Chapter 9 Inflamation, Tissue Repair and Wound Healing

0.0(0)
studied byStudied by 0 people
0.0(0)
full-widthCall with Kai
learnLearn
examPractice Test
spaced repetitionSpaced Repetition
heart puzzleMatch
flashcardsFlashcards
GameKnowt Play
Card Sorting

1/89

encourage image

There's no tags or description

Looks like no tags are added yet.

Study Analytics
Name
Mastery
Learn
Test
Matching
Spaced
Call with Kai

No study sessions yet.

90 Terms

1
New cards

inflammation

response intended to:

  • eliminate initial cause of cell injury

  • remove damaged tissue

  • generate new tissue

2
New cards

endothelial hyperpermeabillity

reaction of vascularized tissues to injury

3
New cards

inflammatory mediators

  • tumor necrosis factor (alpha)

  • vascular endothelial growth factors (VEGF)

  • neutrophils

  • movement of fluid within cells or interstitial fluid

4
New cards

-itis

inflammation

5
New cards

cardinal signs of inflammation

rubor, tumor, calor, dolor, functio laesa

6
New cards

rubor

redness

7
New cards

tumor

swelling

8
New cards

calor

heat

9
New cards

dolor

pain

10
New cards

functio laesa

loss of function

11
New cards

acute inflammation

short duration (minutes to days)

  • exudation(secrete) of fluid and plasma, emigration of leukocytes(neutrophils) into tissues

12
New cards

what causes inflammation?

infections, trauma, immune reactions, physical agents, chemical agents, tissue necrosis from any cause

13
New cards

endothelial cells

barrier between circulating blood in vessels and surrounding tissues

14
New cards

what do endothelial cells produce?

antiplatelet and antithrombotic agents (maintains vessel patency)

15
New cards

vasodilators and vasoconstrictions regulate what?

blood flow

16
New cards

endothelial cells are involved in the formation of new blood vessels, this is called?

angiogenesis

17
New cards

platelets

  • involved in primary hemostasis

  • releases potent inflammatory mediators

    • increases vascular permeability

18
New cards

neutrophils

they are phagocytic leukocytes that arrive within 90 minutes

19
New cards

monocytes/ macrophages

phagocytic leukocyte that produce potent vasoactive mediators

20
New cards

vasoactive mediators

prostaglandins, leukotrienes, platelet activating factor, inflammatory cytokines

21
New cards

leukocytosis

increased white blood cells

22
New cards

bands

immature form of neutrophil

23
New cards

eosinophils

parasitic infection and allergic reactions

24
New cards

basophils

contains histamine

  • binding of IgE triggers release

25
New cards

mast cells

degranulation releases histamine, TNF, IL-16

26
New cards

TNF (tumor necrosis factor)

hypotension, tachycardia associated with sepsis

27
New cards

vasodilation

induced by histamine and nitric oxide mediators

28
New cards

vascular phase

vasodilation, erythema (redness), warmth, edema (swelling)

29
New cards

edema

increased osmotic pressure causes fluid to move into tissues ad produce swelling

30
New cards

cellular stage

margination, chemotaxis, leukocyte activation and phagocytosis, etc.

31
New cards

margination

cytokines cause endothelial cells to express adhesion molecules (leukocyte accumulation to the endothelium)

32
New cards

chemotaxis

chemokines direct trafficking of leukocytes

33
New cards

leukocyte activation and phagocytosis

monocytes, neutrophils and tissue macrophages activated

34
New cards

phagocytosis

engulf and degrade bacterial and cellular debris

35
New cards

what do metabolic burst pathways do?

generates toxic oxygen and nitrogen products that requires oxygen

  • this kills the microbe

36
New cards

histamine and prostaglandins have?

vasoactive and smooth muscle constricting properties

37
New cards

plasma proteases

activate complement system, clotting cascade, kinin system

38
New cards

chemotactic factors

chemokines

39
New cards

reactive molecules and cytokines are liberated from?

leukocytes

40
New cards

histamine

  • found in mast and basophil cells

  • involved IgE antibodies

41
New cards

what cells are first to be released?

mast and basophil cells

42
New cards

histamine causes what?

dilation of vessels, sneezing, runny nose, eye tearing, sinusitis, increased permeability

43
New cards

arachidonic acid metabolites

release leads to production of prostaglandins, induces inflammation, potentiate effects histamine

44
New cards

arachidonic acid metabolites promote?

