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MTAP 1 FINALS > Chapter 14 Stevens (Serology) > Flashcards

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

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2
Q

Devised classification system from these reaction based on their immunologic mechanism in 1960

A

Philip Gell and Robin Coombs

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3
Q

Type I Hypersensitivity other name:

A

Anaphylactic hypersensitivity

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4
Q

Type II Hypersensitivity other name:

A

Antibody-mediated cytotoxicity hypersensitivity

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5
Q

Type III Hypersensitivity other name:

A

Complex mediated hypersensitivity

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6
Q

Type IV Hypersensitivity other name:

A

Cell - mediated hypersensitivity

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7
Q

Anaphylactic hypersensitivity other name:

A

Immediate

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8
Q

Cytotoxic hypersensitivity other name:

A

Antibody mediated

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9
Q

Immune complex hypersensitivity other name:

A

Complement mediated

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10
Q

Delayed hypersensitivity other name:

A

T-cell Mediated

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11
Q

Heterologous antigen is seen in:

A

Type I Hypersensitivity (Anaphylactic)

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12
Q

Autologous and Heterologous antigen is seen in

A

Type II
Type III
Type IV

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13
Q

Time of Latency in Anaphylactic hypersensitivity

A

minutes

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14
Q

Time of Latency in Cytotoxic and immune complex hypersensitivity

A

Hours

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15
Q

Time of latency in delayed hypersensitivity

A

Days

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16
Q

Anaphylactic, Cytotoxic, Immune Complex immune reaction:

A

Humoral

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17
Q

Immune reaction of Delayed Hypersensitivity

A

Cellular

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18
Q

Immune mechanism:

Release of
mediators from
IgE-sensitized
mast cells and
basophils

A

Anaphylactic Hypersensitivity

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19
Q

Immune mechanism:

Cell destruction
caused by
antibody and
complement,
opsonization, or
ADCC

Cell function
inhibited by
antibody binding

A

Cytotoxic

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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

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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

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22
Q

Presence of complement is seen in:

A

Cytotoxic and Immune Complex hypersensitivity

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23
Q

Complement found in delayed hypersensitivity

A

Cellular

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24
Q

Anaphylaxis
Allergies (food,
products
Bronchial Asthma
Hay Fever
Urticaria

Type of hypersensitivity

A

Type I Anaphylactic Hypersensitivity

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25
Q

AHA
HDN
HTR
Thrombocytopenia
Goodpasture
Pemphigus
Vulgaris
Drug Allergies
Hyperacute GVHD
Rheumatic fever
Grave’s Disease
Type II DM

Type of Hypersensitivity:

A

TYPE II HYPERSENSITIVITY Antibody-mediated cytotoxicity

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26
Q

SLE
Arthus
Serum Sickness
Dengue
SLE
RA
Post
Streptococcal
Vasculitis

Type of Hypersensitivity

A

TYPE III HYPERSENSITIVITY Complex mediated hypersensitivity

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27
Q

Dermatitis
Chrons
Celiac
Leprosy
Tuberculin
Poison Ivy
Acute GVHD
Hashimot’s
Type I DM

Type of hypersensitivity

A

TYPE IV HYPERSENSITIVITY Cell - mediated hypersensitivity

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28
Q

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

A

Passive cutaneous anaphylaxis

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29
Q

inherited tendency to develop classic allergic responses to naturally occurring inhaled or ingested allergens

A

Atopy

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30
Q

PHASES OF TYPE I IMMUNE RESPONSE

A

Sensitization Phase
Activation Phase
Late Phase

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31
Q

Sensitization Phase of type I immune response involves

A

Formation of antigen -specific IgE that attaches to mast cells and basophils

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32
Q

Resposure to the same antigen, causing degranulation of mast cells and
basophils and release mediators

A

Activation phase

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33
Q

most abundant preformed mediator; primary mediator

A

Histamine

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34
Q

When mast cells and basophils are triggered to synthesize other reactants such as
secondary reactants

6-8 hours after exposure

A

Late phase

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35
Q

MEDIATOR for primary (preformed)

A

Histamine
Heparin
Eosinophil (ECF-A)
Neutrophil (NCF-A)
Proteases (tryptase, chymase)

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36
Q

Smooth muscle contraction, vasodilation,
increased vascular permeability

Mediator:

A

Histamine, Heparin

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37
Q

Chemotactic for eosinophil

Mediator:

A

Eosinophil (ECF-A)

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38
Q

Chemotactic for neutrophils

Mediator:

A

Neutrophil (NCF-A)

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39
Q

Convert C3 to C3b
Stimulate mucus production
Activate Cytokines

Mediator:

A

Proteases (tryptase, chymase)

40
Q

Secondary
(Newly
Synthesized) mediators:

A

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
Q

Vasodilation
Increased vascular permeability

Mediator:

A

Prostaglandin PGD2

42
Q

Chemotactic factor for neutrophils,
eosinophils

Mediator:

A

Leukotriene LTB4

43
Q

Increased vascular permeability
Bronchoconstriction, mucus secretions

Mediator:

A

Leukotrienes LTC4, LTD4 LTE4

44
Q

Platelet Aggregation Mediator:

A

Platelet-activating factor (PAF)

45
Q

Increase inflammatory cells in area, and
increase IgE production

Mediator:

A

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
Q

Clinical Manifestation of Type I Hypersensitivity

A

Allergic rhinitis
Allergic Asthma
Food Allergies
Skin Reactions
Anaphylaxis
Latex Sensitivity

47
Q

most common form of atopy

A

allergic rhinitis

48
Q

Seasonal allergic rhinitis, triggered by tree and grass pollens in the
air during the spring in temperate climates

49
Q

“Panting” or “breathlessness”’

Airflow obstruction

A

Allergic asthma

50
Q

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

A

Food allergies

51
Q

Manifest acute urticaria or eczema

A

Skin reactions

52
Q

local inflammation of the skin

A

Dermatitis

53
Q

caused by the release of vasoactive mediators from
mast cells in the skin following contact with allergens such as pet dander or
insect venom.

