Immuno USMLE Flashcards

1
Q

a secondary lymphoid organ that has many afferents & 1 or more efferents. It is encapsulated, with trabeculae.

A

lymph node

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2
Q

fxs of lymph node (3)

A

1) filtration by macrophages
2) storage/proliferation of B and T cells
3) antibody production

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3
Q

this part of the lymph node is the site of B-cell localization and proliferation.

A

follicle

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4
Q

these follicules have pale central germinal centers and are active.

A

secondary follicles

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5
Q

this part of the lymph nodes consists of closely packed lymphocytes and plasma cells and sinuses that communicate with efferent lymphatic and contain reticular cells and macrophages

A

medulla

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6
Q

this part of the lymph node houses T cells. It is the region of the cortex between follicles and medulla. It contains high endothelial venules through which T and B cells enter from the blood. In extreme cellular immune response (i.e., viral) the this becomes greatly enlarged.

A

paracortex

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7
Q

paracortex is not well developed in pts with this syndrome

A

DiGeorge syndrome

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8
Q

this duct drains the right arm and right half of the head

A

right lymphatic duct

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9
Q

this duct drains the right arm and right half of the head

A

right lymphatic duct

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10
Q

this duct drains everything besides the right arm and right half of the head

A

thoracic duct

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11
Q

these are long vascular channels in red pulp with fenestrated “barrel hoop” basement membrane. Macrophages are found nearby.

A

sinusoids of the spleen

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12
Q

these cells are found in the periarterial lymphatic sheath (PALS) and in the red pulp of the pleen.

A

T cells

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13
Q

these cells are found in the follicles within the white pulp of the spleen

A

B cells

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14
Q

this is the site of T-cell maturation.

A

thymus

mneu: think of the Thymus as “finishing school” for T cells. They arrive immature and “dense” in the cortex; they are mature in the medulla.

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15
Q

the thymus is from the epithelium of this branchial pouch.

A

3rd

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16
Q

In the thymus, the cortex is dense with this type of T cells; while the medulla is pale with this type of T cells and epithelial reticular cells and Hassall’s corpuscles.

A

immature

mature

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17
Q

In the corticomedulary junction only T cells with MHC restriction are chosen, this is called?
then only T cells that are non-reactive to self are chosen.
what is this called

A

positive selection

negative selecton

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18
Q

this type of T cell produces IL-2 & gamma interfereon in order to activate macrophages and Tc cells

A

Th1 cells

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19
Q

this type of T cell produces IL-4 & IL-5 to help B cells make Ab

A

Th2 cells

B=2nd letter of the alphabet

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20
Q

State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Host defense against infection (opsinize bacteria, neutralize toxins & viruses)

A

Ab mediated immunity (B cells)

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21
Q

State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Host defense against Mycobacterium tuberculosis, virus infected cells, and fungi.

A

Cell mediated immunity (T cells)

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22
Q

State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Host defense against Mycobacterium tuberculosis, virus infected cells, and fungi.

A

Cell mediated immunity (T cells)

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23
Q

State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Allergy (e.g., hay fever, type I hypersensitivity)

A

B (Ab mediated immunity)

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24
Q

State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells: Allergy to poison oak, type IV hypersensitivity

A

Cell-mediated immunity (T cells)

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25
Q

State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Autoimmunity

A

B cell (Ab mediated immunity)

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26
Q

State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
Graft & tumor rejection

A

T cell(Cell mediated immunity)

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27
Q

State whether this is a fx of B (Ab mediated immunity) or T (Cell mediated immunity) cells:
help and supression of Ab response

A

T cell(Cell mediated immunity)

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28
Q

MHC stands for

A

major histocompatibility complex

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29
Q

give the 3 class I genes

A

A,B,C

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30
Q

give the 3 class I genes

A

A,B,C

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31
Q

give the 3 MHC class II genes

A

DP,DQ,DR

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32
Q

this type of MHC has 1 polypeptide, with B2-microglobin

A

Class I

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33
Q

this type of MHC has 2 polypeptides, with an alpha and a beta chain

A

class II

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34
Q

this type of cells have MHC II & MHC I proteins

A

APCs (e.g., macrophages & dendritic cells)

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35
Q

This class of MHC are the main determinants of organ rejection

A

class II

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36
Q

this type of Ag loading occurs in RER (viral Ag)

