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PHARM 310 > Allergy & Hypersensitivity vs Autoimmune Disease > Flashcards

Allergy & Hypersensitivity vs Autoimmune Disease Flashcards

(73 cards)

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1
Q

What causes Type IV Hypersensitivity

A

Antigen Specific Effector T-Cells release products that results in an inflammatory reaction
- CD4 TH1 cause the majority of reactions (Insect bite)
- Cytotoxic CD8 can cause some reactions (Poison Ivy-Pentadecacatechol)

Also involved in Chronic Transplant Rejection and Autoimmune Diseases

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2
Q

Type I Hypersensitivity Reaction

A

Anaphylaxis (Allergy Response)

Soluble antigens trigger release of IgE which triggers mast cell activation

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3
Q

Different methods to treat Allergic Reactions

A
  1. Prevention
  2. Pharmacological
  3. Immunological (Prevent production of allergen-specific IgE)
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4
Q

Type IV Hypersensitivity Reaction
- TH2

A

Delayed Type and Contract Type

Soluble antigens trigger TH2 cells to activate Eosinophils

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5
Q

What is Serum Sickness

A

After administering an IV of therapeutic proteins/Antibodies from another species the body may recognize it as foreign
- Leads to formation of immune Ag:Aby complexes causing symptoms like fever, arthritis, nephritis

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6
Q

Type II Hypersensitivity Reaction

A

Cytotoxic

Cell Surface Receptors or Cell/Matrix associated antigens trigger release of IgG which attract complements to harm those cells or mark Fc receptors on cells

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7
Q

Inhaled Allergen Process

A
  1. Allergen enters the airways and is picked up by APC (Like a B-Cell)
  2. APC (Like a B-Cell) presents antigen to T-Cell
  3. TH2 secretes IL-4
  4. B-Cell develops into Plasma cell and produces IgE
  5. IgE binds to Fc epsilon receptors on mast cells
  6. When allergen antigen binds to IgE on mast cell it triggers degranulation
  7. Mast cell releases inflammatory mediators
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8
Q

How are Hypersensitivity Reactions grouped?

A

Based on the effector mechanisms that produce the reaction

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9
Q

What reactants are synthesized after Eosinophil cell activation (Chemokine)
- What are their biological effects

A

CXCL8
- Promotes influx of leukocytes

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10
Q

Autoimmune Disease and Genetic Factor

A

Susceptibility to an autoimmune disease depends on ones genes (Differs between ethnic groups)

Every autoimmune disease has an HLA gene association
- Between the Polymorphic Class I (A, B, C) and Class II (DQ, DR)

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11
Q

Where are Eosinophils located

A

Found in loose connective tissue under epithelial and mucosal surfaces
- Respiratory, Gastrointestinal, Urogenital
- Small amount found in peripheral blood

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12
Q

Autoimmune Hemolytic Anemia Mechanism

A
  1. IgG and IgM bind to antigens on RBC
  2. Activates complement through the classical pathway
  3. RBC coated with antibody and Opsonins (C3b) are cleared from circulation
    - Done by Fc/Complement receptors on phagocytic cells in spleen
    - Or RBC undergoes lysis after formation of MAC
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13
Q

What are the common sources of allergens?

A
  1. Inhaled Materials
  2. Injected Materials
  3. Ingested Materials
  4. Contacted Materials
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14
Q

Mast Cells and Eosinophils what class of molecules are Pre-Packaged. What classes are Synthesized

A

Enzymes, Toxic Proteins, Cytokines

Cytokines, Chemokines, Lipid Mediators (Eosinophils do not contain pre-packaged cytokines)

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15
Q

What pre-packaged reactants are released by Mast Cells (Enzymes)
- What are their biological effects

A

Tryptase, Chymase, Cathepsin G
- Remodeling of connective tissue matrix

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16
Q

Systemic Lupus Erythematosus
- Type of Disease
- Autoantigen
- Consequence

A
  • Immune-Complex Disease (Type III)
  • DNA, histones, ribosomes, snRNP, snRNP
  • Glomerulonephritis, Vasculitis, arthritis
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17
Q

