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FirstAID > Immunlogy > Flashcards

Immunlogy Flashcards

1
Q

site of B cell localization and proliferation in lymph nodes?

A

Follicle - in outer cortex

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2
Q

Which part of lymph node houses T cells?

A

Paracortex - area of cortex between follicles and medulla

  • becomes enlarged during extreme immune responses
  • not well developed in DiGeorge syndrome pts (b/c no T cells…)
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3
Q

lymph node drainage from upper limb, lateral breast?

A

Axillary lymph nodes

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4
Q

lymph node drainage from stomach

A

celiac nodes

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5
Q

lymph node drainage from duodenum and jejunum

A

superior mesenteric node

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6
Q

lymph node drainage from sigmoid colon

A

colic –> inferior mesenteric node

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7
Q

lymph node drainage from rectum?

A

internal iliac node

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8
Q

lymph node drainage from anal canal?

A

superficial inguinal node

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9
Q

lymph node drainage from testes

A

superficial and deep plexuses –> para-aortic nodes = retroperitoneal nodes

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10
Q

lymph node drainage from thigh (superficial)

A

superficial inguinal nodes

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11
Q

lymph node drainage from lateral side of dorsum of foot

A

popliteal nodes

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12
Q

lymph node drainage of prostate

A

internal iliac nodes

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13
Q

right lymphatic duct vs thoracic duct drains?

A

right lymphatic ducts drains: right arm and right half of head
thoracic duct drains: everything else

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14
Q

Where are B cells found in the spleen?

A

Follicles within white pulp of spleen

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15
Q

Where are T cells found in spleen?

A

PALS = periarterial lymphatic sheath within white pulp of spleen

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16
Q

immunlogic results of/response to splenic dysfunction?

A

splenic dysfunction: decreased IgM–>decreased complement activation –> decreased C3b opsonization –> increased susceptibility to encapsulated organisms (SSHiNK: Salmonella, S. pneum, H. influenza, N. meningitidis, K. pneumonia)

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17
Q

Howell-Jolly bodies, Target cells, and thrombocytosis

A

Post-splenectomy

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18
Q

Thymus is derived from what branchial pouch?

A

3rd branchial pouch

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19
Q

Where in thymus does positive selection occur? Negative selection?

A

positive –> corex

negative –> medulla/corticomedullary jxn

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20
Q

beta-2-microglobulin is found on which class of MHC molecule?

A

MHC I: has a heavy chain and a beta-2-microglobulin chain

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21
Q

Which HLA genes code for MHC I? MHC 2?

A

MHC I: HLA-A, HLA-B, HLA-C

MHC II: HLA-DR, HLA-DP, HLA-DQ

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22
Q

which cell types express MHC I? MHC II?

A

MHC I –> expressed on almost all nucleated cells (not expressed on RBCs)
MHC II: expressed only on APCs

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23
Q

HLA-A3

A

Hemochromatosis

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24
Q

HLA-B27

A

PAIR:

  • Psoriasis
  • Ankylosing spondylitis
  • Inflammatory bowel disease
  • Reiter’s syndrome
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25
Q

HLA-B8

A

Graves disease

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26
Q

HLA-DR2

A
  • Multiple sclerosis
  • Hay fever
  • SLE
  • Goodpasture’s
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27
Q

HLA-DR3

A

Diabetes type I

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28
Q

HLA-DR4

A
  • Rheumatoid arthritis

- Diabetes type I

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29
Q

HLA-DR5

A
  • Pernicious anemia –> B12 deficiency

- Hashimoto’s thyroiditis

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30
Q

HLA-DR7

A

steroid-responsive nephrotic syndrome

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31
Q

only lymphocyte member of innate immune system?

A

natural killer cells

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32
Q

What CD-?’s are expressed on NK cells?

A
  • CD-16

- CD-56

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33
Q

Which cytokines activate natural killer cells?

A

IL-12
IFN-alpha
IFN-beta

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34
Q

which cytokine induces Th2 formation? which cytokines are secreted by Th2 and what are their actions?

