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Immuno and Sero > IS Lec Finals - Hypersensitivity > Flashcards

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

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2
Q

second line of defense against non-self pathogens

A

Innate Immunity

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3
Q

third line of defense against non-self pathogens

A

Adaptive Immunity

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4
Q

Macrophage, Neutrophil, Dendritic cell, Natural killer cell, complement, natural antibodies, epithelial barrier

A

Innate Immunity

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5
Q

Cytokines, B lymphocyte, High-affinity antibodies, Helper and Cytotoxic T lymphocyte

A

Adaptive Immunity

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6
Q

what are the cells present in both innate and adaptive immunity

A

PBMC, dendritic cells, macrophages, NK cells

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7
Q

it is an exaggerated response to a harmless antigen that results in injury to the tissue, disease, or even death

A

Hypersensitivity

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8
Q

heightened state of immune responsiveness

A

Hypersensitivity

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9
Q

immune & inflammatory responses that are harmful to the host

A

Hypersensitivity

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10
Q

required to prime the
immune system

A

PRIMING DOSE

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11
Q

results to injurious consequence

A

SHOCKING DOSE

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12
Q

dose that alerts the immune system

A

PRIMING DOSE

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13
Q

IMMEDIATE, ALLERGIC or Ig-E mediated hypersensitivity reaction

A

Type I Hypersensitivity

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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

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15
Q

Immune mediator for Type 1

A

IgE

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16
Q

responsible for sensitizing mast cells and providing recognition of antigen

A

IgE

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17
Q

IgE degranulation of basophils or mast cells

A

Type I Hypersensitivity

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18
Q

Antigens that trigger formation of IgE

A

atopic antigens, or allergens.

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19
Q

refers to an inherited tendency to respond to naturally occurring inhaled and ingested allergens with continued production of IgE.

A

Atopy

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20
Q

first researchers to show that a serum factor was responsible for type I reactions.

A

Carl Wilhelm Prausnitz and Heinz Küstner

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21
Q

who was allergic to fish?

A

Heinz Küstner

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22
Q

what was responsible for type I reactions that was discovered by Carl Wilhelm Prausnitz and Heinz Küstner?

A

serum factor

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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

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24
Q

what do you call the antibody responsible for sensitizing mast cells and basophils and will recognize the allergens

A

immune mediator

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25
Q

what immunity is when antibody is injected?

A

active immunity

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26
Q

what immunity is when antigen is injected and allows the body to develop its own antibodies

A

passive immunity

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27
Q

what t-helper cell is used in people with allergies?

A

TH2

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28
Q

what t-helper cell is used in people without allergies?

A

TH1

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29
Q

principle effector cells of immediate hypersensitivity

A

mast cells

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30
Q

contains numerous cytoplasmic granules including HISTAMINE

A

Mast cells

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31
Q

contain histamine-rich granules and high-affinity receptors for IgE

A

Basophils

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32
Q

respond to chemotactic stimulation and tend to accumulate in the tissues during an inflammatory reaction

A

Basophils

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33
Q

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

A

mast cells and basophils

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34
Q

we take this during allergic reactions

A

anti-histamine

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35
Q

used to relieve the symptoms of allergy

A

anti-histamine

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36
Q

block histamine receptors

A

anti-histamine

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37
Q

most important mediator of anaphylaxis

A

Histamine

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38
Q

histamine enables…

A

vasodilation, vascular permeability, smooth muscle constriction

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39
Q

Type I Hypersensitivity may occur in two (2) forms:

A

Anaphylaxis and Atopy

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40
Q

Acute, potentially fatal, and systemic manifestation of hypersensitivity reactions

A

Anaphylaxis

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41
Q

It occurs when an allergen (antigen) binds to IgE on the surface of mast cells with subsequent release of several mediators of anaphylaxis.

A

Anaphylaxis

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42
Q

In ____ multiple organs are usually affected and death may occur within 2 hours

A

Anaphylaxis

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43
Q

A condition of familiar hypersensitivity occurring spontaneously in humans

A

Atopy

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44
Q

Recurrent, non-fatal, local manifestation of immediate hypersensitivity reaction

A

Atopy

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45
Q

It is localized to specific tissues (often epithelial surfaces of antigen entry)

A

Atopy

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46
Q

Common manifestations: asthma, rhinitis, urticaria, atopic dermatitis

A

Atopy

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47
Q

classification by immunopathological phenotype can be used to determine management strategies

A

Asthma

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48
Q

food ingestion (eggs, shellfish, peanuts, drug reactions), insect stings

A

Systemic Anaphylaxis

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49
Q

derived from the Greek word for “panting” or “breathlessness”

A

Bronchial asthma

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50
Q

Recurrent airflow obstruction –> Airway resistance –> breathlessness

A

Bronchial asthma

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51
Q

due to bronchial smooth muscle contraction, mucosa edema, and heavy mucus secretion

A

Bronchial asthma

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52
Q

other term for rhinitis

A

hay fever

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53
Q

usually airborne and affect the the conjunctive and respiratory mucus membrane

A

Rhinitis (hay fever)

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54
Q

most common form of atopy, or allergy.

