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NPLEX 1 > Immunology 2 > Flashcards

Immunology 2 Flashcards

1
Q

What do Interferon Alpha and Beta do?

A

Part of the innate immune systems defence against both RNA and DNA. Interferons are glycoproteins synthesized by viral-infected cells that act locally on uninfected cells, “priming” them for viral defense.

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2
Q

What are the two steps of “priming” interferon Alpha and Beta?

A
  1. RNAase L - degradation of viral/host mRNA2. Protein kinase - inhibition of viral/host protein synthesis These two steps essentially result in apoptosis, thereby interrupting viral amplification
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3
Q

Where do we find/see cell surface proteins?

A

All cells except mature RBCs have MHC1

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4
Q

What cell surface receptors are present on T cells?

A

TCR (bind antigen-MHC complex)CD3 (associated with TCR for signal transduction) CD28 (binds B7 and APC)

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5
Q

What cells surface receptors are present on Helper T Cells?

A

CD4, CD40l

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6
Q

What cell surface receptors are present on Cytotoxic T cells?

A

CD8

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7
Q

What cell surface receptors are present on B cells?

A

Ig (binds antigen)CD19, CD20, CD21 (receptor for EBV)CD40MHC2, B7

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8
Q

What cell surface receptors are present on Macrophages?

A

CD14, CD40MHC2, B7Fc and C3b receptors (enhance phagocytosis)

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9
Q

What cell surface receptors are present on NK cells

A

CD16 (binds Fc of IgG)CD56 (unique marker for NK)

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10
Q

Define Anergy

A

A state of immune unresponsiveness

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11
Q

What effects can bacterial toxins have?

A
  • Pathogens like S. progenies and S. aureus, cross-link the Beta region of the T-cell receptor to the MHC class 2 on APCs.
  • Can activate any T cell, leading to massive release of cytokines
  • Endotoxins/lipopolysaccharide (gram-negative bacteria) - directly stimulate macrophages by binding to endotoxin receptor CD14; Th cells are not involved
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12
Q

Define Antigenic Variation

A

Mechanism by which an infectious organism such as a protozoan, bacterium or virus alters its surface proteins in order to evade a host immune response

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13
Q

Provide an example of antigenic variation

A
  • DNA rearrangement

- RNA segment reassortment (eg. influenza major shift)

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14
Q

How do you acquire passive vs. active immunity

A 
passive = receiving preformed antibodies
active = exposure to foreign antigens
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15
Q

Describe the difference in the onset of passive vs. active immunity

A 
Passive = rapid
Active = slow
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16
Q

Compare duration of a passive vs. active immune response

A 
Passive = short lasting 
Active = long lasting
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17
Q

Name 4 pathogens, given as vaccines, that provide passive immunity via preformed antibodies

A

TO BE HEALED RAPIDLY - Tetanus, Botulinum toxin, HBV, Rabies vaccines

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18
Q

What other terms/words are used in the place of active immunity?

A

Active immunity = humoral immunity = cellular immunity

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19
Q

Describe Live Attenuated Vaccines

A

Microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host. Mainly induces a CELLULAR RESPONSE

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20
Q

Describe Inactive or Killed Vaccines

A

Pathogen is inactivated by heat or chemicals; maintains epitope structure on surface antigens is important for immune response. HUMORAL IMMUNITY induced.

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21
Q

List 1 pro and 1 con of live attenuated vaccines

A

PRO - induced strong, often lifelong, immunity

CON - may revert to virulent form, Often contraindicated in pregnancy and immune def.

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22
Q

List 1 pro and 1 con of inactived/killed vaccines

A

PRO - stable and safer than live vaccines

CON - weaker immune response; booster shots are usually required

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23
Q

List some live attenuated vaccines

A

MMRPV

  1. measles
  2. mumps
  3. rubella
  4. polio (Sabin)
  5. influenza
  6. varicella
  7. yellow fever
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24
Q

List some inactivated/killed vaccines

A
  1. cholera
  2. hep A
  3. Polio (Salk)
  4. Influenza (inj)
  5. rabies
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25
Q

What type of reaction is a type 1 hypersensitivity response?

A

Anaphylactic and atopic (First and Fast)

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26
Q

Which types of hypersensitivity reactions are antibody mediated?

A

Types 1,2 and 3

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27
Q

How do type 1 hypersensitivity reactions work?