A
  • IL-4 induces Th2
  • Th2 makes:
  • IL-4 –> stimulates B-cells
  • IL-5 –> stimulates B-cells
  • IL-10 –> inhibits Th-1 cells and macrophages
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35
Q

which cytokine induces Th1 formation? which cytokines are secreted by Th1 and what are their actions? Which cytokine inhibits Th1?

A
  • IL-12 induces Th1
  • Th1 secretes:
  • IL-2 –> stimulates T-cells
  • IFN-gamma –> stimulates macrophages
  • IL-10 (secreted by Th2 cells) inhibit Th1 cells
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36
Q

What are the antigen presenting cells?

A
  • Macrophages
  • Dendritic cells
  • B cells
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37
Q

What are the 2 signals needed for Helper T-cell activation?

A

signal 1: foreign antigen, after being phagocytosed by APC, is presented on MHC II of APC and is recognized by TCR on the Th cell
signal 2 = “co-stimulatory signal”: interaction between B7 (on APC) and CD28 (on Th cell)

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38
Q

2 signals needed for cytotoxic T-cell activation?

A

signal 1: viral or self proteins are presented on MHC I and recognized by TCR on cytotoxic T-cell
signal 2: IL-2 from Th1 cell activates cytotoxic T-cell to kill the virus-infected cell

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39
Q

2 signals needed for B-cell activation and class-switching?

A

First, helper T-cells are activated LOOK UP IN IMMUNO BOOK!

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40
Q

Th1 cells:

  • regulate:
  • secrete which cytokines?
  • activate what?
  • inhibited by?
A
  • regulate cell-mediated response
  • secrete Th1 cytokines: IL-2, IFN-gamma
  • activate macrophages and CD8+ T-cells
  • inhibited by IL-10 (from Th2 cell)
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41
Q

Th2 cells:

  • regulate?
  • secrete which cytokines?
  • another action they do?
  • inhibited by?
A
  • regulate humoral response
  • secrete Th2 cytokines: IL-4, IL-5, IL-6, IL-10
  • help B-cells make antibody (IgE> IgG)
  • inhibited by IFN-gamma (from Th1 cell)
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42
Q

How do natural killer cells induce apoptosis?

A

use perforin and granzymes to induce apoptosis

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43
Q

How do cytotoxic T-cells induce apoptosis?

A

release cytotoxic granules containing preformed proteins:

  • perforin (delievers granules into target cell)
  • granzyme (activates apoptosis inside target cell)
  • granulysin (antimicrobial, induces apoptosis)
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44
Q

Natural Killer vs Cytotoxic T-cells

A

Both induce apoptosis of virally-infected or tumor cells

  • NK cells –> Recognize ABSENCE of MHC-1 on target cell surface
  • Cytotoxic T-cells –> have CD8, which BINDS to MHC-1 on virus-infected cells
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45
Q

What part of the antibody is recognizes antigens?

A

the antigen binding fragment on the Fab part of the antibody; the VL and VH (variable light and variable heavy) chains recognize antigens.

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46
Q

Which part of the antibody fixes complement?

A

Complement binding is at CH2 of the Fc part of the antibody (of IgG and IgM only)

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47
Q

Which part of antibody do macrophages bind to?

A

Fc fragment, below the complement binding area

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48
Q

Which part of the antibody determines the isotype (ie IgG, IgM, IgD, IgE, IgA)? idiotype (ie unique antigen-binding pocket)?

A

Isotype –> determined by the Fc

Idiotype –> determined by Fab

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49
Q

opsonization vs neutralization vs complement activation:

A

opsonization - antibody promotes phagocytosis
neutralization - antibody prevents bacteral adherence
complement activation - antibody activates complement, enhancing opsoninzation and lysis

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50
Q

Main antibody in secondary/delayed response to an antigen, and most abundant antibody in blood?

A

IgG (t1/2 of IgG = 21 days; one reason it’s most abundant!)

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51
Q

Which antibodies can fix complement?

