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PATHOLOGY EXAM 1 > immunity part 2 > Flashcards

immunity part 2 Flashcards

1
Q

immune system dysfunctions:
1
2
3

A

hypersensitivity
autoimmune diseases
immune deficiency diseases

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2
Q

lack of response to antigens that is induced by exposure of lymphocytes to these antigens

A

immunologic tolerance

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3
Q

ability to discriminate between self and nonself antigens

A

immunologic tolerance

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4
Q

if immunologic tolerance fails->

A

autoimmunity

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5
Q

with immunologic tolerance:
normally, microbes are immunogenic[cause immune response], and self-antigens are

A

tolerogenic[do not cause immune response]

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6
Q

developing lymphocytes encounter self antigens in central lymphoid organs(bone marrow)

A

central tolerance

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7
Q

mature lymphocytes encounter self antigens in peripheral tissues (secondary lymphoid organs)

A

peripheral tolerance

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8
Q

central t cell tolerance normally deals with

A

cd4 t cells

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9
Q

central t cell tolerance->
self reactive tcells:

A
  1. negative selection or deletion
  2. development of regulatory t cells
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10
Q

peripheral t cell tolerance 3 ways

A
  1. regulatory t cells
  2. anergy
  3. deletion
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11
Q

blocks the activation of self-reactive lymphocytes

A

regulatory t cells

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12
Q

functional inactivation of t cells (lack of costimulation)

A

anergy

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13
Q

apoptosis of self-reactive lymphocytes

A

deletion

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14
Q

self polysaccharides, lipids, and nucleic acids: induce tolerance in

A

b cells

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15
Q

two types of cell tolerance in b cells

A
  1. central b cell tolerance
  2. peripheral b cell tolerance
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16
Q

-receptor editing
-negative selection (apoptosis)

what type of b cell tolerance is this

A

central b cell tolerance

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17
Q

-anergy
-excluded from lymphoid follicles

what type of b cell tolerance is this

A

peripheral b cell tolerance

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18
Q

immune response against self antigens

A

autoimmunity

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19
Q

the development of autoimmunity may be related to

A
  1. inheritance of susceptibility genes
  2. environmental triggers
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20
Q

must autoimmune diseases are

A

polygenic

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21
Q

autoimmune diseases often associate with particular HLA(MHC) genes that are inefficient at displaying self antigens:

A
  1. defective t cell negative selection
  2. may fail to stimulate regulatory t cells
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22
Q

infections may activate self-reactive lymphocytes in autoimmunity by:

A
  1. increased production of costimulatory molecules on APCs
  2. molecular mimicry
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23
Q

injurious or pathologic immune reactions
-immune response may be inadequately controlled
-directed against normal harmless antigens

A

hypersensitivity

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24
Q

what 3 things causes hypersensitivity

A
  1. autoimmunity :reactions against self antigens (failure of self-tolerance)
  2. reactions against microbes: excessive reactions or unusually persistent microbes
  3. reactions against environment: common allergens (pollen)
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25
Q

types of hypersensitivity

A

type I: immediate
type II: antibody-mediated
type III: immune complex-mediated
type IV: cell mediated (with t cells)

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26
Q

which types of hypersensitivity
-tissue reaction that occurs rapidly after interaction of antigen with IgE antibody bound to mast cell
-often developed in atopic individuals- sensitized to allergens
-environmental and food allergens

mild to severe reaction (asthma example)

A

type I

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27
Q

mediators that are released by mast cells after activation for type 1 immediate hypersensitivity:
1
2
3

A
  1. vasoactive amines
  2. lipid mediators
  3. cyotkines
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28
Q

causes vasodilation, increased vascular permeability, smooth muscle contraction, and increased secretion of mucus

A

histamine-> vasoactive amines
[mediator for type I]

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29
Q

smooth muscle contraction, vascular permeability

A

prostaglandins + leukotrienes-> lipid mediators for type I

30
Q

TNF, chemokines, IL-4, IL-5

A

cytokine mediator for type I

31
Q

anaphlyaxis, bronchial asthma, allergic, rhinitis, sinusitis(hay fever), food allergies

A

type I

32
Q

development of allergies?

A
  1. susceptibility is genetically determined
  2. atopic individuals: 50% have family history of allergy, more TH2 cells, higher serum IgE
  3. environmental factors: pollution, infections
33
Q
  1. caused by antibodies directed against target antigens on cell surfaces
    -target cells for phagocytosis
    -activate complement system
    -interfere with normal cellular functions

which type of hypersens.

A

type II: antibody-mediated diseases

34
Q
  1. in type II hypersens, cells may be opsonized(coated) by autoantibodies which targets these cells for
A

phagocytosis
-induces phagocytosis by neutrophils, macrophages

35
Q
  1. in type II hypersens, antibodies activate the complement system which _____________=triggers inflammation
A

recruits neutrophils, macrophages

which then triggers inflammation

36
Q
  1. in type II hypersens, antibody-mediated cellular dysfunction ->
A

impair or dysregulates important functions

37
Q
  1. autoimmune hemolytic anemia
  2. autoimmune thrombocytopenic purpura
  3. pephigus vulgaris
  4. vasculitis caused by ANCA
  5. goodpasture syndrome
  6. acute rheumatic fever
  7. myasthenia gravis
  8. graves disease
  9. pernicious anemia
A

types of type II hypersens

38
Q

-antigen-antibody complex formed (immune complexes)
-deposit in blood vessels-> complement activation and acute inflammation
-antigen may be foreign protein or endogenous (autoimmunity)
-soluble antigens!!!!!!!!!

