IS Lec Finals - Hypersensitivity Flashcards
1
Q
It is a defense mechanism by which the body rids itself of potentially harmful antigens
A
Immune Response
2
Q
second line of defense against non-self pathogens
A
Innate Immunity
3
Q
third line of defense against non-self pathogens
A
Adaptive Immunity
4
Q
Macrophage, Neutrophil, Dendritic cell, Natural killer cell, complement, natural antibodies, epithelial barrier
A
Innate Immunity
5
Q
Cytokines, B lymphocyte, High-affinity antibodies, Helper and Cytotoxic T lymphocyte
A
Adaptive Immunity
6
Q
what are the cells present in both innate and adaptive immunity
A
PBMC, dendritic cells, macrophages, NK cells
7
Q
it is an exaggerated response to a harmless antigen that results in injury to the tissue, disease, or even death
A
Hypersensitivity
8
Q
heightened state of immune responsiveness
A
Hypersensitivity
9
Q
immune & inflammatory responses that are harmful to the host
A
Hypersensitivity
10
Q
required to prime the
immune system
A
PRIMING DOSE
11
Q
results to injurious consequence
A
SHOCKING DOSE
12
Q
dose that alerts the immune system
A
PRIMING DOSE
13
Q
IMMEDIATE, ALLERGIC or Ig-E mediated hypersensitivity reaction
A
Type I Hypersensitivity
14
Q
short time lag (rapidly occurring), usually seconds to minutes, between exposure to antigen and the onset of clinical symptoms
A
Type I Hypersensitivity
15
Q
Immune mediator for Type 1
A
IgE
16
Q
responsible for sensitizing mast cells and providing recognition of antigen
A
IgE
17
Q
IgE degranulation of basophils or mast cells
A
Type I Hypersensitivity
18
Q
Antigens that trigger formation of IgE
A
atopic antigens, or allergens.
19
Q
refers to an inherited tendency to respond to naturally occurring inhaled and ingested allergens with continued production of IgE.
A
Atopy
20
Q
first researchers to show that a serum factor was responsible for type I reactions.
A
Carl Wilhelm Prausnitz and Heinz Küstner
21
Q
who was allergic to fish?
A
Heinz Küstner
22
Q
what was responsible for type I reactions that was discovered by Carl Wilhelm Prausnitz and Heinz Küstner?
A
serum factor
23
Q
It occurs when serum is transferred from an allergic individual to a nonallergic individual, and then the second individual is challenged with specific antigen.
A
Passive Cutaneous Anaphylaxis
24
Q
what do you call the antibody responsible for sensitizing mast cells and basophils and will recognize the allergens
A
immune mediator
25
what immunity is when antibody is injected?
active immunity
26
what immunity is when antigen is injected and allows the body to develop its own antibodies
passive immunity
27
what t-helper cell is used in people with allergies?
TH2
28
what t-helper cell is used in people without allergies?
TH1
29
principle effector cells of immediate hypersensitivity
mast cells
30
contains numerous cytoplasmic granules including HISTAMINE
Mast cells
31
contain histamine-rich granules and high-affinity receptors for IgE
Basophils
32
respond to chemotactic stimulation and tend to accumulate in the tissues during an inflammatory reaction
Basophils
33
most prominent in the connective tissues, skin, upper and lower respiratory tract, and GI tract, that is why these are the most affected during allergic reactions
mast cells and basophils
34
we take this during allergic reactions
anti-histamine
35
used to relieve the symptoms of allergy
anti-histamine
36
block histamine receptors
anti-histamine
37
most important mediator of anaphylaxis
Histamine
38
histamine enables...
vasodilation, vascular permeability, smooth muscle constriction
39
Type I Hypersensitivity may occur in two (2) forms:
Anaphylaxis and Atopy
40
Acute, potentially fatal, and systemic manifestation of hypersensitivity reactions
Anaphylaxis
41
It occurs when an allergen (antigen) binds to IgE on the surface of mast cells with subsequent release of several mediators of anaphylaxis.
