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Immunology > McPhail Exam 4 > Flashcards

McPhail Exam 4 Flashcards

1
Q

Mechanism of methotrexate

A

inhibits dihydrofolate reductase, which is involved in the de novo synthesis of thymine. Also causes the release of adenosine into the bloodstream and tissues, which has anti-inflammatory effects

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2
Q

Methotrexate interaction

A

NSAIDs increase the blood concentrations of methotrexate

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3
Q

What is the active metabolite of leflunomide

A

A77 1726

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4
Q

A77 1726 mechanism

A

inhibits dihydro-orotate dehydrogenase, which is required for pyrimidine biosynthesis. It also inhibits tyrosine kinase, which would interfere with T and B cell proliferation. The cells become non-responsive to cytokines and inflammatory signals.

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5
Q

Thalidomide mechanism

A

reported to decrease circulating TNF-a in patients with erythema nodosum leprosum but increase it in patients who are HIV seropositive

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6
Q

Methotrexate indication

A

Rheumatoid arthritis

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7
Q

Leflunomide indication

A

Rheumatoid arthritis

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8
Q

Thalidomide indication

A

erythema nodosum

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9
Q

Echinacea mechanism

A

has no direct antibacterial activity, but stimulates the innate immune system by increasing phagocytosis and the release of TNFs and interferons from macrophages and T cells

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10
Q

Levamisole class

A

Immunorestorative agents/immunostimulants

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11
Q

Levamisole mechanism

A

Mimics thymic hormone thymopoietin, which is probably why it’s effective. Restores depressed immune function of B cells, T cells, monocytes, and macrophages caused by chemotherapy.

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12
Q

Imiquimod mechanism

A

toll like receptor 7 agonist that stimulates the immune system to produce interferon-α and other cytokines (IL-1,6,8,10,12, TNF-α) and activates macrophages, NK cells, TH¬1 cells, and B cells

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13
Q

Vaccine definition

A

suspensions of attenuated or dead microorganisms administered for prevention amelioration, or treatment of infectious diseases

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14
Q

What type of T cells do vaccines stimulate

A

TH2

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15
Q

Killed (inactivated) pathogens

A

denaturing disinfectant kills pathogen, allows recovery of the surface antigens, but this risks losing antigenicity

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16
Q

Live/attenuated pathogens

A

pass the pathogen through many generations of host animals to yield low virulent strain. Some viruses are too dangerous even at low virulence and they can regain virulence.

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17
Q

Live/attenuated related strain

A

cowpox virus used in place of smallpox virus

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18
Q

Cellular antigen from a pathogen

A

isolate the surface antigen from the pathogen, purify it and reconstitute into a vaccine preparation

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19
Q

Genetically engineered pathogens

A

clone a piece of DNA encoding the surface antigen from the pathogen and over produce the antigen. This way you don’t have to expose workers to the pathogen and lower risk.

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20
Q

Simple vaccine

A

contains only one kind of antigen or strain

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21
Q

Multivalent vaccine

A

contains two or more kinds of antigens or strains that cause the same disease

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22
Q

Polyvalent vaccine

A

contains two or more kinds of antigens or strains that cause different diseases

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23
Q

Single-dose vaccine

A

needed only once during lifetime

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24
Q

Multiple-dosing regimen

A

several doses needed to get full protection

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25
Q

Booster dose

A

needed to bolster/reinforce protection after some time

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26
Q

Co-administered vaccine

A

only if they don’t interfere with each other

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27
Q

Viral vaccines examples

A

smallpox, influenza, polio, chickenpox, rubella, hepatitis, measles, rotavirus, mumps, HPV

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28
Q

Bacterial vaccines examples

A

pertussis, tuberculosis, meningococcal, cholera, haemophilus influenza type B, pneumococcal

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29
Q

Toxoids

A

denatured pathogens the bacteria would produce

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30
Q

What are the two subtypes of antibodies?

A

immunoglobulins (polyclonal) and monoclonal antibodies

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31
Q

What are the two major uses for antibodies in the treatment of human disease?

A

to neutralize and eliminate toxic molecules or to eliminate target cells

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32
Q

What are the four ways antibodies can eliminate target cells?

