Exam 2: pain inflamaiton medication Flashcards
1
Q
3 phases of Healing
A
- Inflammation
- Proliferation
- Maturation
2
Q
Inflammation Phase (general)
A
Prepares for healing
3
Q
Proliferation phase (general)
A
rebuilds and
strengthens damaged tissue
4
Q
Maturation phase (general)
A
modifies tissue to mature form
5
Q
Inflammation phase (specific)
A
- 1-6 days
- Induced by disease/trauma
- Cardinal signs of inflammation present
- hyperemia
- swelling
- pain from pressure
6
Q
Inflammation phase time
A
1-6 days
7
Q
Cardinal signs of inflammation (5)
A
- Calor
- Rubor
- Tumor
- Dolor
- Functio laessa
8
Q
Hyperemia
A
Increased blood flow (redness, erythema)
occurs with inflammation
9
Q
erythema
A
reddening of skin
occurs with inflamation
10
Q
Calor
A
heat.
one of the 5 cardinal signs of inflammation
11
Q
Rubor
A
Redness.
one of the 5 cardinal signs of inflammation
12
Q
Tumor (in regards to inflammation)
A
swelling.
one of the 5 cardinal signs of inflammation
13
Q
Dolor
A
pain.
(In inflammation: caused by chemical mediators released during inflammation and from pressure from swelling)
one of the 5 cardinal signs of inflammation
14
Q
Functio laessa
A
decrease in function.
one of the 5 cardinal signs of inflammation (this one was recently added)
15
Q
Swelling (in inflammation)
A
also known as tumor
increased permeability of cells and vasodilation
often accompanied by ecchymosis
16
Q
Ecchymosis
A
a discoloration of the skin resulting from bleeding underneath, typically caused by bruising.
17
Q
Injuries causing inflammation: (8)
A
- sprains, strains, & contusions
- Fractures
- Foreign bodies (sutures)
- Autoimmune diseases (RA)
- Microbial agents
- chemical agents
- thermal agents (burns/frostbite)
- Irradiation (UV or radiation)
18
Q
Sprain
A
ligament tear
19
Q
strain
A
tendon tear
20
Q
contusion
A
bruise:
bone or soft tissue
21
Q
How is inflammatory process triggered?
A
mast cells, the most important activator (NOT the trigger)
22
Q
How do mast cells induce inflammation (2 ways)
A
- Degranulation
- release of contents of mast cell granules
- Acute
- Synthesis
- new production and release of mediators in response to stimuli
- Long term
23
Q
Mast cell degranulation
A
Acute: release of contents of mast cell granules within seconds:
- Histamines
- Chemotactic Factors
24
Q
Mast cell synthesis (what it is and 3 things synthesized)
A
Activated mast cells begin new synthesis of inflammatory mediators to be released later:
- Leukotrienes
- Prostaglandins
- platelet-activating factors
Long term response (takes over from histamine response)
25
What do mast cells release during degranulation? (2 things)
Histamines
Chemotactic Factors
26
Histamines cause: (in inflammation)
* temporary rapid constriction of smooth muscle + dilation of veinules (increases blood flow)
## Footnote
* Increases vascular permeability
* Improves adherence of leukocytes to endothelium
VERY QUICK
27
Chemotactic Factors, (what they do and 2 types)
form gradient that cause chemotaxis of cells towards inflammation
1. neutrophil chemoactic factor (attracts neutrophils)
2. Eosinophil chemotactic factor of anaphylaxis (attracts eosinophils)
TNF-a (tumor necrosis factor-alpha) is also a chemotactic factor
28
Leukotrienes
synthesized by mast cells
effects similar to histamine except slower and longer response
Important later in stages of inflammation
29
Prostaglandins
* synthesized by mast cells
* cause increased vascular permeability, neutrophil chemotaxis, & pain
* (NSAIDs inhibit prostaglandins and are non-selective)
30
NSAIDs
Non-Steroidal Anti-Inflammatory Drug
non-selective
inhibit prostaglandins
31
Platelet-activating factor
synthesized by mast cells
cause
1. endothelial retraction to increase vascular permeability,
2. leukocyte adhesion to endothelial cells, and
3. platelet activation
32
What causes leukocyte adhesion to endothelial cells (one for long term and one for short term)
Short term: Histamines released by degranulation of mast cells (early part of inflammatory response)
Long term: Platelet-activating factor synthesized by mast cells after histamines are spent during longer inflammatory response
33
Vascular response to inflammation
Initial (5-10 min after injury): vasoconstriction (chemically induced --\> norepinephrine)
Later (1 hour after injury): Vasodilation (chemically induced--\> histamine, Hageman factor, bradykinin, prostaglandins, and complement fractions)
34
bradykinin
a compound released in the blood during later stages of inflammation that causes vasodilation. It is a peptide comprising nine amino-acid residues.
