6/28 - Diseases of Immune System

Question 1

immune reactant for Type II HS

Answer 1

IgG and some cases IgM

Question 2

antigen for Type II HS

Answer 2

cellular or extracellular matrix antigens

Question 3

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

Answer 3

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

Question 4

mechanisms of type II HS

Answer 4

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

Question 5

describe opsonization and phagocytosis in type II HS

Answer 5

antibody coats cell and and is marked for phagocytosis

Question 6

what causes tissue damage in type II HS

Answer 6

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

Question 7

what do antibodies attack in inflammation of type II HS

Answer 7

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

Question 8

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

Answer 8

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

this directs migration of neutrophils and monocytes and anaphylaxtonins

Question 9

what are the anaphylatoxins? what does it do?

Answer 9

C3a, C4a, and C5a
increase vascular permeability

Question 10

pathway for type II HS inflammation and tissue injury

Answer 10

1. antigen + target cell + antibody
2. • 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

Question 11

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

Answer 11

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

both type II

Question 12

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

Answer 12

autoimmune hemolytic anemia - type II

Question 13

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?

Answer 13

erythroblastosis fetalis - type II

Question 14

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

Answer 14

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

Question 15

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

Answer 15

myasthenia gravis - type II HS

Question 16

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

Answer 16

Grave’s disease = type II HS

Question 17

autoimmune hemolytic anemia

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

Answer 17

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

Question 18

autoimmune thrombolytic purpura

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

Answer 18

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

Question 19

B)

pemphigus vulgaris

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

Answer 19

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

Question 20

vasculitis caused by antineutrophil cytoplasmic AB

target antigen, mechanism of disease, clinical manifestation

Answer 20

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

Question 21

good pasture syndrome

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

Answer 21

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

Question 22

acute rheumatic fever

target antigen, mechanism of disease, clinical manifestation, HS

Answer 22

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

Question 23

myasthenia gravis

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

Answer 23

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

Question 24

insulin-resistant diabetes

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

Answer 24

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

Question 25

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

Answer 25

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

Question 26

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

Answer 26

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

Question 27

immune reactant for type III HS

Answer 27

IgG or IgM

Question 28

antigen for type III HS

Answer 28

solubule antigen

Question 29

type III HS rxn is mediated by formation of what

Answer 29

antigen-antibody aggregates called immune complexes

Question 30

how are type III HS rxns frequently initiated

Answer 30

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

Question 31

how are type III HS rxns less frequently initiated

Answer 31

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

Question 32

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

Answer 32

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

Question 33

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

Answer 33

BOTH! exogenous AND endogenous

Question 34

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

Answer 34

exogenous rxns

Question 35

what are self antigens/autoimmuniy?

Answer 35

endogenous rxns

Question 36

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

Answer 36

acute Arthus rxns - type III

Question 37

what mediates acute Arthus rxns?

Answer 37

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

Question 38

when do acute arthus rxn form

Answer 38

within 4-8 hours

Question 39

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

Answer 39

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

Question 40

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

Answer 40

serum sickness - type III

Question 41

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

Answer 41

serum sickness - type III

Question 42

manifestation of serum sickness depends on what

Answer 42

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

Question 43

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

Answer 43

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

Question 44

systemic lupus erythematosus antigen involved, clinical manifestation, and HS type

Answer 44

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

Question 45

poststreptococcal glomerulonephritis antigen involved, clinical manifestation, and HS type

Answer 45

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

Question 46

polyarteritis nodosa antigen involved, clinical manifestation, and HS type

Answer 46

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

Question 47

reactive arthritis antigen involved, clinical manifestation, and HS type

Answer 47

AI: bacterial antigens CM: acute arthritis HS: III

Question 48

serum sickness antigen involved, clinical manifestation, and HS type

Answer 48

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

Question 49

arthus rxn antigen involved, clinical manifestation, and HS type

Answer 49

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

Question 50

! what HS is cell-mediated delayed rxn

Answer 50

type IV

Question 51

type IV HS invovles interaction of what cells

Answer 51

T cells, monocytes, and macrophages

Question 52

type IV rxn is also called what

Answer 52

delayed-type HS

Question 53

how long does it take for type IV to develop

Answer 53

several days

Question 54

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

Answer 54

type IV

Question 55

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

Answer 55

type IV HS

Question 56

pathway of type IV HS rxn

Answer 56

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

Question 57

do activated CD8+ T cells destroy target cells on contact

Answer 57

YES

Question 58

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

Answer 58

multinucleated giant cells

Question 59

what is also known as purified protein derivative

Answer 59

tuberculin

Question 60

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

Answer 60

tuberculin

Question 61

when is TB test considered positive

Answer 61

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

Question 62

microscopically, what is causing TB test to be positive

Answer 62

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

Question 63

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

Answer 63

macrophages

Question 64

dominated macrophages in TB undergo transformation into ___

Answer 64

epithelioid cells

Question 65

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

Answer 65

granuloma/granulomatous inflammation

Question 66

B! what are the clinical conditions which granulomas are formed

Answer 66

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

Question 67

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

Answer 67

allergic contact dermatitis

Question 68

what is an inflammatory disease of the skin

Answer 68

allergic contact dermatitis

Question 69

what are the best indicators of the offending agent in ACD

Answer 69

morphology and location of the dermatitis

Question 70

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

Answer 70

poison ivy

Question 71

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

Answer 71

nickel

Question 72

what is a common cause of CHRONIC dermatitis

Answer 72

rubber glvoes

Question 73

what cells mediate ACD

Answer 73

CD8+ T cells

Question 74

where are ACD CD8+ T cells primed? recruited?

Answer 74

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

Question 75

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

Answer 75

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

Question 76

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

Answer 76

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

Question 77

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

Answer 77

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

Question 78

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

Answer 78

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

Question 79

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

Answer 79

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

Question 80

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

Answer 80

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