A
  • free antigen cross-links IgE on a pre-sensitized mast cells and basophils.
  • This triggers immediate release of vasoactive amines that act as post capillary venues (i.e histamine).
  • This reactions develops quickly because of preformed antibodies
  • delayed response follows due to production of arachadonic acid metabolites (e.g leukotrienes)
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28
Q

What is responsible for the rapid response of type 1 hypersensitivity?

A

preformed antibodies (e.g. histamine)

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29
Q

What is responsible for the delayed response that follows the rapid response of the type 1 hypersensitivity?

A

arachadonic acid metabolites (e.g leukotrienes)

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30
Q

What types of reaction is a type 2 hypersensitivity?

A

Cytotoxic

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31
Q

How do type 1 hypersensitivity reactions work?

A

IgM, IgG bind to fixed antigen on “enemy” cells, leading to cellular destruction.
3 mechanisms
1. opsonization leading to phagoctosis or compliment activation
2. complement-mediated lysis
3. antibody- dependent cell-mediated cytotoxicity, usually due to NK cells or macrophages

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32
Q

How do type 3 hypersensitivity reactions work?

A

Imagine an immune complex with 3 things stuck together - antigen, antibody, complement.
This complex activates complement, which attracts neutrophils; neutrophils release lysosomal enzymes

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33
Q

What types of hypersensitivity reaction is responsible for serum sickness?

A

Type 3

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34
Q

How does serum sickness arise?

A

A type 3 hypersensitivity response by the immune system.
An immune complex forms in which antibodies to the foreign proteins are produced (takes 5 days). Immune complexes form and are deposited in membranes, where they fix complement (leads to tissue damage). More common than Arhus reaction.

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35
Q

What are the symptoms of serum sickness?

A

Fever, urticaria, arthralgias, proteinuria, lymphadenopathy, 5-10 days after antigen exposure

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36
Q

What is an arthrus reaction?

A

A local, subacute antibody mediated hypersensitivity (type 3) reactions.
Intradermal injection of an antigen induces antibodies, which form antigen 0 antibody complexes in the skin.

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37
Q

What are the symptoms of Arthrus Reactions?

A

Edema, necrosis, activation of complement

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38
Q

What causes Arthrus reactions?

A

Antigen-antibody complexes

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39
Q

What is another name for Type 4 hypersensitivity?

A

Delayed (T cell mediated) hypersensitivity

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40
Q

How does Type 4 hypersensitivity work?

A

Sensitized T lymphocytes encounter antigen and then release lymphokines (leads to macrophage activation; no antibody involved)

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41
Q

List the 4 types of hypersensitivity reaction with their number and name

A

Type 1, anaphylactic and atopic
Type 2, Cytotoxic
Type 3, Immune complex
Type 4, Delayed (T cell mediated) type

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42
Q

What types of hypersensitivity reaction causes anaphylaxis?

A

Type 1

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43
Q

What types of hypersensitivity reaction causes allergies atopically

A

type 1

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44
Q

What types of hypersensitivity reaction causes SLE

A

type 3

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45
Q

What types of hypersensitivity reaction causes Autoimmune hemolytic anemia?

A

type 2

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46
Q

What types of hypersensitivity reaction causes Pernicious anemia?

A

type 2

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47
Q

What types of hypersensitivity reaction causes MS?

A

Type 4

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48
Q

What types of hypersensitivity reaction causes Polyarteritis nodosa?

A

Type 3

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49
Q

What types of hypersensitivity reaction causes idiopatic throbocytopenia purpora

A

Type 2

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50
Q

What types of hypersensitivity reaction causes Erythroblastosis fettles?

A

Types 2

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51
Q

What types of hypersensitivity reaction causes Poststreptococcal glomerulonephritis?

A

Type 3

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52
Q

What types of hypersensitivity reaction causes Acute hemolytic transfusion reactions

A

Type 2

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53
Q

What types of hypersensitivity reaction causes Guillain-Barre Syndrome?

A

Type 4

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54
Q

What types of hypersensitivity reaction causes graft-vs-host disease?

A

Type 4

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55
Q

What types of hypersensitivity reaction causes Serum Sickness

A

Type 3

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56
Q

What types of hypersensitivity reaction causes PPD (test for M. tuberculosis)

A

Type 4

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57
Q

What types of hypersensitivity reaction causes contact dermatitis?

A

Type 4

58
Q

What types of hypersensitivity reaction causes Rheumatic fecer

A

Type 2

59
Q

What types of hypersensitivity reaction causes Goodpastures Syndrome?

A

Type 2

60
Q

What types of hypersensitivity reaction causes Bullous pemphigoid?

A

Type 2

61
Q

What types of hypersensitivity reaction causes Arthus reaction?

