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Pathology > Immuno2 0519FA > Flashcards

Immuno2 0519FA Flashcards

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
Q

function of C3a, C5a

A

anaphylaxis

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26
Q

function of C5a

A

neutrophil chemotaxis

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27
Q

function of C5b-9

A

cytolysis by MAC

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28
Q

what are the primary OPSONINS in bact defense?

A

C3b and IgG

*C3b also helps clear immune complexes

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29
Q

what are the INHIBITORS of complement?

A
  1. decay-accelerating factor (DAF)
  2. C1 esterase inhibitor

–help prevent complement activation on self cells

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30
Q

C1 esterase inhibitor deficiency

A

HEREDITARY ANGIOEDEMA.

decreased C4 bc it is broken down by C1 esterase.

31
Q

what is contraindicated in C1 esterase inhibitor deficiency?

A

ACE inhibitors

32
Q

C3 deficiency

A

severe recurrent pyogenic sinus and resp tract infx.

increased susceptibility to type III hypersens.

33
Q

C5-9 deficiencies

A

recurrent Neisseria bacteremia

34
Q

DAF (GPI anchored enzyme) deficiency

A

complement-mediated lysis of RBCs

and paroxysmal nocturnal hemoglobinuria.

35
Q

TYPE I hypersensitivity

A

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
Q

onset of TYPE I hypersensitivity

A

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
Q

test for TYPE I hypersensitivity

A

scratch test.

radioimmunosorbent assay.

38
Q

TYPE II hypersensitivity

A

ANTIBODY-MEDIATED:

IgM, IgG bind fixed Ag on enemy cell, leading to lysis by complement (MAC) or phagocytosis

39
Q

mechanisms of TYPE II hypersensitivity

A
  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
Q

test for TYPE II hypersensitivity

A

direct and indirect Coombs

41
Q

TYPE III hypersensitivity

A

IMMUNE COMPLEX:

Ag-Ab (IgG) complexes activate complement, which attracts neutrophils that release lysosomal enzymes

42
Q

serum sickness

A

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
Q

presentation of serum sickness

A 
often caused by DRUGS.
fever.
urticaria.
arthralgias.
proteinuria.
lymphadenopathy.

5-10 days after Ag exposure.

44
Q

Arthus reaction

A

local subacute reaction in which INTRADERMAL INJECTION of Ag induces Abs, forming IC in skin. complement is activated.

45
Q

presentation of Arthus reaction

A

edema.

necrosis.

46
Q

which is more common, serum sickness or Arthus reaction?

A

serum sickness

47
Q

test for TYPE III hypersensitivity

A

immunofluorescent staining

48
Q

TYPE IV hypersensitivity

A

DELAYED (CELL-MEDIATED):

sensitized T lymphocytes encounter Ag and release lymphokines to activate MACROPHAGES.

49
Q

4T’s of TYPE IV hypersensitivity

A

T lymphocytes.
Transplant rejection.
TB skin test.
Touching (contact dermatitis).

50
Q

test for TYPE IV hypersensitivity

A

patch test

ex: PPD

51
Q

which is the only hypersensitivity that does NOT involve Abs?

A

TYPE IV hypersensitivity

52
Q

TYPE I hypersensitivity disorders

A

Anaphylaxis: bee sting, food/drug allergies.

Allergic and atopic disorders: rhinitis, hay fever, eczema, hives, asthma.

53
Q

TYPE II hypersensitivity presentation

A

tends to be specific to tissue or site where Ag is found

54
Q

TYPE III hypersensitivity presentation

A

can be assoc with vasculitis and systemic manifestations

55
Q

TYPE III hypersensitivity disorders

other than serum sickness and Arthus rxn

A 
SLE.
rheumatoid arthritis.
polyarteritis nodosum.
PSGN.
hypersensitivity pneumonitis.
56
Q

blood transfusion rxn: allergic rxn

A

type I hypersensitivity.

against plasma proteins in transfused blood.

57
Q

presentation of allergic rxn to blood transfusion

A

urticaria.
pruritus.
wheezing.
fever.

treat w/ antihistamines.

58
Q

blood transfusion rxn: anaphylactic rxn

A

severe rxn.

IgA-deficient pts must receive blood products without IgA.

59
Q

presentation of anaphylactic rxn to blood transfusion

A 
dyspnea.
bronchospasm.
hypotension.
resp arrest.
shock.
60
Q

blood transfusion rxn: febrile nonhemolytic transfusion rxn (FNHTR)

A

type II hypersensitivity rxn.

host Ab against donor HLA Ags and leukocytes.

61
Q

presentation of FNHTR

A

fever.
headache.
chills.
flushing.

62
Q

blood transfusion rxn: acute hemolytic transfusion rxn (HTR)

A

type II hypersens rxn.

intravasc hemolysis: ABO incompatibility.

extravasc hemolysis: host Ab rxn against foreign Ag on donor RBCs.

63
Q

presentation of acute HTR

A 
fever.
hypotension.
tachypnea.
tachycardia.
flank pain.
hemoglobinemia (intra).
jaundice (extra).
64
Q

bacterial infx in T cell deficiency

A

sepsis

65
Q

bacterial infx in B cell deficiency

A 
encapsulated organisms:
S.pneumoniae.
H.Influenzae type B.
Neisseria meningitidis.
Salmonella.
Klebsiella pneumoniae.
group B Strep.

“SHiN SKiS”

66
Q

bacterial infx in granulocyte deficiency

A

BUrkholderia cepacia.
Nocardia.
Staphylococcus.
Serratia.

“no GRAiN for the BUNSS”

67
Q

bacterial infx in complement deficiency (C5-9)

A

Neisseria

68
Q

viral infx in T cell deficiency

A

CMV.
EBV.
VZV.
chronic infx w/ resp and GI viruses.

69
Q

viral infx in B cell deficiency

A

enteroviral encephalitis.

poliovirus (live vaccine contraindicated).

70
Q

fungal/parasitic infx in T cell deficiency

A

candida.

PCP.

71
Q

fungal/parasitic infx in B cell deficiency

A

GI giardiasis (due to no IgA)

72
Q

fungal/parasitic infx in granulocyte deficiency

A

candida.

aspergillus.

73
Q

B cell deficiencies tend to produce?

A

recurrent bacterial infxs

74
Q

T cell deficiencies tend to produce?

A

fungal and viral infxs

Pathology (10 decks)

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