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Immuno2 0519FA Flashcards

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1
Q

what Igs do mature B cells express on surface?

A

IgM, IgD

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2
Q

how do B cells make the other Ig?

A

differentiate by isotype switching (gene rearrangement via cytokines and CD40 L) into PLASMA CELLS that secrete IgA, G, E.

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3
Q

IgM structure

A

monomer on B cell.

PENTAMER in tissue.

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4
Q

how does IgM shape help it function?

A

pentamer shape allows it to efficiently trap free Ags out of tissue while humoral response evolves

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5
Q

function of IgM

A

produced in primary/immediate response to Ag.

fixes complement but does not cross placenta.

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6
Q

IgD

A

unclear fx.

found on surface of many B cells and in serum.

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7
Q

IgA function

A

prevent attachment of bacteria and viruses to MUCOUS MEMBRANES.

does NOT fix complement.

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8
Q

IgA structure

A

monomer in circ.

dimer when secreted.

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9
Q

by what method does IgA cross epithelial cells?

A

transcytosis - pick up secretory component from epith cells before secretion.

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10
Q

where is IgA found?

A

secretions (tears, saliva, mucus).

breast milk/colostrum.

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11
Q

IgG function

A

main Ab in secondary/delayed response to Ag.

fixes complement.
crosses placenta.
opsonizes bacteria.
neutralizes bact toxins and viruses.

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12
Q

what cells does IgE bind?

A

mast cells and basophils - cross-links when exposed to allergen, mediating type I hypersensitivity through release of inflamm mediators (histamine)

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13
Q

which Ig is most abundant in blood?

A

IgG

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14
Q

which Ig provides passive immunity to infants?

A

IgG - CAN CROSS PLACENTA

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15
Q

Which Ig is in lowest conc in serum?

A

IgE

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16
Q

how does IgE also mediate immunity to worms?

A

activate eosinophils

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17
Q

what Ig is released in response to thymus-independent Ags?

A

(Ags lacking peptide component; cannot be presented by MHC to T cells)

IgM ONLY.
no immunologic memory.

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18
Q

what occurs when thymus-DEpendent Ags bind?

A

(Ags contain protein component)

B cells directly interact with Th cells (CD40-CD40), which release IL-4,5,6,10.
cytokines induce class switching and immunologic memory in B cells.
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19
Q

complement is part of what kind of immunity?

A

innate (+ inflammation)

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20
Q

membrane attack complex (MAC) of complement defends against?

A

gram neg bacteria

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21
Q

what activates CLASSIC pathway of complement?

A

IgG or IgM

“GM makes CLASSIC cars”