A

IgM and IgG

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52
Q

Which antibody can cross the placenta?

A

IgG

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53
Q

Which antibody is found in secretions (tears, saliva, mucus) and breast milk (“colustrum”)?

A

IgA

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54
Q

Which antibody is a monomer in circulation, but a dimer when secreted?

A

IgA

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55
Q

Which antibody is produced in primary/immediate response to an antigen?

A

IgM

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56
Q

Which antibody can exist as a pentamer (as well as a monomer)?

A

IgM

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57
Q

Which antibody mediates immediate/type I hypersensitivity reactions through release of histamine?

A

IgE

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58
Q

Which antibody mediates immunity to worms by activating eosinophils?

A

IgE

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59
Q

which antibody is in lowest concentration in serum?

A

IgE

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60
Q

Which blood types of mothers may lead to erythroblastosis fetalis and hemolytic disease of newborn?

A

Type O mothers; because in type O mothers, antibodies are mostly IgG, so can cross placenta and cause fetal hemolysis.
But, maternal blood types A and B: anti-A and anti-B antibodies are IgM, so can’t cross placenta…

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61
Q

3 complement pathways:

A

1) Classic: IgG or IgM mediated; form antigen-antibody complexes
2) Alternative: stimulated by spontaneous and microbe surface molecules
3) Lectin: mannose

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62
Q

Which 2 complement factors are involved in anaphylaxis?

A

C3a and C5a

63
Q

Which 2 complement factors are involved in opsonization of bacteria?

A

C3b and IgG

64
Q

What complement complex stimulates cytolysis by MAC?

65
Q

Hereditary angioedema: have increased bradykinin (so increased vasodilation and vascular permeability), episodes of painless, non-pitting, well-circumscribed edema

A

C1 esterase inhibitor deficiency (C1 esterase inhibitor prevents complement activation on self cells; but, in this case, it is deficient)

66
Q

recurrent pyogenic sinus and respiratory tract infections (esp S. pneum and H. infl), and increased susceptibility to type III hypersensitivity rxns (esp glomerulonephritis)

A

C3 complement deficiency

67
Q

Recurrent Neisseria bacteremia (N. gonococcal and N. meningococcal)

A

C5-C9 complement deficiency

68
Q

DAF (decay accelerating factor) deficiency may cause?

A

DAF is a complement inhibitor, meant to prevent complement activate on self-cells. If deficient, may lead to Paroxysmal Nocturnal Hemoglobinuria and to complement-mediated lysis of RBCs

69
Q

pro-inflammatory cytokines?

anti-inflammatory cytokines?

A

IL-1 and IL-6 –> pro-inflammatory

IL-10 and TGF-Beta –> anti-inflammatory

70
Q

functions IL-1 through IL-5

A

“Hot T-Bone stEAk”
IL-1: Hot –> pyrogen, fever, acute inflammation

IL-2: T –> stimulates growth of helper and cytotoxic T-cells (note: lots of immunosuppressants block IL-2)

IL-3: B–> stimulates Bone marrow stem cells (functions like GM-CSF = granulocyte macrophage colony stimulating factor)

IL-4:E –>stimulates class-switching to IgE and IgG. Also: induces differentiation into Th2 cells, and promotes growth of B cells

IL-5: A –> stimulates class-switching to IgA and stimulates eosinophil production (it’s the mucus-producing IL!); also: promotes differentiation of B cells.

71
Q

Which cytokines are secreted by macrophages?

A

IL-1, IL-6, IL-8, IL-12, TNF-gamma

72
Q

Which cytokines are secreted by all T-cells? by Th1 only? by Th2 only?

A
  • all T-cells secrete IL-3
  • Th1 secrete: IL-2, IFN-gamma
  • Th2 secrete: IL-4, IL-5, IL-10
73
Q

Which cytokine is the major chemotactic factor for neutrophils?

A

IL-8 (“clean up on aisle 8!” –> neutrophils come clear infections!)