A

MHC I

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37
Q

this type of Ag loading occurs in acidified endosome

A

MHC II

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38
Q

Give the 2 T-cell glycoproteins

A

CD4

CD8

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39
Q

helper T cells have CD_, which binds to MHC II on APCs

A

4

mneu: product of CD & MHC =8

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40
Q

Cytotoxic T cells have CD__, which binds to MHC I on virus infected cells

A

8

mneu: product of CD & MHC =8

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41
Q

this is a cluster of polypeptides associated with a T-cell receptor. It is important in signal transduction

A

CD3 complex

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42
Q

give the 3 Ag presenting cells

A

1) macrophage
2) B cell
3) dendritic cells

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43
Q

in this type of T cell activation:

1) foreign body is phagocytosed by APC
2) Foreign Ag is presented on MHC II and recognized by TCR on Th cell
3) “Costimulatory signal” is given by interaction of B7 & CD28
4) Th cell is activated to produce IL-2 and gamma-interferon

A

Th activation

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44
Q

In this type of T cell activation:

1) Endogenously synthesized (viral or self) proteins are presented on MHC I and recognized by TCR on Tc cell
2) IL-2 from Th cell activates killing of the virus infected cell.

A

Tc activation

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45
Q

_______ part of L & H chains recognize Ag.

A

variable

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46
Q

_______ part of H chain of IgM & IgG fixes complement

A

Constant

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47
Q

_______ chain contributes to Fc and Fab fractions

A

Heavy

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48
Q

_____ chain contributes only to Fab fraction

A

light

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49
Q

This fragment of Ab is constant, has a carboxy terminal, is complement-binding (IgG & IgM only) and has carbohydrate side chains

A

Fc fragment

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50
Q

Abs do many things to aid in host defense. This method of host defense refers to when Ab promotes phagocytosis. image. p.184

A

opsonization

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51
Q

Abs do many things to aid in host defense. This method of host defense refers to when Ab prevents bacterial adherance. image. p.184

A

neutralization

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52
Q

Abs do many things to aid in host defense. This method of host defense refers to when Ab activates compliment, enhancing opsinization and lysis. image. p.184

A

complement activation

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53
Q

Ab diversity is generated by:

1) random ______ of VJ (light chain or VDJ (heavy chain) genes)
2) random ______ of heavy chains with light chains
3) Somatic __________
4) addition of DNA during _________ by terminal deoxynucleotidl transferase

A

recombination
combination
hypermutation
genetic recombination

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54
Q

mature B lymphocytes express ______ & _____ on their surfaces.

A

IgM & IgD

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55
Q

mature B lymphocytes express IgM & IgD on their surfaces may differentiate by isotype switching (mediated by cytokines and CD40 ligand) into plasma cells that secrete ____,____ or _____

A

IgA, IgE, or IgG

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56
Q

this immunoglobin isotype is the main Ab in secondary response. It is the most abundant. It fixes complement, crosses the placenta, opsonizes bactera, & neutralizes bacterial toxins & viruses

A

IgG

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57
Q

This immunoglobin isotype prevents attachment of bacteria and viruses to mucous membranes, it does not fix complement. It can be a monomer or dimer. It is found on secretions. It picks up secretory component from epithelial cells before secretion.

A

IgA

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58
Q

this immunoglobin isotype is produces in the primary response to an antigen. It fixes complement but does not cross the placenta. The Ag receptor is on the surface of the B cells. It can be a monomer or pentamer.

A

IgM

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59
Q

this immunoglobin isotype is found on the surface of many B cells and in serum. Its fx is unclear.

A

IgD

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60
Q

this immunoglobin isotype mediates immediate (type I) hypersensitivity by inducing the release of mediators from mast cells and basophils when exposed to allergen. It mediates immunity to worms. It is the lowest Ig isotype in serum

A

IgE

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61
Q

This is an Ig epitope that differs among members of the same species. It can be on light or heavy chain

A

allotype (polymorphism)

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62
Q

This Ig epitope is common to a single class of Ig (5 classes determined by the heavy chain)

A

Isotype (IgG, IgA, etc.)

