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Surgery I > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are Halsted’s Principles?

A 
Gentle tissue handling 
Meticulous Hemostasis 
Preservation of blood supply 
Strict aseptic technique 
Minimum tension 
Accurate tissue apposition 
Obliteration of dead space
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2
Q

What is the basic principle behind inflammation?

A

Protective immunovascular response of tissues to harmful stimuli to remove the initial cause of injury

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3
Q

What are the three most basic things involved in inflammation?

A

Immune cells + Blood vessels + Molecular mediators

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4
Q

What are the four physical signs of acute inflammation?

A

Rubor - Calor - Dolor - Tumor

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5
Q

What is the result of rubor, color, dolor, and tumor?

A

Loss of function

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6
Q

What are the four major acute vascular responses in inflammation?

A

Vasodilation
Increased vascular permeability
Stasis
Leukocyte extravasation

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7
Q

What is the behavior of the blood vessels at the beginning of an insult?

A

Immediate vasoconstriction followed by vasodilation

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8
Q

What are the stimulators for the initial vasocontriction with inflammation? (Four things)

A

Catcholamines + Serotonin + Prostaglandins + NE

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9
Q

How long does it take vasodilation to occur with acute inflammation?

A

Minutes

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10
Q

What happens with vasodilation in acute inflammation?

A

Capillary beds open = Increased blood flow = Local delivery of inflammatory mediators

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11
Q

What are two major factors that increase vascular permeability?

A

Histamine + Serotonin

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12
Q

What is the behavior of serum protein with acute inflammation?

A

Loss of serum protein
Decreased osmotic pressure
Increased blood viscosity

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13
Q

What occurs with edema in interstitial space?

A

Delivery of soluble factors

Localized pain + Loss of Function

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14
Q

What are the three major steps in leukocyte extravasation?

A

Margination + Adherence + Diapedesis/Transmigration

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15
Q

What is occurring during margination of leukocytes?

A

Weak cell to leukocyte interaction

Rolling along endothelium = to BF velocity

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16
Q

What is responsible for adherence of leukocytes to endothelium?

A

Integrins

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17
Q

What occurs during recruitment of a leukocyte?

A

Halts progression of leukocyte within circulation

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18
Q

What are the four major cellular components to inflammation?

A

Neutrophils + Mast cells + Macrophages + Lymphocytes

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19
Q

Which are the first migratory cells to arrive?

A

Neutrophils

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20
Q

What do neutrophils play a predominant role in?

A

Acute inflammation

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21
Q

What is it that neutrophils do?

A

Local killing + Degradation of bacterial macromolecules

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22
Q

How do neutrophils kill/degrade bacteria?

A

Phagocytosis + Superoxide radicals

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23
Q

Are neutrophils pro or anti inflammatory?

A

Pro

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24
Q

What pro-inflammatory cytokines do neutrophils produce?

A

IL-1 + IL-6 + TNF-a

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25
Q

How long do neutrophils last?

A

24 to 48 hours

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26
Q

What ends neutrophils?

A

Macrophages

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27
Q

What are the three big things macrophages play a role in?

A

Inflammatory response + Wound debridement + Tissue Repair

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28
Q

How do macrophages carry out debridement?

A

Phagocytosis

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29
Q

What do macrophages secrete that dissolve damaged tissue?

A

Collagenase + Elastase

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30
Q

Are macrophages pro or anti inflammatory?

A

Pro

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31
Q

What pro-inflammatory cytokines do macrophages secrete?

A

IL-1 + IL-6 + TNF-a

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32
Q

What cell type do macrophages stimulate to produce collagen?

A

Fibroblasts

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33
Q

What type of immunity are lymphocytes?

A

Acquired/Cell-mediated

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34
Q

What are two paths lymphocytes can take?

A

Cytotoxic + Helper

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35
Q

What is another name for helper T cells?

A

CD4

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36
Q

What is another name for cytotoxic T cells?

A

CD8

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37
Q

What are the two types of helper T cells?

A

TH-1 + TH-2

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38
Q

What is it that TH-1 cells do?

A

Maximize bacterial killing potential of macrophages

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39
Q

What is it that TH-2 cells do?