35
Hageman factor
plasma protein that causes later vasodilation during inflammation
36
Vasoconstriction (clot formation)
Blood vessel linings adhere
Neutrophils migrate to injury area - extravasion
Leukocytes line vessel wall - margination
37
Extravasion
Neutrophils migrate to injury area
part of vasoconstriction (clot formation)
38
Margination
Leukocytes line vessel wall
part of vasoconstriction (clot formation)
39
Neutrophils
Short term: predominant phagocytes in early inflammatory process (Arrive 6-13 hrs after injury)
not capable of cell division
become puss (short life)
Primary role: Sterile lesions: remove debris and dead cells Non-sterile lesions: phagocytosis of bacteria
40
Phagocytosis
cell eating (bacteria is more solid)
41
Pinocytosis
cell drinking (bacteria is more liquid)
42
Leukocytes (general, not specific types)
Long term.
Many forms: Monocytes immature form that becomes macrophage after inflammatory site entry. (Eosinophils & Basophils are leukocytes too)
Arrive 24 hrs post injury
Largest normal blood cell
produced in bone marrow
Seen in higher proportions in chronic inflammation
43
Leukocytes (3 types)
Monocytes --\> become macrophages after entry into inflamed site
Eosinophils
Basophils
Long term
44
Eosinophils
* type of leukocyte
* mildly phagocytic
* primary defense against parasites
* help regulate vascular mediators from mast cells
* Help limits inflammation
45
Basophils
type of leukocyte
Mobile mast cells which release similar inflammatory agents
46
Edema
Swelling; accumulation of fluid in extravascular space/interstitial tissues
Diapedesis = leukocytes squeeae through vessel wall
emigration: chemotactic agents attract leukocytes to interstitial tissues
47
Diapedesis in Edema
Leukocytes squeeze through vessel wall
48
Emigration in Edema
Chemoactic agents attract leukocytes to interstitial tissues
49
Effusion: definition and 4 types
swelling contained in cavity.
1. joint effusion
2. Pleural effusion
3. ascites
4. peritoneal effusion
50
Difference between edema and effusion
Edema is more likely in interstitial tissue
Effusion is more likely in joint cavity (or I assume other body cavities??)
51
4 Forms of Edema/Effusion
1. Transudate
2. Exudate
3. Pus
4. Blood
52
Transudate
Dissolved electrolytes and H2O (clear)
can be found in effusions/edema
53
Exudate
plasma proteins, lipids, cellular debris (cloudy)
can be found in effusions/edema
54
Pus
neutrophils, digested tissue, fluid, bacteria
can be found in effusions/edema
55
Aspiration of a joint
stick a needle in in a joint cavity and remove fluid.
Used to determine contents of effusion
56
Increased vascular permeability (4 stages?)
