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My Pathoma > CH2 - Inflammation, Inflammatory Disorders, and Wound Healing > Flashcards

CH2 - Inflammation, Inflammatory Disorders, and Wound Healing Flashcards

1
Q

What does inflammation allow?

A

Allows inflammatory cells, plasma proteins (e.g., complement), and fluid to exit blood vessels and enter the interstitial space

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2
Q

Inflammation is divided into what?

A

Divided into acute and chronic inflammation

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3
Q

What is inflammation characterized by?

A

the presence of edema and neutrophils in tissue

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4
Q

Inflammation arises in response to what?

A

infection (to eliminate pathogen) or tissue necrosis (to clear necrotic debris)

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5
Q

innate immunity

A

Immediate response with limited specificity

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6
Q

What are the mediators of acute inflammation?

A

Toll-like receptors, Arachidonic acid (AA) metabolites, Mast cells, Complement, Hageman Factor

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7
Q

Toll-like receptors

A

Present on cells of the innate immune system (e.g., macrophages and dendritic cells)

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8
Q

How are TLRs attivated?

A

pathogen-associated molecular patterns (PAMPs) that are commonly shared by microbes, CD14 (a TLR) on macrophages recognizes lipopolysaccharide (a PAMP) on the outer membrane of gram-negative bacteria

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9
Q

TLR activation results in what?

A

upregulation of NF-kB, a nuclear transcription factor

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10
Q

What does NF-kB do?

A

activates immune response genes leading to production of multiple immune mediators

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11
Q

TLRs and chronic inflammation?

A

They are also present on cells of adaptive immunity (e.g., lymphocytes) and play an important role in mediating chronic inflammation.

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12
Q

Arachidonic acid (AA) metabolites

A
  1. AA is released from the phospholipid cell membrane by phospholipase A2 and then acted upon by cyclooxygenase or 5-lipoxygenase.
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13
Q

Cyclooxygenase

A

produces prostaglandins (PG) a. PGI2, PGD2 and PGE2 mediate vasodilation and increased vascular permeability. PGE2 also mediates pain.

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14
Q

5-lipoxygenase

A

produces leukotrienes (LT) a. LTB4 attracts and activates neutrophils. b. LTC4, LTD4 and LTE4 (slow reacting substances of anaphylaxis) mediate vasoconstriction, broncho spasm, and increased vascular permeability.

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15
Q

Where are Mast cells located?

A
  1. Widely distributed throughout connective tissue
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16
Q

How are Mast cells activated?

A

(1) tissue trauma (2) complement proteins C3a and C5a (3) cross-linking of cell-surface IgE by antigen

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17
Q

Mast cells immediate response is?

A

involves the release of preformed histamine granules, which mediate vasodilation of arterioles and increased vascular permeability

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18
Q

Mast cells delayed response is?

A

involves production of arachidonic acid metabolites, particularly leukotrienes.

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19
Q

Complement

A

proinflammatory serum proteins that complement inflammation

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20
Q

Where is complement located?

A

Circulate as inactive precursors;

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21
Q

Activation of complement occurs via what?

A

Classical pathway, Alternative pathway, MBL pathway

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22
Q

Classical pathway

A

C1 binds IgG or IgM that is bound to antigen

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23
Q

Alternative pathway

A

Microbial products directly activate complement.

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24
Q

Mannose binding lectin pathway

A

mannose binding lectin (MBL) pathway MBL binds to mannose on microorganisms and activates complement

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25
Q

All pathways of complement result in?

A

production of C3 convertase (mediates C3?>C3a and C3b, producing C5 convertase (mediates C5?>C5a and C5b)

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26
Q

What forms the MAC?

A

C5b complexes with C6-C9 to form the membrane attack complex (MAC)

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27
Q

C5a

A

chemotactic for neutrophils

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28
Q

C5b

A

opsonin for phagocytosis

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29
Q

MAC

A

Lyses microbes by creating a hole in the cell membrane

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30
Q

Where is Hageman factor (Factor XII) produced?

A

Inactive proinflammatory protein produced in liver

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31
Q

How is Hageman factor (Factor XII)?

A

Activated upon exposure to subendothelial or tissue collagen;

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32
Q

Hageman factor (Factor XII) activates what?

A
  1. Coagulation and fibrinolytic systems 2. Complement 3. Kinin system
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33
Q

Kinin system

A

Kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin, which mediates vasodilation and increased vascular permeability (simitar to histamine), as well as pain.

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34
Q

What are the cardinal signs of inflammation?

A

Redness (rubor) and warmth (calor), swelling, pain, fever

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35
Q

What is Redness (rubor) and warmth (calor) due to?

A
  1. Due to vasodilation, which results in increased blood flow
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36
Q

How does Redness (rubor) and warmth (calor) occur?

