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23 General Pathology > 6/28 - Diseases of Immune System > Flashcards

6/28 - Diseases of Immune System Flashcards

1
Q

immune reactant for Type II HS

A

IgG and some cases IgM

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2
Q

antigen for Type II HS

A

cellular or extracellular matrix antigens

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3
Q

what causes type II HS? what does it result in?

A

cause: destruction of cells
result: inflammation or interference w/ normal cell function (dysfunction)

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4
Q

mechanisms of type II HS

A
  1. opsonization and phagocytosis (destruction)
  2. inflammation (destruction)
  3. cellular dysfunction
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5
Q

describe opsonization and phagocytosis in type II HS

A

antibody coats cell and and is marked for phagocytosis

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6
Q

what causes tissue damage in type II HS

A

cellular lysis induced by direct binding of antibody to cell surface antigens

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7
Q

what do antibodies attack in inflammation of type II HS

A

attack leukocytes or RBCs (mobile cells) or bind to fixed cells (part of solid tissues)

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8
Q

what do antibodies involved in inflammation activate? what does this result in

A

activate complement generating by-products , including chemotactic agents (mainly C5a)

this directs migration of neutrophils and monocytes and anaphylaxtonins

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9
Q

what are the anaphylatoxins? what does it do?

A

C3a, C4a, and C5a
increase vascular permeability

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10
Q

pathway for type II HS inflammation and tissue injury

A
  1. antigen + target cell + antibody
    • complement protein (C3a and mainly C5a)
      3a. complement 5b-9MAC
      3b. + membrane attack complex (MAC) insert into cell
      4b. results in osmotic lysis or drill holes in cell membrane
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11
Q

2 main examples of antibody-mediated cellular destruction. what type of HS?

A
  1. autoimmune hemolytic anemia
  2. erythroblastosis fetalis (hemolytic disease of newborn)

both type II

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12
Q

what is the disease where individuals produce antibodies to their own blood? HS type?

A

autoimmune hemolytic anemia - type II

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13
Q

what is the disease where there is an antigenic difference between mother and fetus and IgG antierythrocyte antibodies from the mother cross the placenta and destroy the fetal red cells? HS type?

A

erythroblastosis fetalis - type II

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14
Q

what are the two main examples of cellular dysfunction for type II HS

A
  1. myasthenia gravis (interferes w/ cellular function)
  2. grave’s disease (cellular hyperfunction)
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15
Q

what disease:

antibodies reactive with Ach receptors in motor end plates of skeletal muscles block neuromuscular transmission and cause muscle weakness? what type of HS

A

myasthenia gravis - type II HS

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16
Q

what disease:

antibody-mediated stimulation of cell function is the basis; antibodies against the TSH receptors on thyroid epithelial ells stimulate the cells, resulting in hyperthyroidism

what type of HS

A

Grave’s disease = type II HS

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17
Q

autoimmune hemolytic anemia

target antigen, mechanism of disease, clinical manifestation, HS type

A

TA: red cell membrane protein
MoD: opsonization and phagocytosis of RBCs
CM: hemolysis anemia
HS: type II

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18
Q

autoimmune thrombolytic purpura

target antigen, mechanism of disease, clinical manifestation, HS type

A

TA: platelet membrane protein
MoD: opsonization and phagocytosis of platelets
CM: bleeding
HS: type II

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19
Q

B)

pemphigus vulgaris

target antigen, mechanism of disease, clinical manifestation, HS type

A

TA: protein in intercellular junctions
MoD: antibody-mediated activation of proteases disruption of intercellular adhesion
CM: skin vesicles
HS: type II

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20
Q

vasculitis caused by antineutrophil cytoplasmic AB

target antigen, mechanism of disease, clinical manifestation

A

TA: neutrophil granule proteins released from activated neutrophils
MoD: neutrophil degranulation and inflammation
CM: vasculitis
HS: type II

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21
Q

good pasture syndrome

target antigen, mechanism of disease, clinical manifestation, HS type

A

TA: non collagenous protein in BM of kidneys
MoD: complement and Fc receptor mediated inflammation
CM: nephritis, lung hemorrhage
HS: type II

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22
Q

acute rheumatic fever

target antigen, mechanism of disease, clinical manifestation, HS

A

TA: streptococcal cell wall antigen, antibody-cross react w/ myocardial antigens
MoD: inflammation, macrophage activation
CM: myocarditis, arthritis
HS: type II

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23
Q

myasthenia gravis

target antigen, mechanism of disease, clinical manifestation, HS type

A

TA: Ach receptors
MoD: antibody inhibits acetylcholine binding, down modulates receptors
CM: muscle weakness, paralysis
HS: type II