What reactants are synthesized after Eosinophil cell activation (Cytokine)
- What are their biological effects

A

IL-3, IL-5, GM-CSF
- Amplify eosinophil production by bone marrow
- Cause eosinophil activation

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18
Q

Autoimmune Disease and Lyme Disease

A
  1. Tick transmits Borrelia Bacteria through a bite
  2. Can cause Lyme Arthritis
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19
Q

What reactants are synthesized after mast cell activation (Cytokines)
- What are their biological effects

A

IL-4,13
- Stimulate and amplify T-Helper 2 Cell Response

IL-3, IL-5, GM-CSF
- Promote eosinophil production and activation

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20
Q

What do Mast Cells synthesize through oxidation of fatty acids

A

Produces Prostaglandins and Leukocytes from Arachidonic Acid

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21
Q

Multiple Sclerosis
- Type of Disease
- Autoantigen
- Consequence

A
  • T Cell-mediated Disease (Type IV)
  • Myelin basic protein, Proteolipid protein
  • Brain degeneration, Paralysis
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22
Q

Subacute Bacterial Endocarditis
- Type of Disease
- Autoantigen
- Consequence

A
  • Immune-Complex Disease (Type III)
  • Bacterial Antigen
  • Glomerulonephritis
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23
Q

What kind of Type III diseases can a Subcutaneous injection cause

A

Immune-Complex Deposition in Perivascular area
- Arthus Reaction

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24
Q

What pre-packaged reactants are released by Eosinophils (Toxic Proteins)
- What are their biological effects

A

Major Basic Protein
- Toxic to parasites and mammalian cells
- Triggers histamine release from mast cells