Anaphylaxis
42
In ____ multiple organs are usually affected and death may occur within 2 hours
Anaphylaxis
43
A condition of familiar hypersensitivity occurring spontaneously in humans
Atopy
44
Recurrent, non-fatal, local manifestation of immediate hypersensitivity reaction
Atopy
45
It is localized to specific tissues (often epithelial surfaces of antigen entry)
Atopy
46
Common manifestations: asthma, rhinitis, urticaria, atopic dermatitis
Atopy
47
classification by immunopathological phenotype can be used to determine management strategies
Asthma
48
food ingestion (eggs, shellfish, peanuts, drug reactions), insect stings
Systemic Anaphylaxis
49
derived from the Greek word for “panting” or “breathlessness”
Bronchial asthma
50
Recurrent airflow obstruction --> Airway resistance --> breathlessness
Bronchial asthma
51
due to bronchial smooth muscle contraction, mucosa edema, and heavy mucus secretion
Bronchial asthma
52
other term for rhinitis
hay fever
53
usually airborne and affect the the conjunctive and respiratory mucus membrane
Rhinitis (hay fever)
54
most common form of atopy, or allergy.
Rhinitis
55
sinusitis, otitis media (ear infection), eustachian tube dysfunction, and sleep disturbances may result
Rhinitis
56
(wheal and flare) - mediated by histamine.
Urticaria
57
late-phase reaction to allergen in the skin - inflammation - can be treated with steroids.
Eczema
58
Symptoms limited to the gastrointestinal tract include cramping, vomiting, and diarrhea, while spread of antigen through the bloodstream may cause hives and angioedema on the skin, as well as asthma or rhinitis.
Food Allergies
59
an itchy red skin rash, may be caused by food allergens or exposure to house dust mites.
Eczema
60
what is the first line of defense for the Treatment for Type I Hypersensitivity?
Avoidance of known allergens
61
Antihistamines, decongestants, bronchodilators,
followed by inhaled corticosteroids
Treatment for Type I Hypersensitivity
62
very small quantities of sensitizing antigen are injected into the patient with the idea of building up IgG antibodies
Immunotherapy or hyposensitization
63
This antibody combines with IgE at the same site that IgE would normally use to bind to receptors on mast cells. Blocking of this site does not allow IgE to bind to mast cells, thus helping to alleviate allergic symptoms.
anti-IgE monoclonal antibody
64
In vivo skin test (cutaneous and intradermal tests)
Allergy testing
65
serum level of TOTAL IgE antibody
Radioimmunosorbent assay (RIST)
66
serum level of IgE specific allergen
Radioallergosorbent assay
67
Immunofluorescence method
detection of IgE
68
ELISA and Passive Agglutination
detection of IgE in the serum for diagnosis of atopy
69
other name for Type II Hypersensitivity
Cytotoxic hypersensitivity
70
triggered by antigens found on cell surfaces. These antigens may be altered self-antigens or heteroantigens.
Type II Hypersensitivity
71
Antibody coats cellular surfaces and promotes phagocytosis by both opsonization and activation of the complement cascade
Type II Hypersensitivity
72
what are the mediators of Type II Hypersensitivity
IgG and IgM
73
in type II, Antibody coats cellular surfaces and promotes phagocytosis by
both ___ and ___
OPSONIZATION and COMPLEMENT ACTIVATION
74
have Fc receptors that bind the Fc region of antibody on the target cells, thus enhancing phagocytosis.
Macrophages, neutrophils and NK cells
75
Type II Hypersensitivity: If the complement cascade is activated, complement can trigger cellular destruction in two ways:
by coating cells with C3b, by complement-generated lysis
76
plays a central role in the cellular damage that typifies type II reactions
complement
77
Type II Hypersensitivity examples
Transfusion reaction
Hemolytic disease of the fetus and newborn
Autoimmune hemolytic anemia
Type II Reactions Involving Tissue Antigens (Organ-specific)
78
examples of cellular destruction that result from
antibody combining with heteroantigens.