A

Occurs via relaxation of arteriolar smooth muscle;

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37
Q

Key mediators of Redness (rubor) and warmth (calor) are?

A

histamine, prostaglandins, and bradykinin

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38
Q

Swelling (tumor) is due to what?

A

Due to the leakage of fluid from postcapillary venules into the interstitial space (exudate)

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39
Q

What are the Key mediators of swelling?

A

(1) histamine, which causes endothelial cell contraction and (2) tissue damage, resulting in endothelial cell disruption,

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40
Q

Pain (dolor)

A

Bradvkinin and PGE2 sensitize sensory nerve endings.

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41
Q

Fever

A
  1. Pyrogens (e.g., LPS from bacteria) cause macrophages to release IL-1 and TNF, which increase cyclooxygenase activity in perivascular cells of the hypothalamus, 2. Increased PGE2 raises temperature set point.
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42
Q

What are the steps in neutrophil arrival?

A

Margination, Rolling, Adhesion, Transmigration and Chemotaxis, Phagocytosis, Destruction of phagocytosed material, resolution

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43
Q

Step 1?Marginatum

A
  1. Vasodilation slows blood flow in postcapillary venules. 2. Cells marginate from center of flow to the periphery.
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44
Q

Step 2?Rolling

A
  1. Selectin speed bumps are upregulaled on endothelial cells. 2. Selectins bind sialyl Lewis X on leukocytes. 3. Interaction results in rolling of leukocytes along vessel wall
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45
Q

P-selectin is released from where and what does it mediate?

A

release from Weibel Palade bodies, is mediated by histamine.

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46
Q

E-selectin is induced by what?

A

TNF and IL-1.

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47
Q

Step 3?Adhesion

A
  1. Cellular adhesion molecules (ICAM and VCAM) are upregulated on endothelium by TNF and IL-1 2. Integrins are upregulated on leukocytes by C5a and LTB4 3. Interaction between CAMs and integrins results in firm adhesion of leukocytes to the vessel wall
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48
Q

Step 4?Transmigration and Chemotaxis

A
  1. Leukocytes transmigrate across the endothelium of postcapillary venules and move toward chemical attractants (chemotaxis).
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49
Q

Neutrophils are attracted by

A

bacterial products, IL-8, C5a, and LTB4

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50
Q

Step 5?Phagocytosis

A
  1. Consumption of pathogens or necrotic tissue; phagocytosis is enhanced by opsonins (IgG and C3a). 2. Pseudopods extend from leukocytes to form phagosomes, which are internalized and merge with lysosomes to produce phagolysosomes.
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51
Q

Step 6?Destruction of phagocytosed material

A
  1. O2-dependent killing is the most effective mechanism. 2. HOCl generated by oxidative burst in phagolysosomes destroys phagocytosed microbes.
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52
Q

Step 7?Resolution

A

Neutrophils undergo apoptosis and disappear within 24 hours after resolution of the inflammatory stimulus.

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53
Q

Macrophages

A

Macrophages predominate after neutrophils and peak 2-3 days after inflammation begins.

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54
Q

What are macrophages derived from?

A

monocytes in blood

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55
Q

How do macrophages arrive in tissue?

A

via the margination, rolling, adhesion, and transmigration sequence

56
Q

What do macrophages do?

A

Ingest organisms via phagocytosis (augmented by opsonins) and destroy phagocytosed material using enzymes (e.g., lysozyme) in secondary granules (02-independent killing)

57
Q

What are the outcomes for macrophages managing the next step of the inflammatory process?

A

Resolution and healing, 2. Continued acute inflammation, Abscess, Chronic inflammation

58
Q

Macrophages induce Resolution and healing by?

A

Anti-inflammatory cytokines (1L-10 and TGF-(Beta) are produced by macrophages.

59
Q

Macrophages induce Continued acute inflammation by?

A

persistent pus formation; IL-8 from macrophages recruits additional neutrophils.

60
Q

Macrophages induce Abscess by?

A

acute inflammation surrounded by fibrosis; macrophages mediate fibrosis via fibrogenic growth factors and cytokines.

61
Q

Macrophages induce chronic inflammation by?

A

Macrophages present antigen to activate CD4+ helper T cells, which secrete cytokines that promote chronic inflammation

62
Q

Chronic inflammation is characterized by?

A

presence of lymphocytes and plasma cells in tissue, its a delayed response but more specific (adaptive immunity) than acute inflammation

63
Q

Chronic inflammation stimuli include

A

(1) persistent infection (most common cause); (2) infection with viruses, mycobacteria, parasites, and fungi; (3) autoimmune disease; (4) foreign material; and (5) some cancers.

64
Q

What is granulomatous inflammation?