A

Helminth infections + Allergic reactions

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40
Q

What three basic things can stimulate mast cell degranulation?

A

Physical trauma
Completment factors
Microbial products

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41
Q

What is the major thing mast cells secrete?

A

Histamine

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42
Q

When is histamine released from mast cell? (physiological process)

A

Acute inflammation

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43
Q

Are mast cells pro or anti inflammatory?

A

Pro

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44
Q

What pro-inflammatory mediators do mast cells secrete?

A

Serotonin + Leukotrines + Heparin + Cytokines

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45
Q

What are the six categories of inflammatory mediators?

A 
Vasoactive amines 
Cytokines 
Lipid/cell membrane derived 
ROS 
Gaseous mediators 
Acute phase proteins
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46
Q

What are the two vasoactive amines?

A

Histamine + Serotonin

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47
Q

What are the important pro-inflammatory cytokines?

A

TNF-a + IL-1/6 + Chemokines

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48
Q

What are the important anti-inflammatory cytokines?

A

IL-10

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49
Q

What are the two major lipid membrane derived inflammatory mediators?

A

Eicosanoids + PAF

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50
Q

What are the two types of eicosanoids?

A

Prostaglandins + Leukotrienes

51
Q

What are the two ROS?

A

Hydroxyl radical + Superoxide anion

52
Q

What are the three gaseous mediators?

A

Nitric oxide + Carbon monoxide + Hydrogen sulfide

53
Q

What are negative APP?

54
Q

What are the positive APP?

A

C-reactive protein
Serum amyloid A
Complement proteins
Coagulation factors

55
Q

What releases Histamine?

A

Mast cells

56
Q

What does histamine do?

A

Arteriolar vasodilation
Increased venule permeability
Constriction of large arteries

57
Q

What cells does histamine attract?

A

Eosinophils

58
Q

What does histamine stimulate receptor wise?

A

Pruritic nociceptors

59
Q

What are two Anti-inflammatory mediators?

A

IL-10 + IL-1ra

60
Q

What is the major initiator of acute inflammation?

61
Q

What are the major structural characteristics of TNF-a?

A

Membrane-bound surface proteins

Anti-tumor activity

62
Q

What is TNF-a associated with in chronic diseases?

63
Q

What cytokine does TNF-a stimulate production of?

64
Q

What is a inflammatory process that TNF-a initiates?

A

Cell invasion at site of inflammation

65
Q

What, besides the cytokine, does TNF-a initiate?

A

ROS + Endothieal adhesion molecules

66
Q

What can inhibit the production of TNF-a?

67
Q

What is IL-1 produced by?

A

Macrophages (and others)

68
Q

What basic job does IL-1 have?

A

Mediates increases in other pro-inflammatory cytokines + prostaglandins + NO

69
Q

What four pathologies does IL-1 cause?

A

Hypotension
Leukopenia
Hemorrhage
Pulmonary Edema

70
Q

What is the counter regulatory function to IL-1?

71
Q

What does IL-1ra do?

A

Compete for space at the receptor site with IL-1

72
Q

What does IL-6 in the most basic sense?

A

Increase all inflammatory conditions

73
Q

What is IL-6 produced by?

A

Macrophages + T cells + Epithelial cells + Enterocytes

74
Q

What is important about IL-6 clinically?

A

Mediator + Diagnostic/Prognostic biomarker of inflammation, levels proportional to duration/severity of condition

75
Q

What is IL-10 in the most basic sense?

A

Anti-inflammatory cytokine

76
Q

What is IL-10 produced by?

A

TH-2 cells + Monocytes + B cells

77
Q

What does IL-10 depress the production of?

A

TNF-a + IL-1 + IL-6

78
Q

In a normal immune response what would the levels of IL-10 be in acute phase inflammation?

A

Low, will increase over time

79
Q

What category of disease is there commonly an IL-10 deficiency?

A

Chronic autoimmune diseases

80
Q

What is the fatty acid precursor to all eicosanoids?

A

Arachidonic acid

81
Q

Where is arachidonic acid stored?

A

Cells membranes of endothelial cells + Leukocytes + etc. k

82
Q

When is arachidonic acid released?

A

Stimulation but Phospholipase A2

83
Q

What are two things that arachidonic acid can be metabolized by?

