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Pathoma > Chapter 2 - Inflammation, Inflammatory Disorders and Wound Healing > Flashcards

Chapter 2 - Inflammation, Inflammatory Disorders and Wound Healing Flashcards

1
Q

What 2 things characterize acute inflammation?

A
  1. Edema
  2. Neutrophils
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2
Q

What 2 things cause acute inflammation?

A
  1. Infection
  2. Tissue Necrosis
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3
Q

What 5 things mediate acute inflammation?

A
  1. Toll-like receptors (TLRs)
  2. Arachidonic Acid (AA) Metabolites
  3. Mast Cells
  4. Complement
  5. Hageman Factor (Factor XII)
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4
Q

What activates TLRs?

A

Pathogen-Associated Molecular Patterns (PAMPs)

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5
Q

What receptor recognizes LPS?

A

CD14 on Macrophages

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6
Q

How does activation of TLRs activate the immune response?

A

Upregulation of NF-κB which activates the immune response.

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7
Q

What are the two pathways for AA?

A

Cyclooxygenase (COX) and 5-Lipoxygenase (LOX)

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8
Q

What does the COX pathway produce (be specific)

A

PGI2

PGD2

PGE2

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9
Q

What functions do PGI2, PGD2, and PGE2 share?

A

Vasodilation at arteriole

Increased vascular permeability at postcapillary venuole

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10
Q

What two functions are unique to PGE2?

A

Pain and Fever

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11
Q

What does the 5-LOX pathway produce?

(be specific)

A

LTB4

LTC4

LTD4

LTE4

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12
Q

What are the functions of the Leukotrienes?

A

Vasoconstriction

Bronchospasm

Increased Vascular Permeability

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13
Q

What 4 things attract and activate Neutrophils?

A
  1. LTB4
  2. C5a
  3. IL8
  4. Bacterial Products
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14
Q

What 3 things activate mast cells?

A
  1. Tissue Trauma
  2. C3a and C5a
  3. Cross-linking of cell-surface IgE by antigens
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15
Q

What is the immediate response of Mast cells?

A

Release of preformed histamine granules

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16
Q

What is the delayed response of Mast cells?

A

Production of AA metabolites, especially Leukotrienes

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17
Q

What are the 3 ways to activate Compliment?

A
  1. Classical Pathway (IgG or IgM + antigen)
  2. Alternative Pathway (Microbial Products)
  3. Mannose-Binding Lectin (MBL) Pathway (MBL + Mannose actives compliment)
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18
Q

Which two compliment proteins cause mast cell degradation?

A

C3a and C5a

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19
Q

Which Compliment protein is an opsonin?

A

C3b

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20
Q

What activates Hageman Factor?

A

Exposure to subendothelial or tissue collagen

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21
Q

What does Hageman Factor activate?

A
  1. Coagulation
  2. Complement
  3. Kinin System
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22
Q

What are the functions of Bradykinin?

A

Vasodilation

Increased Vascular Permeability

Pain

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23
Q

What is the mechanism behind Redness and Warmth in inflammation?

A

Vasodilation due to Prostaglandins, Bradykinin and Histamine

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24
Q

What is the mechanism behind Pain in inflammation?

A

Bradykinin and PGE2 sinsitize nerve endings

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25
Q

What is the mechanism behind Swelling in inflammation?

A

leakage of fluid from postcapillary venules due to histamine.

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26
Q

What is the mechanism behind Fever in inflammation?

A

Pyogens cause macrophages to release TNF which increases COX activity in perivascular cells of the hypothalmus.

PGE2 increases temperature set point.

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27
Q

Is this Acute or Chronic inflammation?

A

Acute

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28
Q

What are the 7 steps of Neutrophil arrival and funtion?

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration and Chemotaxis
  5. Phagocytosis
  6. Destruction of phagocytosed material
  7. Resolution
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29
Q

What are the 3 phases of acute inflammation?

A
  1. Fluid
  2. Neutrophil
  3. Macrophage
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30
Q

What is the mechanism of Margination?