A

Subtype of chronic inflammation, Characterized by granuloma, which is a collection of epithelioid histiocytes

65
Q

What are epithelioid histiocytes?

A

macrophages with abundant pink cytoplasm, usually surrounded by giant cells and a rim of lymphocytes

66
Q

What is granulomatous inflammation divided into?

A

noncaseating and caseating subtypes

67
Q

What is noncaseating granulomas?

A

lack central necrosis

68
Q

Common etiologies for noncaseating granulomas?

A

include reaction to foreign material, sarcoidosis, beryllium exposure, Crohn disease, and cat scratch disease,

69
Q

Caseating granulomas

A

exhibit central necrosis and are characteristic of tuberculosis and fungal infections

70
Q

What are the seps involved in granuloma formation?

A
  1. Macrophages process and present antigen via MHC class II to CD4+ helper T cells. 2. Interaction leads macrophages to secrete IL-12, inducing CD4+ helper T cells to differentiate into THl subtype. 3. TH1 cells secrete IFN-y, which converts macrophages to epithelioid histiocytes and giant cells.
71
Q

What is DiGeorge Syndrome?

A

Developmental failure of the third and fourth pharyngeal pouches

72
Q

What is DiGeorge Syndrome?

A

Due to 22qll microdeletion

73
Q

What does DiGeorge Syndrome presents with?

A

T-cell deficiency (lack of thymus); hypocalcemia (lack of parathyroids); and abnormalities of heart, great vessels, and face

74
Q

Severe combined immunodeficiency

A

defective cell-mediated and humoral immunity

75
Q

What are the etiologies for SCID?

A

Cytokine receptor defects, Adenosine deaminase (ADA) deficiency, MHC class II deficiency

76
Q

Cytokine receptor defects

A

Cytokine signaling is necessary for proliferation and maturation of B and T cells.

77
Q

Adenosine deaminase (ADA) deficiency

A

ADA is necessary to deaminate adenosine and deoxyadenosine for excretion as waste products; buildup of adenosine and deoxyadenosine is toxic to lymphocytes

78
Q

What is systemic Lupus Erythematosus?

A

Systemic autoimmune disease, antibodies against tbe host damage multiple tissues via type II (cytotoxic) and type III (antigen-antibody complex) hypersensitivity.

79
Q

Systemic Lupus Erythematosus is more common in?

A

women, especially African American females

80
Q

Clinical features of systemic Lupus Erythematosus include?

A

Fever and weight loss, Malar ‘butterfly’ rash, especially upon exposure to sunlight, Arthritis, Pleuritis and pericarditis (involvement of serosal surfaces), CNS psychosis, Renal damage, Endocarditis, myocarditis, or pericarditis (can affect any layer of the heart), Anemia, thrombocytopenia, or leukopenia (due to autoantibodies against cell surface proteins), Renal failure and infection are common causes of death.

81
Q

Anemia, thrombocytopenia, or leukopenia in SLE is due to?

A

autoantibodies against cell surface proteins

82
Q

Most common causes of death in SLE?

A

Renal failure and infection

83
Q

What is a classic finding for systemic lupus eythematosus?

A

Libman-Sacks endocarditis is and is characterized by small, sterile deposits on both sides of the mitral valve.

84
Q

What is the most common clinical features of systemic Lupus Erythematosus?

A

Diffuse proliferative glomerulonephritis, though other patterns of injury also occur.

85
Q

Systemic Lupus Erythematosus and anemia, thrombocytopenia, or leukopenia is due to?

A

autoantibodies against cell surface proteins

86
Q

What are common causes of death for SLE?

A

renal failure and infection

87
Q

SLE is characterized by

A

antinudear antibody ANA; sensitive, but not specific and anti dsDNA antibodies (highly specific)

88
Q

Antihistone antibody is characteristic of?

A

drug-induced SLE.

89
Q

What are some common causes of drug induced SLE?

A
  1. Hydralazine, procainamide, and isoniazid are common causes 2. Removal of drug usually results in remission.
90
Q

30% of what cases are associated with SLE?

A

Antiphospholipid antibody syndrome

91
Q

What is sjogren syndrome?

A

Autoimmune destruction of lacrimal and salivary glands, lymphocyte-mediated damage (type IV hypersensitivity) with fibrosis

92
Q

How does sjogren syndrome classically present?

A

as dry eyes (keratoconjunctivitis), dry mouth (xerostomia), and recurrent dental carries in an older woman (50-60 years)?Can’t chew a cracker, dirt in my eyes

93
Q

Sjogren syndrome is characterized by?

A

ANA and anti-ribonucleoprotein antibodies anti-SS-A/Ro and anti-SS-B/La)

94
Q

Sjogren syndrome is often associated with?

A

other autoimmune diseases, especially rheumatoid arthritis

95
Q

Sjogren syndrome results in increased risk for?