A

Type 3

62
Q

What types of hypersensitivity reaction causes contact dermatitis?

A

Type 4

63
Q

What types of hypersensitivity reaction causes pemphigus vulgarism?

A

Type 2

64
Q

Describe the pathogenesis of an allergic reaction to blood transfusion

A

Type 1 hypersensitivity
Reaction against plasma proteins in the transfused blood
Presentation: urticaria, pruiritus, wheezing, fever

65
Q

Describe the pathogenesis of an anaphylactic reaction to blood transfusion

A

Severe allergic reaction
IgA-def individuals must receive blood products that lack IgA
Presentation: dyspnea, bronchospasm, hypotension, respiratory arrest, shock

66
Q

Describe the pathogenesis of febrile nonhemolytic transfusion reactions

A

Type 2 hypersensitivity reaction
Host antibodies against donor HLA antigens and leukocytes
Presentation: Fever, HA, chills, flushing

67
Q

Describe the pathogenesis of an acute hemolytic transfusion reaction

A 
Type 2 hypersensitivity
Intravascular hemolysis (ABO bloog gourp incompatible) or extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs)
Presentation: fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinemia (intravascular), jaundice (extravascular hemolysis)
68
Q

What disorder is associated with Anti-ach receptor antibody?

A

Myasthenia gravis

69
Q

What disorder is associated with Anti-basement membrane antibody?

A

Goodpastures syndrome

70
Q

What disorder is associated with Anti-cardiolipin, lupus anticoagulant antibody?

A

SLE, antiphospholipid syndrome

71
Q

What disorder is associated with Anticentromere antibody?

A

Limited scleroderma (CREST syndrome)

72
Q

What disorder is associated with Anti-dsDNA, anti-Smith antibody?

A

SLE

73
Q

What disorder is associated with Anti-glutamate decarboxylase antibody?

A

Type 1 Diabetes Mellitus

74
Q

What disorder is associated with Anti-hemidesmosome antibody?

A

bollous pemphigoid

75
Q

What disorder is associated with antihistone antibody?

A

drug-induced lupus

76
Q

What disorder is associated with Anti-jo-1, anti-SRP, Anti-MI-2 antibody?

A

Polymyositis, dermatomyositis

77
Q

What disorder is associated with antimicrosomal, anti-thyroglobulin antibody

A

hashimoto thyroiditis

78
Q

What disorder is associated with animitochondrial antibody?

A

primary biliary cirrhosis

79
Q

What disorder is associated with antinuclear antibodies

A

SLE, nonspecific

80
Q

What disorder is associated with anti-Scl-70 (anti-DNA topoisomerase 1)

A

scleroderma (diffuse)

81
Q

What disorder is associated with anti-smooth muscle antibody?

A

autoimmune hepatitis

82
Q

What disorder is associated with anti-sea, anti-ssb (anti-Ro, anti-La) antibody?

A

Sjogren syndrome

83
Q

What disorder is associated with Anti-TSH receptor antibody?

A

graves disease

84
Q

What disorder is associated with Anti-U1 RNP (ribonucleoprotein) antibody?

A

mixed connective tissue disease

85
Q

What disorder is associated with c-ANCA (PR-3 ANCA) antibody?

A

Granulomatosis with polyangiitis (Wegener)

86
Q

What disorder is associated with IgA antiendomysia, Iga anti-tissue transglutaminase antibody?

A

celiac disease

87
Q

What disorder is associated with p - ANCA (MPO-ANCA) antibody?

A

Microscopic polyangiitis, Churg-Strauss syndrome

88
Q

What disorder is associated with rheumatoid factor (antibody most commonly IgM, specific to IgG Fc region), Anti-CCP antibody

A

Rheumatoid arthritis

89
Q

What bacterial infection will you likely get if you are missing T cells?

A

sepsis

90
Q

What bacterial infections are you likely to contract if you are missing B cells? (There are 7)

A 
SHiNE SKiS
Strep pneumonia
H. influenza type B
N. meningitidis
E. coli
Salmonella
Klebsiella pneumonia 
group B Strep
91
Q

What bacterial infections are you likely to get if you have NO granulocytes?

A

Staphylococcus: Burkholderia cepacia, Serratia, Nocardia

92
Q

What bacterial infections are you likely to get if you are lacking compliment (immune deficiency)?

A

Neisseria (no membrane attack complex aka MAC)

93
Q

What viral infection are you likely to get if you are missing T cells (immunodeficiency)?

