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Pathophysiology > 6. Innate Immunity: Inflammation & Wound Healing > Flashcards

6. Innate Immunity: Inflammation & Wound Healing Flashcards

1
Q

Lines of defense (3)

A
  • 1st: innate (natura/native) immunity - 2nd: inflammation - 3rd: adaptive (acquired) immunity
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2
Q

What 3 things are part of innate immunity?

A
  • physical barriers - epithelial cell-derived chemicals - normal microbiome
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3
Q

What organ systems are lined w/ physical barriers?

A

the GI, genitourinary, and respiratory tracts

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4
Q

List 5 chemical barriers that are part of the innate immune system

A
  • saliva - tears - ear wax - sweat - mucus
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5
Q

What major problem can occur to the skin? What problems will this cause?

A

skin burns -> cause problems w/ infection and hydration

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6
Q

What can happen if you lose your normal microbiome? List 2 examples.

A

other bacteria can overgrow; yeast in the vagina and clostridium deficile in the intestines (pseudomembranous colitis)

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7
Q

What is the treatment for Cdiff?

A

Oral flagyl and vancomycin or stool transplant if antibiotics don’t work

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8
Q

List 4 characteristics of the inflammatory response

A
  • occurs in vascularized tissues - activates rapidly (in seconds) after damage occurs - depends on activity of both cellular and chemical components - nonspecific
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9
Q

At the beginning of the inflammatory reaction, what are 3 vascular responses that occur?

A
  • vasodilation - increased vascular permeability - WBC adherence to the inner walls of vessels and migration through vessels
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10
Q

List 4 goals of inflammation

A
  • limit and control inflammatory process - prevent/limit infection and further damage - initiate adaptive immune response - initiate healing
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11
Q

What causes edema at the site of injury?

A

increased vascular permeability -> plasma proteins leak from capillary bed -> oncotic pressure -> fluid will follow protein out of capillary -> edema

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12
Q

Who are the 1st and 2nd responders at a site of inflammation?

A

1st responder: neutrophil 2nd responder: macrophage (from monocyte)

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13
Q

What 3 things occur in response to cellular injury and/or pathogenic invasion (infection)?

A
  • mast cell degranulation - activation of plasma systems - release of cellular products
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14
Q

List the 3 plasma systems

A
  • complement - clotting - kinin
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15
Q

Symptoms of acute inflammatory response and causes?

A
  • vasodilation (erythema/warmth) - vascular permeability (edema) - cellular infiltration (pus) - thrombosis (clots) -> helps encapsulate bacteria - stimulation of nerve endings by kinin (pain)
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16
Q

cells filled w/ granules and located in loose connective tissue close to blood vessels

A

mast cells

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17
Q

2 ways mast cells release chemicals

A

degranulation (immediate) and synthesis (delayed)

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18
Q

What 3 types of granules are released by mast cells?

A
  • histamine - chemotactic factor for neutrophils - chemotactic factor for eosinophils
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19
Q

List 3 mediators synthesized by mast cells

A
  • platelet activating factor (PAF) - prostaglandins - leukotrienes
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20
Q

Function of PAF

A

platelet activation and vasodilation

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21
Q

Function of prostaglandins

A

increased vascular permeability, neutrophil chemotaxis, and pain

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22
Q

Function of leukotrienes

A

smooth muscle contraction, increased vascular permeability

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23
Q

Ex. of leukotriene inhibitor

A

Singulair

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24
Q

Ex. of prostaglandin inhibitor (inhibits enzyme for production)

A

Ibuprofen

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25
Q

Explain histamine’s function after being released from mast cells

A

vasoactive: temporary rapid constriction of large blood vessels and dilation of post-capillary venues; retraction of endothelial cells lining capillaries (junctions)

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26
Q

Which receptor is pro- inflammatory and anti-inflammatory for histamine?

A

H1 - pro H2 - anti

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27
Q

Where are H2 receptors abundant and what will activating them cause?

