Hypersensitivity

Question 1

Type 1. Humoral component?

Answer 1

IgE

Question 2

Type 1. Cellular component?

Answer 2

Basophils, Mast cells

Question 3

Type 1. What IL is important?

Answer 3

IL-4, because in type 1 participate basophil, mast cells and IgE

Question 4

Type 1. Sensitization mechanism?

Answer 4

IgE is formed as a result of prior sensitization (i.e., previous contact with the antigen) and coats mast cells and basophils.

Question 5

Type 1. What happens when antigen is encoutered after sensitization?

Answer 5

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

Question 6

Type 1. What means ,,crosslinking”?

Answer 6

free antigen binds to two adjacent IgE antibodies (crosslinking)

Question 7

Type 1. What substances are released from effector cells?

Answer 7

histamine and other mediators (e.g., prostaglandin, platelet-activating factor, leukotrienes, heparin, tryptase)

Question 8

Type 1. What happens once substances are released? what effect?

Answer 8

↑ 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

Question 9

Type 1. What happens in ,,late phase”?

Answer 9

Mast cell secretion of cytokines and other proinflammatory mediators → EOSINOPHIL and NEUTROPHIL chemotaxis → late-phase reaction → inflammation and tissue damage

Question 10

Type 1. Examples?

Answer 10

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

Question 11

Type 2. Humoral component?

Answer 11

1. IgG and IgM

2. Component activation

Question 12

Type 2. Cellular component?

Answer 12

NK cells; Eosinophils, Neutrophils, Macrophages

Question 13

Type 2. what 3 mechanism belong to type 2?

Answer 13

Cellular destruction;
Inflammation;
Cellular dysfunction

Question 14

Type 2. What is patho of IgM and IgG?

Answer 14

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.

Question 15

Type 2. Cell destruction. Antibody-dependent cell-mediated cytotoxicity. What cells?

Answer 15

NK (main) or macrophages

Question 16

Type 2. Cell destruction. Target cell opsonization. What cells?

Answer 16

phagocytosis (eg macrophages) and/or complement activation

Question 17

Type 2. Cell destruction. Examples?

Answer 17

acute hemolytic transfusion reaction,
autoimmune hemolytic anemia,
hemolytic disease of the newborn

Question 18

Type 2. Inflammation. Antibodies bind to cellular surfaces –> ………….. and ……….

Answer 18

activation of the complement system and Fc-receptor mediated immune cell activation

Question 19

Type 2. Inflammation. Examples?

Answer 19

Goodpasture syndrome, rheumatic fever

Question 20

Type 2. Impaired cellular function. Mechanism?

Answer 20

Antibodies bind to cell surface receptors → inhibition or activation of downstream signaling pathways → impaired cellular function

Question 21

Type 2. Impaired cellular function. Examples?

Answer 21

Myastenia gravis, Graves disease

Question 22

Type 3. Humoral component?

Answer 22

Deposition of ANTIBODY (mainly IgG)-ANTIGEN complexes;

Complement activation

Question 23

Type 3. Cellular component?

Answer 23

Neutrophils –> release lysosomal enzymes

Question 24

Type 3. What happens once deposits are present in tissues?

Answer 24

Immune complexes are deposited in tissue, especially blood vessels → initiation of complement cascade → release of lysosomal enzymes from neutrophils → cell death → inflammation → vasculitis

Question 25

Type 3. The most common site of deposit accumulation?

Answer 25

blood vessels

Question 26

Type 3. Type III means three things stuck together: ....+....+......

Answer 26

antigen + antibody + complement

Question 27

Type 3. what two manifestations?

Answer 27

Serum sickness (general) and arthus reaction (local)

Question 28

Type 3. Serum sickness commonly induced by?

Answer 28

Antivenom or antitoxin; Medications most frequently antibiotics (e.g., penicillin, amoxicillin, cefaclor, trimethoprim-sulfamethoxazole); Infections: Hepatitis B virus

Question 29

Type 3. Mechanism of serum sickness?

Answer 29

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

Question 30

Type 3. When occurs symptoms in serum sickness?

Answer 30

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.

Question 31

Type 3. Sypmtoms of serum sickness?

