HYPERSENSITIVITY Flashcards
memorization
A normal but exaggerated or uncontrolled immune response to an antigen that can produce inflammation, cell destruction or tissue injury
Hypersensitivity
Anaphylactic reaction type of hypersensitivity:
TYPE 1 HSR
Cytotoxic reaction type of hypersensitivity:
TYPE 2 HSR
Immune complex type of hypersensitivity:
TYPE 3 HSR
T cell-dependent type of hypersensitivity:
TYPE 4 HSR
Hypersensitivity reactions that can activate complement:
TYPE 2 HSR
TYPE 3 HSR
Antibody mediating in Type 1 HSR:
IgE
Antibody mediating in Type 2 HSR:
IgG/IgM
Antibody mediating in Type 3 HSR:
IgG/IgM
Antibody mediating in type 4 HSR:
None (because of delayed reaction)
Also known as Immediate hypersensitivity:
TYPE 1 HSR
Also known as delayed hypersensitivity:
TYPE 4 HSR
Which of the following is a general characteristic of hypersensitivity
reactions?
a. The immune responsiveness is depressed.
b. Antibodies are involved in all reactions.
c. An exaggerated immune response to an antigen occurs.
d. The antigen triggering the reaction is a harmful one.
c. An exaggerated immune response to an antigen occurs.
Hypersensitivity reactions are characterized by an overactive immune response to harmless or harmless antigens, leading to tissue damage.
Types of hypersensitivity reactions:
1. Type I: Immediate hypersensitivity (allergic reactions, anaphylaxis)
2. Type II: Antibody-dependent cytotoxicity
3. Type III: Immune complex-mediated reactions
4. Type IV: Delayed hypersensitivity (cell-mediated immunity)
Key features:
1. Exaggerated immune response
2. Antigen-specific
3. Immune cells and mediators involved
4. Tissue damage
Which of the following is associated with an increase in IgE
production?
a. Transfusion reaction
b. Activation of Th2 cells
c. Reaction to poison ivy
d. Hemolytic disease of the fetus and newborn
Option b: Activation of Th2 cells
Activation of T-helper 2 (Th2) cells stimulates B cells to produce IgE antibodies, contributing to:
1. Allergic reactions
2. Asthma
3. Atopic diseases (e.g., eczema)
4. Parasitic infections
IgE’s role:
1. Allergen recognition
2. Mast cell activation
3. Histamine release
4. Inflammatory response
Other options:
a. Transfusion reaction: Involves IgG/IgM (Type II hypersensitivity)
c. Reaction to poison ivy: Cell-mediated immunity (Type IV hypersensitivity)
d. Hemolytic disease of the fetus and newborn: Involves IgG (Type II hypersensitivity)
Which of the following would cause a positive DAT test?
a. Presence of IgG on RBCs
b. Presence of C3b or C3d on RBCs
c. A transfusion reaction caused by preformed antibody
d. Any of the above
Option d: Any of the above
A positive Direct Antiglobulin Test (DAT) indicates:
Causes
1. Presence of IgG on RBCs (Option a): Autoantibodies or alloantibodies.
2. Presence of C3b or C3d on RBCs (Option b): Complement activation.
3. Transfusion reaction caused by preformed antibody (Option c): Acute hemolysis.
DAT sensitivity
1. IgG (most common)
2. C3b/C3d (complement)
3. IgM (less common)
Clinical implications
1. Autoimmune hemolytic anemia
2. Alloimmune hemolytic anemia
3. Transfusion reactions
4. Hemolytic disease of the fetus and newborn
All of the following are associated with type I hypersensitivity except
a. release of preformed mediators from mast cells.
b. activation of complement.
c. cell-bound antibody bridged by antigen.
d. an inherited tendency to respond to allergens.
Option b: Activation of complement.
Type I hypersensitivity typically involves:
1. IgE-mediated mast cell activation
2. Release of histamine and other mediators
3. Immediate allergic response
Complement activation is more characteristic of:
1. Type II (cytotoxic)
2. Type III (immune complex)
Which of the following is associated with anaphylaxis?
a. Buildup of IgE on mast cells
b. Activation of complement
c. Increase in cytotoxic T cells
d. Large amount of circulating IgG
Option a: Buildup of IgE on mast cells.