A

parietal cells of gastric mucosa -> activation via histamine will cause secretion of gastric acid

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28
Q

Explain the compliment system

A
  • C3 -> C3b + C3a - C3b -> C5 -> C5b + C5a - C5b -> C6-9 -> membrane attack complex - MAC forms pores in pathogen membrane to damage it
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29
Q

What in the compliment system creates opsonin? What is the function of opsonin?

A
  • C3b - coats surface of bacteria and increases their susceptibility to phagocytosis
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30
Q

potent anaphylatoxin in the compliment system -> mass cell release of histamine

A

C3a

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31
Q

Anaphylatoxin and chemotactic factor in compliment system -> leukocyte (neutrophil) migration

A

C5a

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32
Q

main protein in a blood clot

A

fibrin

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33
Q

3 functions of clots

A
  • plug damaged vessels and stop bleeding - trap microorganisms and prevent spread to other tissues - provide framework for future repair/healing
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34
Q

What activates the extrinsic pathway of the clotting system?

A

tissue factor (TF) - released by damaged endothelial cells in blood vessels (external trauma)

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35
Q

What activates the internal pathway of the clotting system?

A

activated when the vessel wall is damaged (trauma inside the blood vessels)

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36
Q
  • Factor unique to extrinsic pathway - Factor unique to intrinsic pathway - Factor activated by both pathways
A
  • Extrinsic: VIIa - Intrinsic: XII (Hageman Factor) -> XIIa - Both: Xa
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37
Q

Describe the common pathway of the clotting cascade

A

Xa -> thrombin -> fibrinogen -> fibrin -> blood clot

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38
Q

functions to activate and assist inflammatory cells; interacts closely w/ coagulation system

A

Kinin system

39
Q

Primary kinin

A

bradykinin

40
Q

What activates the kinin system?

A

activation of Hageman factor (XII) to XIIa (aka prekallikrein)

41
Q

Functions of bradykinin

A
  • vasodilation (like histamine) - induce pain (w/ prostaglandins) - smooth muscle contraction - increase vascular permeability - leukocyte chemotaxis
42
Q

Cytokines that cause vasodilation (3)

A
  • prostaglandins - histamine - NO
43
Q

Cytokines that cause vascular permeability (4)

A
  • histamine - bradykinin - leukotrienes - PAF
44
Q

Cytokines that cause pain (2)

A
  • prostaglandins - bradykinin
45
Q

Cytokines that cause fever (4)

A
  • IL-1 - IL-6 - TNF-a - prostaglandins
46
Q

Cytokines that activate leukocytes (2)

A
  • IL-1 - TNF-a
47
Q

Cytokines that activate mast cells and eosinophils (2)

A
  • IL-4 - IL-5
48
Q

List acute phase reactants (5)

A

IL-1, IL-6, IL-8, TNF-a, and C-reactive protein

49
Q

What does C-reactive protein tell about inflammation

A

global test for inflammation (doesn’t tell cause or location; only that it exists)

50
Q

Normal WBC count

A

5,000-10,000

51
Q

increased neutrophils?

A

acute bacteria/acute inflammation

52
Q

increased lymphocytes?

A

vital infection/chronic bacterial infection

53
Q

increased monocytes?

A

inflammation

54
Q

increased basophils?

A

allergic reaction

55
Q

increased eosinophils?

A

parasitic infection

56
Q

3 types of granulocytes

A
  • basophils - eosinophils - neutrophils
57
Q

type of innate lymphocyte

A

natural killer cell (NK cell)

58
Q

5 types of WBC found on differential

A
  • lymphocyte - monocyte - neutrophil - basophil - eosinophil
59
Q

How do cytokines limit inflammation?

A
  • inhibit production - inhibit macrophage proliferation - destroy histamine and leukotrienes
60
Q

How do cytokines help w/ repair and healing?

A
  • activate macrophages - stimulate fibroblast growth - stimulate endothelial growth
61
Q

Explain VEGF function and how it relates to cancer and chemo

A
  • VEGF is angiogenic -> vascular growth - found in some cancers to help them develop blood supply - some chemo targets this -> will also delay healing
62
Q

What does the erythrocyte sedimentation rate test?

