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Therapy Modalities Lecture > Therapeutic Interventions > Flashcards

Therapeutic Interventions Flashcards

1
Q

Overall Treatment Appraoch

A
  • Determine problems and limitations and apply treatments that will overcome them
  • Must consider limitations based on surgical precautions or physician orders
    ~ Exercises need to be approved/
    cleared
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2
Q

Common Problems/Limitations

A
  • Common problems/limitations
    ~ Activity deficits
    ~ Pain
    ~ Swelling
    ~ Loss of/abnormal function
    > Muscle weakness/lack of
    endurance
    > Flexibility/ROM deficits
    > Neuromuscular Deficits
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3
Q

How are problems determined?

A
  • Evaluation
  • Re-evaluation
    ~ Helps to determine if treatment is
    working
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4
Q

Overcoming Problems/Limitations

A
  • Apply modalities and rehabilitation that
    SPECIFICALLY address problems/
    limitations
  • Modify inflammation/healing/pain
    response to injury!!
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5
Q

What are the Problems with Therapeutic Interventions in Allied Health?

A
  • Many protocols - Few proven
    ~ Protocols shown to work, do so under
    very controlled circumstances
    ~ What works on one individual with a
    specific problem many times does not
    work on another person with the same
    problem
  • Humans are sheep
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6
Q

“Not so good” Practitioner

A
  • Heavy use of protocols
  • Uses treatment based on injury type/
    area
  • Uses same treatment long term
    regardless of results
  • Has no/little basis for what they’re
    doing
    ~ Can’t answer “why”
    ~ May use some good techniques, but
    not well reasoned
    ~ Copycat/sheep
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7
Q

“Good” Practitioner

A
  • Selects treatment based on evaluation
    findings
  • Modifies treatment based on re-
    evaluation
  • Has some basis/reason for what they’re
    doing
  • Stops using treatment when no change is
    observed
  • Listens to athletes/patients and modifies treatment accordingly
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8
Q

How to be a “good” practitioner

A
  • Learn what specific treatments
    specifically do
    ~ To answer “why”
  • Apply specific treatments for a specific
    effect
    ~ Match treatment to goals
    ~ Utilize “Rifle” rather than “Shotgun”
    approach
    > Rifle: see the problem and be
    specific
    > Shotgun: see the problem and be
    broad
    ~ Think!
    > Understand that it’s an art based on
    experience, research, tradition, and
    theory
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9
Q

Treatment Technique Checklist

A
  • What is this accomplishing?
  • Why select this technique/is this the best
    technique at this time?
  • Where do I go from here?
    ~ Progression
    ~ When do I stop or change?
    > Stop if: pt. is better or no change in
    pt.
    > Change if: pt. is not improving
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10
Q

Movement of materials across membranes: Diffusion & Osmosis

A
  • Diffusion is the movement of dissolved
    particles (solute) from an area of high
    concentration to areas of low
    concentration
    ~ Areas divided by a membrane
    permeable to the solute
  • Osmosis is the movement of water
    molecules from a dilute solution to a
    more concentrated solution
    ~ Areas divided by a membrane
    permeable to water
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11
Q

Osmotic Pressure within the body

A
  • Areas
    ~ Between cells and extracellular fluids
    ~ Between tissues and blood
  • Typically little difference
    ~ Cells maintain normal size
    ~ Blood volume remains fairly constant
    ~ Disease/Injury can alter this imbalance
    and causes water to go somewhere:
    tissues (swelling)
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12
Q

Inflammation

A
  • Body’s reaction to:
    ~ Cell death
    ~ Cell injury
    ~ Exposure to allergen/pathogen
  • Normal reaction has several purposes:
    ~ Limits extent of the injury
    ~ Removes debris
    ~ Prepares site for healing
    ~ Rids area of allergen/pathogen
  • Occurs in somewhat predictable phases
    ~ Progressive, but overlap one another
    > Acute
    > Repair
    > Maturation
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13
Q

Cardinal Signs of Inflammation

A
  • All caused by chemical mediators
    produced during inflammation
    ~ Redness (Rubor): due to increased
    blood flow
    ~ Heat (Calor) : due to increased blood
    flow
    ~ Swelling (Edema): caused by
    movement of blood plasma and
    proteins
    ~ Pain (Dolar): caused by damage to
    nerve endings and release of
    serotonin, HT, PG, and BK
    ~ Functional loss: due to swelling,
    pain, and or neurological damage
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14
Q

Start of the Inflammatory Response

A
  • Cell death, cell injury, or exposure to
    allergen/pathogen causes the formation
    of Bradykinin (BK) from proteins in the
    blood, lymph, or interstitial fluid
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15
Q

Effects of Bradykinin

A
  • 2 different effects
    ~ Binds to MAST cells found in
    connective tissues and binds to blood
    platelets causing a release of
    Histamine (HT)
    > Allergen/pathogen binding to MAST
    cell receptors has the same effect
    ~ Causes activation of an enzyme
    (Phospholipase A2), which mobilizes
    Arachidomic Acid from cell membranes
    > Arachidonic Acid is then
    metabolized
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16
Q