A

Wheal-and-flare reaction

54
Q

actions occur deeper in the dermal tissues

55
Q

—– is the most severe type of allergic response because it is
an acute reaction that simultaneously involves multiple organs.

Means “without protection”

A

Anaphylaxis

56
Q

______ 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

A

Latex Sensitivity

57
Q

first anti-IgE monoclonal antibody drug for treatment of type I hypersensitivity

A

Omalizumab

58
Q

For treatment of severe asthma; Ab against IL-5

Treatment of type I hypersensitivity

A

Mepolizumab

59
Q

treat patients with moderate-severe atopic dermatitis

Treatment of type I hypersensitivity

60
Q

In Vivo Skin Test for type I hypersensitivity

A

Percutaneous Test (Prick and Puncture Test)

Intradermal Test - greater amount of antigen is used and more sensitive than cutaneous

61
Q

In a positive test of in vivo skin test, a ____________ will appear at the site where the allergen was applied

A

wheal-and-flare reaction

62
Q

In vitro Test for type I hypersensitivity

A

Competitive radioimmunosorbent test (RIST)

63
Q

Clinical Manifestation of Type II Hypersensitivity

A

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
Q

Reactions may occur within minutes or hours after
receipt of incompatible blood.

ABO: IgM class

May cause DIC, Renal failure, vascular collapse

A

Acute hemolytic transfusion

65
Q

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

A

Delayed hemolytic reactions

66
Q

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

A

Hemolytic Disease of
the Fetus and
Newborn

67
Q

Reaction directed against self-antigens because individuals with this
disease form antibodies to their own RBCs

A

Autoimmune
Hemolytic Anemia

68
Q

Accounts for more than 70% of autoimmune anemias

Characterized by the formation of IgG antibody, which reacts most
strongly at 37°C.

A

Warm autoimmune hemolytic anemia

69
Q

Drugs are capable of attaching to the RBCs directly or of forming
immune complexes that attach to the RBCs

Acts as haptens

A

Penicillin and Cephalosporin

70
Q

Can stimulate the production of antidrug antibodies that bind to the drug to form soluble immune complexes

A

Quinidine and Phenacetin

71
Q

Can induce hemolytic anemia by stimulating production of autoantibodies against the RBC membrane

A

Methyldopa

72
Q

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

A

Cold Agglutinin
Antibodies

73
Q

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

A

Paroxysmal Cold
Hemoglobinuria

74
Q

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
A

Type II Reactions
Involving Tissue
Antigens

75
Q

Testing for Type II Hypersensitivity

A

Direct Antiglobulin Test
Indirect Antiglobulin Test

76
Q

Detects RBCs that have been sensitized with antibody or complement in vivo

A

Direct Antiglobulin Test

77
Q

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

A

Indirect Antiglobulin Test

78
Q

Clinical Manifestation of Type III Hypersensitivity

A

Arthus Reaction
Serum Sickness
Autoimmune Disease and
Other Causes of Type III
Hypersensitivity

79
Q

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

A

Arthus Reaction

80
Q

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.

A

Serum Sickness

81
Q

SLE and rheumatoid arthritis (RA) are two such examples.

Patients with these diseases commonly produce antibodies
against nuclear constituents such as DNA and histones.

A

Autoimmune Disease and
Other Causes of Type III
Hypersensitivity

82
Q

Testing for Type III Hypersensitivity

A

Indirect immunofluorescence

Enzyme-linked immunosorbent assay (ELISA)

Fluorescent microsphere multiplex immunoassays

83
Q

Rheumatoid factor can be detected by:

A

latex agglutination
nephelometry
other immunoassays

84
Q

Seen individuals infected with Mycobacterium tuberculosis which developed a localized
inflammatory response after receiving intradermal injections of a filtrate from the organism

A

Type IV Hypersensitivity

85
Q

Pathogens that commonly induce delayed hypersensitivity include:

A

M. tuberculosis, Mycobacterium
leprae, Pneumocystis carinii, Leishmania species, and herpes simplex virus

86
Q

are those that come into direct contact with the skin

A

Contact antigens

87
Q

Clinical Manifestation of Type IV Hypersensitivity

A

Contact Dermatitis

Hypersensitivity
Pneumonitis

88
Q

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

A

Contact Dermatitis

89
Q

an allergic disease of the lung parenchyma characterized by inflammation of the alveoli and interstitial spaces

A

Hypersensitivity
Pneumonitis

90
Q

Positive interpretation for mantoux method

91
Q

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

A

Patch test

92
Q

have been developed as an alternative to tuberculin skin
testing to detect latent TB infection

A

Interferon gamma release assays (IGRA)

93
Q

patient blood is drawn into specialized collection tubes containing peptides
that are highly specific for M. tuberculosis (ESAT-6 and CFP-10)

A

Quantiferon TB Gold Plus assay

94
Q

Is based on the enzyme-linked immunospot (Elispot) technique.

A

T-SPOT.TB test

95
Q

Hypersensitivity types I, II, and III are ______

A

antibody-mediated

96
Q

Type IV hypersensitivity is a cell-mediated response involving:

A

T lymphocytes

MTAP 1 FINALS (16 decks)

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