A

type III hypersens: immune complex mediated diseases

39
Q

type III immune complex mediated diseases mechanism:

A
  1. formation of immune complexes
  2. deposition of immune complexes
  3. inflammation and tissue injury
40
Q

antibodies secreted in blood- react with antigen- form antigen-antibody complexes

A

formation of immune complexes in type III

41
Q

circulating antigen-antibody complexes deposited in tissues

A

deposition of immune complexes in type III hypersens

42
Q

once deposited, immune complexes initiate inflammation via complement or engagement of leukocytes

A

inflammation and tissue injury in type III hypersens

43
Q
  1. systemic lupus erythematosus
  2. poststreptococcal glomerulonephritis
  3. polyarteritis nodosa
  4. reactive arthritis
  5. serum sickness
  6. arthus reaction!!!!!!!!
A

type III hypersens

44
Q

-cd4 t cells: cytokine mediated inflammation
-cd8 t cells: direct cell cytotoxicity
-many chronic inflammatory diseases are t cell mediated

A

type IV: cell mediated disease

45
Q
  1. cytokines produced induce inflammation-> tissue destruction
  2. delayed-type hypersens: occurs 48-72 hours after subsequent antigen
  3. most reactions are TH1 mediated, some Th17
A

type IV: CD4 t cell mediated

46
Q

CD8 t cells kill antigen-expressing target cells
-effective in virus-infected cells

A

type IV CD8 t cell

47
Q

poison ivy= lesion

A

type IV examples

48
Q
  1. rheumatoid arthritis
  2. multiple sclerosis
  3. type I diabetes!!!!
  4. inflammatory bowel disease
  5. psoriasis
  6. contact sens. (like poison ivy)
A

type IV

49
Q

immunodeficiency syndromes can either be primary(congenital) or secondary (acquired):

A

primary: inherited genetic disorders
secondary: acquired after challenge to immune system such as cancer or environmental factors

50
Q

clinically manifested by increased infections

A

immunodeficiency syndromes

51
Q

-may affect innate or adaptive immunity
-usually detected in infancy
-most involved disorders of B and T lymphocytes

A

primary immunodeficiencies

52
Q

encompasses many genetically distinct syndromes with defects in both cell-mediated immunity and humoral immunity
-children are susceptible to severe recurrent infections
-death within first year without stem cell transplantation

A

severe combined immunodeficiency (SCID)

53
Q

-deletion on chromosome 22
-caused by congenital defect in thymic development-> deficient t cell maturation
-infants are especially vulnerable to viral, fungal, protozoal infections
-also may include development malformation with parathyroid gland, heart defects, cleft palate, behavioral problems

A

digeorge syndrome

54
Q

CATCH 22

A

Cardiac abnormality
Abnormal facies
Thymic aplasia
Cleft palate
Hypocalcemia/Hypoparathyroidism

for digeorge syndrome

55
Q

-inability of t cells to activate b cells
-production of normal to high levels of IgM antibody!!
-decreased levels: IgG, IgA, IgE!!
-recurrent pyogenic infections, susceptibility to pneumonia

A

hyper-IgM syndrome

56
Q

two examples of defects in innate immunity that may affect leukocyte function:

A
  1. leukocyte adhesion deficiencies (LADs)
  2. Chediak-Higashi syndrome
57
Q

defects in adhesion molecules, impair leukocyte recruitment to site of infection -> increased bacterial infections

A

leukocyte adhesion deficiencies LADs
(defect in innate immunity)

58
Q

defective phagocyte function due to impaired lysosomal trafficking-> recurrent infections

A

Chediak-Higashi syndrome
(defect in innate immunity)

59
Q

dchediak-higashi syndrome causes:

A
  1. defective platelets- easy bruising
  2. melanocyte abnormalities- albinisim
  3. nervous system abnormalities- peripheral neuropathy
60
Q

defects in innate immunity also affect the complement system:

A

C2 deficiency is the most common- increased bacterial and viral infections

61
Q

may be encountered in individuals with cancer, diabetes, malnutrition, chronic infection, patients receiving chemo/radiation therapy, immunosuppressive medications
-more common than primary immunodeficiencies

A

secondary immunodeficiencies

62
Q

caused by human immunodeficiency virus (HIV)- SSRNA
transmission by blood or body fluids by sexual contact, parental, perinatal

A

AIDS
acquired immunodeficiency syndrome

63
Q

what is the primary target for HIV

A

CD4 helper t cells

64
Q

has a viral RNA genome
-reverse transcribed into complementary DNA
-integrates into host cell DNA

A

HIV/AIDS

65
Q

are there antibodies against HIV?

A

yes developed but not protective

66
Q

AIDS/HIV life cycle steps:

A
  1. binding
  2. fusion (to cd4 cell)
  3. reverse transcription
  4. integration
  5. replication
  6. assembly
  7. budding
67
Q

AIDS/HIV clinical features

A
  1. asymptomatic
  2. acute retroviral syndrome: 50-70%
    -1-6 weeks after exposure
    -sore throat, fever, rash, headache, diarrhea
    -oral changes like erythema and ulcerations(candidiasis)
    -viremia
  3. latency period
    -several months to 15 years
    -progression affected by patient age, host immune response, treatment
68
Q

AIDS diagnosis

A
  1. CD4 t cell count declines to 200 cells/nm
  2. CD4 t cell count <14% total lymphocyte
69
Q

HIV treatment

A
  1. anti-retroviral therapy (ART): administered in combination to reduce viral resistance
    -viremia declines: reduction in risk for transition to AIDS, death, transmission
70
Q
A

PATHOLOGY EXAM 1 (12 decks)

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