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1 STEP Uworld immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Type 1. Humoral component?

A

IgE

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2
Q

Type 1. Cellular component?

A

Basophils, Mast cells

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3
Q

Type 1. What IL is important?

A

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

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4
Q

Type 1. Sensitization mechanism?

A

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

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5
Q

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

A

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

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6
Q

Type 1. What means ,,crosslinking”?

A

free antigen binds to two adjacent IgE antibodies (crosslinking)

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7
Q

Type 1. What substances are released from effector cells?

A

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

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8
Q

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

A

↑ 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

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9
Q

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

A

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

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10
Q

Type 1. Examples?

A

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

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11
Q

Type 2. Humoral component?

A
  1. IgG and IgM

2. Component activation

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12
Q

Type 2. Cellular component?

A

NK cells; Eosinophils, Neutrophils, Macrophages

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13
Q

Type 2. what 3 mechanism belong to type 2?

A

Cellular destruction;
Inflammation;
Cellular dysfunction

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14
Q

Type 2. What is patho of IgM and IgG?

A

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.

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15
Q

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

A

NK (main) or macrophages

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16
Q

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

A

phagocytosis (eg macrophages) and/or complement activation

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17
Q

Type 2. Cell destruction. Examples?

A

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

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18
Q

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

A

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

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19
Q

Type 2. Inflammation. Examples?

A

Goodpasture syndrome, rheumatic fever

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20
Q

Type 2. Impaired cellular function. Mechanism?

A

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

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21
Q

Type 2. Impaired cellular function. Examples?

A

Myastenia gravis, Graves disease

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22
Q

Type 3. Humoral component?

A

Deposition of ANTIBODY (mainly IgG)-ANTIGEN complexes;

Complement activation

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23
Q

Type 3. Cellular component?

A

Neutrophils –> release lysosomal enzymes

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24
Q

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

A

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

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25
Q

Type 3. The most common site of deposit accumulation?

A

blood vessels

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26
Q

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

A

antigen + antibody + complement

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27
Q

Type 3. what two manifestations?

A

Serum sickness (general) and arthus reaction (local)

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28
Q

Type 3. Serum sickness commonly induced by?

A

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

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29
Q

Type 3. Mechanism of serum sickness?

A

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

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30
Q

Type 3. When occurs symptoms in serum sickness?

A

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.

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31
Q

Type 3. Sypmtoms of serum sickness?

A 
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

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32
Q

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

A

Vaccination against tetanus, diphtheria

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33
Q

Type 3. What people are predisposed to arthus reaction?

A

Presentisitized people, who have preformed IgG ciculating

34
Q

Type 3. arthus reaction pathophysiology?

A

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

35
Q

Type 3. arthus reaction symptoms?

A

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

36
Q

Type 3. Examples?

A

Vasculitis: Polyarteritis nodosa; Drug-induced hypersensitivity vasculitis

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

Rheumatoid arthritis

Hypersensitivity pneumonitis

37
Q

Type 4. Humoral component?

A

NONE

38
Q

Type 4. Cellular component?

A

T cells and macrophages

39
Q

Type 4. Those reactions are referred as?

A

delayed and cell-mediated

40
Q

Type 4. two major steps?

A

T cell sensitization and Presensitized T cell response

41
Q

Type 4. T cell sensitization mechanism?

A

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

42
Q

Type 4. Presensitized T cell response?

A

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

43
Q

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)

A

Allergic contact dermatitis

44
Q

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)

A

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

45
Q

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)

A

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

46
Q

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)

A

Stevens-Johnson syndrome and toxic epidermal necrolysis

47
Q

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

…………….

A

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

48
Q

Basophils, Mast cells?

A

type 1

49
Q

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

A

type 1

50
Q

Anaphylaxis?

A

type 1

51
Q

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

A

type 1

52
Q

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

A

type 1

53
Q

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

A

type 1

54
Q

Humoral?

  1. IgG and IgM
  2. Component activation
A

type 2

55
Q

NK cells; Eosinophils, Neutrophils, Macrophages?

A

type 2

56
Q

Cellular destruction;
Inflammation;
Cellular dysfunction

A

type 2

57
Q

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

A

type 2

58
Q

NK (main) or macrophages?

A

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

59
Q

phagocytosis (eg macrophages) and/or complement activation?

A

Cell destruction. Target cell opsonization.

60
Q

acute hemolytic transfusion reaction?

A

Type 2. Cell destruction.

61
Q

autoimmune hemolytic anemia?

A

Type 2. Cell destruction.

62
Q

hemolytic disease of the newborn?

A

Type 2. Cell destruction.

63
Q

Goodpasture syndrome

A

Type 2. Inflammation.

64
Q

Rheumatic fever

A

Type 2. Inflammation.

65
Q

Myastenia gravis

A

Type 2. Impaired cellular function.

66
Q

Graves disease

A

Type 2. Impaired cellular function.

67
Q

Neutrophils –> release lysosomal enzymes, what type?

A

Type 3. Cellular component

68
Q

Antivenom or antitoxin?

A

Type 3. Serum sickness

69
Q

Infections: Hepatitis B virus?

A

Type 3. Serum sickness

70
Q

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

A

Type 3. Serum sickness

71
Q

Vaccination against tetanus?

A

Type 3. arthus reaction

72
Q

Vaccination against diphtheria?

A

Type 3. arthus reaction

73
Q

Vasculitis: Polyarteritis nodosa; Drug-induced hypersensitivity vasculitis?

A

Type 3.

74
Q

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

A

Type 3.

75
Q

Rheumatoid arthritis?

A

Type 3.

76
Q

Hypersensitivity pneumonitis?

A

Type 3.

77
Q

T cells and macrophages?

A

type 4

78
Q

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

A

type 4

79
Q

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

A

type 4

80
Q

Stevens-Johnson syndrome and toxic epidermal necrolysis

A

type 4

81
Q

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

A

type 4

82
Q

Allergic contact dermatitis?

A

type 4

1 STEP Uworld immunology (13 decks)

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