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Symptoms Midterm > Gout drugs > Flashcards

Gout drugs Flashcards

1
Q

Blocks formation of uric acid

A

allopurinol

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2
Q

Breaks down uric acid

A

Pegloticase

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3
Q

Increases excreation of uric acid in urine

A

Probenecid

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4
Q

reduces degree of inflammation in pts from gout crystal depois

A

steroids, indomethacin, Colchicine

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5
Q

Goals of gout tx

A

• Increase excretion of uric acid • Inhibit inflammatory cells • Inhibit uric acid biosynthesis • Provide symptomatic relief – Typically with NSAIDS or steroids (short-term)

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6
Q

Why is aspirin contraindicated in tx of gout

A

dose depended effect: low dose see decreased uric acid excreation large dose: see increase uric acid excreation via blocking reabsorpiton by interaction with OAT transporter

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7
Q

A patient that cannot take a NSAID for relief to acute gout symptoms has the following options

A

• Wait until symptoms subside (usually within a few days, in some cases longer) • Take low dose colchicine (within 48 hrs of attack) • Intraarticular glucocorticoid injections • Take celecoxib Low dose oral steroids

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8
Q

What do the following have in common: • Methotrexate • Sulfasalazine • Hydroxychloroquine • Azathioprine • N-penicillamine • Mycophenolate mofetil • Leflunomide

A

NON-Biological DMARDs

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9
Q

What do the following have in common: • Etanercept • Infliximab • Adalimumab • Rituximab • Anakinra • Abatacept • Tocilizumab • Belimumab • Apremilast • Tofacitinib • Secukinamab • Ustekinumab

A

Biological DMARDS

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10
Q

are a class of drugs which includes monoclonal antibodies, receptor analogues, and chimeric small molecules designed to bind to or mimic their molecular targets

A

biologics

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11
Q

Advantages of biological DMARDS

A

advantages over conventional therapy in terms of potency, specificity, and theoretically decreased side effects, since the product is engineered to bind to or interfere with a distinct molecular target

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12
Q

blocks the co-stimulation of T cells.

A

Abatacept

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13
Q

____and____ inhibit the proliferation and activity of T cells and B cells.

A

Methotrexate leflunomide

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14
Q

Etanercept, infliximab, adalimumab, golimumab, and certolizumab work by:

A

inactivate TNF - α.

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15
Q

____blocks the action of IL-1, and_____ inactivates IL-6.

A

Anakinra tocilizumab

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16
Q

that inhibit T-cell activation and IL-2 production by regulation of gene transcription.

A

glucocorticoids

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17
Q

– irreversibly binds to and inhibits dihydrofolate reductase, resulting in inhibition of purine and thymidylic acid synthesis, thus interfering with DNA synthesis, repair, and cellular replication.

A

Methotrexate

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18
Q

– metabolized to sulfapyridine and 5-aminosalicylic acid; Mechanism not known but IgA and IgM rheumatoid factor production are decreased. In vitro suppression of T-cell activation and inhibition of B-cell proliferation; inhibit the release of inflammatory cytokines

A

Sulfasalazine

19
Q

– Mechanism unclear. suppression of T-lymphocyte responses to mitogens, decreased leukocyte chemotaxis, stabilization of lysosomal enzymes, inhibition of DNA and RNA synthesis, and the trapping of free radicals.

A

Hydroxychloroquine

20
Q

– cleaved to 6-mercaptopurine, which in turn is converted to additional metabolites that inhibit de novo purine synthesis; Cell proliferation thereby is inhibited, impairing a variety of lymphocyte functions

A

Azathioprine

21
Q

– Chelates with lead, copper, mercury and other heavy metals to form stable, soluble complexes that are excreted in urine; depresses circulating IgM rheumatoid factor, depresses T-cell but not B-cell activity;

A

N-penicillamine

22
Q

– converted to active metabolite that inhibits inosine monophosphate dehydrogenase, leading to suppression of T- and B-lymphocyte proliferation

A

Mycophenolate mofetil

23
Q

– undergoes rapid conversion to its active metabolite, A77-1726. This metabolite inhibits dihydroorotate dehydrogenase, leading to a decrease in ribonucleotide synthesis and the arrest of stimulated cells in the G1 phase of cell growth. inhibits T-cell proliferation and production of autoantibodies by B cells.

A

Leflunomide

24
Q

MOA of Sirolimus

A

inhibition of IL-2 REceptor signaling

25
Q

What do Ciclosporin and Tacrolimus do?