A

Vasodilation slows blood flow in postcapillary veins

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31
Q

What is the mechanism of Rolling (Step 2)?

A

Selectin is upregulated on endothelial cells.

Selectins bind sialyl Lewis X on leukocytes

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32
Q

What are the two types of Selectin and where do they come from?

A

P-Selectin (comes from Weibel-Palade bodies)

E-Selectin (induced by TNF and IL-1)

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33
Q

What is the mechanism of Adhesion (Step 3)?

A

Cellular Adhesion Molecules (CAMs) on endothelial cells bind to Integrins on leukocytes and adhere them to the vessel wall.

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34
Q

What upregulates CAMs?

A

TNF and IL-1

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35
Q

What upregulates Integrins?

A

C5a and LTB4

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36
Q

What is Leukocyte Adhesion Deficiency?

A

An Autosomal Recessive Defect of Integrins

(subunit CD18)

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37
Q

What are the clinical features of Leukocyte Adhesion Deficiency?

A
  1. Delayed separation of unbilical cord
  2. increased circulating neutrophils
  3. recurrent bacterial infections that lack pus
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38
Q

Where do leukocytes transmigrate?

A

Postcapillary Venules

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39
Q

What are the 2 opsonins in the text?

A

IgG and C3b

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40
Q

What is Chediak-Higashi Syndrome?

A

An Autosomal Recessive Protein Trafficking Defect characterized by impared phagolysosome formation

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41
Q

What are the 6 clinical features of Chediak-Higashi Syndrome?

A
  1. Increased risk of pyogenic infection
  2. Neutropenia
  3. Giant Granules in Leukocytes
  4. Defective Primary Hemostasis
  5. Albinism
  6. Peripheral Neuropathy
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42
Q

Is O2 dependent or O2 independent killing more effective?

A

Dependent

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43
Q

How is O2 used to kill organisms in O2 dependent killing?

A

It is converted to HOCl- (Bleach)

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44
Q

What are the reactions and enzymes used to convert O2 into HOCl-

A

O2 → O2- (NADPH Oxidase)

O2- → H2O2 (Super Oxide Dismutase)

H2O2 → HOCl- (Myeloperoxidase aka MPO)

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45
Q

What is Chronic Granulomatous Disease (CGD)?

A

An NADPH Oxidase defect characterized by poor O2 dependent killing.

(X-linked or Autosomal Recessive)

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46
Q

To what type of microorganisms are people with CGD susceptible?

(Whic 2 of them were emphasized?)

A

Catalse Positive Microorganisms

(Staph aureus and Pseudomonas cepacia)

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47
Q

What symptoms are characteristic of MPO deficiency?

A

Inreased risk of Candida infections, but most patients are Asymptomatic

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48
Q

What test is used for CGD?

A

Nitroblue Tetrazolium (NBT) test

(turns blue if NADPH Oxidase works)

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49
Q

If a patient has MPO deficiency, but not CGD, what color will an NBT test be, and what does that mean?

A

Blue (NADPH Oxidase works normally)

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50
Q

What is the mechanism of O2 independent killing?

A

Enzymes present in leukocyte secondary granules

(Macrophages = Lysozyme)

(Eosinophils = Major Basic Protein)

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51
Q

What is the mechanism of Resolution (Step 7)?

A

Neutrophils undergo Apoptosis within 24 hours of resolution of infection.

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52
Q

What are macrophages derived from?

A

Monocytes in the blood

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53
Q

How do macrophages enter tissues?

A

The same as neutrophils

(margination, rolling, adhesion, transmigration)

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54
Q

How do macrophages kill phagocytized organisms?

A

Lysozyme (and other enzymes)

O2 independent

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55
Q

What are the 4 main outcomes that Macrophages can promote in the inflammatory process?

(think managing)

A
  1. Resolution and Healing
  2. Continued Acute Inflammation
  3. Abscess
  4. Chronic Inflammation
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56
Q

How do macrophages promote resolution and healing?