platelet aggregation and vasoconstriction

45
New cards

platelet- activating factor

induces platelet aggregation and causes bronchospasm

46
New cards

plasma proteins

clotting, complement and kinin systems

47
New cards

clotting

endothelial adhesion, production of PAF

48
New cards

complement

increases vascular permeability, causes vasodilation, improves phagocytosis

49
New cards

kinin

releases bradykinin, increases permeability, contraction of smooth muscle

50
New cards

cytokines

TNF, IL-1 released in response to bacterial toxins, endotoxins, fever, lowers BP

51
New cards

nitric oxide

smooth muscle relaxation; compensatory mechanism that reduces inflammation

52
New cards

free radicals

released during phagocytic process

53
New cards

chronic inflammation

reaction that persists for a prolonged time (weeks to months) without resolution

54
New cards

etiologic agent examples

mycobacterium tuberculi (TB) and treponema pallidum (syphilis)

55
New cards

nonspecific inflammation

non-targeted response

56
New cards

granulomatous inflammation

chronic inflammation often causes a granuloma where there is massing of macrophages surrounded by lymphocytes (1-2 mm lesion)

57
New cards

tuberculosis

prototypical granulomatous chronic inflammatory disease

58
New cards

systemic manifestations of inflammation

acute-phase response, alterations in WBC count, fever, lymph node reaction

59
New cards

lymphadenitis

aka lymphadenopathy; the enlargement of lymph nodes caused by inflammatory processes

60
New cards

where do lymphocytes mature?

in the lymph node; become enlarged and tender during inflammatory process

61
New cards

tissue repair

response to injury in attempt to maintain normal body structure and function

62
New cards

regeneration

injured cells replaced with cells of the same type

63
New cards

replacement

leaves a permanent scar when replaced with connective tissue

64
New cards

body cells involved in tissue regeneration

labile, stable, permanent cells

65
New cards

labile

continue to divide and replicate throughout life, replacing cells that are continually being destroyed (epithelial cells)

66
New cards

what are cancer cells considered as?

labile cells because they are constantly dividing

67
New cards

stable

normally stop dividing when growth ceases; capable of regeneration when confronted with appropriate stimulus (liver and kidney cells)

68
New cards

permanent cells

cannot undergo mitotic division (nerve cells, cardiac muscle cells)

69
New cards

fibrous tissue repair

severe or persistent injury-repair cannot be accomplished with regeneration alone

  • occurs by replacement with connective (granulation) tissue (scars)

70
New cards

granulation tissue

glistening red, moist connective tissue

  • contains new capillaries (angiogenesis) and fibroblasts (fibrogenesis)

71
New cards

phases of wound healing

inflammatory phase, proliferative phase, wound contraction and remodeling phase

72
New cards

inflammatory phase

blood clot forms at time of injury

  • migration of phagocytic WBC to wound site

  • neutrophils arrive first to ingest and remove bacteria and cellular debris

  • macrophages arrive 24 hours later (ingest cellular debris)

73
New cards

hemostasis

constriction, platelet aggregation, increased permeability

74
New cards

proliferative phase

building of new tissue to fill wound space

  • fibroblasts and epithelialization

75
New cards

fibroblast

a connective tissue cell that synthesizes and secretes collagen and other substances needed for wound healing

76
New cards

what do fibroblasts produce?

growth factors that induce angiogenesis

77
New cards

epithelialization

final stage that forms new surface layer during the proliferative phase

78
New cards

remodeling phase

begins approx. 3 weeks (up to 12 months) after injury

  • fibrous scar developed (increase in tensile strength and shrinks to become less visible)

  • decreased vascularity

  • collagen synthesis by fibroblasts

79
New cards

carefully sutured wounds have approx. ___% of strength of unwounded skin

70%

80
New cards

primary intention of wound healing

clean laceration (edges are well approximated)

  • easily brought together, no missing tissue

81
New cards

secondary intention of wound healing

larger wounds that have greater loss of tissue and contamination

82
New cards

factors involved in wound healing

malnutrition, blood flow, oxygen delivery, impaired inflammatory and immune responses, infection, wound separation, foreign bodies, bite wounds

83
New cards

effects of age on wound healing

neonates, children, older adults

84
New cards

neonates and children

  • greater capacity for repair

  • may lack reserves needed to properly heal (electrolytes, temperature, rapid spread of infection)

  • sufficient calories needed

85
New cards

neonates and children have immature?

immune systems

86
New cards

increased water content means?

epidermis at risk

87
New cards

older adults

  • decreased in dermal thickness

  • decline in collagen content

  • loss of elasticity

  • vulnerable to chronic wounds

88
New cards

inspect areas for redness after how many minutes in older adults?

30 minutes and perform position changes

89
New cards

less than 6 hours pressure

ulceration

90
New cards

braden scale

scale used to predict patientโ€™s risk of developing pressure injures

  • sensory perceptions, moisture, activity, mobility, nutrition, fraction shear