BMD 420 Module 2 (Chapter 5) Flashcards


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1

First line of defense

Physical and chemical barriers such as skin mucous membranes tears saliva and gastric acid

2

Second line of defense

Nonspecific inflammatory response phagocytosis and interferons

3

Third line of defense

Specific immune response involving antibodies and sensitized lymphocytes

4

Inflammation

Body's nonspecific response to tissue injury producing redness swelling warmth pain and possible loss of function

5

Common causes of inflammation

Infection, physical injury, chemicals, ischemia, allergic reaction, extreme temperatures, foreign bodies

6

Bradykinin

Chemical released from injured cells that activates pain receptors

7

Histamine

Released from mast cells causing vasodilation and increased capillary permeability

8

Basic steps of inflammatory process

1. Injury 2. Bradykinin released from injured cells that activates pain receptors 3. Pain stimulates mast cells and basophils to release histamine 4. Bradykinin and histamine cause capillary dilation, increase blood flow and capillary permeability. 5. Break in skin allows bacteria to enter tissue; neutrophils and monocytes migrate to injury site 6. Neutrophils and macrophages phagocytize bacteria

9

Normal capillary exchange

Hydrostatic pressure pushes fluid out at arterial end and osmotic pressure pulls fluid back at venous end

10

Capillary change in inflammation

Injured cells release chemical mediators that cause vasodilation and increase permeability to allow proteins, fluid, and leukocytes to leave capillaries to form exudate and move towards site of injury to phagocytize foreign material

11

What are the four physiologies of inflammation and local effects?

1. Vascular Response (Causes local vasodilation and increased capillary permeability) 2. Cellular Response (WBC attracted by chemotaxis) 3. Excess fluid can collect in interstitial space (Exudate) 4. Inactivation of chemical mediators begins resolution of inflammation (Resolvins/metabolites of omega-3 fatty acids and lipoxins/derived from arachidonic acid)

12

Exudate

Fluid rich in protein cells and electrolytes that accumulates in inflamed tissue

13

Chemotaxis

Attraction of white blood cells to the site of injury

14

Diapedesis

Movement of leukocytes through capillary walls into tissue

15

Hyperemia

Increased blood flow to inflamed tissue causing redness and warmth

16

Cardinal signs of inflammation

Redness, heat, swelling, pain, and sometimes loss of function

17

Serous exudate

Watery fluid with protein and white blood cells

18

Fibrinous exudate

Thick sticky exudate with fibrin that increases scar risk

19

Purulent exudate

Pus containing leukocytes microbes and debris usually from bacterial infection

20

Abscess

Localized pocket of purulent exudate in solid tissue

21

Hemorrhagic exudate

Exudate containing blood due to vessel damage

22

Systemic effects of inflammation

Fever (pyrexia), fatigue, malaise (feeling unwell), headache, anorexia (loss of appetite)

23

Cause of fever in inflammation

Pyrogens released by macrophages reset hypothalamic temperature control

24

Leukocytosis

Increased white blood cell count during inflammation

25

C reactive protein

Protein appearing in blood during acute inflammation and necrosis

26

Erythrocyte sedimentation rate

Lab test elevated in inflammation due to increased plasma proteins

27

Chronic inflammation

Long term inflammation with more macrophages, lymphocytes, fibroblasts, tissue destruction, and scarring

28

Granuloma

Mass of necrotic tissue surrounded by connective tissue in chronic inflammation

29

Complications of chronic inflammation

Ulcers, local complications of specific site of inflammation, Infections, Skeletal Muscle spasms

30

Aspirin

Decreases prostaglandin synthesis at the site of inflammation (anti-inflammatory) and reduces pain (analgesic) and reduces fever (antipyretic)

31

NSAIDs

Anti inflammatory drugs that reduce prostaglandin synthesis and relieve pain fever and inflammation. Same thing as aspirin

32

Acetaminophen

Analgesic and antipyretic drug but not anti inflammatory

33

NSAID COX-2 inhibitor

Anti-inflammatory and analgesic drug

34

Corticosteroids

Strong anti inflammatory drugs that decrease permeability and suppress immune response

35

Side effects of corticosteroids

Delayed healing, high blood glucose, fluid retention, tissue atrophy, adrenal suppression

36

RICE therapy

Rest ice compression elevation used to reduce swelling and pain

37

Resolution healing

Minimal tissue damage with complete return to normal structure

38

Regeneration healing

Replacement of damaged tissue with identical new cells through mitosis

39

Replacement healing

Extensive damage repaired by connective tissue forming scar

40

Healing by first intention

Clean wound with edges close together minimal inflammation and small scar

41

Healing by second intention

Large wound with more inflammation slower healing and greater scar formation

42

Healing process

1. Injury 2. Blood clot forms and seals area 3. Inflammation develops in surrounding area 4. Granulation tissue grows into gap 5. Epithelial cells undergo mitosis, closing wound while granulation tissue forms 6. Fibroblasts and connective tissue cells enter area, producing collagen 7. Scar tissue remains, non-functional with no specialized structures

43

Granulation tissue

Fragile vascular connective tissue that fills wound during healing

44

Role of fibroblasts in healing

Produce collagen that strengthens repaired tissue

45

Scar tissue characteristics

Nonfunctional fibrous tissue lacking specialized structures

46

Factors that promote healing

Youth, good nutrition, adequate hemoglobin, effective circulation, clean wound, absence of infection

47

Example good nutrition factor

Protein and vitamins A and C support collagen formation and tissue repair

48

Factors delaying healing

Old age, poor nutrition, anemia, diabetes, infection, radiation, chemotherapy, prolonged steroid use

49

Contracture

Shrinking nonelastic scar tissue causing joint deformity or restricted movement

50

Stenosis

Narrowing of tubes or ducts caused by scar tissue

51

Adhesions

Bands of scar tissue joining surfaces that normally move freely

52

Hypertrophic scar

Excess collagen forming raised thick scar

53

Keloid

Excessive overgrowth of scar tissue beyond wound margins

54

Ulceration

Impaired blood supply around scar area

55

Burn

Thermal electrical or chemical injury causing acute inflammation and tissue destruction

56

First degree burn

Superficial burn affecting epidermis only and healing without scar

57

Second degree burn

Partial thickness burn affecting epidermis and part of dermis causing blisters pain and possible scarring

58

Third degree burn

Full thickness burn destroying all skin layers often charred and requiring grafting

59

Rule of nines

Method estimating percent body surface area burned

60

Eschar

Dead coagulated tissue forming hard crust over full thickness burn

61

Escharotomy

Surgical incision through eschar (damaged tissue) to relieve pressure and restore circulation

62

Major burn complication hypovolemic shock

Loss of fluid and protein from bloodstream decreases blood volume and pressure

63

Major burn complication infection

Loss of skin barrier increases risk of bacterial invasion

64

Burn hypermetabolism

Increased metabolic demand requiring more protein and calories

65

Reason burn healing difficult fluid loss

Massive fluid and protein leakage causes shock and tissue damage

66

Reason burn healing difficult tissue destruction

Extensive loss of regenerative structures requires grafting and prolonged repair

67

Skin graft

Transplantation of skin to cover large burn wounds and promote healing

68

Compression garments

Used after burns to reduce hypertrophic scar formation