Transfusion Reaction
79
Acute HTR is mediated by what Ig?
IgM mediated
80
Delayed HTR is mediated by what Ig?
IgG mediated
81
As soon as cells bearing that antigen are introduced into the patient, intravascular hemolysis occurs because of complement activation, and it results in the release of hemoglobin and vasoactive and procoagulant substances into the plasma.
Transfusion Reaction
82
Result: disseminated intravascular coagulation (DIC), vascular collapse, and renal failure
Transfusion Reaction
83
Rh incompatibility of the mother and the fetus
Hemolytic Disease of the Fetus and Newborn
84
The mother makes IgG antibodies in response, and these cross the placenta to destroy fetal red cells.
Hemolytic Disease of the Fetus and Newborn
85
In Hemolytic Disease of the Fetus and Newborn, what is the Rh of the mother and the baby?
Rh negative mother, Rh positive baby
86
protein, it tells if you are positive or negative
Rh
87
which baby is affected during HDFN?
second baby (subsequent baby)
88
IN HDFN, if enough of the baby’s red cells get into the mother’s circulation, what cells develop?
memory B cells
89
IN HDFN, when memory b-cells are activated upon re-exposure to the same red cell antigen, what Ig is produced?
IgG
90
During 2nd pregnancy, ___ passes through the placenta → mother excretes
Bilirubin
91
Continuous RBC destruction → bilirubin → accumulation (due to underdeveloped liver) →jaundice
Hemolytic Disease of the Fetus and Newborn
92
when bilirubin reaches the brain and cause irreversible brain damage to the baby
kernicterus
93
Severe HDN is called ___
erythroblastosis fetalis
94
Prevention: administration of Rhogam
Hemolytic Disease of the Fetus and Newborn
95
when to administer Rhogam?
28 weeks of gestation and 72 hours after birth
96
Prevents sensitization of fetal cells by inhibiting production of antibody by combining with and destroying the D red blood cells, thus preventing them from being antigenic
Rhogam
97
Warm autoimmune hemolytic anemia is mediated by? at what temp?
IgG, warm reacting antibody
Optimum at 37C
98
Cold agglutinin disease is mediated by? at what temp?
IgM, cold reacting antibody
Optimum at 4C
99
Optimum at 4C
Cold agglutinin disease
100
Optimum at 37C
Warm autoimmune hemolytic anemia
101
Examples of Type II Reactions Involving Tissue Antigens (Organ-specific)
Goodpasture’s syndrome
Graves disease (hyperthyroidism)
Hashimoto’s disease
Myasthenia gravis
102
Testing for Type II Hypersensitivity
Direct antiglobulin testing (DAT)
Indirect antiglobulin testing (IDAT)
Polyspecific antihuman globulin
103
is performed to detect transfusion reactions, hemolytic disease of the newborn, and autoimmune hemolytic anemia.
Direct antiglobulin testing (DAT)
104
is performed to determine the presence of a particular antibody in a patient or to type patient red blood cells for specific blood group antigens.
Indirect antiglobulin testing (IDAT)
105
a mixture of antibodies to IgG and complement components such as C3b and C3d, and it is used for initial testing
Polyspecific antihuman globulin
106
when Polyspecific antihuman globulin tests positive, it should be repeated using ___
monospecific anti-IgG, anti-C3b, and anti-C3d
107
what is the other name for Type III Hypersensitivity?
immune complex disease
108
similar to type II reactions in that IgG or IgM is involved and destruction is complement mediated
Type III Hypersensitivity
109
In the case of type ___ diseases, the antigen is soluble.
Type III Hypersensitivity
110
When soluble antigen combines with antibody, complexes are formed that precipitate out of the serum.
