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3J - IMMUNOSERO LEC (1ST SEM: MIDTERMS ‼️) > LESSON 1: HYPERSENSITIVITY REACTIONS > Flashcards

LESSON 1: HYPERSENSITIVITY REACTIONS Flashcards

1
Q

State of unresponsiveness to a specific antigen in an effort to
prevent destruction from overreactivity of the immune system

A

Immune tolerance

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2
Q

ability of immune system to recognize
= NOT RESPOND against self produced antigens

A

self tolerance

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3
Q

failed self tolerance =

A

autoimmune disease

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4
Q

immune system actively
AVOIDS RESPONDING to external antigens

A

induced tolerance

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5
Q

failed induced tolerance =

A

hypersensitivity reactions

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6
Q

EXCESSIEVE and INAPPROPRIATE immune response = damaged host tissue resulting from
prolonged or repeated antigen exposure

A

Hypersensitivity reaction

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7
Q

end result of hypersensitivity reaction

A

damaged host cells, tissue and organs

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8
Q

All hypersensitivity reactions are consequences of ? = tissue damage

A

adaptive immune response

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9
Q

4 general types of hypersensitivity reaction

A

type 1: immediate or anaphylactic
type 2: cytotoxic
type 3: immune complex
type 4: delayed or cell-mediated

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10
Q

types of hypersensitivity reaction that are ANTIBODY MEDIATED = faster onset of signs and symptoms

A

type 1,2,3

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11
Q

Antigens that stimulate allergies; mostly proteins that naturally triggers an immune
response

A

allergens

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12
Q

factors that are instrumental in the manifestation
of an allergy

A

genetic background
environment

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13
Q

COMPONENTS OF THE IMMUNE SYSTEM INVOLVED IN TYPE I
HYPERSENSITIVITY REACTION

A

IgE
Mast cells
Basophils
Eosinophils
T helper 2 cells
Cytokines and chemokines (IL-4, IL-5, IL-13)

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14
Q

TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

Antibody mediator

A

IgE

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15
Q

TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

Antigen involved

A

soluble antigens

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16
Q

TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

cellular mediators

A

mast cells and basophils

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17
Q

TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

chemical mediators

A

histamine

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18
Q

TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

mechanism

A

CROSS LINKING OF (2) IGE antibodies on mast
cells/basophils and the RELEASE OF HISTAMINE

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19
Q

causes the manifestation of
the signs and symptoms of Type I Hypersensitivity
reactions

A

release of HISTAMINE

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20
Q

TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

Clinical states

A

Hay fever
Asthma
Food allergies
Anaphylactic shock

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21
Q

Involves the second or subsequent exposure to the
same antigen; stage that causes damage to the host cell

A

Effector Stage / Reaction Phase

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22
Q

Involves the first exposure to the antigen

A

sensitization stage

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23
Q

TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

Sensitization stage: Allergen enters the body through ?

A

Direct contact
Inhalation
Ingestion
Puncture

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24
Q

cause the mast cells and basophils to undergo
degranulation

A

crosslinking of IgE

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25
Q

Expresses Fc Epsilon receptors (FcERI) = why IgE has the greatest affinity to mast cells

A

mast cells

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26
Q

Antibody isotype involved in allergy
disorders/parasite immunity

A

IgE

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27
Q

Tetrameric receptor complex that binds specifically to the Fc portion of the epsilon heavy chain of your IgE

A

FcERI

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28
Q

MECHANISM OF TYPE I HYPERSENSITIVITY REACTION

where APC migrates to present processed antigen to the naive T helper cells

A

lymph nodes

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29
Q

MECHANISM OF TYPE I HYPERSENSITIVITY REACTION

migrate to the target site to which the allergen first entered; attach to the receptor site of the APC → start to secrete large amounts of cytokines

A

T helper 2 cell

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30
Q

Allows differentiation of B cells into IgE
producing plasma cells

A

IL-4 and IL-5

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31
Q

MECHANISM OF TYPE I HYPERSENSITIVITY REACTION

allow successful attachment of IgE into the mast
cell and basophils

A

FCeRI

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32
Q

releases Interleukin 4, Interleukin 13 and
Interleukin 5.

