Lec 04: Hypersensitivity Flashcards
- Adaptive response to antigens or allergens which occurs in an exaggerated or inappropriate manner causing tissue damage
- Heightened state of immune response
Hypersensitivity
- Type 1 Hypersensitivity
- Type 2 Hypersensitivity
- Type 3 Hypersensitivity
- Type 4 Hypersensitivity
A. Immune complex
B. Cell mediated/delayed type
C. Immediate/Anaphylactic
D. Cytotoxic
CDAB
Type 1 Hypersensitivity
Antibody:
Effector cell:
Antibody: IgE
Effector cell: Mast cell
Type 1 Hypersensitivity
TOF. The end of the activation phase is when the IgE Ab produced adheres to mast cells.
F (end of sensitization)
Type 1 Hypersensitivity
TOF. There is NO
HYPERSENSITIVITY REACTION during sensitization.
T
Type 1 Hypersensitivity
What activity/event should happen for the activation phase to commence?
Re-exposure
Type 1 Hypersensitivity
TOF. The mediators released by the
mast cell causes anaphylactoid,
which is IgE mediated.
F (anaphylaxis)
Anaphylactoid → Ag will directly activate the mast cell leading to degranulation (no IgE,
thus, no sensitization phase happens)
Type 1 Hypersensitivity
Common Allergen (Ag): Drugs, serum, venom
Route of entry: I/V
Response: Edema, vasodilation, asthma, laryngeal edema, shock, death
A. Food allergy
B. Bronchial asthma
C. Wheal and flare
D. Allergic Rhinitis and hay fever
E. Systemic anaphylaxis
E
Type 1 Hypersensitivity
Common Allergen (Ag): Insect bites, sensitivity testing
Route of entry: Subcutaneous
Response: Local
vasodilation and local edema
A. Food allergy
B. Bronchial asthma
C. Wheal and flare
D. Allergic Rhinitis and hay fever
E. Systemic anaphylaxis
C
Type 1 Hypersensitivity
Common Allergen (Ag): Pollen (ragweed), dust, mites, feces
Route of entry: Inhaled
Response: Edema of the
nose, irritation of nasal mucosa
A. Food allergy
B. Bronchial asthma
C. Wheal and flare
D. Allergic Rhinitis and hay fever
E. Systemic anaphylaxis
D
Type 1 Hypersensitivity
Common Allergen (Ag): Pollen dust, mites, and feces
Route of entry: Inhaled
Response: Bronchial
constriction, increased mucous and
airway inflammation
A. Food allergy
B. Bronchial asthma
C. Wheal and flare
D. Allergic Rhinitis and hay fever
E. Systemic anaphylaxis
B
Type 1 Hypersensitivity
Common Allergen (Ag): Fish, milk, egg, wheat
Route of entry: Oral
Response: Vomiting and
diarrhea, pruritis (itching), urticaria (hives)
A. Food allergy
B. Bronchial asthma
C. Wheal and flare
D. Allergic Rhinitis and hay fever
E. Systemic anaphylaxis
A
Type 1 Hypersensitivity
Matching type:
1. 1000x more potent, Cause erythema (flare) and wheal
formation (umbok)
2. Vasodilation, Smooth muscle contraction, Bronchoconstriction, Increase mucus secretion
A. Histamine
B. Leukotriene
BA
paaral nalang ng table sa primary and secondary, treatment modality and clinical
Type 1 Hypersensitivity
Enumerate clinical manifestations
- Hay fever
- Atopic Dermatitis or Eczema
- Insect Venom
- Anaphylaxis to drugs
- Food and Latex Allergies
- Allergy to animal and animal products
Type 1 Hypersensitivity
Enumerate in vivo screening tests
Skin Prick Test, Intradermal Test, Prausnitz – Kustner Reaction
Type 1 Hypersensitivity
DIAGNOSTIC TESTS (IN VITRO)
1) RAST (Radioallergosorbent Test/Assay)
2) RIST (Radioimmunosorbent Test/Assay)
Type 1 Hypersensitivity
- Negative control: NSS
- Positive control: Histamine
- Result: 15 – 20 minutes
o (+) Wheal/Induration is >3mm
o Presence or absence of Flare
Skin Prick Test also known as Percutaneous or
Puncture test
Type 1 Hypersensitivity
- 0.01 to 0.05 mL of test solution
- Positive result is the same with SPT:
After 15 – 20 minutes,
o (+) Wheal/Induration is >3mm
o Presence or absence of Flar
Intradermal Test
Type 1 Hypersensitivity
- Passive Cutaneous Anaphylaxis
- Obsolete method/test
- Serum passing
- If the injected individual will have wheal formation after 48 hours, it is considered positive
Prausnitz – Kustner Reaction
Type 1 Hypersensitivity
Matching type:
- Used to detect/determine specific IgE that is directed to a specific allergen
- Used to measure the Total IgE in the serum or blood of a px
A. RAST
B. RIST
AB
TYPE II Hypersensitivity
Antibody involved:
IgG and IgM
TYPE II Hypersensitivity
Enumerate the clinical states
- Transfusion Reactions
- Hemolytic Disease of the Newborn
- Autoimmune and Drug Induced Hemolytic Anemia
- Drug-induced thrombocytopenic purpura
- Good Pasture Syndrome
- Myasthenia Gravis
TYPE II Hypersensitivity
TESTS FOR TYPE II
Coomb’s test
TYPE II Hypersensitivity
- Used to determine IN VIVO sensitization
- To check if the red cells of the patient is sensitized inside the body
- It is sensitized because of hemolytic transfusion reaction or HDN if the mother is Rh negative and the baby is Rh positive.
