1. Eosinophil chemotaxis and activation 2. Maturation of B cells to plasma cells 3. Class switching to IgA

[1] Inflammation Flashcards by Jp Reyes

Neutrophils are attracted to these chemical attractants

IL8
C5a
LTB4
Bacterial components

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Where do neutrophils migrate to exert their action?

Post-capillary Venule

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Disease characterized by impairment in protein trafficking

Chediak-Higashi Syndrome

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Clinical Features of Chediak-Higashi Syndrome

Increased risk of pyogenic infections
Neutropenia
Giant granules in leukocytes
Defective primary hemostasis
Albinism
Peripheral Neuropathy

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Most effective mechanism of killing phagocytosed materials?

O2-Dependent Killing Mechanism

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What converts Oxygen to Superoxide

NADPH

Also called oxidative burst

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What converts Superoxide to Hydrogen Peroxide?

Superoxide Dismutase

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What converts Hydrogen Peroxide to HOCl (Bleach)?

Myeloperoxidase

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What is defective in Chronic Granulomatous Disease

NAPDH Oxidase Defect

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Patients with CGD have granuloma formation with these kinds of organisms

How come only these organisms can cause infections?

Catalase-positive

Most bacteria produce hydrogen peroxide, which can be converted to HOCl, but those that produce catalase breakdown H2O2, therefore disrupting the pathway

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Test used to screen for CGD

How?

Nitroblue Tetrazolium Test

Turns blue if NADPH oxidase can convert O2 to O2-

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Patients with MPO deficiency are usually asymptomatic but do have an increased risk for these infections

Candida Infections

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Neutrophils disappear after how many hours via what mechanism?

24 hours via apoptosis

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What leukocyte predominates after the neutrophil phase?

Macrophage

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Macrophages manage the next step of the acute inflammatory process of resolution and healing by secreting?

Resolution and Healing: IL-10 and TGF-B (Anti-inflammatory)

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How do macrophages recruit additional neutrophils?

Secrete IL-8

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4 Possible Endpoints of the Acute Inflammatory Process

Resolution and Healing
Continued Acute Inflammation
Abscess Formation
Chronic Inflammation

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Chronic inflammation is characterized by?

Lymphocytes and plasma cells in tissue

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T Cells are produced in?

Bone Marrow

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TCR Complexes can only recognize antigen when presented by?

MHC

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CD4 and CD8 T-Cells recognize which MHC Class

CD4 :: MHC II

CD8 :: MHC I

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Immature B Cells are produced in?

Bone Marrow

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Function of IL-4

Class Switching of IgG -> IgE

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Function of IL-5

Eosinophil chemotaxis and activation
Maturation of B cells to plasma cells
Class switching to IgA

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Function of IL-10

Inhibits TH1 Phenotype

How are CD8 TCells Activated?

1. Intracellular antigen is presented to MHC I 2. IL-2 from CD4 TH1 Cells provide a 2nd activation signal 3. Cytotoxic T-Cells activated for killing

Key enzyme that mediates apoptosis?

Caspases

How are B-Cells Activated?

1. Antigen binding by surface IgM or IgD 2. Becomes an IgM or IgD secreting Plasma Cell or 1. Antigen presentation to CD4 Helper T Cell via MHC II 2. CD40 receptor on B-Cells bind CD40L on Helper T Cell providing 2nd activation signal (Secretes IL-4,IL-5)

What is the defining characteristic of a granuloma?

Epithelioid histiocytes (macrophages with abundant pink cytoplasm)

How can you differentiate caseating from non-caseating granulomas?

Central Necrosis

Caseating granulomas are characteristic of these diseases

TB and Fungal Infections

Steps involved in Granuloma Formation

1. Macrophages present antigen via MHC II to CD4 Helper T Cells 2. Macrophages secrete IL-12, inducing CD4 to differentiate into TH1 Subtype 3. TH1 Cells secrete IFN-Y which converts macrophages to epitheliod histiocytes

Function: IL-12

Induce CD4 to differentiate into TH1

What do helper T Cells secrete to convert macrophages to granulomas?

IFN-Y

DiGeorge Syndrome is a developmental failure of? | This is due to a deletion of which chromosome?

3rd and 4th Pharyngeal Pouch 22q11 microdeletion

Presentation of DiGeorge Syndrome

1. T-Cell Deficiency (Lack of Thymus) 2. Hypocalcemia (Lack of Parathyroids) 3. Abnormalities of heart, great vessels, and face

Etiologies of SCID

1. Cytokine Receptor Defects 2. Adenosine deaminase deficiency (Adenosine and Adenosine oxide are toxic to lymphocytes) 3. MHC Class II Deficiency

Treatment for SCID

1. Sterile Isolation | 2. Stem Cell Transplant

X-Linked Agammaglobulinemia is a defect in?