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24
Q

insulin-resistant diabetes

target antigen, mechanism of disease, clinical manifestation, HS type

A

TA: insulin receptor
MoD: antibody inhibits binding to insulin
CM: hyperglycemia, ketoacidosis
HS: type II

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25
Q

graves disease

target antigen, mechanism of disease, clinical manifestation, HS type

A

TA: TSH receptors
MoD: antibody mediated stimulation of TSH receptors
CM: hyperthyroidism
HS: type II

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26
Q

pernicious anemia

target antigen, mechanism of disease, clinical manifestation, HS type

A

TA: intrinsic factor of gastric parietal cells
MoD: neutralizatin of intrinsic factor, decreased absorption of Vit B
CM: abnormal erythropoiesis anemia
HS: type II

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27
Q

immune reactant for type III HS

A

IgG or IgM

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28
Q

antigen for type III HS

A

solubule antigen

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29
Q

type III HS rxn is mediated by formation of what

A

antigen-antibody aggregates called immune complexes

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30
Q

how are type III HS rxns frequently initiated

A

when antigens combine with antibodies in circulation (creating immune complexes)

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31
Q

how are type III HS rxns less frequently initiated

A

when immune complexes are formed at sites where antigen has been “planted” previously

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32
Q

type III HS immune complexes can precipitate in various tissues (such as skin, joints, vessels, or glomeruli) resulting in what?

A

tissue damage and inflammation at the site of deposition thru triggering of classical complement pathway

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33
Q

in type III HS rxn, antigens may form immune complexes that are [exogenous OR endogenous]

A

BOTH! exogenous AND endogenous

34
Q

what is a foreign protein that is injected or produced by an infectious microbe

A

exogenous rxns

35
Q

what are self antigens/autoimmuniy?

A

endogenous rxns

36
Q

what is an acute, localized inflammatory response that typically occurs after vaccination? type of HS

A

acute Arthus rxns - type III

37
Q

what mediates acute Arthus rxns?

A

antigen is injected or enters intradermally or subcutaneously, they bind w/ antibody to form localized immune complexes

38
Q

when do acute arthus rxn form

A

within 4-8 hours

39
Q

as acute arthus rxn develops, localized tissue damage and vascular damage results in what?

A

accumulation of fluids (edema) and RBCs (erythema) at site of antigen entry

40
Q

what disease: large amounts of antigen enter blood stream (vaccinations of multiple insect bites) and bind to antibody, circulating immune complex forms? type of HS

A

serum sickness - type III

41
Q

what disease involve immune complexes that are smaller and soluble and not phagocytosed by phagocytic cells leading to abnormal immune rxn? type of HS

A

serum sickness - type III

42
Q

manifestation of serum sickness depends on what

A
  1. quantity of immune complex
  2. overall site of deposition
  3. accumulation of complexes occurring at site of blood filtration
43
Q

generalized type III HS rxn at different site results in what?

A

different diseases:
1. glomerulonephritis - kidney
2. vasculitis - arteries
3. arthritis - synovial joints

44
Q

systemic lupus erythematosus

antigen involved, clinical manifestation, and HS type

A

AI: nuclear antigen (circulated or planted in kidney)
CM: nephritis, skin lesions, arthritis others
HS: III

45
Q

poststreptococcal glomerulonephritis

antigen involved, clinical manifestation, and HS type

A

AI: streptococcal cell wall antigens; may be planted in glomerular basement membrane
CM: nephritis
HS: III

46
Q

polyarteritis nodosa

antigen involved, clinical manifestation, and HS type

A

AI: hep B virus antigen in some cases
CM: systemic vasculitis
HS: III

47
Q

reactive arthritis

antigen involved, clinical manifestation, and HS type

A

AI: bacterial antigens
CM: acute arthritis
HS: III

48
Q

serum sickness

antigen involved, clinical manifestation, and HS type

A

AI: various proteins (e.g. foreign serum protein)
CM: arthritis, vasculitis, nephritis
HS: III

49
Q

arthus rxn

antigen involved, clinical manifestation, and HS type

A

AI: various foreign proteins
CM: cutaneous vasculitis
HS: III

50
Q

!

what HS is cell-mediated delayed rxn

51
Q

type IV HS invovles interaction of what cells

A

T cells, monocytes, and macrophages

52
Q

type IV rxn is also called what

A

delayed-type HS

53
Q

how long does it take for type IV to develop

A

several days

54
Q

what rnx is mediated by T cells that provoke inflmamatory rxn against exogenous or endogenous antigens

55
Q

what HS rxn can occur in response to contact w/ certain allergens (contact dermatitis) or in response to some diagnostic procedures as in the tuberculin skin test

A

type IV HS

56
Q

pathway of type IV HS rxn

A
  1. activated CD4+ T h1 cells recognized foreign antigen in complex w/ MHC class II on surface of antigen presenting cells
  2. secrete: IL2 & interferon gamma thus mediatin immune response
57
Q

do activated CD8+ T cells destroy target cells on contact

58
Q

activated macrophages produce hydrolytic enzymes and on presentation w/ certain intracellular pathogens, transform into what?