Anaphylaxis characteristics:
Immunological Mechanisms
1. IgE antibodies bind to mast cells and basophils.
2. Allergen cross-links IgE, triggering mast cell activation.
3. Release of histamine, tryptase, and other mediators.
Clinical Symptoms
1. Rapid onset
2. Respiratory distress (bronchospasm)
3. Cardiovascular collapse
4. Cutaneous symptoms (hives, itching)
5. Gastrointestinal symptoms (nausea, vomiting)
To determine if a patient is allergic to ryegrass, the best test to
perform is the
a. total IgE test.
b. skin prick test.
c. DAT.
d. complement fixation.
Option b: Skin prick test.
The skin prick test (SPT) is the gold standard for diagnosing allergies, including ryegrass. It:
Benefits
1. Measures immediate allergic reaction
2. Specificity and sensitivity
3. Rapid results
4. Low cost
Procedure
1. Ryegrass allergen extract applied to skin
2. Prick or puncture with small needle
3. Observe for wheal and flare reaction
Alternative tests
1. Specific IgE blood tests (e.g., ImmunoCAP, RAST)
2. In vitro tests (e.g., ELISA)
Incorrect options
1. Total IgE test: Measures overall IgE levels, not specific allergy.
2. DAT (Direct Antiglobulin Test): Detects antibodies against RBCs.
3. Complement fixation: Measures complement activation, not allergy-specific.
Which condition would result in hemolytic disease of the fetus and
newborn?
a. Buildup of IgE on mother’s cells
b. Sensitization of cytotoxic T cells
c. Exposure to antigen found on both mother and baby RBCs
d. Prior exposure to foreign RBC antigen
Option d: Prior exposure to foreign RBC antigen.
Hemolytic Disease of the Fetus and Newborn (HDFN) occurs when:
1. Maternal sensitization to fetal RBC antigens (e.g., Rh, ABO, Kell).
2. Maternal immune response produces IgG antibodies.
3. Antibodies cross placenta, targeting fetal RBCs.
4. Fetal RBC destruction (hemolysis).
Common scenarios
1. Rh-negative mother, Rh-positive fetus (most common).
2. ABO incompatibility.
3. Other RBC antigen mismatches (e.g., Kell, Duffy).
Incorrect options:
1. Option a: IgE buildup (allergic reactions, not HDFN).
2. Option b: Cytotoxic T-cell sensitization (cell-mediated immunity).
3. Option c: Antigen shared by mother and baby RBCs (wouldn’t trigger immune response).
What is the immune mechanism involved in type III hypersensitivity
reactions?
a. Cellular antigens are involved.
b. Deposition of immune complexes occurs in antibody excess.
c. Only heterologous antigens are involved.
d. Tissue damage results from complement-mediated lysis.
Option b: Deposition of immune complexes occurs in antibody excess.
Type III hypersensitivity reactions involve:
Mechanism:
1. Antigen-antibody (IgG/IgM) complex formation.
2. Immune complex deposition in tissues (e.g., skin, kidneys, joints).
3. Complement activation (C3, C5).
4. Neutrophil recruitment.
5. Inflammation and tissue damage.
Characteristics:
1. Immune complex-mediated.
2. Antibody excess.
3. Localized or systemic.
4. Examples: Systemic lupus erythematosus (SLE), rheumatoid arthritis.
Incorrect options:
1. Option a: Cellular antigens (Type IV hypersensitivity).
2. Option c: Heterologous antigens (not specific to Type III).
3. Option d: Complement-mediated lysis (Type II hypersensitivity).
What is the immune phenomenon associated with the Arthus
reaction?
a. Tissue destruction by cytotoxic T cells
b. Removal of antibody-coated RBCs
c. Deposition of immune complexes in blood vessels
d. Release of histamine from mast cells
Option c: Deposition of immune complexes in blood vessels.
The Arthus reaction is a localized Type III hypersensitivity reaction, characterized by:
Immune Mechanism:
1. Antigen-antibody (IgG) complex formation.
2. Immune complex deposition in blood vessel walls.
3. Complement activation (C3, C5).
4. Neutrophil recruitment.
5. Inflammation, vascular damage and necrosis.
Clinical Features:
1. Localized skin lesions.
2. Redness, swelling, and induration.
3. Necrosis.
Examples:
1. Immunization reactions.
2. Serum sickness.
3. Vasculitis.
Incorrect options:
1. Option a: Cytotoxic T-cell activity (Type IV hypersensitivity).
2. Option b: Antibody-mediated RBC removal (Type II hypersensitivity).
3. Option d: Histamine release (Type I hypersensitivity).
Which of the following conclusions can be drawn about a patient
whose total IgE level was determined to be 150 IU/mL?
a. The patient definitely has allergic tendencies.
b. The patient may be subject to anaphylactic shock.
c. Antigen-specific testing should be done.
d. The patient will never have an allergic reaction.