- It can also happen if there is
autoimmune and drug induced hemolytic anemia. - In here, we need to collect a sample of red cells and add a AhG reagent.
- Positive result: agglutination or hemolysis
DIRECT ANTIGLOBULIN TEST
TYPE II Hypersensitivity
- Used to test IN VITRO sensitization
- The principle of crossmatching.
- In crossmatching we need to check if the red cell from the donor is compatible to the patient.
- Sample is the red cell from the donor and then the serum from the patient because the serum contains antibody that is possibly directed to the red cells of the donor that’s why cross matching is performed.
- In major cross-match, sample is donor’s red cell and the patient’s serum.
- Positive result: agglutination or hemolysis
- Now if there is agglutination or hemolysis, this means that the blood of the donor is incompatible
INDIRECT ANTIGLOBULIN TEST
TYPE III Hypersensitivity
Antibody Involved:
IgG and IgM
TYPE III Hypersensitivity
CLINICAL STATES
enumerate
- SLE, RA
- Post Streptococcal Glomerulonephritis
- Polyarteritis nodosa
- Serum Sickness
- Arthus reaction
TYPE III Hypersensitivity
TESTS FOR TYPE III
- C1Q BINDING
- RAJI CELL ASSAY
TYPE III Hypersensitivity
- Based on radiolabeled assay
- Serum of SLE Px + Radioactive C1q + PEG = Radioactivity
C1Q BINDING
TYPE III Hypersensitivity
has receptors for the complement
components such as C3 that are participating in CIC
RAJI Cell Assay
TYPE IV Hypersensitivity
Antibodies:
None
TYPE IV Hypersensitivity
- Reactions involves sensitized (???)and release of its (???) as mediators and amplifiers
- Symptoms peak between (???) to (???) hours after exposure to antigen
- T cells… lymphokines
- 48-72 hours
TYPE IV Hypersensitivity
Antigens that can trigger Type IV hypersensitivity:
- Mycobacterium tuberculosis, Mycobacterium leprae Pneumocystis carinii, Leishmania species, and herpes simplex virus
- Plants such as poison ivy and poison oak; Metals such as nickel salts, and components of hair dyes and cosmetics
A. Contact Antigen
B. Extracellular pathogens
C. Intracellular pathogens
CA
TYPE IV Hypersensitivity
Clinical states
- Contact Dermatitis
- GVHD
- Transplant Rejection
- TB
- Leprosy
- Poison Ivy
TYPE IV Hypersensitivity
→ Gold standard for contact dermatitis
→ After 48 hours, redness with papules or tiny blisters is considered a positive test
SKIN PATCH TEST
TYPE IV Hypersensitivity
- Used to determine exposure to M. tuberculosis antigen
- A screening test but not diagnostic for TB
- injected and after 48 hours, check for induration or wheal formation
TUBERCULIN/ MANTOUX/ PPD (PURIFIED
PROTEIN DERIVATIVE) TEST
PPD
- HIV positive
- Recent contact with an active TB patient
- Nodular or fibrotic changes on chest X-ray
- Organ transplant
A. >15mm
B.>10mm
C. >5mm
C
PPD
- Recent arrivals (< 5 yrs) from high-prevalence countries
- IV drug users
- Resident/employee of high-risk congregate settings
- Mycobacteriology lab personnel
- Comorbid conditions
- Children < 4 yrs old
- Infants, children, & adolescents exposed to high risk categories
A. >15mm
B.>10mm
C. >5mm
B
PPD
- Persons with no known risk factors for TB
A. >15mm
B.>10mm
C. >5mm
A
