentary to therapeutic exercise and interventions to increase participation in active rx programs (modalities = cotherapies)
What are different types of modalities?
thermal - heat & cold
electromagnetic - electrotherapy, diathermy, light
mechanical - traction, compression
hydrotherapy
acoustic - ultrasound
manual - massage
What are the purposes of modalites?
They assist, augment, or complement natural reparative mechanisms of the body (not change how body heals itself) by…
- decreasing pain, edema, and stiffness
- increasing ROM, tissue healing, mm activation
What is a determining factor of which modality to use on a pt?
the phase of tissue healing the pt is in - the wrong modality can delay healing (contraindicated)
Function of cryotherapy (cold)
- reduces blood flow (vasoconstriction) & metabolic activity
- decreases pain (increasing pain threshold), desensitizing peripheral afferent nociceptors
- reduces swelling
Function of applying heat
- facilitate tissue healing (in proliferative & reconstruction phases)
- relax skeletal mm, decrease mm spasms & pain
- promote & increase blood flow (vasodilation)
-prep soft tissues for stretching, mobilization, and exercise (may be used before a pt sesh)
Function of electrotherapy
- strengthening or relaxing skeletal mm
- decreasing pain
- facilitating neuromuscular re-education
- increasing ROM
- promoting tissue & wound healing
- reducing edema
- increasing local blood flow
- deliver medicinal ions transdermally
- attenuating disuse atrophy
function of compression
- prevent, attenuate, or reverse swelling
- alter or minimize scar formation during proliferative & maturation phases, and reduce hypertrophic scarring
inflammatory/acute phase
body’s immediate defense mechanism (days 1-10)
individual factors effecting on the healing of tissues
size of the wound, cardiopulmonary disease, severity of wound/injury, active infection, immunosuppressive disorder or drugs
What brief response occurs in the beginning of the inflammatory phase?
vasoconstriction of BV & lymph vessels, aggregation of platelets for coagulation - to reduce bleeding & minimize bacteria exposure
What is the second part of the inflammatory phase?
vasodilation > edema (fluid released form intracellular space), redness, warm to touch, pain (bc tissues distended & nerve fibers irritated)
- inhibits extra clot formation