A

how fast RBCs settle at the bottom of the test tube -> faster may mean inflammation

63
Q

How do cytokines help w/ phagocytosis?

A
  • adherence and diapedesis - chemotaxis - opsonins - activate and increase macrophages
64
Q

Type I interferons (IFN)

A

INF-a and INF-b

65
Q

What causes production of type I interferons? What do these IFNs do?

A

produced and released by virally infected cells in response to double stranded RNA -> induce production of antiviral proteins

66
Q

Type II interferon (IFN)

A

IFN-y

67
Q

What produces INF-y and what does IFN-y do in response?

A

produced primarily by lymphocytes -> activates macrophages -> increased killing activity by macrophages

68
Q

What produces interleukins (IL)?

A

primarily macrophages and lymphocytes in response to a pathogen or stimulation by other cytokines

69
Q

IL that is pro inflammatory an endogenous pyrogen (causes fever)

A

IL-1

70
Q

IL that directly induces hepatocytes to produce proteins needed for inflammation and stimulate differentiation and growth of BM cells

A

IL-6

71
Q

List 3 systemic effects of TNF-a

A
  • induces fever (endogenous pyrogen) - increased synthesis of inflammation proteins by liver - muscle wasting (cachexia) and intravascular thrombosis in cases of severe infection/cancer
72
Q

What IL is anti-inflammatory?

A

IL-10

73
Q

What cells secrete TNF-a?

A

macrophages

74
Q

attract leukocytes to site of inflammation?

A

chemokines

75
Q

What activates platelets and what does their activation lead to?

A

activated by tissue destruction/inflammation -> leads to interaction w/ clotting cascade

76
Q

macrophages that predominate in early inflammation and become a component of purulent exudate

A

neutrophils (PMNs)

77
Q

Life cycle of monocytes

A

produced in the BM -> travel to site of inflammation about 24 hours after neutrophils -> develop into macrophages

78
Q

defense against parasites and regulation of vascular mediators

A

eosinophils

79
Q

primary phagocytic cells located in the peripheral organs and skin -> migrate though lymphatics to lymph nodes to interact w/ T cells

A

Dendritic cells

80
Q

adherence of leukocytes to endothelial cells

A

margination

81
Q

emigration of cells through endothelial junctions

A

diapedesis

82
Q

protein filled watery exudate that indicates early inflammation

A

serous

83
Q

thick, clotted exudate -> indicates more advanced inflammation

A

fibrinous

84
Q

pus filled exudate that indicates bacterial infection or inflammation (supperative)

A

purulent

85
Q

2 types of exudate that indicate bleeding

A

serosanguinous and sanguinous

86
Q

3 systemic manifestations of acute inflammation

A
  • fever - leukocytosis - increased plasma protein synthesis (ex. CRP, fibrinogen, amyloid etc.)
87
Q

causes of chronic inflammation (5)

A
  • unsuccessful acute inflammation - high lipid/wax content of microorganisms - ability to survive in macrophage - toxins - chemical or physical irritants
88
Q

bacteria circulating in the blood

A

bacteremia

89
Q

presence and multiplication of bacteria in the blood

A

septicemia

90
Q

Explain what happens intracellular after phagocytosis

A

phagosome (carrying microbe) fuses w/ a lysosome (digestive enzymes) -> creates phagolysosome (kill and digest microbes)

91
Q

Risks that lead to dysfunctional wound healing

A
  • hemorrhage - fibrous adhesion - hypovolemia - lack of nutrients - poor control of glucose levels - infection
92
Q

raised scar from original skin level (4mm above skin)

A

keloid scar

93
Q

scar that is larger than it should be

A

hypertrophic

94
Q

Reasons why inflammation is less in older adults

A
  • impaired function phagocytes - impaired inflammation due to chronic illness - chronic medication intake reduces inflammation response

Pathophysiology (20 decks)

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