Isotype=iso (same) common to same class)

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63
Q

This Ig epitope is determined by the Ag binding site

A

Idiotype (specific for a given Ag)

Idiotype=idio (unique)
hypervariable region is unique

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64
Q

This important cytokine is secreted by macrophages. It stimulates T cells, B cells, neutrophils, fibroblasts, and epithelial cells to grow, differentate, or synthesize specific products. It is an endogenous pyrogen

A

IL-1

mneu:
HOT T-BONE stEAk
IL-1: fever (HOT)
IL-2: stimulates T cells (T)
IL-3: stimulates BONE marrow
IL-4: stimulates IgE (E)
IL-5: stimulates IgA (A)
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65
Q

This important cytokine is secreted by Th cells. It stimulates growth of helper and cytotoxic T cells

A

IL-2

mneu:
HOT T-BONE stEAk
IL-1: fever (HOT)
IL-2: stimulates T cells (T)
IL-3: stimulates BONE marrow
IL-4: stimulates IgE (E)
IL-5: stimulates IgA (A)
66
Q

This important cytokine is secreted by activated T cells. It supports the groth and differentiation of bone marrow stem cells. It has a fx similar to GM-CSF

A

IL-3

mneu:
HOT T-BONE stEAk
IL-1: fever (HOT)
IL-2: stimulates T cells (T)
IL-3: stimulates BONE marrow
IL-4: stimulates IgE (E)
IL-5: stimulates IgA (A)
67
Q

This important cytokine is secreted by Th cells. It promotes groth of B cells. It enhances class switching of IgE & IgG

A

IL-4

mneu:
HOT T-BONE stEAk
IL-1: fever (HOT)
IL-2: stimulates T cells (T)
IL-3: stimulates BONE marrow
IL-4: stimulates IgE (E)
IL-5: stimulates IgA (A)
68
Q

This important cytokine is secreted by Th cells. It promotes differentiation of B cells. It enhances class switching of IgA. It stimulates production and activation of eosinophils

A

IL-5

mneu:
HOT T-BONE stEAk
IL-1: fever (HOT)
IL-2: stimulates T cells (T)
IL-3: stimulates BONE marrow
IL-4: stimulates IgE (E)
IL-5: stimulates IgA (A)
69
Q

This important cytokine is secreted by Th cells and macrophages. It stimulates production of acute phase reactants and immunoglobins.

A

IL-6

70
Q

This important cytokine is a major chemotactic factor for neutrophils

A

IL-8

71
Q

This important cytokine is secreted by B cells and macrophages. It activates NK and Th2 cells

A

IL-12

72
Q

This important cytokine is secreted by Th cells. It stimulates macrophages

A

gamma interferon

73
Q

This important cytokine is secreted by macrophages. It increases IL-2 receptor synthesis by Th cells. It increases B cell proliferation. It attracts and activates neutrophils. It stimulates dendritic cell migration to lymph nodes.

A

TNF-alpha

74
Q

given the cell surface proteins give the cell:

CD4,TCR,CD3,CD28,CD40L

A

helper T cells

75
Q

given the cell surface proteins give the cell:

CD8,TCR,CD3

A

cytotoxic T cells

76
Q

given the cell surface proteins give the cell:

IgM,B7,CD19,CD20,CD40, MHC II

A

B cells

77
Q

given the cell surface proteins give the cell:

MHC II,CD14, receptors for Fc & C3b

A

Macrophages

78
Q

given the cell surface proteins give the cell: Receptors for MHC I, CD16

A

NK cells

79
Q

MHC I

A

all cells except mature red cells

80
Q

This system is a system of proteins that interact to play a role in humoral immunity and inflammation

A

compliment

81
Q

complement defends against this type of bacteria

A

G-

82
Q

compliment is activated by Ig_ & Ig_ in the ______ pathway,

and activated by molecules on the surface ofmicrobes (especially endotoxin) in the ________ pathway

A

G & M, classic
alternate

mneu: GM makes CLASSIC cars

83
Q

given the complements give the function:

C1,C2,C3,C4

A

viral neutralization

84
Q

given the complements give the function:

C3b

A

opsonization

85
Q

given the complements give the function:

C3a,C5a

A

anaphylaxis

86
Q

given the complements give the function:

C5a

A

neutrophil chemotaxis

87
Q

given the complements give the function:

C5b-9

A

cytolysis by membrane attack complex (MAC)

88
Q

deficiency of _______ leads to hereditary angioedema (overactive complement)

A

C1 esterase inhibitor

89
Q

deficiency of _______ leads to severe, recurrent pyogenic sinus and respiratory tract infections