A

IL-10 and TGF-β

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57
Q

How do macrophages recruit more neutrophils to continue acute inflammation?

A

IL-8

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58
Q

What is an abscess?

A

Acute inflammation surrounded by fibrosis

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59
Q

How do macrophages promote chronic inflammation?

A

Presenting antigen to activate CD4+ and Helper T-Cells

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60
Q

After how much time is Acute Inflammation considered Chronic Inflammation?

A

FALSE

The differentiation is not based on time, but on the presence of neutrophils vs lymphocytes

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61
Q

Is this Acute or Chronic Inflammation?

A

Chronic

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62
Q

What are the 5 common cuases of Chronic Inflammation?

A
  1. persistent infection
  2. viruses, mycobacteria, parasites, fungi
  3. autoimmune diseases
  4. foreign material
  5. some cancers
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63
Q

Where do T cells mature?

A

Thymus

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64
Q

What is the difference between the TCR on CD4+ and CD8+ cells?

A

CD4+ recognizes antigen on MHC class II (extracelllar)

CD8+ recognizes antigen on MHC class I (intracellular)

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65
Q

What is required for T cell activation?

A
  1. binding of antigen/MHC complex
  2. an additional 2nd signal
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66
Q

What is the second signal to activate CD4+ cells?

A

B7 on APC binds to CD28 on CD4+ cell

( 28 / 7 = 4 )

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67
Q

What do Th1 cells secrete?

(What are the functions of the secretions?)

A

IL-2 (T cell growth and CD8+ activator)

IFN-γ (macrophage activator)

68
Q

What do Th2 cells secrete?

(What are the functions of the secretions?)

A

IL-4 (B-cell slass switching to IgG and IgE)

IL-5 (eosinophil chemotaxis/activation, maturation of B cells to plasma cells, class switching to IgA)

IL-10 (inhibits Th1 phenotype)

69
Q

What is the second activatoin signal for CD8+ cells?

A

IL-2 from Th1 cells

70
Q

How do Cytotoxic T-cells (CD8+) kill?

A
  1. Secretion of perforin and granzyme (activate caspase)
  2. Expression FasL (binds to Fas and induces apoptosis)
71
Q

What do naive B cells express?

A

surface IgM and IgD

72
Q

What happens when atigen binds to the surface IgM or IgD on naive B cells?

A

Matures into IgM or IgD secreting plasma cell

73
Q

What are the 3 steps of the second (not IgM or IgD) method of activation of B cells?

A
  1. B-cell presents antigen to CD4+ cell
  2. CD40 receptor on B cell binds CD40L on T cell (second T cell activation signal)
  3. Th2 cell secretes IL-4 and IL-5 which mediates B cell isotype switching and maturation
74
Q

What are the 4 characteristics of granulomatous inflammation?

A
  1. a granuloma
  2. EPITHELIOD HISTIOCYTES (macrophages with abundant pink cytoplasm)
  3. giant cells
  4. rim of lymphocytes
75
Q

What is the difference between non-caseating and caseating granulomas?

A

Caseating granulomas have central necrosis

(non-caseating do not)

76
Q

What are the 5 common etiologies of non-caseating granulomatous inflammation?

A
  1. Foreign Material
  2. Sarcoidosis
  3. Beryllium exposure
  4. Chron’s disease
  5. Cat Scratch disease (stellate granuloma)
77
Q

BONUS ROUND

What is the histologic hallmark of Ulcerative Colitis?

A

Crypt Abscesses

78
Q

BONUS ROUND

What type of stain is used for TB?

A

AFB stain

79
Q

BONUS ROUND

What type of stain is used for fungal infections?

A

GMS stain

80
Q

What are the 3 steps of granuloma formation?

A
  1. Macrophages present antigen to CD4+ cells
  2. Macrophages then secrete IL-12 causing CD4+ cells to become Th1 cells
  3. Th1 cells secrete INF-γ converting macrophages into epitheliod histiocytes and giant cells
81
Q

What type of inflammation is this?