74
Q

Interferons alpha, beta, and gamma functions:

A
  • all activate NK cells and kills virus-infected cells
  • alpha and beta –> inhibit viral protein synthesis
  • gamma –> stimulate MHC I and II expression and antigen presentation in all cells
75
Q

All T-cells express:

A
  • TCR (binds antigen-MHC complex)
  • CD3
  • CD28 (binds B7 on APC)
  • Th cells –> CD4 also
  • cytotoxic T-cells –> CD8
76
Q

CD19, CD20, CD21 –> all present on what cell type?

77
Q

CD14, CD16, and CD40 are present on what cell type?

A

Macrophages

78
Q

CD16, CD56 are present on what cell type?

A

NK cells (CD16 is also on macrophages; but CD56 is a unique marker for NK cells)

79
Q

How do superantigens work?

A

Superantigens (like from S. aureus, and Group A Strep) –> cross-link the TCR on T-helper cells to the MHC class II on APCs: So, get uncoordinated release of IFN-gamma from Th1 cells; IFN-gamma stimulates macrophages, so get release of IL-1, IL_6, and TNF-alpha from macrophages

80
Q

How do endotoxins/lipopolysaccharides work?

A

ie in gram (-) bacteria –> stimulate macrophages directly (Th cells not involved, unlike with superantigens) by binding to CD14 receptor –> release of acute phase cytokines (IL-1, IL-6, TNF-alpha)

81
Q

After exposure to which diseases/microbes should a person be given preformed/passive antibodies?

A

“To Be Healed Rapidly”

  • Tetanus toxin
  • Botulinum toxin
  • Hepatitis B
  • Rabies virus
    (also: should give RSV abs to premature babies born during winter months)
82
Q

What kind of immune response is induced by live attenuated vaccines? inactivated or killed vaccines?

A
  • live attenuated –> cellular response

- inactivated or killed –>humoral imunnity (weaker response; usually need booster shots)

83
Q

4 types of hypersensitivity reactions (briefly)

A 
"ACID" 
(types 1-3 = antibody-mediated) 
Type 1 - Anaphylactic and Atopic
Type 2 - Cytotoxic
Type 3 - Immune complex
Type 4 - Delayed (cell-mediatedd)
84
Q

What type of hypersensitivity reaction is this: anaphlaxic (“wheal and flare”), atopic; free-antigen cross-links IgE on pre-sensitized mast cells and basophils –> release of histamine, etc. How quickly does this reaction develop?

A

Type I –> happens very rapidly after antigen exposure to pre-formed antibody

85
Q

Hypersensitivity type: IgM, IgG bind fixed antigen on an “enemy” self cell –> lysis by complement or phagocytosis = cytotoxic

86
Q

Hypersensitivity type: Immune complex (antigen-antibody) activates complement–> neutrophils –> release lysosomal enzymes

87
Q

What type of hypersensitivity reaction is serum sickness?

A

type III: serum sickness–>antibodies to foreign proteins form over about 5 days –> form immune complexes –> deposit in membranes –> fix complement –> tissue damage

88
Q

fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure?

A

serum sickness (type III hypersensitivity)

89
Q

Arthrus reaction

A

Type III hypersensitivity reaction

  • test by immunofluorescent staining
  • intradermal injection of antigen induces antibodies–>form antigen-antibody complexes in the skin –> edema, necrosis, activation of complement
  • ex = swelling and inflammation following tetanus vaccine.
90
Q

Type IV hypersensitivity? How long does it take?

A
  • Delayed/T-cell-mediated
  • -> sensitized T-cells encounter antigen–> release lymphokines –> macrophage activation…
  • takes about 48 hours
  • 4 T’s:
  • T-lymphocytes
  • Transplant rejections
  • TB skin tests
  • Touching (contact dermatitis)
91
Q

Direct and Indirect Coombs’ test –> tests for what kind of hypersensitivity rxn?