A

C3

90
Q

deficiency of _______ leads to Neisseria bacteremia

A

C6-C8

91
Q

deficiency of _______ leads to leads to paroxysmal nocturnal hemoglobinuria (PNH)

A

DAF

92
Q

these are proteins taht place uninfected cells in an antiviral state

A

interferons (alpha, beta,gamma)

93
Q

Interferons induce the production of a 2nd protein that inhibits viral ______ by degrading viral mRNA (but not host mRNA)

A

protein synthesis

94
Q

alpha and beta interferons inhibit viral ________

A

protein sythesis

95
Q

gamma interferons increase ________ expresssion and antigen presintation in all cells

A

MHC I & II

96
Q

interferons activate these cells to kill virus-infected cells

A

NK cells

97
Q

this type of immunity is induced after exposure to foreign Ag. It has a slow onset and provides long lasting protection (memory)

A

active immunity

98
Q

this type of immunity is based on recieving preformed Ab from another host. There is a rapid onset but a short life span of the Ab

A

passive immunity

99
Q

what are some common exposures in which pts are given preformed Abs (passive immunity)

A

Tetanus Toxin
Botulism Toxin
HBV
Rabies

mneu: To Be Healed Rapidly

100
Q

Classic examples of antigen variation include this bacteria with 2 flagellar varients

A

salmonella

101
Q

Classic examples of antigen variation include this virus that undergoes antigen shift and antigen drift

A

influenza

102
Q

Classic examples of antigen variation include this parasite that undergoes programmed rearrangement

A

trypanosomes

103
Q

Some mechanisms for Ag variation include DNA rearrangement and RNA segment rearrangement, Which one occurs in an influenza major shift.

A

RNA segment rearrangement

104
Q

this process describes when self-reactive T cells become nonreactive without costimulary molecule

A

anergy

105
Q

can B cells become anergic

A

yes -but tolerence is lest complete than in T cells

106
Q

this type of hypersensitivity involves aaphylactic and atopic reactions

A

Type I

Mneu: First and Fast (anaphylaxic)

107
Q

In this type of hypersensitivity rxn the Ag cross-links IgE on presensitized mast cells and basophils, triggering release of vasoactive amines (i.e., histamine). A reaction develops rapildly after Ag exposure due to preformed Ab. E.g., include anaphylaxis, asthma, hives, local wheal and flare

A

Type I

108
Q

This type of hypersensitivity is Ab mediated. IgM & IgG bind to Ag on “enemy” cell, leading to lysis (by complement or phagocytosis. E.g., include autoimmune hemolytic anemia, Rh dz(erythroblastosis fetalis), goodpasture’s syndrome, rheumatic fever, Graves dz, bullous pemphigoid, myasthenia gravis, ITP

A

type II

mneu: cy-2-toxic

109
Q

In type II hypersensitivity rxns the Ab & complement lead to this complex

A

membrane attack complex

110
Q

these types of hypersensitivity reactions are Ab mediated

A

I,II,III

111
Q

Immune complex, serum sickness, and Arthrus reactions describe this type of hypersensitivity reaction

A

type III

112
Q

In this subtype of a type III hypersensitivity reaction Ag-Ab complexes activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes. Examples include PAN, immune complex glomerulonephritis, SLE,rheumatoid arthritis.

A

immune complex

113
Q

immune complexes are essentially 3 things stuck together. What are they?

A

Ag-Ab-C’

114
Q

pt presents with fever, uticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after Ag exposure

A

serum sickness

115
Q

This subtype of a type III hypersensitivity reaction is an immune complex dz in which Ab to the foreign proteins are produced (takes 5 days). Immune complexes form and are deposited in membranes, where they fix compliment (leads to tissue damage).

A

Serum Sickness

116
Q

most serum sickness is now caused by this not serum

A

drugs

117
Q

This subtype of a type III hypersensitivity reaction is a local subacute Ab mediated hypersensitivity. Intradermal injection of Ag induces Ab, which form Ag-Ab complexes in the skin. It is characterized by edema, necrosis, and activation of complement. Examples include hypersensitivity pneumonitis (farmer’s lung) and thermophilic actinomycetes.