A

Caseating

82
Q

What type of inflammation is this?

A

Non-Caseating

83
Q

How does a patient develop DiGeorge Syndrome?

A

22q11 mutation

84
Q

What is problem in DiGeorge Syndrome?

(i.e. what’s missing or imporoperly developed?)

A

Failure of the 3rd and 4th pharyngeal pouches

(lack of thymus and parathyroids)

85
Q

How does DiGeorge syndrome present?

A

Lack of T-cells

Hypocalcemia

Abnormalities of heart, great vessels, and face

86
Q

What type of infections would expect to see in a person who has DiGeorge Syndrome?

A

Viral or Fungal

(no T-cells to fight those infections)

87
Q

What are the 3 main etiologies of Severe Combined Immunodeficiency (SCID)?

A
  1. Cytokine Receptor defects
  2. Adenosine Deaminase (ADA) deficiency
  3. MHC Class II deficiency
88
Q

What is the end result of the etiology of SCID?

(i.e. what isn’t working, or what is missing?)

A

Defective cell-mediated and humoral immunity

89
Q

Why do lymphocytes need ADA?

A

Buildup of Adenosine and Deoxyadenosine is toxic to lymphocytes.

(they must be deanimated and excreted as waste)

90
Q

SCID is characterized by susceptibility to what 6 things?

A
  1. Fungi
  2. Bacteria
  3. Viruses
  4. Protozoa
  5. Opportunistic infections
  6. Live Vaccines
91
Q

What is the treatment for SCID?

(short term and long term)

A

Sterile Isolation (Short Term)

Stem Cell Transplantation (Long Term)

92
Q

What is the etiology of X-Linked Agammaglobulinemia?

A

Mutated Bruton Tyrosine Kinase (BTK)

(Naive B cells cannot mature to plasma cells)

93
Q

What is missing or not working in X-Linked Agammaglobulinemia?

A

ocmplete lack of immunoglobulin.

94
Q

What 3 infections are characteristic of X-linked Agammaglobulinemia?

A
  1. Recurrent Bacterial
  2. Enterovirus

Giardia lamblia

95
Q

At what age does X-Linked Agammaglobulinemia normally present?

A

Around 6 months

(because maternal antibodies are present up to about 6 months of age)

96
Q

What is the dysfunction in Common Variable Immunodeficiency (CVID)?

A

Low immunoglobulin

(due to B-cell or Helper T-cell defects)

97
Q

For which 3 types of infections are patients with CVID at increased risk?

A
  1. Recurrent Bacterial
  2. Enterovirus
  3. Giardia lamblia
98
Q

For which 2 diseases are patients with CVID at increased risk?

A

Autoimmune disease and lymphoma

99
Q

What is the most common immunoglobulin deficiency?

A

IgA Deficiency

100
Q

What are the symptoms for IgA Deficiency?

A

Asympomatic

(increased risk for mucosal infection. especially viral)

101
Q

What is the etiology of Hyper-IgM Syndrome?

A

Mutated CD40L or CD40 receptor

102
Q

What are the levels of the different immunoglobulins in Hyper-IgM syndrome (in relation to normal levels)?

A

IgM - high

IgD - ? ? ?

IgA - Low

IgG - Low

IgE - Low

103
Q

To which type of infection(s) are patients with Hyper-IgM syndrom more susceptible?

A

Recurrent pyogenic infections (especially at mucosal sites)

104
Q

What is the etiology of Wiskott-Aldrich Syndrome?

A

mutationin the WASP gene (X-linked)

105
Q

Which three conditios are characteristic of Wiskott-Aldrich Syndrome?

A
  1. Recurrent infections
  2. Thryombocytopenia
  3. Eczema
106
Q

For what infection is someone with C5-C9 deficiency at risk?

A

Neisseria

107
Q

What is characteristic of C1 Inhibitor deficiency

A

Hereditray Angioedema

(edema of the skin and mucosal surfaces)

108
Q

What type of edema is most characteristic of Angioedema?

A

Periorbital

109
Q

What condition does this patient have?