Complete lack of immunoglobulin Due to disordered B-cell maturation

X-Linked Agammaglobulinemia is caused by which mutated gene?

Mutated Tyrosine Kinase

These infections are common in patients with X-Linked Agammaglobulinemia

Bacterial Enterovirus Giardia infections (Mucosal infections: IgA deficiency)

How come patients with X-linked Agammaglobulinemia only present with symptoms after 6 months of life?

They have their mother's immunoglobulins (IgA) through breast milk

What is the most common Ig deficiency?

IgA

Which GI disease is commonly associated with IgA deficiency?

Celiac Disease

What is the cause of Hyper IgM Syndrome?

Mutation of the CD40L or CD40 Receptor (Cannot use the alternate pathway of B-Cell Activation)

Which Immunoglobulins would be low in patients with HyperIgM Syndrome?

IgA IgG IgE

Triad of Wiskott-Aldrich Syndrome

1. Thrombocytopenia 2. Eczema 3. Recurrent infections

C5-C9 deficiencies would have an increased risk for what kind of infections?

Neisseria

Autoimmune diseases are caused by a loss of this defense mechanism

Self-tolerance

SLE causes systemic damage via which Hypersensitivity Reactions?

``` Type II (Cytotoxic) Type III (Antigen-Antibody Complexes) ```

This is the most common type of renal damage in patients with SLE

Diffuse proliferative glomerulonephritis

What is unique about Libman-Sacks endocarditis?

Presence of vegetation on both sides of the heart valves

What is characteristic of drug-induced SLE?

Antihistone Antibody

These drugs are common causes of drug-induced SLE?

Hydralazine Procainamide Isoniazid

Which antibodies are associated with Antiphospholipid Syndrome?

Anticardiolipin | Lupus Anticoagulant

Anticardiolipin interferes with this test

Leads to a false-positive syphilis test

Lupus Anticoagulant interferes with this diagnostic test

Elevated PT/PTT

Treatment for APAS

Lifelong anticoagulation

Sjogren Syndrome is associated with destruction of these glands

Lacrimal | Salivary

Classic antibody test for Sjogren Syndrome

ANA | Anti-ribonucleoprotein Antibodies (Anti-SS-A and Anti-SS-B)

Patients with Sjogren syndrome usually present with bilateral parotid gland enlargement. What is the significance of a unilateral enlargement of a parotid gland late in the disease course?

The patient has possibly developed a B-cell Lymphoma

Scleroderma is characterized by these antibodies

Anti-DNA Topoisomerase I Antibody (Scl-70)

Classic Presentation of Crest Syndrome

``` Calcinosis/Anti-Centromere Antibody Raynaud Phenonemon Esophageal Dysmotility Sclerodactyly Telangectasias of Skin ```

Where are the stem cells located in the small and large bowels?

Mucosal Crypts

Where are the stem cells located in the skin?

Basal Layer

Where are the stem cells located in the bone marrow?

Hematopoietic Stem Cells

Where are the stem cells located in the lung?

Type II Pneumocytes

What is the marker for hematopoietic stem cells?

CD34

Which tissues in the body have poor/no regenerative potential?

Skeletal Muscle Neurons Cardiac Muscle

What are the components of granulation tissue?

1. Fibroblasts 2. Capillaries 3. Myofibroblasts

What do fibroblasts do in the initial phase of repair?

Deposit Type III Collagen

When granulation tissue scars, this type of collagen is replaced with what type of collagen?

Type III -> Type I Collagen

Type I Collagen is commonly seen in?

Bone [b-ONE]

Type II Collagen is commonly seen in?

Cartilage [Car-TWO-lage]

Type III Collagen is commonly seen in?

Blood vessels, granulation tissue, embryonic tissue [Seen in tissues that are able to stretch. s-THREE-tch]

Type IV Collagen is commonly seen in?

Basement Membrane

During repair, collagenase removes Type III collagen, but requires what as a co-factor?

Zinc

[Function] FGF

Angiogenesis | Skeletal Development

[Function] VEGF

Angiogenesis

[Function] TGF-A

Epithelial and Fibroblast Growth Factor

[Function] TGF-B

Inhibits Inflammation | Fibroblast Growth Factor

[Function] PDGF

Endothelium, Smooth Muscle, Fibroblast Growth Factor

Differentiate healing via primary versus secondary intention

Primary: Wound edges brought together; minimizes scar formation Secondary: Edges are not approximated, granulation tissue fills in the defect

[1] Inflammation Flashcards

(83 cards)