A

Type II = antibody-mediated

92
Q

List 8 disorders/situations with type IV hypersensitivity:

A
  • diabetes - type I
  • multiple sclerosis
  • contact dermatitis
  • PPD
  • Hashimoto’s thyroiditis
  • Graft-vs-Host disease
  • Granulomatous inflammation
  • Guillain-Barre syndrome
93
Q

List 7 disorders/situations with type III hypersensitivity

A
  • Serum sickness
  • Arthus reaction
  • Post-Strep GN
  • SLE
  • Rheumatoid arthritis
  • Polyarteritis nodosum
  • Hypersensitivity pneumonitis (ie Farmer’s lung)
94
Q

List examples of type II hypersensitivity disorders/reactions

A
  • Anemias (hemolytic anemia, pernicious anemia)
  • erythroblastosis fetalis (Rh incompatibility)
  • acute hemolytic transfusion rxns
  • idiopathic thrombocytopenic purpura
  • rheumatic fever
  • Goodpasture’s syndrome
  • Bullous pemphigoid, Pemphigus vulgaris
  • Grave’s disease
  • Myasthenia gravis
95
Q

What type of hypersensitivty reaction is Goodpastures? PSGN?

A

Goodpastures–> type 2

PSGN–> type 3

96
Q

what type of hypersensitivity rxn is Grave’s disease? Hashimoto’s?

A

Graves–>type 2

Hashimoto’s –> type 4

97
Q

ANA (anti-nuclear antibodies)

A
  • SLE

- nonspecific (Sjogren’s, scleroderma, polymyositis, dermatomyositis, rheumatoid arthritis,juvenile arthritis, MCTD)

98
Q

anti-dsDNA, anti-Smith

A

SLE (anti-dsDNA=specific for renal disease)

99
Q

anti-IgG antibodies

A

=Rheumatoid facor = IgM antibodies that attack IgG –> Rheumatoid arthritis

100
Q

antimitochondrial antibodies

A

primary biliary cirrhosis

101
Q

anti-desmoglein antibodies

A

pemphigus vulgaris

102
Q

anti-microsomal, anti-thyroglobulin antibodies

A

Hashimoto’s thyroidits

103
Q

anti-Jo-1 antibodies

A

polymyositis, dermatomyositis

104
Q

anti-SS-A antibodies

A

=anti-Ro antibodies –> Sjogrens

105
Q

anti-SS-B antibodies

A

=anti-La –> Sjogrens

106
Q

anti-U1-RNP (ribonucleoprotein)

A

mixed connective tissue disease

107
Q

anti-smooth muscle antibodies

A

autoimmune hepatitis

108
Q

anti-glutamate decarboxylase antibodies

A

type 1 diabetes

109
Q

anti-TSH receptor antibodies

110
Q

anti-Ach receptor antibodies

A

Myasthenia gravis

111
Q

p-ANCA antibodies

A

Vasculitides:

  • microscopic polyangitis
  • churg-strauss syndrome
112
Q

Boys with recurrent bacterial infections after 6 months, B-cell deficient, and deficient in all classes of Ig’s. What’s the condition and what gene is defective?

A

Bruton’s agammaglobulinemia; defect in BTK, a tyrosine kinase gene. can form pro-B cells, but not beyond that. X-linked recessive, so increased in males

113
Q

Defect in BTK gene

A

BTK = a tyrosine kinase gene –> defect = Bruton’s agammaglobulinemia

114
Q

Defect that causes hyper-IgM syndrome?

A

defective CD40L on helper T-cells–> can’t class switch

115
Q

anaphylaxis on exposure to blood products with IgA; and: sinus and lung infections, milk allergies, and diarrhea…

A

Selective Ig deficiency, usually to IgA

-caused by a defect in isotype switching to a specific class

116
Q

normal # of B cells, but decreased plasma cells, decreased Immunoglobulin…

A

Defect in B-cell maturation –> CVID = common variable immunodeficiency

117
Q

22q11 deletion

A

90% of pts with DiGeorge syndrome (thymic aplasia) –> failure to develop 3rd and 4th pharyngeal pouches (so, no thymus)