A

Rhinitis

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55
Q

sinusitis, otitis media (ear infection), eustachian tube dysfunction, and sleep disturbances may result

A

Rhinitis

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56
Q

(wheal and flare) - mediated by histamine.

A

Urticaria

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57
Q

late-phase reaction to allergen in the skin - inflammation - can be treated with steroids.

A

Eczema

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58
Q

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.

A

Food Allergies

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59
Q

an itchy red skin rash, may be caused by food allergens or exposure to house dust mites.

A

Eczema

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60
Q

what is the first line of defense for the Treatment for Type I Hypersensitivity?

A

Avoidance of known allergens

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61
Q

Antihistamines, decongestants, bronchodilators,
followed by inhaled corticosteroids

A

Treatment for Type I Hypersensitivity

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62
Q

very small quantities of sensitizing antigen are injected into the patient with the idea of building up IgG antibodies

A

Immunotherapy or hyposensitization

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63
Q

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.

A

anti-IgE monoclonal antibody

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64
Q

In vivo skin test (cutaneous and intradermal tests)

A

Allergy testing

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65
Q

serum level of TOTAL IgE antibody

A

Radioimmunosorbent assay (RIST)

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66
Q

serum level of IgE specific allergen

A

Radioallergosorbent assay

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67
Q

Immunofluorescence method

A

detection of IgE

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68
Q

ELISA and Passive Agglutination

A

detection of IgE in the serum for diagnosis of atopy

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69
Q

other name for Type II Hypersensitivity

A

Cytotoxic hypersensitivity

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70
Q

triggered by antigens found on cell surfaces. These antigens may be altered self-antigens or heteroantigens.

A

Type II Hypersensitivity

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71
Q

Antibody coats cellular surfaces and promotes phagocytosis by both opsonization and activation of the complement cascade

A

Type II Hypersensitivity

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72
Q

what are the mediators of Type II Hypersensitivity

A

IgG and IgM

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73
Q

in type II, Antibody coats cellular surfaces and promotes phagocytosis by
both ___ and ___

A

OPSONIZATION and COMPLEMENT ACTIVATION

74
Q

have Fc receptors that bind the Fc region of antibody on the target cells, thus enhancing phagocytosis.

A

Macrophages, neutrophils and NK cells

75
Q

Type II Hypersensitivity: If the complement cascade is activated, complement can trigger cellular destruction in two ways:

A

by coating cells with C3b, by complement-generated lysis

76
Q

plays a central role in the cellular damage that typifies type II reactions

A

complement

77
Q

Type II Hypersensitivity examples

A

Transfusion reaction
Hemolytic disease of the fetus and newborn
Autoimmune hemolytic anemia
Type II Reactions Involving Tissue Antigens (Organ-specific)

78
Q

examples of cellular destruction that result from
antibody combining with heteroantigens.

A

Transfusion Reaction

79
Q

Acute HTR is mediated by what Ig?

A

IgM mediated

80
Q

Delayed HTR is mediated by what Ig?

A

IgG mediated

81
Q

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.

A

Transfusion Reaction

82
Q

Result: disseminated intravascular coagulation (DIC), vascular collapse, and renal failure

A

Transfusion Reaction

83
Q

Rh incompatibility of the mother and the fetus

A

Hemolytic Disease of the Fetus and Newborn

84
Q

The mother makes IgG antibodies in response, and these cross the placenta to destroy fetal red cells.

A

Hemolytic Disease of the Fetus and Newborn

85
Q

In Hemolytic Disease of the Fetus and Newborn, what is the Rh of the mother and the baby?

A

Rh negative mother, Rh positive baby

86
Q

protein, it tells if you are positive or negative

A

Rh

87
Q

which baby is affected during HDFN?

A

second baby (subsequent baby)

88
Q

IN HDFN, if enough of the baby’s red cells get into the mother’s circulation, what cells develop?

A

memory B cells

89
Q

IN HDFN, when memory b-cells are activated upon re-exposure to the same red cell antigen, what Ig is produced?

A

IgG

90
Q

During 2nd pregnancy, ___ passes through the placenta → mother excretes

A

Bilirubin

91
Q

Continuous RBC destruction → bilirubin → accumulation (due to underdeveloped liver) →jaundice

A

Hemolytic Disease of the Fetus and Newborn

92
Q

when bilirubin reaches the brain and cause irreversible brain damage to the baby

A

kernicterus

93
Q

Severe HDN is called ___

A

erythroblastosis fetalis

94
Q

Prevention: administration of Rhogam

A

Hemolytic Disease of the Fetus and Newborn

95
Q

when to administer Rhogam?