Metabolism of Arachidonic Acid

A
  • 2 enzyme pathways metabolize
    Arachidonic Acid
    ~ Cyclooxygenase (COX): produces
    prostaglandins and thromboxanes
    ~ Lipooxygenase: produces leukotriene
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17
Q

Inflammatory Response Chart

A

Cell death, Cell injury, or Exposure to Allergen/Pathogen → BK → binds to MAST cells and platelets → releases HT

                         - OR -

Cell death, Cell injury, or Exposure to Allergen/Pathogen → BK → PHOS A2 → mobilizes AA

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18
Q

Metabolism of Arachidonic Acid Chart

A

AA → COX → PG & TX

     - OR -

AA → LIPO → LT

19
Q

Acute Phase of Inflammation: 1st Hour

A
  • Typically 2-4 days
  • 1st Hour (very brief)
    ~ Blood vessels in area constrict in
    reaction to release of Norepinephrine
    and Seritonin
    > Epinephrine/Norepinephrine are
    released from Adrenal glands (NE >
    EP)
    > Serotonin is released from
    damaged MAST cells found in
    connective tissue and platelets~ Vasoconstriction allows coagulation
    of broken blood vessels to begin~ Vasoconstriction followed by
    vasodilation and increased blood
    vessel permeability in reaction to BK,
    HT, LT, & PG release
20
Q

Acute Phase of Inflammation: 2nd Hour

A
  • 2nd Hour through Day 4
    ~ Continued vasodilation and increased
    permeability
    > Vasodilation creates gaps in blood
    vessel walls
    > Continued vasodilation and
    increased vessel permeability
    allows passage of blood plasma,
    proteins, and cells (exudate) into
    damaged tissue~ Leukocytes (white blood cells)
    > Leukotaxin release causes
    leukocytes to line up along blood
    vessel walls (margination)
    > Leukocytes pass into surrounding
    tissues
    > Leukocytes are further attracted to
    injured tissues by opsonin and BK
21
Q

Leukocytes

A
  • Neutrophils: die and release digestive
    enzymes that kill bacteria, ingest small
    debris and bacteria
  • Monocytes: arrive after the neutrophils,
    ingest large debris and dead neutrophils
  • Lymphocytes: kill bacteria and virus
22
Q

Exudate

A
  • In an orthopedic injury, Exudate causes
    Edema
  • Exudate can be seen oozing from
    wounds and infected tissues
  • Descriptions
    ~ Serous (clear fluid)
    ~ Purulent/Pus
    ~ Fibrinous
    ~ Hemorrhagic
23
Q

What is the purpose of modalities?

A

To manage some of the cardinal signs of inflammation

24
Q

Repair/Proliferation Phase of Inflammation

A
  • Begins during the first few hours after
    injury and can last 4-6 weeks
  • Blood Vessel Repair
    ~ Endothelial cells begin to grow and
    repair the damaged blood vessels
    > Blood flow returns to the site of
    injury delivering oxygen and
    nutrients and removing waste
  • Fibroplasia - Healing
    ~ Begins with the formation of
    granulation tissue
    > Delicate Connective Tissue
    > Derived from Exudate
    > Fills the gaps between damaged
    tissues
    ~ Collagen and elastin fibers continue
    to proliferate forming minimal scar
    tissue
25
Q

Fibroblasts

A
  • Produce collagen and elastin forming a
    random matrix of weak connective tissue
  • blast cells build
  • plast cells break down
26
Q

Regeneration

A
  • Most injured tissue is replaced with scar tissue
    ~ Scar tissue can be beneficial in certain
    cases as long as it’s controlled and not
    bulky
  • Actual regeneration is only possible in a
    handful of tissue:
    ~ Bone marrow
    ~ Epidermis (deformity can’t be major)
    ~ Intestines
    ~ Liver
27
Q

Maturation/Remodeling Phase of Inflammation

A
  • Davis’s Law: With increased stress and
    strain the collagen fibers of the matrix
    realign and strengthen in a position of
    maximum efficiency parallel to the lines
    of tension
    ~ (Body lays down more tissue in the
    direction of the stress)
    ~ 3-4 weeks for good healing, can take
    years for full healing
    ~ Exercise and movement can
    encourage this process
    ~ Graston/massage puts stress on area
    ~ Controls scar tissue build up which is
    good
28
Q

Is inflammation the injured athlete’s friend?

A
  • Yes and No
  • Yes because the result of the
    inflammatory response is tissue healing
    ~ Healing can’t occur unless
    inflammation occurs
  • No because pain and swelling can lead to
    loss of function
    ~ Can also lead to secondary damage:
    damage caused after initial injury
    (primary)
    ~ Enzymes released by dead cells that
    digest debris can cause damage to
    normal cells
    ~ Lymphocyte over activity
    ~ Hypoxia
29
Q

Should inflammation be managed/minimized?

A

Yes!