A

antibody-mediated cell growth control (bound antibodies block binding of growth factors)
antibody-mediated reticuloendothelial clearance aka macrophage system (antibody-costed target cells can be engulfed by phagocytes)
complement-mediated cytotoxicity aka CMC (IgG and IgM binding to cells elicits complement, leading to the formation of a membrane attack complex)
antibody-dependent cell-mediated cytotoxicity aka ADCC (large cells can be killed by cytotoxic substances released by macrophages and killer cells)

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33
Q

human immunoglobulin examples

A

rabies, tetanus, hepatitis B, rho

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34
Q

Digibind origin

A

Fab fragment of the IgG isolated from sheep immunized against digoxin

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35
Q

Digibind mechanism

A

It tightly binds digoxin, shifting the equilibrium away from drug receptor complex formation

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36
Q

What are the two types of anti-thymocyte globulin and what is the difference?

A

Thymoglobulin is from rabbits

Atgam is from horses

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37
Q

Indication for anti-thymocyte globulin

A

Rejection of transplanted kidney, aplastic anemia in patients who are not suitable for bone marrow transplant, interim treatment until bone marrow transplant

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38
Q

anti-thymocyte globulin mechanism

A

depletes circulating T-lymphocytes by direct killing, blocks lymphocyte function by binding to cell surface molecules involved in the regulation of cell function, which suppresses the cascade of immune cells.

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39
Q

monoclonal antibody definition

A

an antibody synthesized from a single clone of B-lymphocytes or plasma cells

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40
Q

polyclonal antibody definition

A

multiple immunoglobulins responding to different epitopes on an antigen molecule

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41
Q

chimeric antibody

A

66% human

constant region from human, antigen-binding region from mouse

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42
Q

humanized antibody

A

> 90% human

only specific antigen binding sites (sugar fragments) from mice

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43
Q

How do we make chimeric/humanized/fully human antibodies?

A

recombinant genetic engineering

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44
Q

amab

A

rat

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45
Q

emab

A

hamster

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46
Q

imab

A

primate

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47
Q

omab

A

mouse

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48
Q

umab

A

human

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49
Q

ximab

A

chimerized

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50
Q

zumab

A

humanized

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51
Q

Indication for MAbs that attach to a T cell receptor

A

used to stop rejection of transplanted organs

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52
Q

What compounds did we cover that attach to a T cell receptor

A

muromonab-CD3 (OKT3), basiliximab, belatacept

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53
Q

OKT3 generic

A

muromonab-CD3

54
Q

OKT3 mechanism of action

A

Interacts with the CD3 marker of human T cells and flags them for destruction. Decreases T cell numbers in the blood within minutes

55
Q

Basiliximab mechanism of action

A

binds to the IL-2 receptor of activated T cells as a competitive antagonist

56
Q

Mechanism of action for belatacept

A

cytotoxic T lymphocyte associated antigen 4 (CTLA4) interrupts CD28 costimulation of T cell, resulting in an attenuation of interleukin 2 and interleukin 2 receptor (T cell anergy) and arrest of T cells at the G1 phase of the cell cycle (T cell apoptosis). Belatacept is a soluble recombinant fusion protein that mimics CTLA4

57
Q

What MAbs did we cover for lymphomas?

A

rituximab, alemtuzumab, brentuximab vedotin, tositumomab I-131, and Y-90-labeled ibritumomab tiuxetan

58
Q

Indications for rituximab

A

cancer, follicular lymphoma, Wegener’s granulomatosis, and microscopic polyangiitis

59
Q

Rituximab mechanism of action

A

binds to CD20, which is distributed on more than 90% of B cell non-Hodgkin’s lymphomas but also present on normal B cells. However, since the cancer results in an overproduction of B cells, more of them are wiped out than the normal B cells.

60
Q

Indication and target for alemtuzumab

A

indication: B-cell chronic lymphocytic leukemia
target: CD52

61
Q

Bentuximab vedotin indication

A

Hodgkin’s lymphoma and systemic anaplastic large cell lymphoma

62
Q

Three components of bentuximab vedotin

A

The chimerized IgG1 antibody cAC10, specific for human CD30
The microtubule disrupting agent MMAE
A protease-cleavable linker that covalently attaches MMAE to cAC10

63
Q

Bentuximab vedotin mechanism of action

A

CD30 is prevalent in HL and sALCL but has limited expression in healthy cells. Binding of brentuximab to CD30 on the cell surface initiates internalization of the ADC-CD30 complex. Inside the cell, MMAE is released via proteolytic cleavage. Binding of released MMAE to tubulin disrupts the microtubule network, which interferes with cell division, inducing apoptotic cell death.

64
Q

Tositumomab I-131 target

A

CD20

65
Q

Tositumomab mechanism of action

A

induces normal immunological reactions and radioimmunoconjugates deliver cytotoxic ionization radiation. High energy beta particles emitted by I-131 are cytotoxic over distances of about 1-2mm, therefore also kills cells that are inaccessible to the antibody.