A

CMV, EBV, VZV, chronic infection with reps/GI viruses

94
Q

What viral infections are you likely to get if you are missing B cells (immunodeficiency)?

A 
Enteroviral encephalitis
Polio virus (live vaccine contraindicated)
95
Q

What fungal infections are you likely to get if you are deficient in T cells?

A

Candida

PCP

96
Q

What fungal/paracidic infections are you likely to get if you are deficient in B cells?

A

GI giardiasis (no IgA)

97
Q

What fungal/parasite infections are you likely to get if you are deficient in granulocytes?

A

Candida

Aspergillus

98
Q

B-cell deficiencies tend to produce recurrent ________ infections.
Whereas, T- cell deficiencies produce more _________ and ________ infections

A

B-cell deficiencies tend to produce recurrent BACTERIAL infections
Whereas, T- cell deficiencies produce more FUNGAL and VIRAL infections

99
Q

List 3 immune deficiencies that are B-cell linked

A
  1. X-linked (Bruton) agammaglobulinemia
  2. Selective IgA deficiency
  3. Common variable immunodeficiency
100
Q

List 4 immune deficiencies that are T-cell linked

A
  1. Thymic aplasia (DiGeorge’s syndrome)
  2. IL-12 receptor deficiency
  3. Autosoma dominant hyper-IgE syndrome (Job syndrome)
  4. Chronic mucocutaneous candidasis
101
Q

What is the most common primary immunodeficiency?

A

Selective IgA def

102
Q

Describe the defect associated with X-linked (Bruton) agammaglobulinemia (immunodeficiency)

A

Defect in BTK, a tyrosine kinase gene - no B cell matuartion. X-linked recessive (increased in boys)

103
Q

Describe the presentation of X-linked (Bruton) agammaglobulinemia (immunodeficiency)

A

Recurrent bacterial and enteroviral infections after 6 months (decreased material IgG).

104
Q

Describe the presentation of Selective IgA deficiency (immunodeficiency)

A

Majority asymptomatic. Can see airway and GI infections, Autoimmune disease, Atropy, Anaphylaxis to IgA containing products

105
Q

Describe the defect seen in Common Variable Immunodeficiency (immunodeficiency)

A

Defect in B-cell differentiation. Many causes

106
Q

Describe the presentation of Common Variable Immunodeficiency (immunodeficiency)

A

Can be acquired in 20s-30s; increased risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmonary infections

107
Q

Describe the defect associated with Thymic aplasia (DiGeorge’s syndrome) (immunodeficiency)

A

22q11 deletion; failure to develop 3rd and 4th pharyngeal pouches –> absent thymus and parathyroids

108
Q

Describe the clinical presentation of Thymic aplasia (DeGeorge Syndrome) (immunodeficiency)

A 
Tetany (hypocalcemia)
Recurrent viral/fungal infections (T-Cell deficiency)
Conotruncal abnormalities (e.g. tetralogy of Fallot, truncus  arteriosus)
109
Q

Describe the defect associated with IL-12 receptor deficiency (immunodeficiency)

A

Decreased Th1 response.

Autosomal recessive

110
Q

Describe the clinical presentation of IL-12 receptor deficiency (immunodeficiency)

A

Disseminated mycobacterial and final infections;

may present after administration of BCG vaccine

111
Q

Describe the defect associated with Autosomal dominant hyper-IgE syndrome (Job Syndrome) (immunodeficiency)

A

Deficiency of Th17 cells due to STAT3 mutation –> impaired rectruitement of neutrophils to sites of infection

112
Q

Describe the clinical presentation of Autosomal dominant hyper IgE syndrome (Job Syndrome) (immunodeficiency)

A

FATED: Coarse Facies, Cold (non inflammed) stphylococcal, Abscesses, retained primary Teeth, increase IgE, Dermatologic problems (eczema).

113
Q

Describe the defect associated with Chronic mucocuteneous candidiasis (immunodeficiency)

A

T cell dysfunction. Many causes

114
Q

Descirbe the clinical presentation of Chronic mucocutaneous candidiasis (immunodeficiency)

A

Non-invassive Candida albicans infections of the skin and mucous membranes

115
Q

List 4 immunodeficiencies that result from EITHER B and/or T cells disorders

A
  1. Severe combined imminodeficiency (SCID)
  2. Ataxia-telangiectasia
  3. Hyper-IgM syndrome
  4. Wiskott-Aldrich syndrome
116
Q

Describe the defect associate with SCID (sever combines immunodef)

A

Several types including defective IL-2R gamma chain (most common, X-linked), adenosine deaminase deficiency (autosomal recessive)

117
Q

Describe the clinical presentation of SCID (immunodeficiency)

A

Failure to thrive, chronic diarrhea, thrush. Recurrent viral, bacterial, fungal, and protozoal infections.

