Hypersensitivity Flashcards
Type 1. Humoral component?
IgE
Type 1. Cellular component?
Basophils, Mast cells
Type 1. What IL is important?
IL-4, because in type 1 participate basophil, mast cells and IgE
Type 1. Sensitization mechanism?
IgE is formed as a result of prior sensitization (i.e., previous contact with the antigen) and coats mast cells and basophils.
Type 1. What happens when antigen is encoutered after sensitization?
Subsequent encounter with antigen results in an IgE-mediated reaction by preformed IgE antibodies: free antigen binds to two adjacent IgE antibodies (crosslinking) → degranulation of cells
Type 1. What means ,,crosslinking”?
free antigen binds to two adjacent IgE antibodies (crosslinking)
Type 1. What substances are released from effector cells?
histamine and other mediators (e.g., prostaglandin, platelet-activating factor, leukotrienes, heparin, tryptase)
Type 1. What happens once substances are released? what effect?
↑ Smooth muscle contraction → bronchospasm, abdominal cramping
Peripheral vasodilation and ↑ vascular permeability → hypovolemia, hypotension
Extravasation of capillary blood → erythema
Fluid shift into the interstitial space → edema, pulmonary edema
Pruritus
Type 1. What happens in ,,late phase”?
Mast cell secretion of cytokines and other proinflammatory mediators → EOSINOPHIL and NEUTROPHIL chemotaxis → late-phase reaction → inflammation and tissue damage
Type 1. Examples?
Anaphylaxis
Allergies (food: nuts, shellfish, eggs, soy, wheat; drugs: penicillin, muscle relaxants; insect venom allergies (e.g., bee, wasp)
Allergic or anaphylactic transfusion reactions (e.g., in patients with IgA deficiency)
Reactions to inhaled or other environmental allergens (e.g., dust mites, animal dander, pollen, latex) → asthma, allergic rhinitis, atopy
Type 2. Humoral component?
- IgG and IgM
2. Component activation
Type 2. Cellular component?
NK cells; Eosinophils, Neutrophils, Macrophages
Type 2. what 3 mechanism belong to type 2?
Cellular destruction;
Inflammation;
Cellular dysfunction
Type 2. What is patho of IgM and IgG?
IgM and IgG mistakenly bind to surface antigens of the cells in the body (aka Cell is opsonized (coated) by antibodies) that results in those 3 mechanisms.
Type 2. Cell destruction. Antibody-dependent cell-mediated cytotoxicity. What cells?
NK (main) or macrophages
Type 2. Cell destruction. Target cell opsonization. What cells?
phagocytosis (eg macrophages) and/or complement activation
Type 2. Cell destruction. Examples?
acute hemolytic transfusion reaction,
autoimmune hemolytic anemia,
hemolytic disease of the newborn
Type 2. Inflammation. Antibodies bind to cellular surfaces –> ………….. and ……….
activation of the complement system and Fc-receptor mediated immune cell activation
Type 2. Inflammation. Examples?
Goodpasture syndrome, rheumatic fever
Type 2. Impaired cellular function. Mechanism?
Antibodies bind to cell surface receptors → inhibition or activation of downstream signaling pathways → impaired cellular function
Type 2. Impaired cellular function. Examples?
Myastenia gravis, Graves disease
Type 3. Humoral component?
Deposition of ANTIBODY (mainly IgG)-ANTIGEN complexes;
Complement activation
Type 3. Cellular component?
Neutrophils –> release lysosomal enzymes
Type 3. What happens once deposits are present in tissues?
Immune complexes are deposited in tissue, especially blood vessels → initiation of complement cascade → release of lysosomal enzymes from neutrophils → cell death → inflammation → vasculitis
Type 3. The most common site of deposit accumulation?
blood vessels
Type 3. Type III means three things stuck together: ….+….+……
antigen + antibody + complement
Type 3. what two manifestations?
Serum sickness (general) and arthus reaction (local)
Type 3. Serum sickness commonly induced by?