A

T helper 2

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33
Q

causes T helper cells to DIFFERENTIATE into T
helper 2 cells

A

IL-4

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34
Q

enhances MUCUS production of epithelial cells

A

IL-13

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35
Q

recruit EOSINOPHILS from the bone marrow to the site of infection

A

IL-5

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36
Q

PATHOGENESIS OF TYPE 1 HYPERSENSITIVITY

bronchi of the lungs

A

bronchochostriction

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37
Q

PATHOGENESIS OF TYPE 1 HYPERSENSITIVITY

intestine

A

(!) Bowel Peristalsis (due to increased peristaltic movement)
(2) Diarrhea (attempt to dilute food)
(3) Epigastric pain (increased prod of HCl)

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38
Q

PATHOGENESIS OF TYPE 1 HYPERSENSITIVITY

blood vessel

A

vasodilation permeability = hypotension

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39
Q

fluid will accumulate
underneath the skin showing skin manifestation is called

A

urticaria

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40
Q

PATHOGENESIS OF TYPE 1 HYPERSENSITIVITY

nerves

A

pruritus/itching

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41
Q

TYPE 1: LOCALIZED HYPERSENSITIVITY REACTIONS

also known as?

A

atopy

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42
Q

TYPE 1: LOCALIZED HYPERSENSITIVITY REACTIONS

examples of atopy

A

asthma
allergic rhinitis (hay fever)
atopic dermatitis

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43
Q

Reaction affects the entire body; exterme allergic reactions

A

SYSTEMIC HYPERSENSITIVITY REACTIONS

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44
Q

Severe type of allergic reaction that involves airway obstruction
and circulatory collapse

A

anaphylaxis

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45
Q

drugs for anaphylaxis

A

penicillin

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46
Q

SYSTEMIC HYPERSENSITIVITY REACTIONS

clinical picture

A
  • decrease in BP = SHOCK
  • bronchospasm, cyanosis, edema and urticaria = respiratory distress
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47
Q

TREATMENT OF TYPE I HYPERSENSITIVITY REACTIONS

localized HSR

A

antihistamine

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48
Q

TREATMENT OF TYPE I HYPERSENSITIVITY REACTIONS

systemic HSR

A

(1) epinephrine
(2) corticosteroids (mmunosuppresant)
(3) antihistamine

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49
Q

TREATMENT OF TYPE I HYPERSENSITIVITY REACTIONS

Address the decrease in the blood pressure; reverse
the symptoms of decreasing blood pressure

A

epinephrine

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50
Q

Type II: Cytotoxic Hypersensitivity Reaction

Antibody mediator

A

IgG and IgM

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51
Q

Type II: Cytotoxic Hypersensitivity Reaction

Antigens involved

A

cell-bound

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52
Q

Type II: Cytotoxic Hypersensitivity Reaction

End result when the complement system is triggered by the activation of classical pathway

A

Membrane
Attack Complex (MAC) = cause the lysis
of the cell

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53
Q

Type II: Cytotoxic Hypersensitivity Reaction

Substance used for opsonization; used to coat the cell surface
and enhance the phagocytic activity of
macrophage which leads to lysis

A

C3B

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54
Q

Type II: Cytotoxic Hypersensitivity Reaction

Cellular mediators

A

macrophages

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55
Q

Type II: Cytotoxic Hypersensitivity Reaction

chemical mediators

A

complement proteins

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56
Q

Type II: Cytotoxic Hypersensitivity Reaction

mechanism

A

IgG and IgM bind to epitopes -> promote opsonization, complement mediated lysis, and ADCC

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57
Q

These Type 2 Hypersensitivity reactions are triggered by antigens
present on the cell surface, which are?