118
Q

absent thymic shadow

A
  • DiGeorge syndrome (thymic aplasia)

- SCID

119
Q

tetany, recurrent viral infections, congenital heart and great vessel/aortic arch defects, cleft palate, mandible deformities…

A

DiGeorge syndrome = thymic aplasia: no thymus or parathyroids, so: deficient T-cells, PTH, Calcium
-absent thymic shadow on CXR

120
Q

Disseminated mycobacterial infections, decreased levels of IFN-gamma

A

IL-12 receptor deficiency –> so decreased Th1 response –> decreased IFN-gamma secretion

121
Q

Job’s syndrome

A

=Hyper-IgE syndrome

  • Th cells don’t produce IFN-gamma –> neutrophils can’t respond to chemotactic stimuli
  • increased levels of IgE
  • presentation = FATED:
  • -coarse Facies
  • -non-inflamed staph Abscesses
  • -retained primary Teeth
  • -increased IgE
  • -Dermatological problems = eczema
122
Q

Abscesses + still have primary teeth + eczema + high levels of IgE

A

think Job’s syndrome = Hyper-IgE syndrome

123
Q

Recurrent infections, Chronic diarrhea, FTT; have NK cells, but no B or T cells

A 
SCID
Variable causes:
-defective IL-2 receptor (most common, X-linked)
-Adenosine Deaminase deficiency
-failture to synthesize MHC II antigens
124
Q

Most common cause of SCID?

A

-defective IL-2 receptor (X-linked)

125
Q

Cerebellar deficits + spider angiomas + IgA deficiency (so increased risk of sinopulmonary infections)

A

=Triad of symptoms in Ataxia-telangiectasia:

  • cerebellar deficits =ataxia
  • spider angiomas = telangiectasia
  • IgA deficiency

–>d/t defects in ATM (Ataxia Telangiectasia Mutated) gene, which codes for DNA repair mechansims –> so, also hypersensitive to x-ray radiation, b/c causes chromosomal breaks

126
Q

In which immune deficiency are patients hypersensitive to X-ray radiation (b/c it causes chromosomal breaks)?

A

Ataxia-Telangiectasia –> mutation in ATM gene, which codes for DNA repair enzymes

127
Q

Thrombocytopenic purpura, recurrent pyogenic Infections, Eczema; Low IgM

A

Triad of symptoms in Wiskott-Aldrich syndome –> “TIE” = Thrombocytopenic purpura, Infections, Eczema

  • X-linked recessive
  • get progressive deletion of B and T cells
  • decreased IgM; increased IgE and IgA
128
Q

Defect in LFA-1 integrin/CD18 protein; poor wound healing – no pus formation, delayed separation of umbilicus

A

Leukocyte adhesion deficiency (type 1)

–>defect in LFA-1 integrin (CD18) protein on phagocytes

129
Q

recurrent infections with staph and strep, partial albinism, peripheral neuropathy/neuro defects; defect in LYST gene

A

Chediak-HIgashi syndrome:

  • autosomal recessive
  • defect in LYST: lysosomal trafficking regulator gene
  • microtubule dysfunction in phagosome-lysosome fusion
  • see abnormal giant lysosomal inclusions on LM of peripheral smear
130
Q

absent respiratory burst in neutrophils, increased susceptibility to catalase positive organisms (ie S. aureus, E. coli, Aspergillus, Serratia, Nocardia…); negative nitroblue tetrazolium dye reduction test

A

Chronic granulomatous disease

131
Q

vascular fibroid necrosis, neutrophil infiltration, and infarction of graft within minutes after a transplant:
-what type of hypersensitivity reaction is this?

A

Hyperacute transplant rejection: antibody-mediated (type II hypersensitivity) d/t prefored anti-donor antibodies in the recipient

132
Q

Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate, weeks after a transplant:
-is this reversible?

