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CV Perf Tech II > Immune Response & Inflammation (Part 2)-Exam 3 > Flashcards

Immune Response & Inflammation (Part 2)-Exam 3 Flashcards

1
Q

What type of a response is inflammation?

A

Non-specific; response to a cute is the same as a burn/radiation/infection, etc.

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2
Q

What are some causes of tissue damage?

A

Pathogens, abrasions, chemical irritations, distortion/cell disturbance, extreme temps

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3
Q

How does the body response to tissue damage?

A

Inflammation

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4
Q

What are 4 signs of inflammation?

A

Redness
Pain
Heat
Swelling

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5
Q

What is the goal of inflammation?

A

To dispose of microbes/ toxins/ foreign materials; prevents the spread, prepares for repair (restores homeostasis)

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6
Q

Where does inflammation occur?

A

At the sight of injury

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7
Q

What are the 3 stages of inflammation?

A
  1. Vasodilation: Increases permeability of blood vessels
  2. Emigration: Movement of phagocytes from blood to interstitial fluid
  3. Tissue repair
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8
Q

What is the purpose of increased permeability?

A

Allows antibodies and clotting factors to leave the blood

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9
Q

What is the purpose of vasodilation?

A

Allows more blood into an area

Helps remove microbial toxins and dead cells

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10
Q

What are some factors that cause vasodilation and increased permeability?

A

Histamine, Kinins, prostaglandins, leukotriens, complement

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11
Q

What cells release histamine?

A

Mast cells

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12
Q

What simulate the release of histamine in the blood?

A

Basophils and platelets

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13
Q

What does histamine cause?

A

Dilation and increased permeability

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14
Q

What are kinins? What do they do?

A

Polypeptides; induce vasodilation and increase permeability; act as chemotaxic agent phagocytes

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15
Q

What’s an example of a kinin?

A

Bradykinin

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16
Q

What are prostaglandins? What releases them? What do they stimulate?

A

Lipids, released by damaged cells, stimulate emigration of phagocytes

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17
Q

What are leukotrienes? What do they do?

A

Basophils and mast cells produce; increase permeability

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18
Q

What does complement do?

A

Stimulate histamine release, attract neutrophils, promote phagocytosis

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19
Q

What do clotting factors moving into the tissues initiate?

A

Clotting Cascade; fibrinogen converted to fibrin and forms fibrin mesh

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20
Q

What is the function of the fibrin mesh?

A

Localizes and traps invading organisms; blocks the spread of organism

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21
Q

How long after the start of the inflammatory process of phagocytes start to appear?

A

Phagocytes appear

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22
Q

What do neutrophils do during inflammation?

A

Stick to the blood vessel wall with increased blood flow; squeeze through blood vessel wall to tissues “emigration”
Depends on chemotaxis

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23
Q

Neutrophils attempt to destroy via what process?

A

Phagocytosis

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24
Q

What cells follow neutrophils? What do they transform into?

A

Monocytes; transform into macrophages

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25
Q

Which is a more potent phagocyte: neutrophils or macrophages?

A

Macrophages are more potent phagocytes than neutrophils; macrophages eventually die

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26
Q

What is left behind when macrophages die?

A

Dead cells and fluid (pus)

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27
Q

What are 4 signs of inflammation due to vasodilation and increased permeability?

A

Heat, redness, swelling, pain

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28
Q

Why is there redness in inflammation?

A

Large amount of blood in damaged area
Local temperatures increase
Metabolic reactions speed up
More heat is released

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29
Q

What is associated with swelling?

A

Increased permeability, more fluid in the area

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30
Q

Why is there pain during inflammation?

A

Neuron injury or increased pressure (edema)

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31
Q

What causes fever?

A

Bacteria toxin increases body temperature; trigger release of interleukin-1

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32
Q

What does fever help do?

A

Inhibit the growth of some microbes, helps to speed up body reactions, aids in repair

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33
Q

What are the two major components of the complex reaction to injurious agents associated with inflammation?

A

Vascular reaction

Cellular reaction

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34
Q

Acute response

A

Rapid onset; short duration, emigration of neutrophils

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35
Q

Chronic response

A

Long duration, lymphocyte involvement, proliferation of blood vessels, tissue necrosis

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36
Q

What cells are involved in inflammation?

