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Modalities > Intro to Physical Agents > Flashcards

Intro to Physical Agents Flashcards

1
Q

What are Physical Agents?

A

Energy and material applied to patients to assist in rehabilitation

Include:
Heat
Cold 
Water
Pressure
Sound
Electromagnetic radiation
Electrical currents
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2
Q

Categories of Physical Agents

A

Thermal

Mechanical

Electromagnetic

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3
Q

Thermal

A

Transfer energy to a patient to increase or decrease tissue temperature

Can be superficial or deep

Examples:
Hot packs, Cold packs, US, Whirlpool or Diathermy

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4
Q

Mechanical

A

Applies force to either increase or decrease pressure on the body

Examples:
Water, Traction, Compression and Sound

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5
Q

Electromagnetic

A

Applies energy via electromagnetic radiation or an electrical current

Examples:
UV radiation, infrared, laser, diathermy, and electrical stimulation

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6
Q

History: Why change in use?

A

Ineffective
-IR lamps for wounds – dried out

Inefficient
-Sunlight for Tuberculosis

Cumbersome
-Diathermy

Excessive risks
-Diathermy

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7
Q

Level at which physical agents have a direct effect…

A

Impaired body function and structure

Ex) Muscle paresis, hypotonicity, pain, sensory deficits, atrophy, soft tissue tightness

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8
Q

Can modalities be used alone?

A

NO! it’s not PT

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9
Q

Evaluation and Planning for the Use of Physical Agents

A
  • Physician referral as needed
  • Medical Diagnosis
  • Precautions/Contraindications
  • Examination
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10
Q

Documentation of PA used

A

Physical agents used

Area of body treated

Patient position during treatment

Intervention duration

Parameters

Outcomes including progress towards goals

Regressions or complications

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11
Q

Precaution

A

Conditions under which a particular form of treatment should be applied with special care or limitations

Relative

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12
Q

Contraindication

A

Conditions under which a particular treatment should NOT be applied

Absolute

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13
Q

General Contraindications/Precautions

A

Pregnancy

Malignancy

Pacemaker or other implanted device

Impaired Sensation or Mentation (lack of communication)

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14
Q

Selection of Physical Agents

A

Goals and Effects of Treatment

Contraindications and Precautions

Evidence for Physical Agent Use

Cost, Convenience, and Availability

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15
Q

Quality Research

A

Patient / Population

  • Question should apply to a specific population
  • More specific = less evidence

Intervention
-Specific

Comparison
-Control

Outcome
-Defined as precisely as possible

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16
Q

Effects of Physical Agents

A

Modification of tissue
inflammation and healing

Relief of pain

Modification of muscle tone

Alteration of collagen extensibility and motion restriction

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17
Q

3 phases of tissue healing

A

1) Inflammation (Days 1-6)
2) Proliferation (Days 3-20)
3) Maturation (Days 9+)

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18
Q

Cardinal Signs of Inflammation

A 
Heat = increased vascularity
Redness = increased vascularity
Swelling = lymphatic drainage blockage
Pain = pressure or irritation of pain sensitive areas
Loss of function = pain and swelling
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19
Q

Inflammation Phase

A

1) Vasoconstriction
2) Vasodilation
3) Clot Formation
4) Phagocytosis

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20
Q

Proliferation Phase

A

1) Epithelialization
2) Collegen production
3) Wound contracture
4) Neovascularization

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21
Q

Maturation Phase

A

1) Collegen Synthesis/Lysis balance

2) Collegen Fiber organization

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22
Q

Vascular Response

A

1) Vasoconstriction followed by vasodilation at the capillaries, postcapillary venules and lymphatics
- Vasodilation mediated by chemical mediators

2) Leukocyte Extravasation
- Movement out of the circulatory system and towards the site of tissue damage or infection

3) Accumulation of fluid in the interstitial tissue (outside the vessels) resulting in edema

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23
Q

Hemostatic response

A

Controls blood loss when vessels are damaged or ruptured.

Retracts and sealing off of blood vessels

Platelets form clots and assist in building of fibrin lattice, which serves as wound’s source of tensile strength

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24
Q

Cellular Response

A

Phagocytosis
-Neutrophils rid the injury site of bacteria and debris
(24 hrs then disintegrate)

Monocytes

  • Predominate for 24-48 hrs
  • Convert to macrophages when they migrate from capillaries into the tissue spaces

Macrophages

  • Most important cell in inflammation!
  • Produce while range of chemicals
    - Facilitate the removal of necrotic tissue and bacteria
    - Promote cell proliferation
    - Influence the number of fibroblastic repair cells
  • Most effective when oxygen is present.

Resident macrophages

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25
Q

Proliferation Purpose

A

cover the wound and regain some of it’s initial strength.

