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HYPERSENSITIVITY Flashcards

(59 cards)

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1
Q

• Normal but exaggerated or uncontrolled immune response to an antigen that can produce inflammation, cell destruction, or tissue injury

A

HYPERSENSITIVITY

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2
Q

antigen can persist, and the immune response can cause damage to the host

A

Hypersensitivity

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3
Q

Time of exposure

A

Immediate
Delayed

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4
Q

• Time of exposure
• Immediate-
Delayed-

A

antibody mediated
IgE, IgG, IgM

cell mediated
T-helper cells
48-72 hours

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5
Q

TYPES OF ANTIGENS AND REACTIONS

A

Latex allergies
Environmental substances
Infectious agents
Food allergies

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6
Q

Latex Allergies
• High-risk group:
- Latex:

A

children with frequent medical treatment or lengthy surgeries

natural rubber product

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7
Q

Reactions:
• IgE-mediated allergic reactions
• Cell-mediated contact dermatitis
• Irritant dermatitis

A

Latex

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8
Q

Environmental Substances

A

Allergens
Haptens
Toxin and irritants
Drug administration

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9
Q

• Influenza virus
• Damage epithelial cells in the respiratory tract
• Cytokine storm

A

Infectious Agents

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10
Q

• Cow’s milk, soy, chicken eggs, peanuts, tree nuts, wheat, fish, and crustaceans
• No current treatment available

A

Food Allergies

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11
Q

TYPE I HYPERSENSITIVITY
Aka

A

(Anaphylactic Hypersensitivity)

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12
Q

•______ derived from the Greek word atopos (meaning “out of place”): an inherited tendency to develop classic allergic responses to naturally occurring inhaled or ingested allergens

A

Atopy

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13
Q

• passive cutaneous anaphylaxis

A

Carl Wilhelm Prausnitz and Heinz Küstner (1921):

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14
Q

• Triggered by allergens (peanuts, eggs, and pollen)
• Immediate allergic reactions

A

TYPE I HYPERSENSITIVITY
(Anaphylactic Hypersensitivity)

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15
Q

TYPE I HYPERSENSITIVITY
IMMUNOLOGIC MECHANISM
-

A

Sensitization Phase
Activation phase
Late phase

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16
Q
  • Sensitization Phase
  • First exposure leads to\____ production and mast cell sensitization.
    • Th2 cells release cytokines (3)
    • These cytokines prompt B cells to turn into plasma cells, which produce IgE antibodies specific to that allergen.
    • The IgE antibodies attach to mast cells and basophils, preparing them for future encounters with the allergen.
A

IgE

like IL-4, IL-5, and IL-13.

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17
Q

• Re-exposure triggers the immediate release of histamine and other mediators, causing rapid allergic symptoms.

A

Activation Phase

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18
Q

Inflammatory mediators:

A

histamine, heparin and tryptase

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19
Q
  • Chronic inflammation results from the recruitment of immune cells, leading to prolonged symptoms.
A
  • Late Phase
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20
Q

TYPE I HYPERSENSITIVITY
CLINICAL MANIFESTATIONS

A

Allergic rhinitis
Asthma
Urticaria
Angioedema
Anaphylaxis
Food allergies
Drug allergies
Eosinophilic esophagitis

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21
Q

: Sneezing, nasal congestion, and itchy eyes.

: Wheezing, shortness of breath, and coughing.

: Red, itchy, raised hives on the skin.

: Swelling of deeper tissues, especially in the face and throat.

A
  • Allergic Rhinitis
  • Asthma
  • Urticaria
  • Angioedema
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22
Q

: Severe, systemic reaction with rapid onset of symptoms, including difficulty breathing and hypotension.

: Oral, gastrointestinal, skin, and
respiratory symptoms after ingesting allergenic foods.

: Skin reactions, respiratory symptoms, and anaphylaxis.

: Swallowing difficulties and chest pain due to allergic inflammation in the esophagus.