A

Circulating White Cells ( and plts)
Connective tissue cells
extracellular matrix

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37
Q

What are some examples of connective tissue cells?

A

Mast cells (surround blood vessels)
Fibroblasts
Macrophages
Lymphocytes

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38
Q

What is in the extracellular matrix?

A

Structural fibrous protein (collagen, elastin)
Adhesive glycoproteins
Proteoglycans
Basement membrane of capillary

39
Q

What chemical factors mediate inflammation?

A

Derived from plasma proteins and/or cells

Produced in response to or activated by inflammation

40
Q

Where does the acute inflammation response deliver mediators? What mediators?

A

Delivers mediators of host defense to site of injury (leukocytes/plasma proteins)

41
Q

What are the components of acute inflammation?

A

Dilation of capillaries and vessels- increase BF
Structural changes in capillaries- allow plasma proteins and leukocytes to enter interstitial space
Emigration of leukocytes from capillaries where they accumulate in focus of injury- activation to eliminate offending agent

42
Q

What are the stimuli for acute inflammation?

A 
Infections and microbial toxins 
Trauma
Physical and chemical agents
Tissue necrosis
Foreign bodies
Immune reactions
43
Q

What are some examples of microbial toxins?

A

Bacterial, viral, parasitic

44
Q

What are some physical and chemical agents that stimulate acute inflammation?

A

Thermal injury (burns, frostbite)
Irradiation
Environmental chemicals

45
Q

What are some foreign bodies that are stimuli for acute inflammation?

A

Splinters
Dirt
Sutures

46
Q

What is the purpose of vascular changes?

A

Maximize movement of plasma proteins and appropriate circulating cells into the site of injury or infection

47
Q

How does the body create vascular changes?

A

Vasodilation

Increased capillary permeability

48
Q

What is the early manifestation of vascular changes?

A

Vasodilation

49
Q

What vasodilates first? Followed by what?

A

Arterioles involved first, followed by opening of new capillary beds

50
Q

What induces vasodilation?

A

Variety of mediators (histamine/ nitric oxide)

51
Q

What is the result of vasodilation?

A

Increased BF which increased redness and warmth of tissue

52
Q

What does increased capillary permeability result in on the capillary level?

A

Movement of protein rich fluid into extravascular tissue and concentration of RBCs (viscosity change)

Physical changes in endothelial structure of capillaries

53
Q

What is the result of capillary permeability (big picture)?

A

Osmotic and hemodynamic change force fluid into interstitial space (results stasis)
neutrophils begin adhering to endothelium and moving into interstitial space
Physical openings in endothelium allow more fluid/protein/cells to migrate

54
Q

What is extravasation?

A

Movement of leukocytes from vessel lumen to interstitial space

55
Q

Margination

A

movement of leukocytes toward the wall of the capillary

56
Q

Rolling

A

leukocytes tumble slowly along endothelium, adhere transiently, then are finally attached, endothelium completely lines with white cells

57
Q

Transmigration (diapedesis)

A

insert pseudopods into junctions between endothelial cells; move through the junction

58
Q

Chemotaxis

A

migrate through interstitial fluid to source of problem; locomotion along chemical gradient

59
Q

What are the most common exogenous agents of chemotaxis?

A

Bacterial products

60
Q

What are the most common endogenous agents?

A

Components of complement (C5a)
Products of lipoxygenase pathway (leukotriene B4)
cytokines

61
Q

What is leukocyte activation induced by?

A

Microbes, products necrotic cells, antigen-antibody complexes, cytokines

62
Q

What are the results of leukocyte activation?

A

Production of arachidonic acid metabolites
Degrannulation and secretion of lysosomal enzymes
Secretion of cytokines
Modulation of surface receptors
Phagocytosis

63
Q

What do chemical mediators originate from?

A

Plasma or cells

  • Plasma derived must be activated
  • Cell-derived usually stored in intracellular granules
64
Q

What is the production of active mediators triggered by?

A

Microbial products or host proteins (complement, etc.)

65
Q

Where do chemical mediators usually bind?

A

Specific receptors on target cells

66
Q

What could one mediator stimulate?

A

The release of other mediators; mediators can also act on more than one target

67
Q

Once a chemical mediator is activated and released, how long do most live?

A

Most are short-lived; most have the potential to do great harm

68
Q

What are mediators/sources of preformed mediators in secretory granules?

