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D2 Fall - Pathology Exam 1 > 9/10: Immunity II > Flashcards

9/10: Immunity II Flashcards

1
Q
  1. What are 3 examples of immune system dysfunction?
A

a. Hypersensitivity
b. Autoimmune disease
c. Immune deficiency disease

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2
Q
  1. This describes the ability to discriminate between self and nonself antigens (big thing, not MHC)
A

a. Immunologic tolerance

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3
Q
  1. If mechanisms to immunologic tolerance fail, what happens?
A

a. Autoimmune disease

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4
Q
  1. The tolerance is when developing lymphocytes encounter self antigens in central lymphoid organs
A

a. Central tolerance

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5
Q
  1. This tolerance is when mature lymphocytes encounter self antigens in peripheral tissues
A

a. Peripheral tolerance

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6
Q
  1. Developing T cells =
A

a. Central tolerance

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7
Q
  1. Mature T cells =
A

a. Peripheral tolerance

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8
Q
  1. Central T cell tolerance will have what cells? (other word for developing)
A

a. Self reactive T cells

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9
Q
  1. How does Central T cell tolerance work?
A

a. Self-reactive T cells - Negative selection or deletion
b. Self reactive T cells - Development of regulatory T cells

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10
Q
  1. In peripheral T cell tolerance, what do the regulatory T cells do?
A

a. Block activation of self-reactive lymphocytes

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11
Q
  1. In peripheral T cell tolerance, what does Anergy do?
A

a. Functional inactivation of T cells

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12
Q
  1. In peripheral T cell tolerance, what does Deletion do?
A

a. Apoptosis of self-reactive lymphocytes

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13
Q
  1. How does Peripheral T cell tolerance work?
A

a. Regulatory T cells
b. Anergy
c. deletion

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14
Q
  1. What induces tolerance in B cells?
A

a. Self polysaccharides
b. Lipids
c. Nucleic acids

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15
Q
  1. What occurs in Central B cell tolerance?
A

a. Receptor editing
b. Negative selection (apoptosis)

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16
Q
  1. What occurs in Peripheral B cell tolerance?
A

a. Anergy
b. Excluded from lymphoid follicles

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17
Q
  1. Most autoimmune disease are _____
A

a. Polygenic

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18
Q
  1. Having an autoimmune disease will cause what to happen?
A

a. Defective T cell negative selection or deletion

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19
Q
  1. How can infections activate self-reactive lymphocytes?
A

a. Increased proliferation of costimulatory molecules on APCs
b. Molecular mimicry

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20
Q
  1. These are injurious or pathologic immune reactions
A

a. Hypersensitivity

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21
Q
  1. What are the 3 hypersensitivity causes?
A

a. Autoimmunity
b. Reaction against microbes
c. Reactions against environmental antigens

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22
Q
  1. Type 1 hypersensitivity includes which antibody?
A

a. IgE

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23
Q
  1. What does Type 1 hypersensitivity cause?
A

a. Anaphylaxis (can be from allergies)

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24
Q
  1. What is involved with Type 1 hypersensitivity?
A

a. Vasoactive amines
b. Lipid mediators
c. Cytokines

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25
Q
  1. What is an example of a vasoactive amine?
A

a. Histamine

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26
Q
  1. What does histamine cause?
A

a. Vasodilation, smooth muscle contraction, secretion of mucus

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27
Q
  1. What are examples of lipid mediators?
A

a. Prostaglandins + leukotrienes

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28
Q
  1. What does prostaglandin and leukotrienes do?
A

a. Smooth muscle contraction, vascular permeability

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29
Q
  1. What are the cytokines used in Type 1?
A

a. TNF
b. Chemokines
c. IL-4, IL-5

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30
Q
  1. Atopic individuals with allergies have what?
A

a. Higher TH2 cells
b. Higher serum IgE

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31
Q
  1. Can the development of allergies be from environmental factors?
A

a. Yes

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32
Q
  1. What is the hygiene hypothesis?
A

a. Too much hygiene may increase allergies

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33
Q
  1. Does early childhood exposure to microbial antigens increase or decrease incidence of allergies?
A

a. Decrease

34
Q
  1. What is an example of a Type 1 disease?
A

a. Anaphylaxis
b. asthma

35
Q
  1. Type II hypersensitivity is
A

a. Antibody mediated disease

36
Q
  1. Describe how type II works
A

a. Opsonization by autoantibodies → activates complement system → cellular dysfunction

37
Q
  1. What are a few examples of type II?
A

a. Autoimmune hemolytic anemia
b. Goodpasture syndrome
c. Myasthenia gravis

38
Q
  1. Type III hypersensitivity is
A

a. Immune complex mediated disease

39
Q
  1. Describe how Type III works
A

Circulating immune complexes are deposited in blood vessels and activate the complement system