A

28 weeks of gestation and 72 hours after birth

96
Q

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

A

Rhogam

97
Q

Warm autoimmune hemolytic anemia is mediated by? at what temp?

A

IgG, warm reacting antibody
Optimum at 37C

98
Q

Cold agglutinin disease is mediated by? at what temp?

A

IgM, cold reacting antibody
Optimum at 4C

99
Q

Optimum at 4C

A

Cold agglutinin disease

100
Q

Optimum at 37C

A

Warm autoimmune hemolytic anemia

101
Q

Examples of Type II Reactions Involving Tissue Antigens (Organ-specific)

A

Goodpasture’s syndrome
Graves disease (hyperthyroidism)
Hashimoto’s disease
Myasthenia gravis

102
Q

Testing for Type II Hypersensitivity

A

Direct antiglobulin testing (DAT)
Indirect antiglobulin testing (IDAT)
Polyspecific antihuman globulin

103
Q

is performed to detect transfusion reactions, hemolytic disease of the newborn, and autoimmune hemolytic anemia.

A

Direct antiglobulin testing (DAT)

104
Q

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.

A

Indirect antiglobulin testing (IDAT)

105
Q

a mixture of antibodies to IgG and complement components such as C3b and C3d, and it is used for initial testing

A

Polyspecific antihuman globulin

106
Q

when Polyspecific antihuman globulin tests positive, it should be repeated using ___

A

monospecific anti-IgG, anti-C3b, and anti-C3d

107
Q

what is the other name for Type III Hypersensitivity?

A

immune complex disease

108
Q

similar to type II reactions in that IgG or IgM is involved and destruction is complement mediated

A

Type III Hypersensitivity

109
Q

In the case of type ___ diseases, the antigen is soluble.

A

Type III Hypersensitivity

110
Q

When soluble antigen combines with antibody, complexes are formed that precipitate out of the serum.

A

Type III Hypersensitivity

111
Q

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

A

Type III Hypersensitivity

112
Q

There they bind complement, causing damage to the particular tissue. Deposition of antigen–antibody complexes is influenced by the relative concentration of both components.

A

Type III Hypersensitivity

113
Q

who demonstrated Arthus Reaction?

A

Maurice Arthus in 1903

114
Q

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.

A

Arthus Reaction

115
Q

The inflammatory response is caused by antigen–antibody combination and subsequent formation of immune complexes that deposit in small dermal blood vessels.

A

Arthus Reaction

116
Q

(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.

A

Arthus Reaction

117
Q

generalized type III reaction that is seen in humans, although not as frequently as it used to be

A

Serum sickness

118
Q

results from passive immunization with animal serum, usually horse or bovine, used to treat such infections as diphtheria, tetanus, and gangrene.

A

Serum sickness

119
Q

Serum sickness results from passive immunization with ___

A

animal serum, usually horse or bovine

120
Q

Vaccines and bee stings may also trigger this type of reaction.

A

Serum sickness

121
Q

Generalized symptoms appear in 7 to 21 days after injection and recovery takes between 7 and 30 days.

A

Serum sickness

122
Q

antibodies are directed against constituents such as DNA and nucleohistones,

A

Systemic lupus erythematosus (SLE)

123
Q

In Systemic lupus erythematosus (SLE), where does the main damage occur?

A

glomerular basement membrane in the kidney.

124
Q

an antibody called rheumatoid factor is directed against IgG. Immune complex deposition occurs in the membranes of inflamed joints.

A

Rheumatoid arthritis

125
Q

it detects specific diseases such as SLE and rheumatoid arthritis

A

agglutination reactions

126
Q

what testing uses antigen-coated carrier particles, including red blood cells or latex particles, or enzyme immunoassays.

A

agglutination reactions

127
Q

determine deposition of immune complexes in the tissues.

A

Fluorescent staining

128
Q

what type is Delayed hypersensitivity

A

Type IV Hypersensitivity

129
Q

Type IV Hypersensitivity is first described by ____

A

Robert Koch in 1890

130
Q

individuals infected with Mycobacterium tuberculosis (Mtb) developed a localized inflammatory response when injected intradermally with a filtrate from the organism

A

Type IV Hypersensitivity

131
Q

who observed that individuals infected with Mycobacterium tuberculosis (Mtb) developed a localized inflammatory response when injected intradermally with a filtrate from the organism

A

Robert Koch

132
Q

what is the bacteria in Type IV Hypersensitivity?