A

Angioedema (periorbital edema)

(possibly C1 Inhibitor deficiency)

110
Q

What percent of American’s have autoimmune disorders?

A

1 %

111
Q

What demographic most commonly has autoimmune disorders?

A

Women of child-bearing age

112
Q

What is the etiology of autoimmune disorders?

A
  1. Environmental Trigger
  2. Genetic Susceptability
113
Q

What is the mechanism of Systemic Lupus Erythematosus (SLE)?

A

Type II (Cytotoxic) Hypersensativity

Type III (Antigen-Antibody Complex) Hypersensativity

114
Q

What are the 8 clinical features of SLE ?

(good luck..)

A
  1. Fever and Weight Loss
  2. Malar ‘butterfly’ rash
  3. Arthritis
  4. Pleuritis/Pericarditis (serosal surface involvement)
  5. CNS Psychosis
  6. Renal Damage (Diffuse Proliferative Glomerulonephritis)
  7. Endocarditis, Myocarditis, Pericarditis
    • Libman-Sacks Endocarditis
  8. ​Anemia, Thrombocytopenia, leukopenia
115
Q

What are the 2 most common causes of death in SLE?

A

Renal failure

infection

116
Q

What is the classic finding in Liebman-Sacks endocarditis?

A

sterile deposits on both sides of the valve

117
Q

What 2 antibodies are characteristic of SLE?

Which is the most specific for SLE?

A

Antinuclear Antibodies (ANA)

Anti dsDNA (more specific)

118
Q

What antibody is characteristic of Drug-induced SLE?

A

Antihistone Antibody

119
Q

What 3 drugs can cause Drug-Induced SLE?

A
  1. Hydralazine
  2. Procainamide
  3. Isoniazid
120
Q

What 2 antibodies are associated with Antiphospholipid antiobody sundrome?

A

Anticardiolipin and Lupus Anticoagulant

121
Q

What can Anticardiolipin lead to?

A

False-Positive Syphilis test

122
Q

How does Lupus Anticoagulant manifest clinically?

A

Falsely-elevated PTT

123
Q

What effects can Antiphospholipid antiobody syndrome have?

A

Arterial and Venous Thromboses

(deep vein, hepatic vein, placental, stroke)

124
Q

How is Antiphospholipid antiobody syndrome treated?

A

Lifelong anticoagulation

125
Q

What is the etiology of Sjogren Syndrome?

A

Type IV Hypersensitivity with Fibrosis

126
Q

What is attacked by the immune system in Sjogrens System?

A

Lacrimal and Salivary Glands

127
Q

In what 3 ways does Sjogren Syndrome present clinically?

A
  1. Dry Eyes
  2. Dry Mouth
  3. Recurrent Caries
128
Q

If a patient complains that they “can’t chew a cracker” or that they “have dirt in my eyes” they probably have what?

A

Sjogren Syndrome

129
Q

What antibodies are characteristic of Sjogren Syndrome?

A

ANA and Anti-Ribonucleoprotein Antibodies

130
Q

What other diseases is Sjogren Syndrome associated with?

A

Autoimmune diseases like Rheumatoid Arthritis

131
Q

Sjogren Syndrome puts a patient at risk for what?

(What is the main symptom?)

A

B-cell Lymphoma

(unilateral enlargement of the parotid)

132
Q

What is Scleroderma?

A

Autoimmune tissue damage with activation of fibroblasts and deposition of collagen

133
Q

What is affected by Diffuse Scleroderma?

A

Any organ

(Commonly the esophagus with dysphagia for solids and liquids)

134
Q

What is Diffuse Scleroderma characterized by?

(what type of antibody?)

A

ANA

Anti-DNA Toperisomerase I

135
Q

What is characteristic of Localized Scleroderma?

A

CREST

Calcinosis/Anti-Centromere Antibodies

Raynaud phenomenon

Esophageal dysmotility

Sclerodactyly

Telangiectasis of the skin

136
Q

How does Mixed Connective Tissue Disease present?