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22
Q

what activates ALTERNATIVE pathway of complement

A

microbe surface molecules

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23
Q

function of C1, 2, 3, 4

A

viral neutralization

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24
Q

function of C3b

A

opsonization

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25
function of C3a, C5a
anaphylaxis
26
function of C5a
neutrophil chemotaxis
27
function of C5b-9
cytolysis by MAC
28
what are the primary OPSONINS in bact defense?
C3b and IgG | *C3b also helps clear immune complexes
29
what are the INHIBITORS of complement?
1. decay-accelerating factor (DAF) 2. C1 esterase inhibitor --help prevent complement activation on self cells
30
C1 esterase inhibitor deficiency
HEREDITARY ANGIOEDEMA. | decreased C4 bc it is broken down by C1 esterase.
31
what is contraindicated in C1 esterase inhibitor deficiency?
ACE inhibitors
32
C3 deficiency
severe recurrent pyogenic sinus and resp tract infx. increased susceptibility to type III hypersens.
33
C5-9 deficiencies
recurrent Neisseria bacteremia
34
DAF (GPI anchored enzyme) deficiency
complement-mediated lysis of RBCs | and paroxysmal nocturnal hemoglobinuria.
35
TYPE I hypersensitivity
ANAPHYLAXIS AND ATOPIC: free Ag cross-links IgE on presensitized mast cells and basophils, triggering release of vasoactive amines that act at postcapillary venules.
36
onset of TYPE I hypersensitivity
rxn develops RAPIDLY after Ag exposure due to PREFORMED Ab. *first contact with Ag is ASYMPTOMATIC. class switch to IgE. IgE binds receptors on cells, ready for re-exposure.
37
test for TYPE I hypersensitivity
scratch test. | radioimmunosorbent assay.
38
TYPE II hypersensitivity
ANTIBODY-MEDIATED: | IgM, IgG bind fixed Ag on enemy cell, leading to lysis by complement (MAC) or phagocytosis
39
mechanisms of TYPE II hypersensitivity
1. opsonize cells or activate complement. 2. Ab recruit neutrophils and macrophages to incite tissue damage. 3. bind to normal cellular receptors and interfere with functioning.
40
test for TYPE II hypersensitivity
direct and indirect Coombs
41
TYPE III hypersensitivity
IMMUNE COMPLEX: | Ag-Ab (IgG) complexes activate complement, which attracts neutrophils that release lysosomal enzymes
42
serum sickness
TYPE III hypersensitivity. Abs to foreign proteins are produced (takes 5 days). IC form and are deposited in membranes, where they fix complement to cause tissue damage.
43
presentation of serum sickness
``` often caused by DRUGS. fever. urticaria. arthralgias. proteinuria. lymphadenopathy. ``` 5-10 days after Ag exposure.
44
Arthus reaction
local subacute reaction in which INTRADERMAL INJECTION of Ag induces Abs, forming IC in skin. complement is activated.
45
presentation of Arthus reaction
edema. | necrosis.
46
which is more common, serum sickness or Arthus reaction?
serum sickness
47
test for TYPE III hypersensitivity
immunofluorescent staining
48
TYPE IV hypersensitivity
DELAYED (CELL-MEDIATED): | sensitized T lymphocytes encounter Ag and release lymphokines to activate MACROPHAGES.
49
4T's of TYPE IV hypersensitivity
T lymphocytes. Transplant rejection. TB skin test. Touching (contact dermatitis).
50
test for TYPE IV hypersensitivity
patch test | ex: PPD
51
which is the only hypersensitivity that does NOT involve Abs?
TYPE IV hypersensitivity
52
TYPE I hypersensitivity disorders
Anaphylaxis: bee sting, food/drug allergies. Allergic and atopic disorders: rhinitis, hay fever, eczema, hives, asthma.
53
TYPE II hypersensitivity presentation
tends to be specific to tissue or site where Ag is found
54
TYPE III hypersensitivity presentation
can be assoc with vasculitis and systemic manifestations
55
TYPE III hypersensitivity disorders | other than serum sickness and Arthus rxn
``` SLE. rheumatoid arthritis. polyarteritis nodosum. PSGN. hypersensitivity pneumonitis. ```
56
blood transfusion rxn: allergic rxn
type I hypersensitivity. | against plasma proteins in transfused blood.
57
presentation of allergic rxn to blood transfusion
urticaria. pruritus. wheezing. fever. treat w/ antihistamines.
58
blood transfusion rxn: anaphylactic rxn
severe rxn. | IgA-deficient pts must receive blood products without IgA.
59
presentation of anaphylactic rxn to blood transfusion
``` dyspnea. bronchospasm. hypotension. resp arrest. shock. ```
60
blood transfusion rxn: febrile nonhemolytic transfusion rxn (FNHTR)
type II hypersensitivity rxn. | host Ab against donor HLA Ags and leukocytes.
61
presentation of FNHTR
fever. headache. chills. flushing.
62
blood transfusion rxn: acute hemolytic transfusion rxn (HTR)
type II hypersens rxn. intravasc hemolysis: ABO incompatibility. extravasc hemolysis: host Ab rxn against foreign Ag on donor RBCs.
63
presentation of acute HTR
``` fever. hypotension. tachypnea. tachycardia. flank pain. hemoglobinemia (intra). jaundice (extra). ```
64
bacterial infx in T cell deficiency
sepsis
65
bacterial infx in B cell deficiency
``` encapsulated organisms: S.pneumoniae. H.Influenzae type B. Neisseria meningitidis. Salmonella. Klebsiella pneumoniae. group B Strep. ``` "SHiN SKiS"
66
bacterial infx in granulocyte deficiency
BUrkholderia cepacia. Nocardia. Staphylococcus. Serratia. "no GRAiN for the BUNSS"
67
bacterial infx in complement deficiency (C5-9)
Neisseria
68
viral infx in T cell deficiency
CMV. EBV. VZV. chronic infx w/ resp and GI viruses.
69
viral infx in B cell deficiency
enteroviral encephalitis. | poliovirus (live vaccine contraindicated).
70
fungal/parasitic infx in T cell deficiency
candida. | PCP.
71
fungal/parasitic infx in B cell deficiency
GI giardiasis (due to no IgA)
72
fungal/parasitic infx in granulocyte deficiency
candida. | aspergillus.
73
B cell deficiencies tend to produce?
recurrent bacterial infxs
74
T cell deficiencies tend to produce?
fungal and viral infxs

Pathology (10 decks)

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