Chapter 14 Stevens (Serology) Flashcards
1
Q
exaggerated response to a typically harmless antigen that results in tissue injury, disease, or even death
A
Hypersensitivity
2
Q
Devised classification system from these reaction based on their immunologic mechanism in 1960
A
Philip Gell and Robin Coombs
3
Q
Type I Hypersensitivity other name:
A
Anaphylactic hypersensitivity
4
Q
Type II Hypersensitivity other name:
A
Antibody-mediated cytotoxicity hypersensitivity
5
Q
Type III Hypersensitivity other name:
A
Complex mediated hypersensitivity
6
Q
Type IV Hypersensitivity other name:
A
Cell - mediated hypersensitivity
7
Q
Anaphylactic hypersensitivity other name:
A
Immediate
8
Q
Cytotoxic hypersensitivity other name:
A
Antibody mediated
9
Q
Immune complex hypersensitivity other name:
A
Complement mediated
10
Q
Delayed hypersensitivity other name:
A
T-cell Mediated
11
Q
Heterologous antigen is seen in:
A
Type I Hypersensitivity (Anaphylactic)
12
Q
Autologous and Heterologous antigen is seen in
A
Type II
Type III
Type IV
13
Q
Time of Latency in Anaphylactic hypersensitivity
A
minutes
14
Q
Time of Latency in Cytotoxic and immune complex hypersensitivity
A
Hours
15
Q
Time of latency in delayed hypersensitivity
A
Days
16
Q
Anaphylactic, Cytotoxic, Immune Complex immune reaction:
A
Humoral
17
Q
Immune reaction of Delayed Hypersensitivity
A
Cellular
18
Q
Immune mechanism:
Release of
mediators from
IgE-sensitized
mast cells and
basophils
A
Anaphylactic Hypersensitivity
19
Q
Immune mechanism:
Cell destruction
caused by
antibody and
complement,
opsonization, or
ADCC
Cell function
inhibited by
antibody binding
A
Cytotoxic
20
Q
Immune mechanism:
Antigen–antibody
complexes
activate
complement
proteins.
Neutrophils are
recruited and
release lysosomal
enzymes that
cause tissue
damage
A
Immune complex hypersensitivity
21
Q
Immune mechanism:
Antigen Sensitized
Th1 cells release
cytokines that
recruit
macrophages and
induce
inflammation or
activate cytotoxic
T cells to cause
direct cell
damage
A
Delayed hypersensitivity
22
Q
Presence of complement is seen in:
A
Cytotoxic and Immune Complex hypersensitivity
23
Q
Complement found in delayed hypersensitivity
A
Cellular
24
Q
Anaphylaxis
Allergies (food,
products
Bronchial Asthma
Hay Fever
Urticaria
Type of hypersensitivity
A
Type I Anaphylactic Hypersensitivity
25
AHA
HDN
HTR
Thrombocytopenia
Goodpasture
Pemphigus
Vulgaris
Drug Allergies
Hyperacute GVHD
Rheumatic fever
Grave’s Disease
Type II DM
Type of Hypersensitivity:
TYPE II HYPERSENSITIVITY Antibody-mediated cytotoxicity
26
SLE
Arthus
Serum Sickness
Dengue
SLE
RA
Post
Streptococcal
Vasculitis
Type of Hypersensitivity
TYPE III HYPERSENSITIVITY Complex mediated hypersensitivity
27
Dermatitis
Chrons
Celiac
Leprosy
Tuberculin
Poison Ivy
Acute GVHD
Hashimot’s
Type I DM
Type of hypersensitivity
TYPE IV HYPERSENSITIVITY Cell - mediated hypersensitivity
28
Serum is transferred from an allergic individual to a non-allergic individual
1967 - Immunoglobulin E was identified as the serum factor responsible for this reaction
Passive cutaneous anaphylaxis
29
inherited tendency to develop classic allergic responses to naturally occurring inhaled or ingested allergens
Atopy
30
PHASES OF TYPE I IMMUNE RESPONSE
Sensitization Phase
Activation Phase
Late Phase
31
Sensitization Phase of type I immune response involves
Formation of antigen -specific IgE that attaches to mast cells and basophils
32
Resposure to the same antigen, causing degranulation of mast cells and
basophils and release mediators
Activation phase
33
most abundant preformed mediator; primary mediator
Histamine
34
When mast cells and basophils are triggered to synthesize other reactants such as
secondary reactants
6-8 hours after exposure
Late phase
35
MEDIATOR for primary (preformed)
Histamine
Heparin
Eosinophil (ECF-A)
Neutrophil (NCF-A)
Proteases (tryptase, chymase)
36
Smooth muscle contraction, vasodilation,
increased vascular permeability
Mediator:
Histamine, Heparin
37
Chemotactic for eosinophil
Mediator:
Eosinophil (ECF-A)
38
Chemotactic for neutrophils
Mediator:
Neutrophil (NCF-A)
39
Convert C3 to C3b
Stimulate mucus production
Activate Cytokines
Mediator:
Proteases (tryptase, chymase)
40
Secondary
(Newly
Synthesized) mediators:
Prostaglandin PGD2
Leukotriene LTB4
Leukotrienes LTC4, LTD4 LTE4
Platelet-activating factor (PAF)
Cytokines IL-1, IL-3, IL-4, IL-5, IL-6,
IL-9, IL-13, IL-14, IL-16, tumor necrosis
factor-α (TNF-α), granulocyte
macrophage colony-stimulating factor
(GM-CSF)
41
Vasodilation
Increased vascular permeability
Mediator:
Prostaglandin PGD2
42
Chemotactic factor for neutrophils,
eosinophils
Mediator:
Leukotriene LTB4
43
Increased vascular permeability
Bronchoconstriction, mucus secretions
Mediator:
Leukotrienes LTC4, LTD4 LTE4
44
Platelet Aggregation Mediator:
Platelet-activating factor (PAF)
45
Increase inflammatory cells in area, and
increase IgE production
Mediator:
Cytokines IL-1, IL-3, IL-4, IL-5, IL-6,
IL-9, IL-13, IL-14, IL-16, tumor necrosis
factor-α (TNF-α), granulocyte
macrophage colony-stimulating factor
(GM-CSF)
46
Clinical Manifestation of Type I Hypersensitivity
Allergic rhinitis
Allergic Asthma
Food Allergies
Skin Reactions
Anaphylaxis
Latex Sensitivity
47
most common form of atopy
allergic rhinitis
48
Seasonal allergic rhinitis, triggered by tree and grass pollens in the
air during the spring in temperate climates
Hay fever
49
“Panting” or “breathlessness”’
Airflow obstruction
Allergic asthma
50
Symptoms limited to the gastrointestinal tract include cramping,
vomiting, and diarrhea, whereas spread of antigen through the
bloodstream may cause hives and angioedema on the skin, asthma,
rhinitis, or anaphylaxis
Food allergies
51
Manifest acute urticaria or eczema
Skin reactions
52
local inflammation of the skin
Dermatitis
53
caused by the release of vasoactive mediators from
mast cells in the skin following contact with allergens such as pet dander or
insect venom.
Wheal-and-flare reaction
54
actions occur deeper in the dermal tissues
Angiodema
55
----- is the most severe type of allergic response because it is
an acute reaction that simultaneously involves multiple organs.
Means “without protection”
Anaphylaxis
56
______ became a significant problem in the late 1980s after the
implementation of Universal Precautions by the Centers for Disease Control and
Prevention (CDC) and regulations by the Occupational Safety and Health
Administration (OSHA) that required health-care workers to wear gloves when
performing laboratory procedures and working with patients
Latex Sensitivity
57
first anti-IgE monoclonal antibody drug for treatment of type I hypersensitivity
Omalizumab
58
For treatment of severe asthma; Ab against IL-5
Treatment of type I hypersensitivity
Mepolizumab
59
treat patients with moderate-severe atopic dermatitis
Treatment of type I hypersensitivity
Dupilumab
60
In Vivo Skin Test for type I hypersensitivity
Percutaneous Test (Prick and Puncture Test)
Intradermal Test - greater amount of antigen is used and more sensitive than cutaneous
61
In a positive test of in vivo skin test, a ____________ will appear at the site where the allergen was applied
wheal-and-flare reaction
62
In vitro Test for type I hypersensitivity
Competitive radioimmunosorbent test (RIST)
63
Clinical Manifestation of Type II Hypersensitivity
Transfusion
Reaction
Hemolytic Disease of
the Fetus and
Newborn
Autoimmune
Hemolytic Anemia
Cold Agglutinin
Antibodies
Paroxysmal Cold
Hemoglobinuria
Type II Reactions
Involving Tissue
Antigens
64
Reactions may occur within minutes or hours after
receipt of incompatible blood.
ABO: IgM class
May cause DIC, Renal failure, vascular collapse
Acute hemolytic transfusion
65
occur days to weeks following a transfusion and
are caused by an anamnestic response to the antigen to which the patient has
previously been exposed.
Rh, Kell, Kidd, Duffy Antigens
IgG class
Delayed hemolytic reactions
66
Appears in infants whose mothers have been exposed to blood-group
antigens on the baby’s cells that differ from their own.