A

Arthrus reaction

118
Q

these complexes cause the arthrus reaction

A

Ab-Ag complex

119
Q

This type of hypersensitivity involves delayed (T cell mediated) reactions. Sensitized T lymphocytes encounter Ag and then release lymphokines which leads to macrophage activation

A

Type IV

mneu: 4th & last-delayed

120
Q

Type IV hypersensitivity reactions are cell mediated–therefore are they transferable by serum

A

No

121
Q

Give the 4 Ts of type IV hypersensitivity reactions

A

T lymphocytes, Transplant reactons, TB skin tests, Touching (contact dermatitis)

122
Q

Use the ACID mneumonic for the types of hypersensitivity. . . .

A

A-Anaphylactic and Atopic(I)
C-Cytotoxic (Ab mediated[II]
I-Immune complex (III)
D-Delayed (cell mediated[IV]

123
Q

Give the immune deficiency:
this is an X linked recessive defect in a tyrosine kinase gene associated with low levels of all classes of immunoglobins. It is Associated with recurrent BACTERIAL infections after 6 mo. of age, when levels of maternal IgG Ab decline. It occurs in BOYS (X-linked)

A

Bruton’s agammaglobulinemia (decreased production of B cells)

124
Q

Give the immune deficiency:
This occurs when the THYMUS and paraTHYROIDS fail to develop owing to failure of development of the THIRD and fourth pharyngeal puches. It presents with TETANY owing to hypocalcemia. Pt often has recurrent viral and fungal infections due to T-cell deficiency. Congenital defects of heart and great vessels often accompany. There is a 22q11 deletion

A

Thymic aplasia (DiGeorge syndrome) decrease production of T cells

125
Q

Give the immune deficiency:
This is a defect in early stem-cell differentiation. It presents with recurrent viral, bacterial, fungal and protozoal infections. It may have multiple causes (e.g., failure to synthesize MHC II Ag, defective IL-2 receptors or adenosine deaminase deficiency.

A

Severe combined immunodeficiency (SCID)

decreased production of B & T cells

126
Q

Give the immune deficiency:

Pt presents with disseminated mycobacterail infections.

A

IL-12 receptor deficiency

T cell activation problem

127
Q
Give the immune deficiency:
Defect in the CD40 ligand on CD4 T helper cells leads to inability to class switch.  Presents early in life with severe pyogenic infections.  High levels of IgM; very low levels of IgG, IgA, & IgE
A

Hyper IgM syndrome

B cell activation problem

128
Q

Give the immune deficiency:
X linked defect in the ability to mount an IgM response to capsular polysaccharides of bacteria. Associated with elevated IgA levels, normal IgE levels, and low IgM levels. Triad of symptoms includes recurrent pyogenic Infections, thrombocytopenic Purpura, Eczema (WIPE).

A

Wiskott-Aldrich Syndrome

B cell activation problem

129
Q

Give the immune deficiency:
Failure of gamma-interferon production by helper T cells. Neutrophils fail to respond to chemotactic stimuli. Presents with recurrent “cold” (noninflamed) staphylococcal abscesses, eczema, coarse facies, retained primary teeth, and high levels of IgE

A

Jobs syndrome-

decreased activation of macrophages

130
Q

Give the Immune deficiency:
Defect in LFA-1 adhesion proteins on phagocyts. Presents early with sever pyogenic and fungal infections and delayed seperation of umbilicus

A

Leukocyte adhesion deficiency syndrome

Phagocytic cell deficiency

131
Q

Give the Immune deficiency: Autosomal recessive defect in microtubular fx and lysosomal emptying of phagocytic cells. Presents with recurrent pyogenic infxns by staphylococci and streptococci, partial albinism, and peripheral neuropathy

A

Chediak-Higashi dz

phagocytic cell deficiency

132
Q

Give the Immune deficiency: Defect in phagocytosis of neutrophils owing to lack of NADPH oxidase activity or similar enzymes. Presents with marked susceptibility to opportunistic infxns with bacteria, especially S. aureus, E. coli, and Aspergillus. Diagnosis is confirmed with negative nitroblue tetrazolium dye reduction test

A

Chronic granulomatous dz

phagocytic cell deficiency

133
Q

Give the Immune deficiency:

T-cell dysfunction specificallly against Candida albicans. Presents with skin and mucous membrane Candida infections.