Antivenom or antitoxin;
Medications most frequently antibiotics (e.g., penicillin, amoxicillin, cefaclor, trimethoprim-sulfamethoxazole);
Infections: Hepatitis B virus
Type 3. Mechanism of serum sickness?
exposure to an antigen (e.g., antivenom, drug) → formation of antibodies (takes few days) → deposition of antibody-antigen complexes in tissue → activation of the complement cascade → tissue damage and systemic inflammation
Type 3. When occurs symptoms in serum sickness?
Symptoms appear 1–2 weeks following initial exposure (because antibodies take several days to form), and usually resolve within a few weeks after discontinuation of the offending agent.
Type 3. Sypmtoms of serum sickness?
Fever Rash (urticarial or purpuric) Arthralgias, myalgia Lymphadenopathy Proteinuria Hand edema Headache, blurred vision Abdominal pain, diarrhea, nausea/vomiting Mucosal involvement is uncommon
OCCUR 1-2 weeks after exposure
Type 3. Etiology arthus reaction (its subacute reaction)?
Vaccination against tetanus, diphtheria
Type 3. What people are predisposed to arthus reaction?
Presentisitized people, who have preformed IgG ciculating
Type 3. arthus reaction pathophysiology?
Intradermal antigen injection in a presensitized individual (previously exposed to the antigen, with preformed, antigen-specific IgG in the serum) → formation of antigen-antibody complexes in the skin → complement activation → local inflammation and possibly necrosis
Type 3. arthus reaction symptoms?
Localized swelling, erythema, hemorrhage
Sometimes superficial skin necrosis a few hours after booster vaccination
Reaction peaks 12–36 hours later.
Its SUBACUTE REACTION
Type 3. Examples?
Vasculitis: Polyarteritis nodosa; Drug-induced hypersensitivity vasculitis
Nephropathy: Poststreptococcal glomerulonephritis, Lupus nephritis, IgA nephropathy, Membranous nephropathy
Rheumatoid arthritis
Hypersensitivity pneumonitis
Type 4. Humoral component?
NONE
Type 4. Cellular component?
T cells and macrophages
Type 4. Those reactions are referred as?
delayed and cell-mediated
Type 4. two major steps?
T cell sensitization and Presensitized T cell response
Type 4. T cell sensitization mechanism?
T cell sensitization: skin penetration by the antigen → uptake of the antigen by Langerhans cell → migration to lymph nodes → formation of sensitized T lymphocytes
Type 4. Presensitized T cell response?
Presensitized T cell response (after repeated contact with the antigen)
–> CD4+ T cells recognize antigens on antigen-presenting cells → release of inflammatory lymphokines cytokines (e.g., IFNγ, TNF α) → macrophages activation → phagocytosis of target cells
–> CD8+ T cells recognize antigens on somatic cells → cell-mediated cytotoxicity → direct cell destruction
Type 4. Examples?
………………..
Skin tests: Candida skin test (to test the immune function of T cells); Mantoux tuberculin skin test for latent tuberculosis
Systemic disorders: Guillain-Barré syndrome, Hashimoto thyroiditis, Multiple sclerosis, Type 1 DM
Stevens-Johnson syndrome and toxic epidermal necrolysis
DRESS syndrome (drug reaction with eosinophilia and systemic symptoms syndrome; also known as drug-induced hypersensitivity syndrome)
Allergic contact dermatitis
Type 4. Examples?
Allergic contact dermatitis
…………..
Systemic disorders: Guillain-Barré syndrome, Hashimoto thyroiditis, Multiple sclerosis, Type 1 DM
Stevens-Johnson syndrome and toxic epidermal necrolysis
DRESS syndrome (drug reaction with eosinophilia and systemic symptoms syndrome; also known as drug-induced hypersensitivity syndrome)
Skin tests: Candida skin test (to test the immune function of T cells); Mantoux tuberculin skin test for latent tuberculosis
Type 4. Examples?
Allergic contact dermatitis
Skin tests: Candida skin test (to test the immune function of T cells); Mantoux tuberculin skin test for latent tuberculosis
………………
Stevens-Johnson syndrome and toxic epidermal necrolysis
DRESS syndrome (drug reaction with eosinophilia and systemic symptoms syndrome; also known as drug-induced hypersensitivity syndrome)
Systemic disorders: Guillain-Barré syndrome, Hashimoto thyroiditis, Multiple sclerosis, Type 1 DM
Type 4. Examples?