Also known as Erythroblastosis fetalis
Major cause: D antigen of Rh blood group
Most common: ABO incompatibility
Hemolytic Disease of
the Fetus and
Newborn
67
Reaction directed against self-antigens because individuals with this
disease form antibodies to their own RBCs
Autoimmune
Hemolytic Anemia
68
Accounts for more than 70% of autoimmune anemias
Characterized by the formation of IgG antibody, which reacts most
strongly at 37°C.
Warm autoimmune hemolytic anemia
69
Drugs are capable of attaching to the RBCs directly or of forming
immune complexes that attach to the RBCs
Acts as haptens
Penicillin and Cephalosporin
70
Can stimulate the production of antidrug antibodies that bind to the drug to form soluble immune complexes
Quinidine and Phenacetin
71
Can induce hemolytic anemia by stimulating production of autoantibodies against the RBC membrane
Methyldopa
72
Less frequent cause of immune hemolytic anemias. By definition, cold
agglutinins are autoantibodies that react with antigens on the RBC
membrane at cold temperatures.
Reversible upon exposure to warm temp
Cold Agglutinin
Antibodies
73
This condition occurs most often after infection with certain viral
illnesses, including measles, mumps, chickenpox, and infectious
mononucleosis
Anemia with hemoglobin in urine
Transient in children and young adults
Paroxysmal Cold
Hemoglobinuria
74
Organ-specific autoimmune diseases in which antibody is directed
against a particular tissue are in this category.
1. Goodpasture’s syndrome - Anti-glomerular basement
membrane
2. Hashimoto’s disease
3. Myasthenia gravis
4. Insulin dependent Diabetes
Type II Reactions
Involving Tissue
Antigens
75
Testing for Type II Hypersensitivity
Direct Antiglobulin Test
Indirect Antiglobulin Test
76
Detects RBCs that have been sensitized with antibody or complement in vivo
Direct Antiglobulin Test
77
Used in the crossmatching of blood to prevent a transfusion reaction.
It is also used to determine the presence of a particular antibody in patient plasma or to
type patient RBCs for specific blood group antigens
Indirect Antiglobulin Test
78
Clinical Manifestation of Type III Hypersensitivity
Arthus Reaction
Serum Sickness
Autoimmune Disease and
Other Causes of Type III
Hypersensitivity
79
The reaction, which is characterized by erythema and
edema, peaks within 3 to 8 hours and is followed by a
hemorrhagic necrotic lesion that may ulcerate.
can be seen in humans following booster injections with tetanus, diphtheria, or measles vaccines
Arthus Reaction
80
Results from passive immunization of humans with animal
serum.
Usually this is a self-limiting disease, and recovery takes a
few weeks after the offending antigen is eliminated.
Serum Sickness
81
SLE and rheumatoid arthritis (RA) are two such examples.
Patients with these diseases commonly produce antibodies
against nuclear constituents such as DNA and histones.
Autoimmune Disease and
Other Causes of Type III
Hypersensitivity
82
Testing for Type III Hypersensitivity
Indirect immunofluorescence
Enzyme-linked immunosorbent assay (ELISA)
Fluorescent microsphere multiplex immunoassays
83
Rheumatoid factor can be detected by:
latex agglutination
nephelometry
other immunoassays
84
Seen individuals infected with Mycobacterium tuberculosis which developed a localized
inflammatory response after receiving intradermal injections of a filtrate from the organism
Type IV Hypersensitivity
85
Pathogens that commonly induce delayed hypersensitivity include:
M. tuberculosis, Mycobacterium
leprae, Pneumocystis carinii, Leishmania species, and herpes simplex virus
86
are those that come into direct contact with the skin
Contact antigens
87
Clinical Manifestation of Type IV Hypersensitivity
Contact Dermatitis
Hypersensitivity
Pneumonitis
88
Reactions are usually caused by low-molecular-weight
compounds that touch the skin
Most of these substances probably function as haptens that bind
to glycoproteins on skin cells
Contact Dermatitis
89
an allergic disease of the lung parenchyma characterized by inflammation of the alveoli and interstitial spaces
Hypersensitivity
Pneumonitis
90
Positive interpretation for mantoux method
> 15 mm
91
is considered the gold standard in testing for contact dermatitis. This test must be done
when the patient is free of symptoms or at least has a clear test site
Patch test
92
have been developed as an alternative to tuberculin skin
testing to detect latent TB infection
Interferon gamma release assays (IGRA)
93
patient blood is drawn into specialized collection tubes containing peptides
that are highly specific for M. tuberculosis (ESAT-6 and CFP-10)
Quantiferon TB Gold Plus assay
94
Is based on the enzyme-linked immunospot (Elispot) technique.
T-SPOT.TB test
95
Hypersensitivity types I, II, and III are ______
antibody-mediated
96
Type IV hypersensitivity is a cell-mediated response involving:
T lymphocytes