1. Endothelial cell contraction- 15-30 minutes – Opens spaces between cells
2. Endothelial injury- altered substance release – Contents of vessel spill into interstitium
3. Leukocyte bind to injured area – Release chemicals and enzymes creating injury
4. Regenerating capillaries- – In later stages of healing tight junctions yet to form
57
Hemostatic Response
Platelets bind to collagen, release fibrin
Fibrin and fibronectin limit fluid drainage and hemorrhaging
clot formed
58
Cellular Response
* Hematoma- erythrocytes (RBC’s) present in injured tissue ( hemarthrosis )- usually severe
* Leukocytes (WBC’s)- present in different concentrations in different healing phases
* Neutrophils, eosinophils , basophils, monocytes, lymphocytes, macrophages
* Phagocytosis- enzymes
59
Immune response
* \* Lymphocyte and phagocyte leukocytes (WBC’s)
* \*Complement system
* ---20 Enzymatic plasma proteins (just know it released a bunch of protein - most important are C3 & C5)
60
Compliment System
Consists of large number of proteins (20) that are activated.
Most important are C3 & C5:
* result in following subunits:
* Opsonins
* Chemotactic factors
* Anaphlatoxins
61
Proliferative Phase (general and length of time)
3-20 days
Prepared for by inflammation phase
Main tissues:
* Epithelial cells & connective tissue
* Cover and strengthen injury site
* Epitheliazation, collagen production, wound contracture, & neovascularization
62
When do we start to see callous formation on a broken bone in an x-ray?
The proliferation phase
63
Epithelialization
Healing:
Primary intention: close approximation of tissues (with sutures)
Secondary intention: indirect union (without sutures)
64
Fibroplastia/Collagen Production
* Granulation tissue
* Type III collagen
* Formation of scar
* Type I collagen day 12
65
Type III collagen
Initial type of collagen in proliferative phase collagen production
weak and thin
66
Type I collagen
type of collegen produced by day 12 (proliferatave phase) - I think it can be converted from type III colagen
more mature and stronger than type III collagen
67
Scar formed from (2 things) during proliferation.
Glycosaminoglycan (GAG)
and
Collagen
68
Wound Contraction
myofibroblasts help pull edges together through creation of smooth muscle cells
not the same as a wound CONTRACTURE (which is pathological)
69
Neovascularization
development of new blood supply (angiogenesis)
70
Maturation phase
day 9 on (may take 1-2 years from injury)
Goal: return function (depends on what kind of structure is healing:
* Type I collagen: bone, skin, tendon, and mature scars
* Type II collagen: replaces former fibrocartilage & articular
* Type III collagen: GI tract, uterus, and blood vessels
71
Hypertrophic scars
synthesis greater than lysis
treatment: pressure garments
kind of looks like keloid but not
72
Keloid
scar beyond boundaries of injury
treatment: surgical, poor outcomes
73
Importance of scar management techniques during scar maturation phase
If not moved, tissue underneath can bind to scar
74
scar management techniques
after scab falls off:
* scar massage
* lotion with vitamin E
* Cross-friction massage
Ideally for one year
TKR a good example of when to use
75
cross-friction massage
* if scar is vertical go across it
* usually done daily for 3-5 min
* usually can begin about 3 weeks post surgery
76
Determination of final collagen structure (6)
1. muscle tension
2. joint movement
3. soft tissue loading/unloading
4. facial gliding
5. temperature changes
6. mobilization
77
Chronic Inflammation
1. progression of active inflammation
2. tissue destruction
3. healing
78
Tendonitis
acute
79
tendonosis
chronic and weaker than tendonitis
80
Inflammation (define acute, sub-acute, and chronic normal expected time periods)
* acute: 0-2 weeks
* sub-acute: \> 4weeks
* chronic: several months or years
## Footnote
(this is not consistently defined, but this is a good normal expectation)
81
Two types of factors affecting healing process