118
Q

What is the treatment for SCID? (immunodeficiency)

A

Bone marrow transplant (no concern for rejection)

119
Q

Describe the defect associated with Ataxia-telangiectasia (immunodeficiency)

A

Defects in ATM gene –> DNA double strand breaks –> cell cycle arrest

120
Q

Describe the clinical presentation of Ataxia-telangiectasia (immunodeficiency)

A

Triad: cerebellar defects (ataxia), spider antgiomas (telangiectasis), IgA deficiency

121
Q

Describe the defect associated with Hyper-IgM syndrome (immunodeficiency)

A

Most commonly due to defective CD40L on Th cells = class switching defect; X-linked recessive

122
Q

Describe the clinical presentation of Hyper IgM syndrome (immunodeficiency)

A

Severe pyogenis infections early in life; opportunistic infection with Pneumocystitis, Cryptosporidium, CMV

123
Q

Describe the defects associate withe Wiskott-Aldrich syndrome (immunodeficiency)

A

Mutations in WAS gene (X-linked recessive); T cells unable to reorganize actin cytoskeleton

124
Q

Describe the clinical presentation associated with Wiskott-Aldrich syndrome

A

WATER: Wiscott-Aldrich; Thrombocytopenic purpura, Eczema, Reccurent infections. Increased risk of autoimmune disease and malignancy

125
Q

List 3 immunodeficiencies that are linked to phagocyte dysfunction

A
  1. Leukocyte adhesion def (type 1)
  2. Chediak-Higashi syndrome
  3. Chronic granulomatous disease
126
Q

Describe the defect associated with Leukoadhesion deficiency (type 1) (immunodeficiency)

A

Defect in LFA-1 integrin (CD18) protein on phagocyte; impaired migration and chemotaxis; autosomal recessive

127
Q

Describe the clinical presentation of Leukoadhesion deficiency (type 1) (immunodeficiency)

A

Recurrent bacterial skin and mucosal infections, absent pus formation, impaired wound healing, delayed separation of umbilical cord (>30 days).

128
Q

Describe the defects associated with Chediak-Higashi syndrome (immunodeficiency)

A

Defect in lysosomal traffecking regulator gene (LYST). Microtubule dysfunction in phagosome-lysosome fusion; autosomal recessive.

129
Q

Describe the clinical presentation of Chediak-Higashi syndrome (immunodeficiency)

A

Recurrent pyogenic infection by staphylococci and streptococci, partial albinism, peripheral neuropathy, progressive neuro-degeneration, infiltrative lymphohistocytosis

130
Q

Describe the defects associated with Chronic granulomatous disease

A

Defect of NADPA oxidase –> decrease reactive oxygen species (e.g., superoxide) and absent respiratory burst in neutrophils; X-linked recessive

131
Q

Describe the clinical presentation of Chronic granulomatous disease

A

increased susceptibility to catalase positive organisms ( acronym = PLACESS)
Pseudomonas, Listeria, Asperillus, Candida, E. Coli, S. aureus, Serratia

132
Q

Where do we attain AUTOGRAPHS?

A

from self

133
Q

Where do we attain SYNERGEIC GRAFTS?

A

from identical twin or clone

134
Q

Where do we attain ALLORAPHS?

A

from non-indentical individual of same species

135
Q

Where do we attain XENOGRAPHS?

A

from different species

136
Q

List the 4 types of transplant rejections and their related speed.

A
  1. Hyper-actute - within minutes
  2. Acute - weeks to months
  3. Chronic - months to years
  4. Graft-versus-host-disease - varies
137
Q

Describe the pathogenesis of hyper acute transplant rejection.

A

Pre-existing recipient antibodies react to donor antigen (type 2 reaction), activate complement.

138
Q

Describe the pathogenesis of acute transplant rejection

A

Cellular: CTLs actuated against donor MHCs
Humoral: similar to hyper acute, except antibodies develop after transplant

139
Q

Describe the pathogenesis of chronic transplant rejection

A

Recipient T cells perceive donor T MHC as recipient MHC and react against donor antigens presented.
Both cellular and hum oral components

140
Q

Describe the pathogenesis of graft-vs-host disease

A

Grafted immuno-compentent T cells proliferate in the immunocompromised host and reject host cells with “foreign” proteins –> severe organ dysfunction

NPLEX 1 (10 decks)

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