A

Mycobacterium tuberculosis (Mtb)

133
Q

play the major role in the manifestations in Type IV Hypersensitivity

A

sensitized T cells

134
Q

how many weeks does initial sensitization phase in Type IV Hypersensitivity take place?

A

1-2 weeks

135
Q

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

A

48 to 72 hours

136
Q

What type: Langerhans cells in the skin and macrophages in the tissue capture and present antigen to T helper cells of the Th1 subclass.

A

Type IV Hypersensitivity

137
Q

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.

A

Type IV Hypersensitivity

138
Q

they recruit macrophages and neutrophils

A

cytokines

139
Q

what cells cause tissue destruction in type IV?

A

Cytotoxic T cells

140
Q

a form of delayed hypersensitivity that accounts for a significant number of all occupationally acquired illnesses.

A

contact dermatitis

141
Q

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

A

contact dermatitis

142
Q

In contact dermatitis, what cell functions as the antigen-presenting cell at the site of antigen contact.

A

Langerhans cells

143
Q

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.

A

Langerhans cells

144
Q

A skin eruption characterized by erythema, swelling, and the formation of papules appears anywhere from 6 hours to several days after the exposure.

A

Contact dermatitis

145
Q

The papules may become vesicular, with blistering, peeling, and weeping and there is usually itching at the site.

A

Contact dermatitis

146
Q

It is mediated predominantly by sensitized T lymphocytes that respond to inhaled allergens.

A

Hypersensitivity Pneumonitis

147
Q

in Hypersensitivity Pneumonitis, what 2 antibodies are formed, but these are thought to play only a minor part.

A

IgG and IgM antibodies

148
Q

This is an allergic disease of the lung parenchyma, characterized by inflammation of the alveoli and interstitial spaces.

A

Hypersensitivity Pneumonitis

149
Q

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

A

Hypersensitivity Pneumonitis

150
Q

Hypersensitivity Pneumonitis is most often seen in ____

A

men between the ages of 30 and 50 years

151
Q

Testing for exposure to tuberculosis is a classic example of a delayed hypersensitivity reaction.

A

Tuberculin-Type Hypersensitivity

152
Q

In Tuberculin-Type Hypersensitivity, they induce a reaction in people who have or have had tuberculosis.

A

Soluble antigens from Mycobacterium tuberculosis

153
Q

When challenged with antigen intradermally, previously sensitized individuals develop an area of ___ and ___ at the injection site.

A

erythema and induration

154
Q

The blood vessels become lined with mononuclear cells, and the reaction reaches a peak by 72 hours after exposure.

A

Tuberculin-Type Hypersensitivity

155
Q

This is the result of infiltration of T lymphocytes and macrophages into the area.

A

Tuberculin-Type Hypersensitivity

156
Q

gold standard in testing for contact dermatitis.

A

Patch test

157
Q

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.

A

Patch test

158
Q

when is the final evaluation of patch test conducted? (in hours)

A

96 to 120 hours.

159
Q

It is performed in much the same manner as testing for the presence of IgE.

A

Mantoux method

160
Q

Typically, 0.1 mL of the antigen is injected intradermally, using a syringe and a fine needle.

A

Mantoux method

161
Q

what test considers induration of 5 mm or more a positive test?

A

Mantoux method

162
Q

what is the indication of a positive result in a patch test?

A

Redness with papules or tiny blisters

163
Q

Immune Mechanism: Release of mediators from mast cells and basophils

A

Type I

164
Q

Immune Mechanism: Cytolysis due to antibody and complement

A

Type II

165
Q

Immune Mechanism: Deposits of antigen and antibody complexes

A

Type III

166
Q

Immune Mechanism: Release of cytokines

A

Type IV

167
Q

What types of hypersensitivity have Complement Involvement?

A

Types II and III

168
Q

Immune Mediator for type I

A

IgE

169
Q

Immune Mediator for type II

A

IgG

170
Q

Immune Mediator for type III

A

IgG or IgM

171
Q

Immune Mediator for type IV

A

t-cells

172
Q

antigen of type I

A

Heterologous

173
Q

antigen of type II

A

Autologous or heterologous

174
Q

antigen of type III

A

Autologous or heterologous

175
Q

antigen of type IV

A

Autologous or heterologous

176
Q

Anaphylaxis, hay fever, food allergies, asthma

A

Type I

177
Q

Transfusion reactions, autoimmune hemolytic anemia, HDFN

A

Type II

178
Q

Serum sickness, Arthus reaction, Lupus Erythematosus

A

Type III

179
Q

Contact dermatitis, tuberculin test, pneumonitis

A

Type IV

180
Q

Contact dermatitis, tuberculin test, pneumonitis

A

Type IV

Immuno and Sero (4 decks)

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