Clinical signs:

  • Granulation tissue is generated which is characterized by red, beefy, shiny tissue with a granular appearance
  • Wound begins to fill
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26
Q

Proliferation at the cellular level

A

Cell activity consists of macrophages-stimulated collagen synthesis, capillary formation, wound contraction and wound epithelialization

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27
Q

Epithelialization

A

The reestablishment of the epidermis

Early with superficial wound
Later with deeper injury
-After collagen production and neovascularization

28
Q

Components Involved in Tissue Healing

A

Fibronectin
Prteogylcans
Elastin
Collagen

29
Q

Collagen Production

A

Fibroblasts make collagen

Fibroblasts migrate to the injured area and fibroplasia (fibroblast growth) occurs

Fibroblast initially produce type III collagen

  • Thin, weak, and no consistent organization.
  • By day 12, immature type III starts to be replaced by type I which is more mature and strong.
30
Q

Fibronectin

A

Tensile strength

“Glue” substances together

31
Q

Proteoglycans

A

Secreted by fibroblasts early in tissue repair
Bind to fibronectin and collagen and help stabilize tissue
Retain water to assist in hydration

32
Q

Elastin

A

Protein that is cross-linked to provide elasticity

33
Q

Collagen

A

Most important protein, provides structural support and tensile strength
3 chains of amino acids coiled around each other in a triple helix
27 types identified

34
Q

Wound Contraction

A

Pulls the edges of the injured site together and in effect shrinks the defect

Begins at day 5 and peaks at 2 weeks

Myofibroblasts are primary cells responsible

Speed of contraction
Linear > Square/rectangular > circular

35
Q

Neovascularization

A

Development of new blood supply or the growth of new vessels = angiogenesis

Healing cannot occur without it
Supplies oxygen and nutrients to injured/healing tissue

Forms capillary loops
Gives scar it’s pinkish to bright red hue

These loops cease as the wound heals leading to more mature scars
Whitish appearance.

36
Q

Maturation

Stop here for Quiz#1

A

Day 9 up to 2 years

Clinical Signs:
Shrinking and thinning of scar and loss of redness

37
Q

Maturation at the Cellular level

A

The collagen fibers remodel, mature, and gain tensile strength

38
Q

Outcomes of Acute Inflammation

A

Complete resolution and replacement of injured tissue with like tissue
(Most beneficial)

Healing by scar formation
(Most common)

Formation of abscess

Progression to chronic inflammation

39
Q

Chronic Inflammation

A

Months to years
Occurs in 1 of 2 ways:

1) Cumulative trauma
- Interference of healing process

2) Immune response to altered host tissue / foreign material or the result of an autoimmune disease (RA)

40
Q

Normal Acute Inflammatory Process

A

no more than 2 weeks

41
Q

Sub acute Inflammation

A

if more than 4 weeks

42
Q

Local Factors that Effect Healing

A

Size, type and location of injury

  • Small vs. Large
  • Surgical incision vs. blunt trauma
  • Scalp vs areas of ischemia – excessive pressure

Infection
-Affect collagen metabolism reducing production increasing lysis.

Vascular supply

  • Muscle vs. Tendon
  • Meniscus

External forces
-Physical Agents

Movement
-Immobilization vs CPM

43
Q

Systemic Factor that Effect Healing

A

Age
-Pediatrics vs Geriatrics

Disease
-Diabetes
-Problems with circulatory system
(Atherosclerosis, sickle cell disease, hypertension)

Medications
-Corticosteriods – at time of injury can decreasing inflammatory response at this stage delays subsequent phases of healing and increases the incidence of infection
(Prednisone, dexamethasone)
-NSAIDs are less likely to impair healing
(Ibuprophen)

Nutrition
-Deficiency in AAs, vitamins, minerals, water
(Protein-calorie malnutrition more than depletion of a single nutrient)

44
Q

Specific Tissue Healing: Cartilage

A

Limited ability to heal because it lacks lymphatics, blood vessels and nerves

Cartilage itself does not form clots healing fails

Different if subchondral bone is involved

45
Q

Specific Tissue Healing: Tendon and Ligaments

A

Inflammation occurs in the first 72 hours

Collagen synthesis occurs in the first week

Intrinsic and extrinsic cells participate in repair

Orientation of cells/collagen are perpendicular to tendon early

  • Changes to parallel around day 10 and last up to 2 months
  • Ultimate maturation depends on sufficient physiological loading
46
Q

Specific Tissue Healing: Skeletal Muscles

A

cannot proliferate once injured

However stem or reserve cells can form new skeletal muscle cells
-Satellite cells

After severe contusion, a calcified hematoma may develop
-Myositis ossificans

47
Q

Specific Tissue Healing: Bone

A

Heals with “like-tissue”.