A

Chronic mucocutaneous Candidiasis-

Idiopathic dysfunciton of T cells

134
Q
Give the Immune deficiency:
Deficiency in a specific class of immunoglobulins--possibly due to a defect in isotype switching.  Selective IgA deficiency is the most common selective immunoglobin deficiency.   Presents with sinus and lung infections.  Milk allergies and diarrhea are common.
A

Selective immunoglobin deficiency

Idiopathic dysfunction of B cells

135
Q

Give the Immune deficiency:
Defect in DNA repearin enzymes with associated IgA deficiency. Presents with cerebellar problems (ataxia) and spider angiomas (telangiectasia.

A

ataxiatelangiectasia-

idiopathic dysfunction of B cells

136
Q
Given the autoantibody, give the associated disorder:
antinuclear Ab (ANA)
A

SLE

137
Q

Given the autoantibody, give the associated disorder: Anti-dsDNA, anti-Smith

A

specific for SLE

138
Q

Given the autoantibody, give the associated disorder:

Antihistone

A

drug induced lupus

139
Q

Given the autoantibody, give the associated disorder: Anti-IgG (rheumatoid factor)

A

rheumatoid arthritis

140
Q

Given the autoantibody, give the associated disorder: antineutrophil (C-ANCA, P-ANCA)

A

Vasculutis

141
Q

Given the autoantibody, give the associated disorder: Anticentromere

A

Scleroderma (CREST)

142
Q

Given the autoantibody, give the associated disorder:

Anti-Scl-70

A

Scleroderma (diffuse)

143
Q

Given the autoantibody, give the associated disorder: antimitochondrial

A

primary biliary cirrhosis

144
Q

Given the autoantibody, give the associated disorder: Antigliadin

A

Celiac dz

145
Q

Given the autoantibody, give the associated disorder:

Anti-basement membrane

A

Goodpasture’s syndrome

146
Q

Given the autoantibody, give the associated disorder:

Anti-epithelial cell

A

Pemphigus vulgaris

147
Q

Given the autoantibody, give the associated disorder:

Antimicrosomal

A

Hashimoto’s thyritis

148
Q

Given the autoantibody, give the associated disorder: Anti-Jo-1

A

polymositis, dermatomyositis

149
Q

Hive the HLA subtype that coincides with the following disorders: Psoriasis, Ankylosing spondylitis, Inflammatory bowel dz, Reiter’s syndrome.

A

B27

mneu: PAIR

150
Q

Give the HLA subtype which cooresponds to the following dz:

Graves’ dz, celiac sprue

A

B8

151
Q

Give the HLA subtype which cooresponds to the following dz:

MS, hay fever, SLE, Goodpasture’s

A

DR2

152
Q

Give the HLA subtype which cooresponds to the following dz: DM type I

A

DR3

153
Q

Give the HLA subtype which cooresponds to the following dz:

Rheumatoid arthritis, DM type 1

A

DR4

154
Q
Give the HLA subtype which cooresponds to the following dz:
Pernicous anemia (B12 deficiency) Hashimoto's thyroiditis
A

DR5

155
Q

Given the autoantibody, give the associated disorder:

Steroid-responsive nephrotic syndrome

A

DR7

156
Q

This type of transplant rejection is Ab mediated due to presence of preformed antidonor Ab in the transplant recipient. It occurs within minutes after transplantation.

A

hyperacute rejection

157
Q

This type of transplant rejection is cell mediated due to cytotoxic T lymphocytes reacting against foreign MHCs. It occurs weeks after transplantation. It is reversible with immunosuppressants such as cyclosporin and OKT3

A

Acute rejection

158
Q

This type of transplant rejection is Ab mediated vascular damage (fibrinoid necrosis) it occurs months to years after transplantation. It is irreversible.

A

Chronic rejection

159
Q

This type of transplant rejection happens when grafted immunocompetent T cells proliferate in the irradiated immunocompromised host and reject cells with “foreign” proteins, resulting in severe organ dysfunction. Major symtoms include maculopapular rash, jaundice, hepatosplenomegly, and diarrhea

A

Graft v. Host dz

160
Q

This type of transplant rejection is Ab mediated vascular damage (fibrinoid necrosis) it occurs months to years after transplantation. It is irreversible.

A

Chronic rejection

161
Q

This type of transplant rejection happens when grafted immunocompetent T cells proliferate in the irradiated immunocompromised host and reject cells with “foreign” proteins, resulting in severe organ dysfunction. Major symtoms include maculopapular rash, jaundice, hepatosplenomegly, and diarrhea

A

Graft v. Host dz