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
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
3
Q
How are problems determined?
A
- Evaluation
- Re-evaluation
~ Helps to determine if treatment is
working
4
Q
Overcoming Problems/Limitations
A
- Apply modalities and rehabilitation that
SPECIFICALLY address problems/
limitations - Modify inflammation/healing/pain
response to injury!!
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
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
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
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
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
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
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)
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
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
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
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
16
Q
Metabolism of Arachidonic Acid
A
- 2 enzyme pathways metabolize
Arachidonic Acid
~ Cyclooxygenase (COX): produces
prostaglandins and thromboxanes
~ Lipooxygenase: produces leukotriene
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
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