A
  • Anaphylaxis

• Food Allergies

• Drug Allergies

  • Eosinophilic Esophagitis
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23
Q

TYPE I HYPERSENSITIVITY
TREATMENT

  • Pharmacological
A

• Antihistamines
- Corticosteroids
• Leukotriene Receptor Antagonist
• Beta-2-Adrenergic Agonists
• Mast cell stabilizers
• Epinephrine

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24
Q

TYPE I HYPERSENSITIVITY
TREATMENT

(Allergen-specific)

Study These Flashcards
A

• Immunotherapy

25
TYPE I HYPERSENSITIVITY TREATMENT • Emergency treatment of anaphylaxis
• Epinephrine • Oxygen • Intravenous fluids • Antihistamine and corticosteroids
26
TYPE I HYPERSENSITIVITY DETECTION/TESTS
Skin testing Serological tests Challenge testing Others Nasal smear Exhaled Nitric Oxide (FeNO)
27
- Skin testing (3) - Serological tests (2)
- Skin Prick Test (SPT) • Intradermal test - Patch test • Total Serum IgE - Allergen-Specific (RAST)
28
TYPE II HYPERSENSITIVITY Aka
(Antibody-Mediated Cytotoxic Hypersensitivity)
29
• Involves IgG and IgM antibodies directed against antigens found on cell surfaces. • antigens may be altered self-antigens or heteroantigens
TYPE II HYPERSENSITIVITY (Antibody-Mediated Cytotoxic Hypersensitivity)
30
TYPE II HYPERSENSITIVITY (Antibody-Mediated Cytotoxic Hypersensitivity) • Binding of the antibody to a cell can have one of three major effects
• cell can be destroyed • function of the cell can be inhibited - function of the cell can be increased above normal
31
TYPE II HYPERSENSITIVITY MAJOR EFFECTS: Cell Damage Cytotoxicity Mechanism: Examples:
• Complement activation • Opsonization - Antibody-Dependent Cellular Cytotoxicity (ADCC) - Blood Transfusion reactions • Hemolytic Disease of the Newborn (HDN) • Autoimmune Hemolytic Anemia
32
TYPE II HYPERSENSITIVITY MAJOR EFFECTS: Inhibition/Stimulation of Cell Function • Dysfunction of the affected tissue or organ • Enhance activity beyond normal levels
• Functional Impairment • Overactivation
33
TYPE II HYPERSENSITIVITY MAJOR EFFECTS: Inhibition/Stimulation of Cell Function • Autoantibody binds to ACH receptor= MUSCLE WEAKNESS • TSI bind to TSH receptor on thyroid cells=excessive thyroid hormone production= HYPERTHYROIDISM
- Myasthenia Gravis • Grave's Disease
34
TYPE II HYPERSENSITIVITY CLINICAL EXAMPLES - Transfusion Reactions • Mechanism
- Mismatched blood transfusion • Antibody-Antigen binding - Complement activation • Hemolysis and tissue damage
35
TYPE II HYPERSENSITIVITY CLINICAL EXAMPLES - Clinical Manifestation
• Immediate Symptoms: Fever, chills, back pain, tachycardia, and hypotension • Hemoglobinuria • Jaundice
36
TYPE II HYPERSENSITIVITY CLINICAL EXAMPLES • Mechanism • Rh incompatibility • Sensitization of the Mother • Subsequent pregnancy • Destruction of fetal RBCs
• Hemolytic Disease of the Newborn
37
- Clinical Manifestation • Anemia - Hydrops Fetalis • Jaundice - Enlarged Liver and Spleen
• Hemolytic Disease of the Newborn
38
TYPE II HYPERSENSITIVITY CLINICAL EXAMPLES
- Autoimmune hemolytic Anemia (AIHA) • Goodpasture Syndrome - Grave's Disease • Myasthenia Gravis • Pernicious Anemia
39
TYPE II HYPERSENSITIVITY DETECTION/TESTS
• Direct Antiglobulin Test (DAT) or Direct Coombs Test • Indirect Antiglobulin Tests (IAT) or Indirect Coombs Test
40
TYPE II HYPERSENSITIVITY DETECTION/TESTS • Detects Abs/complement on the surface of RBCs • Detects free Abs in the serum that can bind to RBC Ags
• Direct Antiglobulin Test (DAT) or Direct Coombs Test • Indirect Antiglobulin Tests (IAT) or Indirect Coombs Test
41
TYPE II HYPERSENSITIVITY DETECTION/TESTS - Measure specific autoantibodies • Quantifies surface-bound antibodies on cells • Detects Abs deposition in tissues
• Enzyme-Linked Immunosorbent Assay (ELISA) • Flow Cytometry • Tissue Biopsy with Immunofluorescence
42
TYPE III HYPERSENSITIVITY Aka
(Immune Complex-Mediated)
43
Mechanism • ***Immune complex formation*** • Ag-Ab complex in circulation • ***Immune complex deposition*** • Blood vessel walls, kidneys, joints and lungs - ***Activation of complement*** • Release of C3a and C5a (inflammatory mediators) - ***Inflammatory response*** • Release lysosomal enzymes and reactive oxygen species - ***Tissue injury*** • Vasculitis, glomerulonephritis, arthritis