A

B-cell (marginal zone) lymphoma, which presents as unilateral enlargement of the parotid gland late in disease course

96
Q

When is healing initiated?

A

when inflammation begins.

97
Q

Wound healing occurs via?

A

a combination of regeneration and repair

98
Q

In wound healing regeneration occurs via?

A

Replacement of damaged tissue with native tissue; dependent on regenerative capacity of tissue

99
Q

Tissues are divided into three types based on?

A

regenerative capacity: labile, stable, and permanent.

100
Q

Labile tissues

A

possess stem cells that continuously cycle to regenerate the tissue.

101
Q

Examples of Labile tisues

A
  1. Small and large bowel (stem cells in mucosal crypts) 2. Skin (stem cells in basal layer) 3. Bone marrow (hematopoietic stem cells)
102
Q

Stable tissues are

A

comprised of cells that are quiescent G0, but can reenter the cell cycle to regenerate tissue when necessary.

103
Q

What is a classic example of regeneration?

A

In the liver by compensatory hyperplasia after partial resection. Each hepatocyte produces additional cells and then reenters quiescence.

104
Q

Permanent tissues

A

lack significant regenerative potential (myocardium, skeletal muscle, and neurons).

105
Q

Repair

A

Replacement of damaged tissue with fibrous scar, Occurs when regenerative stem cells are lost (e.g., deep skin cut) or when a tissue lacks regenerative capacity (e.g., healing after a myocardial infarction

106
Q

Granulation tissue

A

Its formation is the initial phase of repair

107
Q

In the initial phase of repair what does the fibroblasts do?

A

deposit type III collagen

108
Q

In the initial phase of repair what does the capillaries do?

A

provide nutrients

109
Q

Granulation tissue consists of?

A

fibroblasts (deposit type III collagen), capillaries (provide nutrients), and myofibroblasts (contract wound)

110
Q

Granulation tissue eventually results in?

A

scar formation, in which type 111 collagen is replaced with type 1 collagen

111
Q

Type III collagen is

A

pliable and present in granulation tissue, embryonic tissue, uterus, and keloids.

112
Q

Type I collagen

A

has high tensile strength and is present in skin, bone, tendons, and most organs,

113
Q

Collagenase

A

removes type 111 collagen and requires zinc as a cofactor.

114
Q

Tissue regeneration and repair is mediated by?

A

paracrine signaling via growth factors (e.g macrophages secrete growth factors that target fibroblasts)

115
Q

What results in gene expression and cellular growth?

A

Interaction of growth factors with receptors (e.g.. epidermal growth factor with growth factor receptor)

116
Q

Examples of mediators of tissue repair and regeneration

A

TGF-alpha, TGF-beta, platelet, fibroblast growth factor, VEGF

117
Q

TGF-alpha

A

epithelial and fibroblast growth factor

118
Q

TGF-beta

A

important fibroblast growth factor; also inhibits inflammation

119
Q

Platelet-derived growth factor

A

growth factor for endothelium, smooth muscle, and fibroblasts

120
Q

Fibroblast growth factor

A

important for angiogenesis; also mediates skeletal development

121
Q

Vascular endothelial growth factor (VEGF)

A

important for angiogenesis

122
Q

Cutaneous healing occurs via

A

primary or secondary intention.

123
Q

Primary intention

A

Wound edges are brought together (e.g., suturing of a surgical incision); leads to minimal scar formation

124
Q

Secondary intention

A

Edges are not approximated. Granulation tissue fills the defect; myofibroblasts then contract the wound, forming a scar.

125
Q

Delayed wound healing occurs in

A
  1. Infection (most common cause; S aureus is the most common offender)
126
Q

Vitamin C is

A

an important cofactor in the hydroxylation of proline and lysine procollagen residues; hydroxylation is necessary for eventual collagen cross-linking.

127
Q

What is necessary for the formation of stable collagen?

A

Copper is a cofactor forlysyl oxidase, which cross-links lysine and hydroxy lysine to form stable collagen.

128
Q

What is a cofactor for collagenase?

A

Zinc which replaces the type III collagen of granulation tissue with stronger type I collagen

129
Q

What are some causes for delayed wound healing?

A

foreign body, ischemia, diabetes, and malnutrition,

130
Q

Dehiscence is

A

rupture of a wound; most commonly seen after abdominal surgery

131
Q

Hypertrophic scar is

A

excess production of scar tissue that is localized to the wound

132
Q

Keloid is

A

excess production of scar tissue that is out of proportion to the wound

133
Q

Keloid is characterized by

A

excess type III collagen

134
Q

Keloid genetic predisposition

A

more common in African Americans

135
Q

Keloid classically affects

A

earlobes, face, and upper extremities

My Pathoma (3 decks)

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