* Local factors
* Systemic factors
82
Local factors affecting healing process (4)
1. injury type, size & location
2. infection
3. vascular supply external forces (modalities affect here)
4. movement
83
Systemic factors affecting healing process (6)
1. age
2. disease
3. medications
4. nutrition
5. smoking status
6. fitness level
84
Tendonitis pain (sharp or dull)
sharp
85
Tendonosis pain (sharp or dull)
dull
86
Specific healing: Cartilage - both types
poor blood supply
poor healing
87
Specific Tissue Healing: Tendons/ligaments
* 72 hr inflammation
* collegen synthesis - 1 wk
* Tendons no AROM x 3 wks
* PROM indicated for both tissues within limits
88
Specific Tissue Healing: muscle
no proliferation
myocitis ossificans risk
89
myocitis ossificans
calcium build up in the muscle
Typically occurs when a muscle is bruised or from muscle contusion
A reason it is really important to use ice, not heat, on muscle right away
90
Specific Tissue Healing: bone
1. Inflammation
2. soft callus
3. hard callus (3 wks - 4 months)
4. Remodeling (months to years)
## Footnote
can see callus on x-ray around 3 weeks
6-8 wks before you can put stress on bone after fracture
91
3 phases of Tissue healing
1. Inflammation
2. Proliferation
3. maturation
92
Timeline for three phases of tissue healing
1. Inflammation: 1-6 days
2. Proliferation: 3-20 days
3. Maturation: day 9 on (can be as many as 1-2 years)
93
What is the fifth vital sign?
pain
94
What is the most common symptom prompting patients to seek medical attention including rehabilitation?
Pain
95
What are the five vital signs?
1. HR
2. RR
3. BP
4. Body Temp
5. Pain
96
Three goals of treating pain
1. Resolving the cause (find belt & fix)
2. modify patient's perception
3. maximize function within pain limits
97
4 main Types of pain
1. Nociceptive (Somatic & Visceral)
2. Neuropathic (Central & Peripheral)
3. Psychogenic (non-organic)
4. Carcinogenic (cancerous)
98
Somatic pain
A type of nociceptive pain all tissues except neural tissues:
Acute:
Chronic: persists beyond normal tissue healing time
99
Visceral pain:
A type of nociceptive pain
organs
often referred
100
2 types of nociceptive pain
Somatic
Visceral
101
2 types of Somatic pain
(nociceptive pain)
Acute:
Chronic: beyond normal tissue healing time
102
Visceral pain:
(nociceptive pain)
organs
referred
103
acute pain
SNS response: increased muscle tone, HR, BP and skin conductance.
Sudden onset
Lasts days to weeks
normal pain behavior
good response to treatment
localized
104
chronic pain
1. persists beyond normal tissue healing time
2. Caused from acute pain,
3. several failed treatments
4. medication tried & failed but continues to take unbearable or incapacitating alterations in SNS
5. Gradual/diffuse and/or reffered lasts months-years (much more gradual onset)
6. often abnormal pain behavior
7. poor treatment response
105
Neuropathic pain (2 types)
Peripheral
Central
106
some treatments for Acute pain
Cryotherapy, cold laser, pulsed US
Stop aggravating activity to allow healing (if it hurts don't do it)
107
Is acute or chronic pain easier to treat?
Acute
108
Will we likely see acute or chronic pain most often?
chronic pain
109
What are the most common pain types we will see? (2)
Somatic pain
peripheral nervous system pain
110
What is a test that can be used to detect psychogenic sources of pain?
Waddell signs and symptoms for back pain
111
Referred Pain
* hip to knee
* L5-S1 nerve root to lateral leg
* MI or angina to LA, Jaw
* Diaphragm to lateral tip of either shoulder
* spleen to left shoulder gall bladder to R shoulder or inferior angle of R
* scapula
## Footnote
Referred pain is dull
112
Wound Contrature (not contraction)
* Contractures: pathological wound contraction that causes adhesions, muscle shortening, and tissue damage.
* This is different than the normal wound contraction that is part of healing.
* I think it is when the normal process gets out of control