A

Acute transplant rejection

  • cell-mediated: Cytoplasmic T-cells reacting against foreign MHCs
  • can reverse with immunosuppressants
133
Q

obliterative vascular fibrosis; fibrosis of graft tissue and blood vessels, months to years after a transplant:
-is this reversible?

A

Chronic transplant rejection

  • cytoplasmic T-cells see non-self-MHC I as self-MHC I presenting a non-self antigen–> get T-cell and antibody-mediated vascular damage
  • irreversible
134
Q

Maculopapular rash, jaundice, hepatosplenomegaly, diarrhea at variable point after a transplant:

  • what’s the pathogenesis?
  • what types of transplants is this most common in?
A
  • Graft-vs-Host disease
  • usually follows a bone marrow or liver transplant (b/c they’re organs rich in lymphocytes)
  • Pathogenesis: grafted immunocompetent T-cells proliferate in the irradiated immunocompromised host/pt –> graft cells reject cells with “foreign” proteins (ie self) –> get severe organ dysfunction
135
Q

Which immunosuppressant drug is a precursor of 6-mercaptopurine?

A

Azathioprine

136
Q

Mannitol diuresis may prevent nephrotoxicity caused by what immunosuppressant drug?

A

Cyclosporine

137
Q

Which immunosuppressant drug is a monoclonal antibody that binds to CD3 on T-cells?

A

Muromonab-CD3 (OKT3)

138
Q

Which immunosuppressant drug is a monoclonal antibody that binds IL-2 receptor on activated T-cells?

A

Daclizumab

139
Q

Which immunosuppressant drug inhibits IMP (inosine monophosphate dehydrogenase)?

A

Mycophenolate

140
Q

Which immunosuppressant drug inhibits calcineurin–>loss of IL-2 production –> blockage of T-cell differentiation and activation?

A

Cyclosporine

141
Q

Which immunosuppressive drug binds FK-binding protein–> get loss of IL-2 production?

A

Tacrolimus

142
Q

Which immunosuppressive drug inhibits mTOR (mammalian target of rapamycin)–> inhibits T-cell production?

A

Sirolimus (rapamycin)

143
Q

Which immunosuppressive drug is metabolized by xanthine oxidase, so allopurinol increases its toxicity?

A

Azathioprine

144
Q

Clinical use of Filgrastim and Sargramostim?

A
  • ->recombinant cytokines, used to treat post-chemo patients for recovery of bone marrow
  • Filgrastim =granulocyte-colony-stimulating factor
  • Sargramostim =granulocty-macrophage colony stimulating factor
145
Q

Clinical use for recombinant erythropoietin?

A

Anemias, especially:

  • renal failure –> because EPO comes from kidneys
  • pts undergoing chemo
146
Q

clinical use for recombinant alpha-interferon?

A
  • Hepatitis B and C
  • Kaposi’s sarcoma
  • Leukemias
  • Malignant melanoma
147
Q

clinical use for recombinant Beta-interferon?

A

Multiple sclerosis

148
Q

clinical use for recombinant gamma-interferon?

A

Chronic granulomatous disease

149
Q

Infliximab: target? uses?

A

anti-TNF-alpha

-used to treat: Crohn’s disease, Rheumatoid arthritis, Psoriatic Arthritis, Ankylosing spondylitis

150
Q

Adalimumab: target? uses?

A

anti-TNF-alpha

-used to treat: Crohn’s disease, Rheumatoid arthritis, Psoriatic arthritis

151
Q

Abciximab: target? uses?

A

targets Glycoprotein IIb/IIIa

-clinical uses: prevent cardiac ischemia in unstable angina, and in pts treated with percutaenous coronary intervention

152
Q

Herceptin = Trastuzumab: target? clinical use?

A
  • targets erb-B2

- used to treat HER-2-overexpressing breast cancer

153
Q

Rituximab: target? uses?

A
  • targets CD20 (so, B-cells!)

- used to treat B cell-non Hodgkin’s lymphoma

154
Q

Omalizumab: target? uses?

A
  • targets IgE

- used as an additional line of treatment for severe asthma

FirstAID (24 decks)

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