66
Q

Y-90-labeled ibritumomab tiexetan target

A

CD20

67
Q

HER2

A

an oncogene in breast cancer that stimulates cell division

68
Q

Anti-HER2 MAbs

A

Tratuzumab, Ado-tratuzumab emtansine

69
Q

Trastuzumab mechanism of action

A

Anti-HER2 antibodies inhibit HER2-mediated signaling in cancer cells by blocking the extracellular receptor of HER2/neu, ultimately upregulating the levels and activity of p27 (Kip1) protein (an important cell dependent kinase (Cdk) inhibitor), which leads to cell cycle G1 arrest and growth inhibition.
At least six signaling targets and pathways are modulated by trastuzumab

70
Q

mechanism of emtansine/DM1

A

a maytansinoid that disrupts microtubule function

71
Q

MAbs that bind to epidermal growth factor receptor

A

Cetuximab, panitumumab

72
Q

Indication for cetuximab and panitumumab

A

EGFR expressing metastatic colorectal cancer (after disease progression following all available chemotherapy regimens).

73
Q

cetuximab and panitumumab mechanism of action

A

prevents ligand binding at the epidermal growth factor receptor, which inhibits cancer cell growth

74
Q

MAbs for rheumatoid arthritis and Crohn’s disease

A

infliximab, adalimumab, tocilizumab, etanercept

75
Q

Infliximab mechanism of action

A

binds to both free and membrane bound TNF-α. Blocking TNF-α slows the progression of the disease

76
Q

infliximab indications

A

rheumatoid arthritis, Crohn’s disease, and ankylosing spondylitis

77
Q

adalimumab target

A

TNF-alpha

78
Q

tocilizumab target

A

IL-6 receptor

79
Q

etanercept mechanism of action

A

binds TNF-α, slowing down/stopping joint damage by preventing it from binding to immune cells

80
Q

MAbs for asthma and allergic rhinitis

A

omalizumab, mepolizumab

81
Q

omalizumab mechanism of action

A

selectively binds to circulating IgE, so prevents binding of IgE to mast cells and other effector cells. Without surface-bound IgE, these cells are unable to recognize allergens, so prevents cellular activation by antigens and the subsequent allergic reactions

82
Q

mepolizumab target

A

IL-5 receptor on eosinophils

83
Q

efalizumab indication

A

psoriasis

84
Q

efalizumab mechanism of action

A

Inhibits the interaction of CD11a (LFA-1) with various ICAM molecules. Because ICAM-1 (CD54) is expressed on activated endothelial cells and antigen presenting cells (APCs), the antibody inhibits both the APC-T cell interaction and the T cell adhesion to endothelial cells, preventing trans-endothelial migration so immune cells can’t get into the tissues

85
Q

Interferon alpha 2b indications

A

Hairy cell leukemia, malignant melanoma, follicular lymphoma, Kaposi’s sarcoma, chronic hepatitis B, Roferin-A also has the indication of Chronic Granulomatous Disease

86
Q

Interferon beta-1a indications

A

neurological exacerbations in relapsing-remitting multiple sclerosis

87
Q

Interferon beta-1b indications

A

neurological exacerbations in relapsing-remitting MS

88
Q

How does commercial IL-2 differ from natural IL-2

A

commercial IL-2 differs from native IL-2 in that it’s not glycosylated, has no terminal alanine, and a serine is substituted for cysteine-125 (serine has an OH and cysteine has an SH)

89
Q

IL-2 indications

A

cancer, especially metastatic renal cell carcinoma

90
Q

IL-11 indications

A

following myelosupressive chemotherapy in patients with nonmyeloid malignancies

91
Q

Effects on anakinra

A

When given alone or in combination with methotrexate it improves clinical signs and symptoms, decreases radiographic progression, improves patient function, decreases pain and fatigue, and slows bone erosion and degradation of the joint.

92
Q

Target for anakinra

A

blocks the binding of IL-1

93
Q

growth factor definition

A

control the expansion, proliferation, and differentiation of myeloid cells

94
Q

G-CSF

A

granulocyte colony stimulating factor

95
Q

M-CSF

A

macrophage colony stimulating factor

96
Q

GM-CSF

A

granulocyte macrophage colony stimulating factor

97
Q

Multi-CSF

A

multi-lineage colony stimulating factor

98
Q

EPO

A

erythropoietin

99
Q

TPO

A

thrombopoietin

100
Q

What produces/secretes CSFs

A

activated T cells or macrophages

101
Q

What produces/secretes erythropoietin

A

endothelial cells and fibroblasts

102
Q

What is the difference between filgrastim and pegfilgrastim?