Stages of fracture healing
-Impaction, induction, inflammation, soft callus, hard callus, remodeling

48
Q

Types of Pain

A

Acute
Chronic
Referred
Trigger Points

49
Q

Acute Pain

A

-Is experienced when tissue damage is impending and after injury has occurred
(Calor, rubor, tumor)

-Underlying pathology can be identified

50
Q

Chronic Pain

A

-Persists beyond normal time for tissue healing
(3-6 months)

  • Result of activation of dysfunctional neurological or psychological responses
  • Continue to experience pain even when no damaging or threatening stimulus is present
51
Q

Pain Reception and Transmission: Nociceptors

A
  • Free peripheral nerve endings
  • “String-of-beads” appearance
  • Present in almost all types of tissues
  • Activated by intense thermal, mechanical (brick / broken bone), or chemical (acid/bleach / histamine) stimuli
  • Convert stimulus to electrical impulses (action potentials) through transduction along afferent nerves towards the spinal cord.
  • Peripheral sensitization
52
Q

Peripheral Sensitization

A

Release chemicals to increase the response to noxious stimuli

Resulting in activities and stimuli are perceived as painful even though they are not damaging

53
Q

Nociceptors are the terminals of what two types of primary afferent neurons?

A

C-fibers

A-delta fibers

Mechanical trauma activates both!

54
Q

C-Fibers

A

Small, Unmyelinated, Slow (1-4 m/s)

“Dull, throbbing, aching, burning”

Slow onset after initial noxious stimulus

Long lasting, diffusely localized – emotionally difficult

55
Q

A-delta Fibers

A

Small-diameter but myelinated, Fast (30 m/s)

Sensitive to high-intensity mechanical stimulation but also respond to heat/cold.

“Sharp, stabbing, prickling”.

Quick onset, last a short time, localized – not emotional

56
Q

Spinal Cord Pathway

A

C and A-delta nerves –> interneurons (T-cells) –> neurons in the superficial dorsal horn of the grey matter of the spinal cord

57
Q

T-cells (Transmission cells)

A
  • Integrate info from nociceptive and non-nociceptive (A-beta) primary afferent fibers, other T-cells, and supraspinal sites (brain stem and cortex)
  • This balance from excitatory (nociceptors) and inhibitory (sensory nerves) and descending fibers from the brain influence whether or not the person feels pain and how severe it is
  • Can cause muscles spasms through efferent anterior horn cells…Result in pain-spasm-pain cycle
58
Q

Pain-transmitting neurons

A

Cross midline and ascend to thalamus via lateral or anterospinalthalmic tracts

59
Q

Referred Pain

A

At a location distant from its source

From one joint to another

Peripheral nerve to a distal area of innervation

Internal organ to an area of musculoskeletal tissue

60
Q

Gate Control Theory

A

Melzack and Wall in 1965

Severity of pain sensation is determined by the balance of excitatory and inhibitory inputs (A-beta) to the T-cells in the spinal cord

PA and interventions for pain relief

  • Inhibit activation of pain transmission cells
  • Pre-synaptic inhibition of T-cells
  • Closing the gate to the transmission of pain
61
Q

The Endogenous Opioid System / Theory

A

Control pain by binding specific opiate receptors in the nervous system

Paradoxical pain-relieving effects of painful stimulation and acupuncture

Noxious TENS (Acupuncture like)

62
Q

Measuring Pain

A

Visual Analogue Scale (VAS)
Numeric Scale (NPRS)
(Best for quick estimating pain)

Verbal Pain Intensity Scale
Thermometer Scale
Wong-Baker FACES Rating Scale (poor communication population)

McGill Pain Questionnaire (MPQ) [takes a long time!]

63
Q

Documenting Pain

A 
Pain location
Quality
Severity
Timing
Better/worse
Setting
How pain affects function, activities and participation
64
Q

Pain Management Approaches

A

Pharmacological

Physical Agents

65
Q

Physical Agents for pain management

A

Stimulate large diameter afferent fibers

  • TENS
  • Massage
  • Analgesic balms

Decrease pain fiber transmission velocity

  • Cold
  • Ultrasound

Stimulate small diameter afferent fibers

  • Acupressure
  • Deep massage
  • TENS

Stimulate a release of endorphins
-`TENS

66
Q

Other useful Pain Strategies

A

Cognitive process and encouragement

  • Motivation
  • Tension diversion
  • Focusing
  • Relaxation techniques
  • Positive thinking

Minimize tissue damage by application of proper first aid and immobilization

Maintain line of communication with the patient and let them know what to expect

All pain, even psychosomatic, is very real to the patient

Encourage supervised exercise

Modalities (2 decks)

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