  • Even though inflammation is overall
    positive; pain, swelling, and secondary
    damage should be minimized
  • There are no management techniques
    including drug administration that can
    completely shut down inflammation
    ~ Inflammation can be minimized to a
    certain extent, but healing will still
    occur
30
Q

Chronic Inflammation = Bad

A
  • Becomes a never ending cycle instead of
    a straight-line progression
  • Causes
    ~ Driven by LT, PG, and HT presence
    > Repeated use/overuse
    > Resistant infectious organisms
    > Non-living irritant
    > Unknown reasons
  • Complications
    ~ Excess scarring
    ~ Phagocytosis of normal cells
    ~ Dysfunction due to pain
31
Q

Pain’s Purpose

A
  • Warning for withdrawal
    ~ Hot object
  • Alert of something wrong
    ~ #1 reason person seeks treatment
  • Protection
    ~ Results in muscle spasm and
    guarding to protect the injured area
    > Pain - spasm - stasis
32
Q

Cycle of Pain

A

Pain stressor → Muscle tension → Decrease in circulation → Increase in pain → Even more tension → Even less circulation → More pain

33
Q

Pain Sensation

A
  • Neurogenic Pain
    ~ Pain due to damage to a nervous
    system structure
  • Pain Receptor/Nociceptor
    ~ Afferent (toward brain) nerves that
    send impulse to the CNS resulting in
    pain perception
34
Q

Types of Nociceptors

A
  • Smaller and have less myelin therefore
    they’re slower compared to other
    sensory nerves
  • Mechanical Nociceptor: A-delta
    ~ Located in the skin, initiate pain
    transmission in reaction to mechanical
    stress
  • Polymodal Nociceptor: C
    ~ Widely distributed, initiate pain
    transmission in reaction to several
    different stimuli:
    > Heat
    > Mechanical Pressure
    > Inflammatory Chemicals
    • HT
    • BK
    • PG
    • Seritonin
35
Q

Neural Transmission of Pain

A
  • Afferent Nerves (sensory)
    ~ First Order
    > Originates outside the CNS and
    terminate in the dorsal horn of the
    spinal cord
    • Nociceptor
    ~ Second Order
    > Originate in the dorsal horn of the
    spinal cord and terminate in the
    thalamus of the brain
    • Pain is now perceived, only as
    pain
    ~ Third Order
    > Originates in the thalamus and
    terminates in the sensory cortex of
    the cerebrum
    • Exact location and intensity of
    pain is perceived
36
Q

Pain Transmission Chart

A

1st Order: Stressor → Dorsal Horn of
Spinal Cord

2nd Order: Dorsal Horn of Spinal Cord → Thalamus

3rd Order: Thalamus → Cortex of Brain

37
Q

Ascending Pain

A
  • Pain modulation technique interrupts the
    pain impulse from progressing up the
    Ascending path to sensory cortex
38
Q

Descending Pain

A
  • Pain modulation technique causes CNS
    to send impulse down through CNS to
    stop the pain impulse
    ~ An initial reception in the brain
    triggers this response
39
Q

“Gate Theory”: Not Accurate

A
  • Substantia Gelatinosa
    ~ Gate control system, small, tightly
    packed neurons, determines the
    stimulus input sent to the
    transmission cells
    > Transmission cells are neurons
    within the dorsal horn that
    organize stimulus input from
    from afferent nerve fibers and
    pass them to the 2nd order
    neurons~ Active when both pain and sensory
    impulses are sent to the dorsal horn
    ~ Sensory impulses travel faster and
    reach the Substantia Gelantinosa
    before the pain impulses
    ~ Sensory input causes the SG to inhibit
    passage of the pain impulse to the
    transmission cells
    > Ratio of sensory and pain inputs
    determines how much of the pain
    message is blocked
40
Q

Endogenous Analgesics (dorsal horn): Ascending Pain - Very Accurate

A
  • Sensory impulses trigger a release of
    Enkephalin from interneurons in the
    dorsal horn
    ~ Inhibits A-Delta and C afferent nerve
    transmission
    ~ Massage and stim trick the brain into
    decreasing pain
41
Q

Endogenous Analgesics (Hypothalamus): Ascending Pain - Very Accurate

A
  • A-Delta and C impulses stimulate the
    hypothalamus
    ~ Pituitary gland releases Beta-
    endorphins
    ~ Beta-endorphins circulate in the blood
    and act on opiate receptors
    throughout the body
    > Inhibit Nociceptor
    > Increase Dopamine
42
Q

Central Biasing: Descending Pain - Not Accurate

A
  • Impulses from the thalamus and brain
    stem are carried into the dorsal horn on
    efferent fibers
  • Efferent impulse acts to close “the gate”
    and block the pain message at the dorsal
    horn
43
Q

Endogenous Analgesics: Descending Pain - Very Accurate

A
  • Impulse from the thalamus and brain
    stem are carried into the dorsal horn on
    efferent fibers
  • Triggers a release of Enkephalin from
    interneurons in the dorsal horn
  • Inhibits A-Delta and C afferent nerve
    transmission
44
Q

Central Control: a Person’s Relationship with Pain

A
  • Previous experiences, emotional
    influences, sensory perception, and other
    factors influence the response of the
    brain to pain impulse
    ~ Pain perception can be due to
    biological factors and or
    environmental factors throughout
    childhood

Therapy Modalities Lecture (9 decks)

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