TYPE III HYPERSENSITIVITY (Immune Complex-Mediated)
44
TYPE III HYPERSENSITIVITY CLINICAL EXAMPLES • autoantibodies form against nuclear components • Immune complexes deposit in kidneys, skin, joints and other organs
- Systemic Lupus Erythematosus (SLE)
45
TYPE III HYPERSENSITIVITY CLINICAL EXAMPLES • autoantibodies form immune complexes with IgG • deposit in the synovial joints, leading to chronic inflammation and joint damage.
Rheumatoid Arthritis (RA)
46
TYPE III HYPERSENSITIVITY CLINICAL EXAMPLES
Serum sickness Post-streptococcal Glomerulonephritis Arthus reaction
47
TYPE III HYPERSENSITIVITY CLINICAL EXAMPLES • foreign proteins are introduced into the body • formation of immune complexes that deposit in blood vessels. • formation of immune complexes • deposit in the kidneys, leading to glomerular inflammation - Ag is injected into an individual with high levels of circulating Abs • Immune complexes form at the site of injection, leading to localized inflammation.
• Serum Sickness • Post-Streptococcal Glomerulonephritis - Arthus Reaction
48
TYPE III HYPERSENSITIVITY DETECTION/TESTS
• Immune Complex Detection • Complement Levels (C3, C4). • Tissue Biopsy with Immunofluorescence - ANA and Anti-dsDNA Tests. • Rheumatoid Factor Test • Cryoglobulin Test
49
TYPE IV HYPERSENSITIVITY Aka
(Delayed-Type Hypersensitivity)
50
TYPE IV HYPERSENSITIVITY (Delayed-Type Hypersensitivity) - Described by_____ -______ to develop after antigen exposure • driven by________
Robert Koch (1890) 48 to 72 hours T cells and macrophages
51
TYPE IV HYPERSENSITIVITY Mechanisms:
• Sensitization Phase - Effector Phase (Subsequent Exposure) - Inflammation and Tissue Damage
52
TYPE IV HYPERSENSITIVITY (Delayed-Type Hypersensitivity) 1-2 weeks after the first contact with Ag APCs process the Ag and present it to CD4+ helper (Th1) cells - Th1 cells become sensitized to the antigen and proliferate, generating a population of memory T cells that are specific to the antigen.
Sensitization Phase
53
TYPE IV HYPERSENSITIVITY (Delayed-Type Hypersensitivity) • Upon re-exposure to the same antigen, these sensitized Th1 cells recognize the antigen and become activated. • Activated Th1 cells==IFN-y and TNF==macrophages to site of antigen exposure • Macrophages==lysosomal enzymes, ROS, pro-inflammatory cytokines==tissue damage
Effector Phase (Subsequent Exposure)
54
Inflammation and Tissue Damage • The influx of immune cells leads to inflammation and tissue damage at the site of antigen exposure, which manifests clinically as a delayed hypersensitivity reaction.
TYPE IV HYPERSENSITIVITY (Delayed-Type Hypersensitivity)
55
TYPE IV HYPERSENSITIVITY (Delayed-Type Hypersensitivity) • Development of granulomas that release large amounts of lytic enzymes that can destroy surrounding tissue and promote fibrin deposition
Chronic Type
56
TYPE IV HYPERSENSITIVITY (Delayed-Type Hypersensitivity) Chronic Type Triggers: : M. tuberculosis, M. leprae, P. carinii, Leishmania spp and herpes simplex virus : poison ivy, poison oa, metals, hair dyes and cosmetics
Intracellular Contact Ag
57
TYPE IV HYPERSENSITIVITY CLINICAL EXAMPLES • Contact Dermatitis • Common Cause:_______ • poison ivy, poison oak, and poison sumac • Signs: • erythema, swelling, and the formation of papules that appears from 6 hours to several days after the exposure • Duration:_____
URUSHIOL 3-4 weeks
58
TYPE IV HYPERSENSITIVITY CLINICAL EXAMPLES • inflammation of the alveoli and interstitial spaces. • Common Cause - Bacterial and fungal spores • Symptoms • a dry cough, shortness of breath, fever, chills, weight loss, and general malaise
• Hypersensitivity Pneumonitis
59
TYPE IV HYPERSENSITIVITY DETECTION/TESTS
- Patch Testing • Tuberculin Skin Test (Mantoux Test) - Candida and Other Skin Antigens • Granuloma Formation (via Biopsy)

Immuno-Sero LEC (30 decks)

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