A

Self-antigen
Modified/Altered self-antigen
Alloantigen

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58
Q

THREE MAIN MECHANISM OF TYPE II HYPERSENSITIVITY REACTION

A

Complement activation
Opsonization
Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)

59
Q

end result here is the destruction of Red Blood Cell due to
transfusion incompatibility

A

hemolytic transfusion reactions

60
Q

Reasons why Hemolytic Disease of the Newborn occurs

A

ABO incompatibility
Rh incompatibility

61
Q

HEMOLYTIC DISEASE OF THE NEWBORN

Antibodies are naturally occurring

A

ABO blood group

62
Q

HEMOLYTIC DISEASE OF THE NEWBORN

does not have naturally occurring
antibodies; requires exposure to the antigen

A

Rh blood group

63
Q

HEMOLYTIC DISEASE OF THE NEWBORN

acts as a barrier
where Rh antigen of the baby will not go to
the mother

A

placenta

64
Q

HEMOLYTIC DISEASE OF THE NEWBORN

Administered To Prevent
Antibody Formation

A

Rhesus Immune Globulin Injection (Rhogam injection)

65
Q

HEMOLYTIC DISEASE OF THE NEWBORN

An intramuscular injection is given when ?

A

■ At 28 weeks into the pregnancy.
■ Within 72 hours of birth of a confirmed Rh
positive baby.

66
Q

Anemia that results from lack of intrinsic factor

A

pernicious anemia

67
Q

Disease that is characterized by the presence of
autoantibodies in the form of IgG and IgM; autoantibodies will lead to the DESTRUCTION OF THE PARIETAL CELLS

A

PERNICOUS ANEMIA

68
Q

PARIETAL CELLS of the stomach produces ?

A

HCl and intrinsic factor

69
Q

Pernicious Anemia

absent intrinsic factor will cause?

A

not absorbed VitB12

70
Q

Antibodies attack the BASEMENT MEMBRANE in lungs and kidneys → leading to bleeding from the lungs and kidney
failure

A

GOODPASTURE SYNDROME

71
Q

GOODPASTURE SYNDROME

Circulating antibodies are directed against the collagen of the
part of the kidney known as ?

A

Glomerular Basement
Membrane (GBM)

72
Q

Circulating antibodies directed at KIDNEY will result to what kind of disease?

A

Acute or Rapidly Progressive
Glomerulonephritis

73
Q

resuling condition if the circulating antibodies also attack the collagen of the air sacs of the LUNG (alveoli)

A

Pulmonary Hemorrhage

74
Q

TWO MANIFESTATIONS present in patient→ probable diagnosis would be the Goodpasture syndrome.

A

hemoptysis
hematuria

75
Q

Hypersensitivity reaction against Streptococcus pyogenes

A

ACUTE RHEUMATIC FEVER

76
Q

causative agent for tonsillitis

A

Streptococcus pyogenes

77
Q

what organ has an antigen w a similar structure to M protein of S. pyogenes

A

human heart

78
Q

ACUTE RHEUMATIC FEVER

attacking the heart due to its similar structure w S. pyogenes M protein will lead to ?

A

destructction of the MITRAL VALVE of the heart = Rheumatic
heart disease or Acute Rheumatic Fever.

79
Q

Autoimmune disorder caused by an antibody-mediated blockade of NEUROMUSCULAR TRANSMISSION resulting in SKELETAL MUSCLE WEAKNESS

A

Myasthenia Gravis

80
Q

MYASTHENIA GRAVIS

autoimmune attack occurs when autoantibodies form
against the - at the -

A

nicotinic acetylcholine postsynaptic receptors ; neuromuscular junction of skeletal muscles

81
Q

autoimmune disorder that is characterized by the production of autoantibodies against the acetylcholine receptors found in the muscle.

A

myasthenia gravis

82
Q

MYASTHENIA GRAVIS

Binding of antibodies (Ab) to the ACh receptors → in
people with myasthenia gravis → leads to the MANIFESTATION OF ?

A

paralysis

83
Q

Graves’ disease is an autoimmune disease characterized by ?