A

pegfilgrastim has polyethylene glycol attached

103
Q

mechanism of action of the G-CSF analogs

A

stimulates the bone marrow to produce more white blood cells

104
Q

G-CSF analog examples

A

filgrastim, pegfilgrastim

105
Q

G-CSF analog indication

A

neutropenia due to non-myeloid cancer chemotherapy or severe chronic neutropenia or after bone marrow transplant

106
Q

G-CSF risk

A

could promote growth of malignant myeloid cells in blood cancers

107
Q

GM-CSF examples

A

sargramostim, erythopoietin

108
Q

sargramostim indication

A

autologous bone marrow replacement

109
Q

sargramostim mechanism

A

hastens myeloid reconstitution

110
Q

epoetin alfa indications

A

kidney dialysis, chemotherapy in non-myeloid malignancies

111
Q

Difference between epoetin alfa and darbepoetin alfa

A

Darbepoetin alfa differs from epoetin alfa by having two extra carbohydrate chains, which gives it greater metabolic stability – it has a three-fold longer half-life

112
Q

Indications for darbepoetin alfa

A

anemia associated with chronic renal failure, cancer chemotherapy

113
Q

induction of immunosuppression

A

Medications given immediately after transplantation in intensified doses for the purpose of preventing acute rejection (up to 30 days)
Not used for long-term for immunosuppressive maintenance
Includes methylprednisolone, atgam, thymoglobulin, OKT3, and basiliximab

114
Q

maintenance of immunosuppression

A

Medications given before, during or after transplant with the intention to maintain them long-term
Maintenance immunosuppression does not include any immunosuppressive medications given to treat rejection episodes or for induction of immunosuppression
Includes prednisone, cyclosporine, tacrolimus, mycophenolate mofetil, azathioprine, or rapamycin

115
Q

anti-rejection immunosuppression

A

Medications given for the purpose of treating an acute rejection episode during the initial post-transplant period or during a specific follow up period, usually up to 30 days after the diagnosis of acute rejection
Includes methylprednisolone, atgam, OKT3, thymoglobulin, and basiliximab

116
Q

role of analgesics in treating RA

A

relieve pain

117
Q

role of NSAIDs in treating RA

A

relieve pain and reduce inflammation

*only stops the prostaglandin inflammation process, the other pathways keep going

118
Q

role of steroids in treating RA

A

relieve pain and reduce inflammation

119
Q

role of DMARDs in treating RA

A

reduce pain, swelling, and tenderness as well as slow joint damage

120
Q

role of biologic medicines in treating RA

A

targeted treatment to relieve pain and swelling and slow joint damage

121
Q

old treatment for RA

A

used to relieve symptoms until it got too bad then address the disease

122
Q

new treatment for RA

A

treat to stop it from progressing as far as the patient gets older

123
Q

RA pathophysiology

A

Activated T cells stimulate macrophages and fibroblast-like synoviocytes. These generate proinflammatory mediators and proteases, which induces a synovial inflammatory response and destroys the cartilage and bone. Proinflammatory cytokines released by synovial macrophages include TNF-α, IL-1, 6, 12, 15, 18, and 23.

124
Q

Biologic agents whose main indication is RA

A

infliximab, adalimumab, ankinra, rituximab, tocilizumab, etanercept

125
Q

nonpharmacological treatments for RA

A

exercise, diet (less animal products and more leaves), stress reduction, physical therapy, and surgery

126
Q

Medication based therapies for RA

A

NSAIDs, nonbiologic and biologic DMARDs, immunosuppressants, and corticosteroids

127
Q

Comparison of DMARDs and biologics in regards to deliver method

A

DMARDs are usually oral, and methotrexate is usually given just once a week. Biologics are usually injected under the skin or given IV, and administration ranges from daily to monthly

128
Q

Comparison of DMARDs and biologics in regards to drug target

A

DMARDs target the entire immune system, while biologics work by targeting specific steps in the inflammatory process.

129
Q

Comparison of DMARDs and biologics in regards to response time

A

it can take months before it is known whether a DMARD is working. With biologics, results are likely seen within 4-6 weeks, after just a few treatments. In the meantime, an NSAID or a steroid medication may relieve pain and swelling.

130
Q

Comparison of DMARDs and biologics in regards to risks

A

both DMARDs and biologics can increase risk for infections. Serious infections, such as pneumonia, are the biggest risk of taking a biologic.

Immunology (4 decks)

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