Type III Hypersensitivity
111
Normally such complexes are cleared by phagocytic cells, but if the immune system is overwhelmed, these complexes deposit in the tissues vascular endothelium, joint linings, and pulmonary alveolar membranes
Type III Hypersensitivity
112
There they bind complement, causing damage to the particular tissue. Deposition of antigen–antibody complexes is influenced by the relative concentration of both components.
Type III Hypersensitivity
113
who demonstrated Arthus Reaction?
Maurice Arthus in 1903
114
Using rabbits that had been immunized to produce an abundance of circulating antibodies, It showed that when these rabbits were challenged with an intradermal injection of the antigen, a localized inflammatory reaction resulted.
Arthus Reaction
115
The inflammatory response is caused by antigen–antibody combination and subsequent formation of immune complexes that deposit in small dermal blood vessels.
Arthus Reaction
116
(A) Antigen is injected into the skin of an individual who has circulating antibody of that specificity.
(B) Immune complexes are formed and deposit on the walls of blood vessels, activating complement.
(C) Complement fragments cause dilation and increased permeability of blood vessels, edema, and accumulation of neutrophils.
Arthus Reaction
117
generalized type III reaction that is seen in humans, although not as frequently as it used to be
Serum sickness
118
results from passive immunization with animal serum, usually horse or bovine, used to treat such infections as diphtheria, tetanus, and gangrene.
Serum sickness
119
Serum sickness results from passive immunization with ___
animal serum, usually horse or bovine
120
Vaccines and bee stings may also trigger this type of reaction.
Serum sickness
121
Generalized symptoms appear in 7 to 21 days after injection and recovery takes between 7 and 30 days.
Serum sickness
122
antibodies are directed against constituents such as DNA and nucleohistones,
Systemic lupus erythematosus (SLE)
123
In Systemic lupus erythematosus (SLE), where does the main damage occur?
glomerular basement membrane in the kidney.
124
an antibody called rheumatoid factor is directed against IgG. Immune complex deposition occurs in the membranes of inflamed joints.
Rheumatoid arthritis
125
it detects specific diseases such as SLE and rheumatoid arthritis
agglutination reactions
126
what testing uses antigen-coated carrier particles, including red blood cells or latex particles, or enzyme immunoassays.
agglutination reactions
127
determine deposition of immune complexes in the tissues.
Fluorescent staining
128
what type is Delayed hypersensitivity
Type IV Hypersensitivity
129
Type IV Hypersensitivity is first described by ____
Robert Koch in 1890
130
individuals infected with Mycobacterium tuberculosis (Mtb) developed a localized inflammatory response when injected intradermally with a filtrate from the organism
Type IV Hypersensitivity
131
who observed that individuals infected with Mycobacterium tuberculosis (Mtb) developed a localized inflammatory response when injected intradermally with a filtrate from the organism
Robert Koch
132
what is the bacteria in Type IV Hypersensitivity?
Mycobacterium tuberculosis (Mtb)
133
play the major role in the manifestations in Type IV Hypersensitivity
sensitized T cells
134
how many weeks does initial sensitization phase in Type IV Hypersensitivity take place?
1-2 weeks
135
in type IV hypersensitivity, upon subsequent exposure to the antigen, symptoms typically take several hours to develop and reach a peak ___ hours after exposure to antigen
48 to 72 hours
136
What type: Langerhans cells in the skin and macrophages in the tissue capture and present antigen to T helper cells of the Th1 subclass.
Type IV Hypersensitivity
137
What type: Th1 cells are activated and release cytokines, including IL-3, interferon gamma (IFN-., tumor necrosis factor-beta (TNF-), and tumor necrosis factor alpha (TNF-), that recruit macrophages and neutrophils, produce edema, promote fibrin deposition, and generally enhance an inflammatory response.
Type IV Hypersensitivity
138
they recruit macrophages and neutrophils
cytokines
139
what cells cause tissue destruction in type IV?
