Hypersensitivity Reactions Flashcards

1
Q

Inappropriate/ exaggerated immune responses to •Harmless environmental antigens •Infections •Auto-antigens
causing tissue damage.
Is?

A

Hypersensitivity

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2
Q

Four types according to mechanism of tissue damage ?

A
Type I (Immediate/ anaphylactic) “IgE- mediated” • 
Type II (cytolytic) ”IgG/ IgM   - mediated” 

Type III (immune-complex mediated) ”IgG/IgM-mediated

Type IV (delayed /cell-mediated)

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3
Q

Exaggerated immune responses to harmless environmental antigens (allergens).
?

A

Type “I” hypersensitivity

Immediate/Anaphylactic

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4
Q

Mediated by IgE ?

A

Type “I” hypersensitivity

Immediate / anaphylactic

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5
Q

degranulation of Mast cells and eosinophils ?

A

Type “I” hypersensitivity

Immediate/ anaphylactic

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6
Q

ffects are felt within minutes of exposure

A

Type “I” hypersensitivity

immediate hypersensitivity”

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7
Q

Type” I” hypersensitivity

Mechanism: ?

A

A- Sensitization (1st Exposure):

B- Re-exposure to the same allergen:

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8
Q

Type” I” hypersensitivity

Mechanism: A- Sensitization (1st Exposure): Normally, antigenic stimulation ? And condition ?

A

production of extremely low levels of IgE.
Certain individuals have a genetic predisposition to allergy, respond to certain antigens (allergens) by forming large amounts of IgE. ●IgE molecules bind to Fc receptors on mast cells & basophils
●Thus, 1st exposure to an allergen →
sensitization of Mast cells & Basophils

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9
Q

1st exposure to an allergen →

sensitization of ?

A

Mast cells & Basophils

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10
Q

Type “I” hypersensitivity

Mechanism: B- Re-exposure to the same allergen: ?

A
Antigen binds 2 adjacent IgE  molecules on
mast cells (cross-linking)   → Degranulation of mast cells        “release granules and mediators”.

Degranulation: release 2 kinds of mediators:
• Preformed mediators:

Histamine and platelet activating factor (PAF)

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11
Q

Which type of hypersensitivity and clinical form? symptoms are localized in one organ or system Urticaria (+ itching) Gastrointestinal symptoms
Bronchial asthma

A

Type “I” hypersensitivity Clinical Forms

1. Localized form (Atopy):

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12
Q

Type and clinical form? insect venom (e.g., honey bee sting) Symptoms: ● Itching, severe bronchoconstriction and hypotension

shock

A

Type “I” hypersensitivity Clinical Forms

II. Systemic anaphylaxis:

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13
Q

Detection of the antigen to which the individual is sensitive

extracts of various antigens are introduced into the skin of the patient.
Positive cases show
a wheal and flare reaction that appears
within 15-25 min.

A

Type “I” hypersensitivity Diagnosis

1- Skin test:

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14
Q

Type “I” hypersensitivity Diagnosis through ?

A

1- Skin test

2- Measurement of serum levels of total IgE and IgE specific for a particular allergen.

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15
Q

Mediated by IgG / IgM antibodies reacting with Cell-bound antigen (surface antigen).
?

A

Type “II” hypersensitivity / cytolytic / cytotoxic

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16
Q

Mechanism of tissue damage 1. Complement activation
➢Lysis of target cells
2. Antibody-dependent cell-mediated cytotoxicity (ADCC) through the action of natural killer (NK) cells.
3. Opsonization of target cells
?

A

Type “II” hypersensitivity Mechanism

Cytotoxic/ cytolytic

17
Q
Type of hypersensitivity? 
Transfusion reactions        (Blood group ABO incompatibility).
A

Type 2 cytotoxic

18
Q

Hemolytic disease of the newborn (Rh incompatibility)

Type of hypersensitivity?

A

Type 2 cytotoxic

19
Q

A drug may become attached to a cell surface (e.g., RBCs/platelets) Antibodies to the drug reacting at the cell surface lead to destruction of the cell in presence of complement

Type hypersensitivity?

A

Type 2 hypersensitivity

20
Q

Autoimmune diseases
e.g., Autoimmune hemolytic anemia
(autoantibodies to an individual’s own red blood cells)
Gave’s Disease (antibodies against TSH receptors”agonist effect”)
4. Graft rejection

Type of hypersensitivity?

A

Type 2 cytotoxic

21
Q

When antibodies combine with their specific antigen,
immune complexes are formed
Type of reaction ?

A

Type “III” hypersensitivity IMMUNE-COMPLEX

22
Q

Antibodies (IgG or IgM) formed against ?

A

Type “III” hypersensitivity immune complex

23
Q

Formation of soluble immune complexes antigen and IgG / IgM.

Immune complexes penetrate the endothelium of blood vessel walls & become deposited on the vascular basement membrane.

Complement is activated
& C3a and C5a (anaphylatoxins) are released Platelets are aggregated →
Type of hypersensitivity?

A

Type “III” hypersensitivity immune complex

24
Q

Post-streptococcal glomerulonephritis / Autoimmune diseases e.g., SLE (systemic lupus erythematosis) / Graft rejection
Ex of ?

A

Type “III” hypersensitivity / immune complex

25
Q

Exaggerated cell-mediated immune response ?

A

Type “IV” hypersensitivity : delayed

26
Q

Antibodies have NO role

The main cell involved is the activated Th1

A

Type “IV” hypersensitivity delayed

27
Q

Sensitized Th1 cells recognize antigens and release •pro-inflammatory cytokines.?

A

Type “IV” hypersensitivity Mechanism

28
Q
Tuberculin skin test (TST):      A small amount of the antigen, purified
protein derivative (PPD) of tubercle bacilli, is injected intradermally into a person.

Interpretation of results: after 48-72 hours
This induration is due to accumulation of macrophages and lymphocytes.
(diameter !!)

Type of hypersensitivity?

A

Type “IV” hypersensitivity

29
Q

Granuloma formation

Type of hypersensitivity?

A

Type “IV” hypersensitivity Examples