A

Cyclooxygenase + Lipoxygenase

84
Q

What medication can decrease PLA2 production?

A

Corticosteriods

85
Q

What are the functions of prostaglandin?

A

Leukocyte recruitment
Vasodilation
Pain
Fever

86
Q

What are the functions of Leukotrienes?

A

Activate neutrophils

87
Q

What does activation of neutrophils entail?

A

Extravasation + Degranulation + Free-radical production

88
Q

What are the two cyclooxygenase pathways?

A

COX-1 and COX-2

89
Q

What medication works on the COX pathways?

90
Q

What is the major characteristic of COX-1?

A

Constitutively expressed

91
Q

What is the major characteristic of COX-2?

92
Q

What is important medically for control the LOX pathway?

93
Q

What are leukotrienes secreted by?

A

Leukocytes + Platlets + Endothelial cells

94
Q

What is platelet-activating factor metabolized by?

95
Q

What is PAF produced by?

A

Endothelial cells + Neutrophils + Platelets + Macrophages + Eosinophils

96
Q

What does PAF do?

A 
Stimulate Aracodonic Acid release 
Pro-inflammatory effects on neutrophils 
Platelet aggregation 
Degranulation + ROS production in EOS 
Vascular effects
97
Q

What are the vascular effects of PAF?

A

Vascular permeability
Bronchoconstriction
Pulmonary Vasoconstriction

98
Q

What are the PAF effects on neutrophils?

A

Enhanced Adhesion + Motility + Degranulation

99
Q

What are ROS?

A

Unstable molecules with unpaired electrons

100
Q

What are three important affects of ROS?

A

Antibacterial + Intercellular signaling + Tissue damage

101
Q

What are two examples of free radicals?

A

Hydroxyl radical + Superoxide anion

102
Q

What is an example of a non-free radical?

A

Hydrogen peroxide

103
Q

What is myeloperoxidase? Where is it found?

A

ROS generating enzyme found in NEU

Catalyzes Hypochlorous acid from H2O2

104
Q

What is NO synthesized from?

A

L-arginine by NO synthase

105
Q

What are the three forms of NO?

A

Endothelial-derived + Neuronal Derived + Inducible

106
Q

What cell types produce the inducible type of NO?

A

Hepatocytes + Keratinocytes + Macrophages + Neutrophils

107
Q

What conditions will upregulate NO?

A

Inflammatory

108
Q

What does NO do?

A

Regulation of vascular tone via smooth muscle relaxation = vasodilation

109
Q

How is CO produced in the body?

A

Enzymatic break down of heme to bilirubin by heme oxygenase

110
Q

When is heme oxygenase upregulated?

A

Inflammation

111
Q

When is hydrogen sulfide produced in the body?

A

Cysteine metabolism

112
Q

What is the function of hydrogen sulfide?

A

Regulates BP + Visceral analgesia

113
Q

Where do acute phase proteins come from?

114
Q

What are the cytokines that stimulate the production of ACP?

A

IL-6 + IL-1 + TNF-a

115
Q

What is the most basic function of positive ACP?

A

Minimize tissue damage and enhance repair processes after infection/trauma/stress

116
Q

What are the outcomes of inflammation?

A 
Resolution 
Systemic Inflammation 
Multiple Organ Failure 
Immunosupression 
Chronic Inflammation
117
Q

What is occurring during resolution?

A

Decreased NEU recruitment
Increased mononuclear cell infiltration
Macrophages undergo apoptosis
Pro to anti inflammatory factors

118
Q

What is systemic inflammatory response syndrome?

A

Imbalance of inflammatory mediators = inflammation throughout the body

119
Q

What are some of the signs of SIRS?

A

Changes in Temp + HR + BP + RR + WBC

120
Q

What else needs to occur with SIRS for it to be considered sepsis?

121
Q

When can inflammation lead to immunosuppression?

A

Overwhelming anti-inflammatory response

122
Q

What cell change occurs with chronic inflammation?

A

Fibroblasts –> Myofibroblasts

123
Q

What are the basic characteristics of myofibroblasts?

A

Increased collagen production + Fibrosis

Surgery I (17 decks)

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