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PHARM 310 > Allergy & Hypersensitivity vs Autoimmune Disease > Flashcards

Allergy & Hypersensitivity vs Autoimmune Disease Flashcards

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
Q

Kinds of Type I Reactions

A

Allergic Rhinitis, Asthma, Systemic Anaphylaxis

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26
Q

Acute Allergic Asthma vs Chronic Allergic Asthma

A

Acute
- Mast Cell Mediated

Chronic
- Eosinophil and Cytokine mediated

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27
Q

Kinds of Type III Reactions

A

Serum Sickness, Arthus Reaction

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28
Q

What is Autoimmune Hemolytic Anemia

A

A type II autoimmune disease that targets Erythrocytes

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29
Q

Tissue Specific Effects of Degranulation
- Blood Vessels

A
  • Increased blood flow
  • Increased permeability
    –> Edema, Inflammation, Increased lymph flow of antigen to lymph nodes
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30
Q

Penicillin Allergy Process

A
  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
  7. Activation of complement components C1-C3 leads to covalent bonding of C3b and phagocytosis of antibody and complement coated RBC
31
Q

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

A

Histamine, Heparin
- Toxic to parasites
- Increase vascular permeability
- Causes smooth muscle contraction

32
Q

Rheumatoid Arthritis
- Type of Disease
- Autoantigen
- Consequence

A
  • T Cell-mediated Disease (Type IV)
  • Unknown synovial joint antigen
  • Joint inflammation and destruction
33
Q

Delayed-Type Hypersensitivity
- Antigens and Consequences

A

Proteins
- Insect Venom
- Mycobacterial Proteins (Tuberculin, lepromin)

Results in Local Skin Swelling
- Erythema
- Induration
- Cellular infiltrate
- Contact Dermatitis

34
Q

Treatment for Type IV Hypersensitivity

A
  • Avoid contact with agent that cases hypersensitivity
  • Monitor for local infection risk
  • Corticosteroids, Cyclosporins, and Immunotherapy
35
Q

What commonly triggers Type I Hypersensitivity

A

Inhaled particulate Antigen causing Anaphylaxis

36
Q

Relation between infections and autoimmune disease

A

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
Q

Symptoms of Serum Sickness

A
  • Fever
  • Lymphadenopathy
  • Arthralgia
  • Cutaneous Eruptions (Urticarial Rash)
  • GI Disturbances (Vomiting, Diarrhea)
  • Proteinuria
  • Decrease serum complement levels
38
Q

Type IV Hypersensitivity Reaction
- CTL

A

Delayed Type and Contract Type

Cell-Associated Antigens trigger Cytotoxic T-Cells to induces Cytotoxicity of target cells

39
Q

What are the different classes of Autoimmune Disease

A

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
Q

Tissue Specific Effects of Degranulation
- Gastrointestinal

A
  • Increased Fluid Secretion
  • Increased Peristalsis
    –> Expulsion of GI tract contents (diarrhea, vomiting)
41
Q

Immune Complex Stoichiometry

A

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
Q

What kind of Type III diseases can a inhaled dose cause

A

Immune-Complex Deposition in Alveolar Capillary interface
- Farmer’s lung

43
Q

Arthus Reaction Process

A
  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
Q

Mechanism of Type I Hypersensitivity

A
  1. IgE binds to Fc Epsilon receptors on granulocyte cells. (Mast Cells, Eosinophils, Basophils)
  2. Antigen binds to IgE triggering granulocyte cell
  3. Degranulation of cell releasing pre-packaged inflammatory mediators
  4. Later stage mediators are also synthesized by the cells after activation
45
Q

What is an Arthus Reaction

A

Occurs after injection of sub-cutaneous Ag
- Results in localized area of erythema and hard swelling caused by immune complex formation

46
Q

Kinds of Type IV TH1 Reactions

A

Contact Dermatitis, Tuberculin Reaction

47
Q

Tissue Specific Effects of Degranulation
- Airways

A
  • Decreased diameter
  • Mucus secretion
    –> Expulsion of airway contents (phlegm, coughing)
48
Q

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

A

Eosinophil Peroxidase
- Toxic to target by catalyzing halogenation
- Triggers histamine release in mast cells

Eosinophil Collagenase
- Remodels connective tissue matrix

49
Q

What causes Type III Hypersensitization

A

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
Q

What causes a bullseye rash

A

Lyme Disease

51
Q

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

A

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
Q

What causes Type II Hypersensitivity

A
  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
Q

Kinds of Type II Reactions

A

Drug Allergies (Penicillin)

54
Q

Type 1 diabetes (insulin-dependent diabetes mellitus)
- Type of Disease
- Autoantigen
- Consequence

A
  • T Cell-mediated Disease (Type IV)
  • Pancreatic Beta-Cell antigen
  • Beta-Cell Destruction
55
Q

Mixed Essential Cryoglobulinemia
- Type of Disease
- Autoantigen
- Consequence

A
  • Immune-Complex Disease (Type III)
  • Rheumatoid factor IgG complexes (With or without hepatitis C antigens)
  • Systemic Vasculitis
56
Q

What are the difference in the granules of Basophils vs Mast Cells

A

Similar
- Both have same stem-cell precursor

Difference
- Mast Cells secrete IL-4 and IL-13 to initiate TH2 lymphocyte activation

57
Q

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

A

TNF-alpha
- Promote inflammation
- Activates leaky endothelium
- Stimulates cytokine production

58
Q

Allergic Reaction Treatment
(Pharmacological)

A
  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
Q

What is an Autoimmune Response

A

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
Q

What are Urticarial Rashes

A

Type III Hypersensitivity reaction
- Oral edema without mucosal involvement resulting in red wheal-like swellings that overlap each other

61
Q

Treatment Strategies for Type II and Type III Hypersensitivity Reactions

A
  • 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
Q

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

A

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
Q

What are the different types of Type IV Hypersensitivity Reactions

A

Delayed-type Hypersensitivity

Contact Hypersensitivity

64
Q

Type III Hypersensitivity Reaction

A

Immune Complex

Soluble antigens trigger release of IgG which acts on complement phagocytes triggering immune complex and downstream inflammatory effects

65
Q

Allergic Reaction Treatment
(Immunological)

A
  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
Q

Serum sickness process

A
  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
Q

What kind of Type III diseases can an IV High Dose injection cause

A

Immune-Complex Deposition in Blood Vessel Walls
- Vasculitis

Immune-Complex Deposition in Renal Glomeruli
- Nephritis

Immune-Complex Deposition in Joint Spaces
- Arthritis

68
Q

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

A

CCL3
- Chemotactic for monocytes, macrophages, and neutrophils

69
Q

What do Eosinophils do

A
  • Regulates expression of Fc epsilon and Complement receptors after simulation by inflammation environment
  • Releases highly toxic molecules after degranulation
70
Q

What is linkage disequilibrium

A

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
Q

What is autoimmune disease

A

Adaptive immune responses that become misdirected at healthy cells and tissues developing into chronic diseases

72
Q

Type IV Hypersensitivity Reaction
- TH1

A

Delayed Type and Contract Type

Soluble antigens trigger TH1 cells to activate macrophages

73
Q

Kinds of Type IV Reactions

A

Chronic Asthma, Chronic Allergic Rhinitis

PHARM 310 (8 decks)

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