A

Mixed features of

  • SLE
  • Systemic Sclerosis
  • Polymyositis
137
Q

What is characteristic of Mixed Connective Tissue Disorder?

A

Serum antibodies against U1 Ribonucleoprotein

138
Q

When does healing begin (in relation to inflammation)?

A

Healing is intitiated when inflammation begins.

139
Q

Tissues can be divided into 3 categories based on regenerative capacity. What are they?

A
  1. Labile
  2. Stable
  3. Permanent
140
Q

What is the definition of Labile tissues?

A

Possess stem cells that continuously cycle to regenerate the tissue

141
Q

What are 3 examples of labile tissues?

(Where are their stem cells located?)

A
  1. Small and large bowel
    • (mucosal crypts)
  2. Skin
    • (Basal Layer)
  3. Bone Marrow
    • Hematopoetic Stem cells
142
Q

How are stem cells in bone marrow identified clinically?

A

Presence of CD34

143
Q

What is the definition of a stable tissue?

(What is the main example?)

A

comprised of quiescent cells that can reenter the cell cycle to regenerate tissue when necessary

(Hyperplasia of the liver)

144
Q

What is the definition of Permanent tissues?

A

Lack significant regenerative potential

145
Q

What are the 3 types of permanent tissue?

A
  1. Myocardium
  2. Skeletal Muscle
  3. Neurons
146
Q

What is the definition of tissue repair?

A

Replacement of damaged tissue with a fibrous scar

147
Q

What are the two situations when repair occurs?

A
  1. When Regenerative Stem Cells are lost
  2. When a tissue lacks regenerative capacity.
148
Q

What is the initial phase of wound repair?

A

Granulation tissue

149
Q

What 3 things make up granulation tissue?

A

Fibroblasts

Capillaries

Myofibroblasts

150
Q

What causes the shift from granulation tissue to scar formation?

A

The shift from Type III Collagen to Type I Collagen

151
Q

What enzyme is responsible for the change from Type III to Type I Collagen?

(What is the important cofactor?)

A

Collagenase

(Zinc)

152
Q
A
153
Q

What type of signalling mediates regeneration and repair, paracrine, endocrine, or autocrine?

A

Paracrine

(via Macrophage growth factors)

154
Q

What are the 5 mediators of regeneration and repair?

A
  1. TGF-α
  2. TGF-β
  3. Platelet-Derived Growth Factor (PDGF)
    • Endothelium, smooth muscle, and fibroblasts
  4. Fibroblast Growth Factor
    • angiogenesis
  5. Vascularendothelial growth factor (VEGF)
155
Q

What is the difference between healing by Primary Intention versus Secondary Intention?

A

Edges are surgically approximated in Primary Intention

156
Q

How is the wound closed in Secondary Intention?

A

Myofibroblasts contract to close the wound

157
Q

What are the 6 things that cause delayed wound healing?

A
  1. Infection (the most common reason)
  2. Vit C, Copper, or Zinc deficiency
  3. Foreign Body
  4. Ischemia
  5. Diabetes
  6. Malnutrition
158
Q

What is the definition of a Hypertrophic Scar?

A

excess production of scar tissue localized to the wound

(consists of Type I Collage)

159
Q

What is the definition of a Keloid?

A

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

(Consists of Type III Collagen)

160
Q

What demographic most often gets Keloids?

A

African Americans

(Genetic Predisposition)

161
Q

What part of the body is most classically affected by Keloids?

A

Earlobes

(also, face and upper extremeties)

162
Q

Where are Types I - IV Collagen normally found?

A

I. Bone (high tensile strength)

II. Cartilage (cartwolage)

III. Embryo, Blood Vessels, Granulation Tissue (pliable)

IV. Basement Membrane

163
Q

How would you diagnose this scar?

A

Hypertrophic Scar

164
Q

How would you diagnose this scar?

A

Keloid

165
Q

What is the area outlined in red on this heart?

A

Fibrous scarring from infarct

Pathoma (4 decks)

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