A

multinucleated giant cells

59
Q

what is also known as purified protein derivative

A

tuberculin

60
Q

what is a combination of proteins that are used in the diagnosis of TB

A

tuberculin

61
Q

when is TB test considered positive

A

after 48-72 hours, if there is more than 5-10 mm area of swelling

62
Q

microscopically, what is causing TB test to be positive

A

CD4+, TH1 cells secrete cytokines (most importantly INF-gamma) causing vascular leakage leading to edema and fibrin deposition

63
Q

with persistent or nondegradable antigens colonizing the lungs or other tissues, the infiltration in TB is dominated by ___ over a period of 2-3 weeks

A

macrophages

64
Q

dominated macrophages in TB undergo transformation into ___

A

epithelioid cells

65
Q

what is a microscopic aggregation of epithelioid cells, usually surrounded by a collar of lymphocytes

A

granuloma/granulomatous inflammation

66
Q

B!

what are the clinical conditions which granulomas are formed

A
  1. myobacteria tuberculosis
  2. deep fungal infections
  3. parasitic infections
  4. foreign bodies
67
Q

what results from the contact of an offending chemical or antigen w/ the skin, and the subsequent T-cell mediated response

A

allergic contact dermatitis

68
Q

what is an inflammatory disease of the skin

A

allergic contact dermatitis

69
Q

what are the best indicators of the offending agent in ACD

A

morphology and location of the dermatitis

70
Q

what is a common cause of ACD and presents as linear streaks where the plant encounters the skin

A

poison ivy

71
Q

what is a common cause of ACD and presents as dermatitis where necklaces and earrings containing this are worn

72
Q

what is a common cause of CHRONIC dermatitis

A

rubber glvoes

73
Q

what cells mediate ACD

A

CD8+ T cells

74
Q

where are ACD CD8+ T cells primed? recruited?

A

primed: lymphoid organs during sensitization phase
recruited: into the skin upon exposure to antigen

75
Q

rheumatoid arthritis

specificity of pathogenic T cells, mechanism of tissue injury, clinical manifestation, and HS type

A

specificity: collagen, citrullinated self-protein
MoT: inflammation mediated by cytokines, role of antibodies and immune complexes?
CM: chronic arthritis w/ inflammation, destruction of articular cartilage
HS: III

76
Q

multiple sclerosis

specificity of pathogenic T cells, mechanism of tissue injury, clinical manifestation, and HS type

A

specificity: protein antigen in myelin sheath
MoT: inflammation mediated by cytokines, myeline destruction by activated macrophages
CM: demylenination in CNS w/ perivascular inflammation; paralysis
HS: IV

77
Q

type I DM

specificity of pathogenic T cells, mechanism of tissue injury, clinical manifestation, and HS type

A

specificity: antigen of pancreatic islet of beta cell
MoT: t cell mediated inflammation; destruction of islet cells by CTLs (CD8 T lymphocytes??)
CM: chronic inflammation of islets, destruction of beta cells, diabetes
HS: IV

78
Q

inflammatory bowel disease

specificity of pathogenic T cells, mechanism of tissue injury, clinical manifestation, and HS type

A

specificity: enteric bacteria, self antigens?
MoT: inflammation by cytokines
CM: chronic intesetinal inflammation
HS: IV

79
Q

psoriasis

specificity of pathogenic T cells, mechanism of tissue injury, clinical manifestation, and HS type

A

specificity: unkown
MoT: inflammation mediated by cytokines
CM: destructive plaques in the skin
HS: IV

80
Q

contact dermatitis

specificity of pathogenic T cells, mechanism of tissue injury, clinical manifestation, and HS type

A

specificity: various environmental chemicals (uroshiol from poison ivy or poison oak)
MoT: inflammation mediated by cytokines
CM: epidermal necrosis, dermal inflammation, causing skin rash and blisters
HS: IV

23 General Pathology (24 decks)

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