Option c: Antigen-specific testing should be done.
Elevated total IgE (150 IU/mL) indicates:
Possible Conditions
1. Allergic predisposition
2. Atopic dermatitis
3. Parasitic infections
4. Asthma
Limitations
1. Doesn’t confirm specific allergy
2. Doesn’t predict severity
3. Non-allergic conditions can elevate IgE
Next Steps
1. Antigen-specific IgE testing (e.g., ImmunoCAP, RAST)
2. Skin prick testing
3. Clinical evaluation
Incorrect options:
a. Elevated IgE suggests, but doesn’t confirm, allergic tendencies.
b. Anaphylactic shock requires specific allergen exposure.
d. Elevated IgE doesn’t rule out non-allergic conditions.
Which of the following explains the difference between type II and
type III hypersensitivity reactions?
a. Type II involves cellular antigens.
b. Type III involves IgE.
c. IgG is involved only in type III reactions.
d. Type II reactions involve no antibody.
Option a: Type II involves cellular antigens.
Type II Hypersensitivity:
Characteristics
1. Antibody-dependent (IgG, IgM)
2. Target: Cellular antigens (RBCs, platelets, tissues)
3. Mechanisms: Complement activation, antibody-dependent cellular cytotoxicity (ADCC)
4. Examples: Hemolytic disease of the newborn (HDN), autoimmune hemolytic anemia
Type III Hypersensitivity:
Characteristics
1. Immune complex-mediated (IgG, IgM)
2. Target: Small vessels, connective tissue
3. Mechanisms: Complement activation, neutrophil recruitment
4. Examples: Systemic lupus erythematosus (SLE), rheumatoid arthritis
Key differences:
1. Antigen location: Type II (cell-bound), Type III (soluble immune complexes)
2. Mechanism: Type II (ADCC, complement), Type III (immune complex deposition)
3. IgE involvement: Neither Type II nor Type III (IgE is associated with Type I hypersensitivity)
Incorrect options:
b. Type III involves IgG/IgM, not IgE.
c. IgG is involved in both Type II and Type III.
d. Type II reactions involve antibodies.
Two days after administration of the tuberculin skin test, a female health-care worker developed an area of redness and induration 12mm in size at the injection site. This result means that she has
a. an active case of TB.
b. been exposed to M. tuberculosis.
c. developed protective immunity against TB.
d. a result in the normal range for her risk group.
Option b: Been exposed to M. tuberculosis.
Tuberculin Skin Test (TST) Interpretation:
Reaction Size
1. 0-4 mm: Negative (no infection)
2. 5-9 mm: Indeterminate (repeat test recommended)
3. ≥10 mm: Positive (exposure or infection)
Interpretation
1. ≥10 mm:
- Confirmation of M. tuberculosis infection (active or latent)
- Further testing (chest X-ray, sputum smear) recommended
2. Not necessarily active TB disease
A young woman developed red, itchy papules on her wrist 2 days after wearing a new bracelet. This reaction was caused by
a. IgE-sensitized mast cells in the skin.
b. antigen–antibody complexes in the skin.
c. damage to the skin cells by antibodies and complement.
d. an inflammatory response induced by cytokines released from Th1
cells.
Option d: An inflammatory response induced by cytokines released from Th1 cells.
This reaction is consistent with:
Type IV Hypersensitivity (Delayed Hypersensitivity)
Characteristics:
1. Cell-mediated immunity (T-cell response)
2. Th1 cells activate macrophages
3. Cytokine release (e.g., IFN-γ, TNF-α)
4. Inflammatory response
5. Delayed onset (48-72 hours)
Common causes:
1. Contact dermatitis (e.g., nickel, latex)
2. Allergic reactions to jewelry (e.g., nickel)
Incorrect options:
1. Option a: IgE-mediated response (Type I hypersensitivity, immediate reaction)
2. Option b: Immune complex-mediated response (Type III hypersensitivity)
3. Option c: Antibody-dependent cellular cytotoxicity (Type II hypersensitivity)
Reactions to latex are caused by
a. type I hypersensitivity.
b. type IV hypersensitivity.
c. skin irritation.
d. all of the above
Option d: All of the above.