40
Q
  1. How do you form immune complexes in Type III?
A

a. Antibodies secreted in blood → react with antigen → form antigen-antibody complexes

41
Q
  1. What is an example of Type III hypersensitivity?
A

a. Systemic lupus erythematosus

42
Q
  1. Type IV hypersensitivity is
A

a. Cell-mediated disease

43
Q
  1. What does CD4 cause in type IV?
A

a. Cytokine mediated inflammation

44
Q
  1. What does CD8 cause in type IV?
A

a. Direct cell cytotoxicity

45
Q
  1. Many chronic inflammatory disease are ________ mediated
A

a. T-cell mediated

46
Q
  1. Describe Type IV CD4 mediated
A

a. Cytokines produce inflammation → tissue destruction
b. Delayed hypersensitivity reaction (48-72) hours

47
Q
  1. Most type IV CD4 are mediated how?
A

a. TH1 and TH17

48
Q
  1. Describe type IV CD4 mediated
A

a. CD8 cells kill antigen-expressing target cells

49
Q
  1. What are examples of type IV hypersensitivity?
A

a. Type 1 diabetes mellitus

50
Q
  1. What are the 2 kinds of immunodeficiency syndromes?
A

a. Primary
b. Secondary

51
Q
  1. How is primary immunodeficiency syndrome acquired?
A

a. Congenitally

52
Q
  1. How is secondary immunodeficiency syndrome acquired?
A

a. After a challenge to the immune system such as cancer

53
Q
  1. Can you clinically manifest immunodeficiency syndromes? And how?
A

a. Yes, by increased infections

54
Q
  1. Do the primary immunodeficiencies affect innate or adaptive immunity?
A

a. Both

55
Q
  1. When do you detect primary immunodeficiencies?
A

a. 6 months - 2 years

56
Q
  1. Is primary or secondary immunodeficiencies more common?
A

a. secondary

57
Q
  1. Most primary immunodeficiencies involve disorders of
A

a. B and T cells

58
Q
  1. What is severe combined immunodeficiency (SCID)?
A

a. Multiple genetic defects causing defects in humoral and cell-mediated immunity

59
Q
  1. In you have SCID, you are dead within the 1st year without
A

a. Stem cell transplantation

60
Q
  1. This is deletion of chromosome 22
A

a. Digeorge syndrome

61
Q
  1. Digeorge syndrome is caused by what? (not 22 here)
A

a. Congenital defect in thymic development → deficient T cell maturation

62
Q
  1. What is the acronym to remember Digeorge?
A

a. CATCH 22
i. Cardiac abnormalities
ii. Abnormal facies
iii. Thymic aplasia
iv. Cleft palate
v. hypocalcemia/hypoparathyroidism

63
Q
  1. What is hyper-igm syndrome?
A

a. Inability of T cells to activate B cells

64
Q
  1. Describe Hyper-igm syndrome
A

a. Cant activate B cells
b. Normal or high IgM
c. Low levels of G,A,E

65
Q
  1. Hyper-IgM syndrome can have what infections and is susceptible to what?
A

a. Recurrent pyogenic infectious, susceptible to pneumonia

66
Q
  1. Defects in the innate immunity may affect leukocyte function and cause what 2 diseases?
A

a. Leukocyte adhesion deficiency (LAD)
b. Chediak-Higashi

67
Q
  1. This is a defect in adhesion molecules, repair leukocytes recruitment to the site of infection → increased bacterial infections
A

a. LAD

68
Q
  1. This is defective phagocyte function due to impaired lysosomal trafficking
A

a. Chediak-higashi

69
Q
  1. What deficiency in complement function is the most common
A

a. C2

70
Q
  1. Deficiency in C2 in the complement function increases what?
A

a. Bacterial and viral infections

71
Q
  1. Are primary or secondary immunodeficiencies more common?
A

a. Secondary

72
Q
  1. SSRNA is associated with what?
A

a. AIDs

73
Q
  1. How many people with AIDs are affected and dead?
A

a. 80M affected, 35M dead

74
Q
  1. When was the 1st published report of AIDs?
A

a. 1981

75
Q
  1. How is AIDs transmitted?
A

a. Blood or bodily fluids

76
Q
  1. AIDs/HIV targets what cells?
A

a. CD4 T cells

77
Q
  1. What kind of genome do you have in AIDs?
A

a. Viral RNA genome

78
Q
  1. What is the life cycle of AIDs?
A

a. Binding
b. Fusion
c. Reverse transcriptase
d. Integration
e. Replication
f. Assembly
g. Budding

79
Q
  1. Describe the progression of AIDs
A

a. Asymptomatic
b. Acute retroviral symptoms: 1-6 weeks after exposure
c. Latency period: several months to 15 years

80
Q
  1. What is HIV treatment?
A
  1. What is HIV treatment?

D2 Fall - Pathology Exam 1 (8 decks)

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