Answer 31

``` 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

Question 32

Type 3. Etiology arthus reaction (its subacute reaction)?

Answer 32

Vaccination against tetanus, diphtheria

Question 33

Type 3. What people are predisposed to arthus reaction?

Answer 33

Presentisitized people, who have preformed IgG ciculating

Question 34

Type 3. arthus reaction pathophysiology?

Answer 34

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

Question 35

Type 3. arthus reaction symptoms?

Answer 35

Localized swelling, erythema, hemorrhage Sometimes superficial skin necrosis a few hours after booster vaccination Reaction peaks 12–36 hours later. Its SUBACUTE REACTION

Question 36

Type 3. Examples?

Answer 36

Vasculitis: Polyarteritis nodosa; Drug-induced hypersensitivity vasculitis Nephropathy: Poststreptococcal glomerulonephritis, Lupus nephritis, IgA nephropathy, Membranous nephropathy Rheumatoid arthritis Hypersensitivity pneumonitis

Question 37

Type 4. Humoral component?

Answer 37

NONE

Question 38

Type 4. Cellular component?

Answer 38

T cells and macrophages

Question 39

Type 4. Those reactions are referred as?

Answer 39

delayed and cell-mediated

Question 40

Type 4. two major steps?

Answer 40

T cell sensitization and Presensitized T cell response

Question 41

Type 4. T cell sensitization mechanism?

Answer 41

T cell sensitization: skin penetration by the antigen → uptake of the antigen by Langerhans cell → migration to lymph nodes → formation of sensitized T lymphocytes

Question 42

Type 4. Presensitized T cell response?

Answer 42

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

Question 43

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)

Answer 43

Allergic contact dermatitis

Question 44

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)

Answer 44

Skin tests: Candida skin test (to test the immune function of T cells); Mantoux tuberculin skin test for latent tuberculosis

Question 45

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)

Answer 45

Systemic disorders: Guillain-Barré syndrome, Hashimoto thyroiditis, Multiple sclerosis, Type 1 DM

Question 46

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)

Answer 46

Stevens-Johnson syndrome and toxic epidermal necrolysis

Question 47

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 ................

Answer 47

DRESS syndrome (drug reaction with eosinophilia and systemic symptoms syndrome; also known as drug-induced hypersensitivity syndrome)

Question 48

Basophils, Mast cells?

Answer 48

type 1

Question 49

histamine and other mediators (e.g., prostaglandin, platelet-activating factor, leukotrienes, heparin, tryptase)?

Answer 49

type 1

Question 50

Anaphylaxis?

Answer 50

type 1

Question 51

Allergies (food: nuts, shellfish, eggs, soy, wheat; drugs: penicillin, muscle relaxants; insect venom allergies (e.g., bee, wasp)?

Answer 51

type 1

Question 52

Allergic or anaphylactic transfusion reactions (e.g., in patients with IgA deficiency)?

Answer 52

type 1

Question 53

Reactions to inhaled or other environmental allergens (e.g., dust mites, animal dander, pollen, latex) → asthma, allergic rhinitis, atopy?

Answer 53

type 1

Question 54

Humoral? 1. IgG and IgM 2. Component activation

Answer 54

type 2

Question 55

NK cells; Eosinophils, Neutrophils, Macrophages?

Answer 55

type 2

Question 56

Cellular destruction; Inflammation; Cellular dysfunction

Answer 56

type 2

Question 57

IgM and IgG mistakenly bind to surface antigens of the cells in the body (aka Cell is opsonized (coated) by antibodies)?

Answer 57

type 2

Question 58

NK (main) or macrophages?

Answer 58

Type 2. Cell destruction. Antibody-dependent cell-mediated cytotoxicity.

Question 59

phagocytosis (eg macrophages) and/or complement activation?

Answer 59

Cell destruction. Target cell opsonization.

Question 60

acute hemolytic transfusion reaction?

Answer 60

Type 2. Cell destruction.

Question 61

autoimmune hemolytic anemia?

Answer 61

Type 2. Cell destruction.

Question 62

hemolytic disease of the newborn?

Answer 62

Type 2. Cell destruction.

Question 63

Goodpasture syndrome

Answer 63

Type 2. Inflammation.

Question 64

Rheumatic fever

Answer 64

Type 2. Inflammation.

Question 65

Myastenia gravis

Answer 65

Type 2. Impaired cellular function.

Question 66

Graves disease

Answer 66

Type 2. Impaired cellular function.

Question 67

Neutrophils --> release lysosomal enzymes, what type?

Answer 67

Type 3. Cellular component

Question 68

Antivenom or antitoxin?

Answer 68

Type 3. Serum sickness

Question 69

Infections: Hepatitis B virus?

Answer 69

Type 3. Serum sickness

Question 70

Medications most frequently antibiotics (e.g., penicillin, amoxicillin, cefaclor, trimethoprim-sulfamethoxazole)?

Answer 70

Type 3. Serum sickness

Question 71

Vaccination against tetanus?

Answer 71

Type 3. arthus reaction

Question 72

Vaccination against diphtheria?

Answer 72

Type 3. arthus reaction

Question 73

Vasculitis: Polyarteritis nodosa; Drug-induced hypersensitivity vasculitis?

Answer 73

Type 3.

Question 74

Nephropathy: Poststreptococcal glomerulonephritis, Lupus nephritis, IgA nephropathy, Membranous nephropathy?

Answer 74

Type 3.

Question 75

Rheumatoid arthritis?

Answer 75

Type 3.

Question 76

Hypersensitivity pneumonitis?

Answer 76

Type 3.

Question 77

T cells and macrophages?

Answer 77

type 4

Question 78

Skin tests: Candida skin test (to test the immune function of T cells); Mantoux tuberculin skin test for latent tuberculosis

Answer 78

type 4

Question 79

Systemic disorders: Guillain-Barré syndrome, Hashimoto thyroiditis, Multiple sclerosis, Type 1 DM

Answer 79

type 4

Question 80

Stevens-Johnson syndrome and toxic epidermal necrolysis

Answer 80

type 4

Question 81

DRESS syndrome (drug reaction with eosinophilia and systemic symptoms syndrome; also known as drug-induced hypersensitivity syndrome)

Answer 81

type 4

Question 82

Allergic contact dermatitis?

Answer 82

type 4