A

inhbition of IL-2 Expression

26
Q

What does Sulfasalazine, Hydroxycloroquine and Thalidomide have in common?

A

all inhbit excpression of TNF allpha and other cytokines

27
Q

MTX, azothioprine and Mycophenolate mofetil all ahve what in common?

A

inhibit de novo purine synthesis

28
Q

umab

momab

ximab

zumab

mean what?

A

human: umab

murine = momab

chimeric = ximiab

humanized = zumab

29
Q

PharmakoK of MABs

do they cross teh BBB??

dif between SubQ, IM and IV bioavalability

A

• Administration and Absorption
– Subcutaneous- 24-95% bioavailability – Intramuscular-24-95% bioavailability – Intravenous-100% bioavailability

• Distribution
– Extracelluar
– Do not cross blood brain barrier

30
Q

catabolsim and elemination of antibodies

A

catabolism via proteolysis in biological fluids, uptake via endocytosis and catabolism via target tissue

renal and biliary emilnation unimportant

IF human derived have LONGER half life (end in umab or zumab)

31
Q

In general, what is mechanism for longer biological half life for human MABs vs mouse MABs?

A
  • Concept of neonatal Fc receptor (FcRn) for IgG
  • Transfers passive immunity from mother to fetus
  • Role for FcRn to protect IgG from degradation throughout life

Mouse IgG does not bind FcRn and Fab or F(ab)2 antibody fragments lack Fc region-do not bind FcRn

32
Q

What do these drugs have in common?

Infliximab

Adalimumab

Etanercept

A

inhibit TNF-a

33
Q

What is the MOA of Therapeutic antibodies?

A
  • Antagonism or neutralization
  • Antibody binds and inactivates a soluble antigen
  • Antibody acts a competitive inhibitor of ligand binding to cellular receptor
34
Q

B lymphocyte stimulator (BLyS or BLSP), also known as B cell-activating factor (BAFF), is the

A

costimulator for B-cell survival and function.

35
Q

_____is a monoclonal antibody directed against BLyS. Specific binding to soluble BLyS prevents the interaction of BLys with it receptor and decreases the B-cell survival and production of autoantibodies

A

Belimumab

36
Q

a humanized anti-human interleukin (IL)-6 receptor antibody

competes for both the membrane-bound and the soluble forms of human IL-6 thereby inhibiting the binding of the native cytokine to its receptor and interfering with the cytokine’s effects

A

Toclizumab

37
Q

MOA of rituximab

A

A. Complement-dependent cytotoxicity (CDC)

B. Antibody-dependent cellular cytotoxicity (ADCC)

38
Q

Antibody binds cell surface antigen on target cell

Fc region binds complement protein and activates complement system resulting in cell lysis

A

Complement-dependent cytotoxicity (CDC)

39
Q
  • Antibody binds cell surface antigen on target cell
  • Fc region binds Fc receptors on NK cell, neutrophil or macrophage
  • Results in lysis or phagocytosis of target cell by immune cell
A

Antibody-dependent cellular cytotoxicity (ADCC)

40
Q

Adverse effects of Therapeutic Antibodies

A
  • Generally safe and well tolerated
  • Immunogenicity: generation of endogenous

antibodies against the therapeutic antibody

– Concerns

  • neutralizes the effect of therapeutic antibody
  • Hypersensitivity reaction-either localized to injection site or systemic
41
Q

Write in order the antiB that have the greatest potential for immunogenicity:

  • Omab (mouse)
  • Zumab (humanized)
  • Umab (full human)
  • Ximab (chimeric)
A

potential for immunogenicity is less for more human

omab (mouse)> ximab (chimeric) > zumab (humanized) > Umab (human)

42
Q

MOA of Abatacept

A

– After a T cell has engaged an antigen- presenting cell (APC), a second signal is produced by CD28 on the T cell that interacts with CD80 or CD86 on the APC, leading to T-cell activation.

– Abatacept (contains the endogenous ligand CTLA-4) binds to CD80 and 86, thereby inhibiting the binding to CD28 and preventing the activation of T cells.

treatment of patients with rheumatoid arthritis who have had an inadequate response to other drugs

43
Q

Recombinant protein that it is an competitive antagonist of the interleukin-1 (IL-1) receptor

Subq administration

A

Anakinra

44
Q

Treatment of moderately- to severely- active RA in adult patients who have failed one or more DMARDs; may be used alone or in combination with DMARDs

A

Anakinra

Symptoms Midterm (12 decks)

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