Exam 2 supplement: pain inflamaiton medication from Summer 2014, feel free to add/modify to reflect Dr. Thompson's class Flashcards Preview

Thompson class fall 2015 > Exam 2 supplement: pain inflamaiton medication from Summer 2014, feel free to add/modify to reflect Dr. Thompson's class > Flashcards

Flashcards in Exam 2 supplement: pain inflamaiton medication from Summer 2014, feel free to add/modify to reflect Dr. Thompson's class Deck (112):
1

3 phases of Healing

  1. Inflammation
  2. Proliferation
  3. Maturation

2

Inflammation Phase (general)

Prepares for healing

3

Proliferation phase (general)

rebuilds and

strengthens damaged tissue

4

Maturation phase (general)

modifies tissue to mature form

5

Inflammation phase (specific)

  • 1-6 days
  • Induced by disease/trauma
  • Cardinal signs of inflammation present
  • hyperemia
  • swelling
  • pain from pressure

6

Inflammation phase time

1-6 days

7

Cardinal signs of inflammation (5)

  1. Calor
  2. Rubor
  3. Tumor
  4. Dolor
  5. Functio laessa

8

Hyperemia

Increased blood flow (redness, erythema)

occurs with inflammation

9

erythema

reddening of skin

occurs with inflamation

10

Calor

heat.

one of the 5 cardinal signs of inflammation

11

Rubor

Redness.

one of the 5 cardinal signs of inflammation

12

Tumor (in regards to inflammation)

swelling.

one of the 5 cardinal signs of inflammation

13

Dolor

pain.

(In inflammation: caused by chemical mediators released during inflammation and from pressure from swelling)

one of the 5 cardinal signs of inflammation

14

Functio laessa

decrease in function.

one of the 5 cardinal signs of inflammation (this one was recently added)

15

Swelling (in inflammation)

also known as tumor

increased permeability of cells and vasodilation

often accompanied by ecchymosis

16

Ecchymosis

a discoloration of the skin resulting from bleeding underneath, typically caused by bruising.

17

Injuries causing inflammation: (8)

  1. sprains, strains, & contusions
  2. Fractures
  3. Foreign bodies (sutures)
  4. Autoimmune diseases (RA)
  5. Microbial agents
  6. chemical agents
  7. thermal agents (burns/frostbite)
  8. Irradiation (UV or radiation)

18

Sprain

ligament tear

19

strain

tendon tear

20

contusion

bruise:

bone or soft tissue

21

How is inflammatory process triggered?

mast cells, the most important activator (NOT the trigger)

22

How do mast cells induce inflammation (2 ways)

  1. Degranulation    
    • release of contents of mast cell granules    
    • Acute
  2. Synthesis
    • new production and release of mediators in response  to stimuli  
    • Long term 

23

Mast cell degranulation

Acute: release of contents of mast cell granules within seconds:

  • Histamines
  • Chemotactic Factors

24

Mast cell synthesis (what it is and 3 things synthesized)

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)

 

  • 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

(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)

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: < 6 months with known source

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: < 6 months with known cause

Chronic: beyond normal tissue healing time

102

Visceral pain:

(nociceptive pain)

organs

referred

103

acute pain

< 6 months, known source

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

 

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