Eosinophilcationic Protein
- Toxic to parasites
- Neurotoxin

Eosinophil-derived neurotoxin
- Neurotoxin

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25
Kinds of Type I Reactions
Allergic Rhinitis, Asthma, Systemic Anaphylaxis
26
Acute Allergic Asthma vs Chronic Allergic Asthma
Acute - Mast Cell Mediated Chronic - Eosinophil and Cytokine mediated
27
Kinds of Type III Reactions
Serum Sickness, Arthus Reaction
28
What is Autoimmune Hemolytic Anemia
A type II autoimmune disease that targets Erythrocytes
29
Tissue Specific Effects of Degranulation - Blood Vessels
- Increased blood flow - Increased permeability --> Edema, Inflammation, Increased lymph flow of antigen to lymph nodes
30
Penicillin Allergy Process
1. Penicillin modifies proteins of RBC creating foreign epitopes 2. B-Cells activated by antigen and present it to TH2 Cells 3. TH2 Cells activate B-Cells and they differentiate into Plasma Cells 4. Plasma Cells secrete penicillin- specific IgG 5. IgG binds to penicillin modified RBC 6. Activation of complement components C1-C9 and formation of membrane attack complex lyses RBC OR 6. Activation of complement components C1-C3 leads to covalent bonding of C3b and phagocytosis of antibody and complement coated RBC
31
What pre-packaged reactants are released by Mast Cells (Toxic Proteins) - What are their biological effects
Histamine, Heparin - Toxic to parasites - Increase vascular permeability - Causes smooth muscle contraction
32
Rheumatoid Arthritis - Type of Disease - Autoantigen - Consequence
- T Cell-mediated Disease (Type IV) - Unknown synovial joint antigen - Joint inflammation and destruction
33
Delayed-Type Hypersensitivity - Antigens and Consequences
Proteins - Insect Venom - Mycobacterial Proteins (Tuberculin, lepromin) Results in Local Skin Swelling - Erythema - Induration - Cellular infiltrate - Contact Dermatitis
34
Treatment for Type IV Hypersensitivity
- Avoid contact with agent that cases hypersensitivity - Monitor for local infection risk - Corticosteroids, Cyclosporins, and Immunotherapy
35
What commonly triggers Type I Hypersensitivity
Inhaled particulate Antigen causing Anaphylaxis
36
Relation between infections and autoimmune disease
Autoimmune can be an adverse side-effect of an immune response to infection - Antibodies interact with and are specific to infection. However, cells elsewhere in the body may be similar to the infection causing the antibody to attack the body 1. Streptococcal cell wall stimulates antibody response 2. Some antibodies cross-react with heart tissue 3. Rheumatic fever
37
Symptoms of Serum Sickness
- Fever - Lymphadenopathy - Arthralgia - Cutaneous Eruptions (Urticarial Rash) - GI Disturbances (Vomiting, Diarrhea) - Proteinuria - Decrease serum complement levels
38
Type IV Hypersensitivity Reaction - CTL
Delayed Type and Contract Type Cell-Associated Antigens trigger Cytotoxic T-Cells to induces Cytotoxicity of target cells
39
What are the different classes of Autoimmune Disease
Type II - Antibody reacting with cell surface/matrix antigen Type III - Immune complexes Type IV - T-Cell Mediated Cytotoxicity No Type I as no autoimmune disease is mediated by IgE
40
Tissue Specific Effects of Degranulation - Gastrointestinal
- Increased Fluid Secretion - Increased Peristalsis --> Expulsion of GI tract contents (diarrhea, vomiting)
41
Immune Complex Stoichiometry
Early - Too little antibody, lots of antigens --> Small immune complexes are formed however, complement is not activated, and are not cleared from circulation Intermediate - Amount of antigens is comparable to antibody --> Immune complexes are formed that can fix complement and are cleared from circulation Late - Large amounts of antibody, little antigen --> Immune complexes of intermediate size can fix complement are cleared from circulation
42
What kind of Type III diseases can a inhaled dose cause
Immune-Complex Deposition in Alveolar Capillary interface - Farmer's lung
43
Arthus Reaction Process
1. Antigen introduced into subcutaneous tissue 2. Local AGC process the antigen and present it to T-Cells 3. TH1 Cells recognize antigen and release cytokines which act on vascular endothelium 4. Recruitment of T cells, phagocytes, fluid, and proteins to the site of antigen injection 5. Visible legions form
44
Mechanism of Type I Hypersensitivity
1. IgE binds to Fc Epsilon receptors on granulocyte cells. (Mast Cells, Eosinophils, Basophils) 2. Antigen binds to IgE triggering granulocyte cell 2. Degranulation of cell releasing pre-packaged inflammatory mediators 3. Later stage mediators are also synthesized by the cells after activation
45
What is an Arthus Reaction
Occurs after injection of sub-cutaneous Ag - Results in localized area of erythema and hard swelling caused by immune complex formation
46
Kinds of Type IV TH1 Reactions
Contact Dermatitis, Tuberculin Reaction
47
Tissue Specific Effects of Degranulation - Airways
- Decreased diameter - Mucus secretion --> Expulsion of airway contents (phlegm, coughing)
48
What pre-packaged reactants are released by Eosinophils (Enzymes) - What are their biological effects
Eosinophil Peroxidase - Toxic to target by catalyzing halogenation - Triggers histamine release in mast cells Eosinophil Collagenase - Remodels connective tissue matrix
49
What causes Type III Hypersensitization