Latex reactions can manifest through:
Type I Hypersensitivity (Immediate Allergic Reaction)
1. IgE-mediated response
2. Symptoms: Hives, itching, swelling, anaphylaxis
Type IV Hypersensitivity (Delayed Hypersensitivity)
1. Cell-mediated immunity (T-cell response)
2. Symptoms: Contact dermatitis, redness, itching
Irritant Contact Dermatitis (Non-Immune)
1. Skin irritation (non-allergic)
2. Symptoms: Redness, itching, dryness, cracking
Prevalence:
1. Healthcare workers (8-17%)
2. Patients with spina bifida (73%)
3. Individuals with frequent latex exposure
Prevention
1. Use latex-free products
2. Wear protective gloves
3. Implement latex-safe protocols
To determine a cold agglutinin titer,
a. patient serum should be separated from whole blood at 4°C and tested at 4°C.
b. patient serum should be separated from whole blood at 4°C and tested at 37°C.
c. patient serum should be separated from whole blood at 37°C and tested at 4°C.
d. patient serum should be separated from whole blood at 37°C and tested at 37°C.
Option c: Patient serum should be separated from whole blood at 37°C and tested at 4°C.
Rationale:
1. Separate serum at 37°C to prevent cold agglutinins from binding to RBCs.
2. Test serum at 4°C to detect cold agglutinins.
This method:
1. Prevents in vitro agglutination during separation.
2. Allows detection of cold agglutinins at low temperatures.
In vitro methods to detect a cell-mediated response to M. tuberculosis measure production of which of the following immunologic components?
a. IgE antibody
b. Interleukin-1
c. Interleukin-2
d. Interferon-gamma
Option d: Interferon-gamma
Cell-mediated immunity (CMI) to M. tuberculosis involves T-cell activation, producing cytokines like interferon-gamma (IFN-γ). In vitro tests measure IFN-γ production:
Examples of tests:
1. QuantiFERON-TB Gold (QFT-G)
2. QuantiFERON-TB Gold Plus (QFT-Plus)
3. T-SPOT.TB
Why other options are incorrect:
1. IgE antibody (Option a): Associated with Type I hypersensitivity, not CMI.
2. Interleukin-1 (Option b): Involved in inflammation, not specific to CMI.
3. Interleukin-2 (Option c): Important for T-cell growth, but not directly measured in TB tests.
Examples of TYPE 1 HSR:
Hay Fever
Asthma
Food allergies
Environmental allergies
Examples of TYPE 2 HSR:
Transfusion reactions
HDN
Autoimmune Hemolytic Anemia
Examples of TYPE 3 HSR:
SLE
Post strep GN
Arthus Reaction
Farmer’s lung
Serum sickness
Examples of TYPE 4 HSR:
Contact Dermatitis
Mantoux reaction
Hypersensitivity pneumoliths
Two types of IN VIVO SKIN TESTS for type 1 HSR:
- Cutaneous testing or a prick test
- Intradermal test
IN VITRO tests for Type 1 HSR:
RIST
RAST
RIST stands for:
Radioimmunosorbent test
RAST stands for:
Radioallergosorbent test
In vitro test that measures total IgE by capturing the antibody with solid phase anti-IgE. A second anti-IgE immunoglobulin with an enzyme label is used to produce a visible reaction
RIST (Radioimmunosorbent test)
In vitro test that measures antigen-specific IgE by using solid-phase to capture patient antibody. Then a second antibody, enzyme-labeled anti-IgE immunoglobulin is added
RAST (Radioallergosorbent test)
Very small quantities of sensitizing antigens are injected into the patient with the idea of building IgG antibodies.
HYPOSENSITIZATION
It is the most severe type of allergic response because it is an acute reaction that simultaneously involves multiple organs
Anaphylaxis
Tests used in TYPE 2 HSR:
DAT (Direct Antiglobulin Test)
IAT (Indirect Antiglobulin Test)
Type 2 HSR test that detects HTR, HDN, and AIHA
Direct Antiglobulin Test (DAT)
A mixture of antibodies to detect IgG, C3b, and C3d
Polyspecific AHG
Used to identify the presence of IgG, and C3b or C3d
Monospecific AHG
Which T helper subset plays a role in TYPE 1 HSR?
T helper subset 2/T helper 2 (Th2)
Which T helper subset plays a role in TYPE 4 HSR?
T helper subset 1/T helper 1 (Th1)
Tests used in TYPE 4 HSR:
- Patch test
- Mantoux reaction
Gold standard for contact dermatitis; nonabsorbent adhesive patch containing the suspected allergen is applied on the patient’s back, and the skin is checked for a reaction over the next 48 hours
PATCH TEST
A test where 0.1 mL of the antigen is injected intradermally, using a syringe and a fine needle. The test site is read at 48 and 72 hours for the presence of induration:
MANTOUX REACTION