Allergic contact dermatitis
Skin tests: Candida skin test (to test the immune function of T cells); Mantoux tuberculin skin test for latent tuberculosis
Systemic disorders: Guillain-Barré syndrome, Hashimoto thyroiditis, Multiple sclerosis, Type 1 DM
…………
DRESS syndrome (drug reaction with eosinophilia and systemic symptoms syndrome; also known as drug-induced hypersensitivity syndrome)
Stevens-Johnson syndrome and toxic epidermal necrolysis
Type 4. Examples?
Allergic contact dermatitis
Skin tests: Candida skin test (to test the immune function of T cells); Mantoux tuberculin skin test for latent tuberculosis
Systemic disorders: Guillain-Barré syndrome, Hashimoto thyroiditis, Multiple sclerosis, Type 1 DM
Stevens-Johnson syndrome and toxic epidermal necrolysis
…………….
DRESS syndrome (drug reaction with eosinophilia and systemic symptoms syndrome; also known as drug-induced hypersensitivity syndrome)
Basophils, Mast cells?
type 1
histamine and other mediators (e.g., prostaglandin, platelet-activating factor, leukotrienes, heparin, tryptase)?
type 1
Anaphylaxis?
type 1
Allergies (food: nuts, shellfish, eggs, soy, wheat; drugs: penicillin, muscle relaxants; insect venom allergies (e.g., bee, wasp)?
type 1
Allergic or anaphylactic transfusion reactions (e.g., in patients with IgA deficiency)?
type 1
Reactions to inhaled or other environmental allergens (e.g., dust mites, animal dander, pollen, latex) → asthma, allergic rhinitis, atopy?
type 1
Humoral?
- IgG and IgM
- Component activation
type 2
NK cells; Eosinophils, Neutrophils, Macrophages?
type 2
Cellular destruction;
Inflammation;
Cellular dysfunction
type 2
IgM and IgG mistakenly bind to surface antigens of the cells in the body (aka Cell is opsonized (coated) by antibodies)?
type 2
NK (main) or macrophages?
Type 2. Cell destruction. Antibody-dependent cell-mediated cytotoxicity.
phagocytosis (eg macrophages) and/or complement activation?
Cell destruction. Target cell opsonization.
acute hemolytic transfusion reaction?
Type 2. Cell destruction.
autoimmune hemolytic anemia?
Type 2. Cell destruction.
hemolytic disease of the newborn?
Type 2. Cell destruction.
Goodpasture syndrome
Type 2. Inflammation.
Rheumatic fever
Type 2. Inflammation.
Myastenia gravis
Type 2. Impaired cellular function.
Graves disease
Type 2. Impaired cellular function.
Neutrophils –> release lysosomal enzymes, what type?
Type 3. Cellular component
Antivenom or antitoxin?
Type 3. Serum sickness
Infections: Hepatitis B virus?
Type 3. Serum sickness
Medications most frequently antibiotics (e.g., penicillin, amoxicillin, cefaclor, trimethoprim-sulfamethoxazole)?
Type 3. Serum sickness
Vaccination against tetanus?
Type 3. arthus reaction
Vaccination against diphtheria?
Type 3. arthus reaction
Vasculitis: Polyarteritis nodosa; Drug-induced hypersensitivity vasculitis?
Type 3.
Nephropathy: Poststreptococcal glomerulonephritis, Lupus nephritis, IgA nephropathy, Membranous nephropathy?
Type 3.
Rheumatoid arthritis?
Type 3.
Hypersensitivity pneumonitis?
Type 3.
T cells and macrophages?
type 4
Skin tests: Candida skin test (to test the immune function of T cells); Mantoux tuberculin skin test for latent tuberculosis
type 4
Systemic disorders: Guillain-Barré syndrome, Hashimoto thyroiditis, Multiple sclerosis, Type 1 DM
type 4
Stevens-Johnson syndrome and toxic epidermal necrolysis
type 4
DRESS syndrome (drug reaction with eosinophilia and systemic symptoms syndrome; also known as drug-induced hypersensitivity syndrome)
type 4
Allergic contact dermatitis?
type 4