A

hyperthyroidism

84
Q

GRAVES’ DISEASE

– controls the metabolic rate of the body

A

thyroid gland

85
Q

GRAVES’ DISEASE

– responds to the drop in metabolic rate

A

hypothalamus

86
Q

GRAVES’ DISEASE

– responsible in increasing/correcting the metabolic
rate

A

T3 and T4

87
Q

GRAVES’ DISEASE

stimulates thyroid gland to release t3 and T4

A

TSH (thyroid-stimulating
hormone)

88
Q

autoimmune disease characterized by
autoantibodies binding to TSH receptors → stimulates
hormone synthesis → OVERPRODUCTION OF THYROID HORMONES

A

GRAVES’ DISEASE

89
Q

DIABETES MELLITUS TYPE 2 (DM 2)

Adult-onset diabetes, is a form of diabetes that is characterized
by ?

A

increased blood sugar
insulin resistance

90
Q

DIABETES MELLITUS TYPE 2 (DM 2)

the presence of autoantibodies binding to insulin receptors, preventing insulin to bind to the receptor →
inability of the cell to absorb glucose WILL CAUSE WHAT CONDITION

A

hyperglycermia (increased glucose in the blood)

91
Q

TYPE III HYPERSENSITIVITY: IMMUNE
COMPLEX HYPERSENSITIVITY REACTION

Antibody mediators

A

IgG and IgM

92
Q

TYPE III HYPERSENSITIVITY: IMMUNE
COMPLEX HYPERSENSITIVITY REACTION

Antigen involved

A

Soluble bound antigens

93
Q

TYPE III HYPERSENSITIVITY: IMMUNE
COMPLEX HYPERSENSITIVITY REACTION

Cellular mediators

A

Neutrophils

94
Q

TYPE III HYPERSENSITIVITY: IMMUNE
COMPLEX HYPERSENSITIVITY REACTION

Chemical mediators

A

complement proteins

95
Q

TYPE III HYPERSENSITIVITY: IMMUNE
COMPLEX HYPERSENSITIVITY REACTION

Mechanism

A

ANTIGEN-ANTIBODY complexes in
tissues activate complement and
attract neutrophils that release LYTIC MOLECULES

96
Q

unremoved immune complexes can be deposited on the
following preferred sites

A

Blood bessels
Glomerules of the kidney
Joints
Skin

97
Q

TYPE III HYPERSENSITIVITY: s IMMUNE
COMPLEX HYPERSENSITIVITY REACTION

Most preferred site of complex deposition
since

A

GLOMERULUS OF THE KIDNEY

98
Q

TYPE III HYPERSENSITIVITY: s IMMUNE
COMPLEX HYPERSENSITIVITY REACTION

byproducts of the complement system and
a powerful chemotaxin, will recruit more neutrophils toward the area where the immune complex are deposited

A

C5A

99
Q

2 TYPES OF TYPE III HYPERSENSITIVITY REACTION

A

Local: Arthus reaction
Systemic: Serum sickness

100
Q

Discovered Arthus reaction

A

Nicolas Maurice Arthus in 1903

101
Q

Caused by SUBCUTANEOUS or INTRADERMAL introduction of soluble antigen which later forms immune complexes

A

Arthus reaction

102
Q

ARTHUS REACTION

immune complexes deposited in the blood vessels can cause

A

vasculitis
necrosis

103
Q

ARTHUS REACTION

antibody formed upon repeated administration of horse serum into the rabbit

A

high levels of IgG

104
Q

PATHOPHYSIOLOGY OF ARTHUS REACTION

Time period of severe pain, swelling, induration, edema,
hemorrhage, and occasionally by necrosis

A

4-12 hours

105
Q

Arthus reactions (type III hypersensitivity reactions) are rarely
reported after vaccination and can occur after - and -

A

TETANUS
toxoid-containing or DIPTHERIA toxoid-containing vaccines

106
Q

Autoantibody formation against the soluble antigens of the
host (DNA, histones, nucleolar antigens and RNA)

A

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

107
Q

SLE is characteried by

A

production of
antibodies against NUCLEIC ACID and their associated proteins

108
Q

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

anti-DNA complexes are deposited in different tissues in the body, such as ?