Small, insoluble immune complexes of Antigen and Specific Antibody are deposited on walls of blood vessels (kidneys) or lung alveoli - Activates complement on tissue surface leading to inflammatory response and tissue damage
50
What causes a bullseye rash
Lyme Disease
51
What reactants are synthesized after mast cell activation (Lipid Mediator) - What are their biological effects
Leukotriene C4, D4, and E4 - Causes smooth muscle contraction - Increases vascular permeability - Causes mucus secretion Platelet-activating factor - Chemotactic for leukocytes - Amplifies production of lipid mediators - Activates neutrophils, eosinophils, and platelets
52
What causes Type II Hypersensitivity
1. Small molecules that covalently bind to surface of human cells 2. Produce modified structure that is recognized as foreign by immune system 3. Cell destruction through IgG antibody formation, complement protein, and phagocytosis
53
Kinds of Type II Reactions
Drug Allergies (Penicillin)
54
Type 1 diabetes (insulin-dependent diabetes mellitus) - Type of Disease - Autoantigen - Consequence
- T Cell-mediated Disease (Type IV) - Pancreatic Beta-Cell antigen - Beta-Cell Destruction
55
Mixed Essential Cryoglobulinemia - Type of Disease - Autoantigen - Consequence
- Immune-Complex Disease (Type III) - Rheumatoid factor IgG complexes (With or without hepatitis C antigens) - Systemic Vasculitis
56
What are the difference in the granules of Basophils vs Mast Cells
Similar - Both have same stem-cell precursor Difference - Mast Cells secrete IL-4 and IL-13 to initiate TH2 lymphocyte activation
57
What pre-packaged reactants are released by Mast Cells (Cytokines) - What are their biological effects
TNF-alpha - Promote inflammation - Activates leaky endothelium - Stimulates cytokine production
58
Allergic Reaction Treatment (Pharmacological)
1. Block effector pathways (Histamine receptor blocker) 2. Suppress leukocyte function (Corticosteroids) 3. Prevent degranulation (Cromolyn Sodium) 4. Treat anaphylactic reaction (Epinephrine --> Produces a vasoconstriction effect)
59
What is an Autoimmune Response
Antibody and T-Cells attack healthy cells and tissues as though they were infected with a pathogen - Remains throughout lifetime of patient - Increases in severity and can contribute to cause of death
60
What are Urticarial Rashes
Type III Hypersensitivity reaction - Oral edema without mucosal involvement resulting in red wheal-like swellings that overlap each other
61
Treatment Strategies for Type II and Type III Hypersensitivity Reactions
- Discontinue any drug that elicits hypersensitivity - For blood products be careful of cross matching ABO and Rhesus antigens - For mild cases (Urticaria) use antihistamines - For Anaphylaxis use epinephrine, oxygen supplementation, airway management, ECG monitoring, IV fluids/dialysis
62
What reactants are synthesized after Eosinophil cell activation (Lipid Mediators) - What are their biological effects
Leukotrienes C4, D4, E4 - Cause smooth muscle contraction - Increase vascular permeability - Cause mucus secretions Platelet-Activating Factor - Chemotactic to leukocytes - Amplifies production of lipid mediators - Activates neutrophil, eosinophils, and platelets
63
What are the different types of Type IV Hypersensitivity Reactions
Delayed-type Hypersensitivity Contact Hypersensitivity
64
Type III Hypersensitivity Reaction
Immune Complex Soluble antigens trigger release of IgG which acts on complement phagocytes triggering immune complex and downstream inflammatory effects
65
Allergic Reaction Treatment (Immunological)
1. Desensitization Procedure - Shift away from IgE towards IgG4 isotype 2. Series of allergen injections - Small initial dose and gradual increase 3. Vaccination wit discrete allergen-derived peptides - Promotes TH1 response, or anti idiotype antibody vaccine
66
Serum sickness process
1. Body sees antigens from a IV Ag injection as foreign 2. Leads to formation of immune complexes between IgG and antigen 3. Activation of complement releases inflammatory mediators like C5a, C3a, and C4a. 4. C5a induces mast cell degranulation 5. Local inflammation, movement of fluid and protein into tissues
67
What kind of Type III diseases can an IV High Dose injection cause
Immune-Complex Deposition in Blood Vessel Walls - Vasculitis Immune-Complex Deposition in Renal Glomeruli - Nephritis Immune-Complex Deposition in Joint Spaces - Arthritis
68
What reactants are synthesized after mast cell activation (Chemokines) - What are their biological effects
CCL3 - Chemotactic for monocytes, macrophages, and neutrophils
69
What do Eosinophils do
- Regulates expression of Fc epsilon and Complement receptors after simulation by inflammation environment - Releases highly toxic molecules after degranulation
70
What is linkage disequilibrium
Particular alleles of polymorphic HLA genes are combine in HLA haplotypes at higher frequency for a particular disease - More likely for alleles to combine and form the phenotype for a disease
71
What is autoimmune disease
Adaptive immune responses that become misdirected at healthy cells and tissues developing into chronic diseases
72
Type IV Hypersensitivity Reaction - TH1
Delayed Type and Contract Type Soluble antigens trigger TH1 cells to activate macrophages
73
Kinds of Type IV Reactions
Chronic Asthma, Chronic Allergic Rhinitis

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