A

Histamine- mast cells, basophils, platelets
Serotonin- platelets
Lysosomal enzymes- neutrophils, macrophages

69
Q

What are newly synthesized mediators and sources?

A

Prostaglandins (all leukocytes, plts, EC)
Leukotrienes (All leukocytes)
Plt-activating facotrs (All leukocytes, EC)
Activated oxygen species (all leukocytes)
Nitric oxide (macrophages)
Cytokines (lymphocytes, macrophages, EC)

70
Q

What mediators are involved in vasodilation?

A

Prostaglandins
Nitric Oxide
Histamine

71
Q

What mediators are involved in increased vascular permeability?

A 
Vasoactive amines
C3a and C5a (through liberating amines)
Bradykinin
Leukotrienes C4, D4, E4
PAF
Substance P
72
Q

What mediators are involved in chemotaxis,leukocyte recruitment and activation?

A 
C5a
Leukotriene B4
Chemokines
IL-1, TNF
Bacterial products
73
Q

What mediators are involved in fever?

A

IL-1, TNF

Prostagladins

74
Q

What mediators are involved in pain?

A

Prostaglandins

Bradykinin

75
Q

What mediators are involved in tissue damage?

A

Neutrophil and macrophage lysosomal enzymes
Oxygen metabolites
Nitric oxide

76
Q

SIRS

A

systemic inflammatory response syndrome

77
Q

What is SIRS?

A

Common systemic response to a wide variety of insults

78
Q

2 or more of this list must be present for diagnosis of SIRS

A
  1. Body temp above 38C or below 36C
  2. HR > 90 BPM
  3. RR >20 /min or PaCO2 < 32 mmHg
  4. Leukocyte count > 12,000 cell/mm^2
    (or < 4000 cells/mm^3)
    (or present of < 10% immature neutrophils)
79
Q

SIRAB

A

Systemic inflammatory response after bypass

80
Q

Wide spectrum of injuries for SIRAB

A

Pulmonary, Renal, Gut, CNS, Myocardial Dysfunction, Coagulopathy, Hemolysis, fever, increase susceptibility to infection, Leukocytosis

81
Q

Who gets SIRS?

A

Widely accepted that SIRS is induced in all patients undergoing bypass

82
Q

What is the incidence and severity of SIRS?

A

Variable; most have few clinical symptoms. Minority develop severe hemodynamic changes or organ failure after bypass

83
Q

What is the response of patients to bypass?

A

Degree of response is not predictable nor type of response.

84
Q

What is a risk factor for SIRAB?

A

Length of CPB; frequently a risk factor but not necessarily

85
Q

What does SIRAB set into motion?

A

Cytokine mediated events that activate vascular endothelium; allow further neutrophil mediated inflammatory injury

86
Q

What is the most common culprit of SIRAB?

A

Contact with foreign surfaces

87
Q

What are other factors of developing SIRAB?

A 
Altered arterial blood flow patterns
Shear stress (blood pumps)
Cardiotomy suction
Tissue ischemia
Reperfusion
Hypothermia
Relative anemia
anticoagulants (low temps, blood more viscous)
88
Q

What is relative anemia?

A

Accepting a lower HCT on bypass; better for out circuit

89
Q

What is involved in contact activation in developing SIRAB?

A

ECC (coated?)

Activation of contact proteins (XII, XI, prekallikrein, HMWK)

90
Q

What is the end result of SIRAB?

A

Formation of bradykinin
Conversion of plasminogen into plasmin
Initiates fibrinolysis
Triggers classical complement cascade

91
Q

What does exposure to ECC result in?

A

Multiple inflammatory mediators released
Disrupts homeostasis
Generalized whole inflammatory response
Stimulate or catalyze other reactions in cycle of SIRAB

92
Q

What is the general whole inflammatory response mediated by?

A

Chemokine mediated; activates vascular endothelium, further neutrophil-mediate injury

93
Q

What happens to patients post operatively?

A

Pts more susceptible to infections
Serum immunoglobulins/complement decreased
Chemotaxis ability of granulocytes decreased
Natural killer cells decreased (#/fcn)
CD3+/CD4+ cells decreased
CD8 + cells slightly increased
Leukocyte number remains low for about 1 week post bypass

CV Perf Tech II (17 decks)

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