A

skin
joints
glomerulus
serous membranes

109
Q

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

Skin: characteristic - is seen along the bridge of the nose and cheek

A

butterfly rash

110
Q

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

Joints

A

Non-Erosive inflammation with no to little deformity of the
joints

111
Q

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

GLOMERULUS

A

Kidney damage

112
Q

most affected organ in cases of SLE

A

kidney

113
Q

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

SEROUS MEMBRANES: most common affected body cavity in cases of SLE

A

pericardial and pleural cavities

114
Q

POST-STREPTOCOCCAL GLOMERULONEPHRITIS occurs after - of untreated Streptococcal infection of the pharynx and skin

A

1-4 weeks

115
Q

S. pyogenes infection in the pharynx

A

Streptococcal pharyngitis

116
Q

S. pyogenes skin infection

A

Impetigo

117
Q

Autoimmune disorder that may affect many organs but
primarily attacks the JOINTS

A

RHEUMATOID ARTHRITIS

118
Q

RHEUMATOID ARTHRITIS

caused by autoantibodies formed againts - in the blood

A

citrullinated proteins

119
Q

abnormal stiffening and
immobility of a joint due to the fusion of the bones

A

ankylosis

120
Q

allows for distal end of bones of the joints to glide smoothly, no friction

A

articular cartilage

121
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

Antibody mediator

A

none

122
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

Antigen involved

A

SOLUBLE and CELL-BOUND

123
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

Cellular mediators

A

T HELPER 1 CELLS and MACROPHAGES

124
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

Chemical mediators

A

cytokines

125
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

Mechanism

A

Released of mediators by SENSITIZED T CELLS
provoke tissue destruction by MONONUCLEAR cells

126
Q

PATHOPHYSIOLOGY OF TYPE IV HYPERSENSITIVITY

Reaction will be evident in - (time)

A

24-72 hours

127
Q

chemicals that bind in the glycoproteins
present in the skin cells (poison ivy)

A

urushiol

128
Q

condition caused by contact w poison iyivy

A

contact dermatitis

129
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

act on the T helper
cells = T helper cells
will transform into a T
helper 1

A

IL-12

130
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

T HELPER 1 functions to release -

A

IFN-gamma

131
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

Act on to recruit more macrophages
toward the site of infection

A

IFN-gamma

132
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

recruited macrophages will release -

A

lysosomal enzymes and reactive
oxygen species

133
Q

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY

Skin lesions (poison ivy contact): responsible for
causing the skin
lesions or tissue
damage

A

Recruited macrophages

134
Q

Occurs due an exposure to nickel metal

A

CONTACT DERMATITIS - NICKEL

135
Q

Other causes of Contact Dermatitis

A

○ Bleach and Detergents
○ Shampoos
○ Rubber
○ Latex gloves

136
Q

Skin disorder that causes skin cells to multiply up to 10 times
faster than normal

A

psorriasis

137
Q

commonsnites of psoriasis

A

elbows
lumbosacral areas
galns penis

138
Q

MULTIPLE SCLEROSIS

A

Autoimmune demyelinating diseases caused by immune
responses (t cells & macrophages) directed against the
component of the myelin sheath of the neurons in the central
nervous system

139
Q

cause the destruction of the
certain areas of the myelin sheath of the axons of
the nerves from the central nervous system.

A

cytokins

140
Q

Characterized by the absence of insulin

A

DIABETES MELLITUS TYPE 1

141
Q

Qualitative skin test done to screen in vivo sensitization by M. Tuberculosis

A

Mantoux test

142
Q

Mantoux test

Antigen introduced through intradermal route

A

PPD purified derivative protein

142
Q

Mantoux test

> 15 mm

A

Positive

142
Q

Mantoux test

<15 mm

A

Negative

3J - IMMUNOSERO LEC (1ST SEM: MIDTERMS ‼️) (1 decks)

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