Cytotoxic T cells
140
a form of delayed hypersensitivity that accounts for a significant number of all occupationally acquired illnesses.
contact dermatitis
141
caused by Poison ivy, nickel, rubber, formaldehyde; hair dyes and fabric finishes, cosmetics, medications applied to the skin, such as topical anesthetics, antiseptics, and antibiotics, latex allergy
contact dermatitis
142
In contact dermatitis, what cell functions as the antigen-presenting cell at the site of antigen contact.
Langerhans cells
143
In contact dermatitis, these cells may migrate to regional lymph nodes and generate sensitized Th1 cells there. This sensitization process takes several days, but once it occurs, its effects last for years.
Langerhans cells
144
A skin eruption characterized by erythema, swelling, and the formation of papules appears anywhere from 6 hours to several days after the exposure.
Contact dermatitis
145
The papules may become vesicular, with blistering, peeling, and weeping and there is usually itching at the site.
Contact dermatitis
146
It is mediated predominantly by sensitized T lymphocytes that respond to inhaled allergens.
Hypersensitivity Pneumonitis
147
in Hypersensitivity Pneumonitis, what 2 antibodies are formed, but these are thought to play only a minor part.
IgG and IgM antibodies
148
This is an allergic disease of the lung parenchyma, characterized by inflammation of the alveoli and interstitial spaces.
Hypersensitivity Pneumonitis
149
It is caused by chronic inhalation of a wide variety of antigens, and it is most often seen in men between the ages of 30 and 50 years
Hypersensitivity Pneumonitis
150
Hypersensitivity Pneumonitis is most often seen in ____
men between the ages of 30 and 50 years
151
Testing for exposure to tuberculosis is a classic example of a delayed hypersensitivity reaction.
Tuberculin-Type Hypersensitivity
152
In Tuberculin-Type Hypersensitivity, they induce a reaction in people who have or have had tuberculosis.
Soluble antigens from Mycobacterium tuberculosis
153
When challenged with antigen intradermally, previously sensitized individuals develop an area of ___ and ___ at the injection site.
erythema and induration
154
The blood vessels become lined with mononuclear cells, and the reaction reaches a peak by 72 hours after exposure.
Tuberculin-Type Hypersensitivity
155
This is the result of infiltration of T lymphocytes and macrophages into the area.
Tuberculin-Type Hypersensitivity
156
gold standard in testing for contact dermatitis.
Patch test
157
a 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. Redness with papules or tiny blisters is considered a positive test.
Patch test
158
when is the final evaluation of patch test conducted? (in hours)
96 to 120 hours.
159
It is performed in much the same manner as testing for the presence of IgE.
Mantoux method
160
Typically, 0.1 mL of the antigen is injected intradermally, using a syringe and a fine needle.
Mantoux method
161
what test considers induration of 5 mm or more a positive test?
Mantoux method
162
what is the indication of a positive result in a patch test?
Redness with papules or tiny blisters
163
Immune Mechanism: Release of mediators from mast cells and basophils
Type I
164
Immune Mechanism: Cytolysis due to antibody and complement
Type II
165
Immune Mechanism: Deposits of antigen and antibody complexes
Type III
166
Immune Mechanism: Release of cytokines
Type IV
167
What types of hypersensitivity have Complement Involvement?
Types II and III
168
Immune Mediator for type I
IgE
169
Immune Mediator for type II
IgG
170
Immune Mediator for type III
IgG or IgM
171
Immune Mediator for type IV
t-cells
172
antigen of type I
Heterologous
173
antigen of type II
Autologous or heterologous
174
antigen of type III
Autologous or heterologous
175
antigen of type IV
Autologous or heterologous
176
Anaphylaxis, hay fever, food allergies, asthma
Type I
177
Transfusion reactions, autoimmune hemolytic anemia, HDFN
Type II
178
Serum sickness, Arthus reaction, Lupus Erythematosus
Type III
179
Contact dermatitis, tuberculin test, pneumonitis
Type IV
180
Contact dermatitis, tuberculin test, pneumonitis
Type IV
