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Symptoms > Joint Pain Pharmacology > Flashcards

Joint Pain Pharmacology Flashcards

1
Q

Drugs to know for the exam?

A
  • Etanercept
  • Allopurinol
  • Adalimumab
  • Belimumab
  • Colchicine
  • Tocilizumab
  • Probenecid
  • Tofacitinib
  • Pegloticase
  • Abatacept
  • Rituximab
  • Febuxostat
  • Steroid
  • NSAIDs
  • Methotrexate
  • Anakinra
  • Infliximab
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2
Q

Match the following drugs with site of action:

  • Colchicine
  • Indomethacin
  • Allopurinol
  • Probenecid
  • Glucocorticoid (Steroid)
  • Pegloticase
A
  • Colchicine - D
  • Indomethacin - D
  • Allopurinol - A
  • Probenecid - C
  • Glucocorticoid (Steroid) - D
  • Pegloticase - B
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3
Q

What are the therapeutic goals of gout medications?

A
  • Increase excretion of uric acid
  • Inhibit inflammatory cells
  • Inhibit uric acid biosynthesis
  • Provide symptomatic relief
    • NSAIDs or steroids (short term)
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4
Q

Identify the risk of NSAID therapy for acute gout:

Male patient (75 YO) w/ renal disease

A

Dependent on vasodilatory PGs to maintain renal blood flow

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5
Q

Identify the risk of NSAID therapy for acute gout:

55 YO woman w/ peptic ulcer

A

NSAIDs block cytoprotective PGs in GI

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6
Q

Identify the risk of NSAID therapy for acute gout:

68 YO male w/ previous MI & FaHx of heart disease

A
  • NSAIDs (not aspirin) may increase risk (or not prevent) of MI
  • Blocks PGI2 & TXA2
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7
Q

Identify the risk of NSAID therapy for acute gout:

Female patient w/ nasal polyps & previous rxn to aspirin

A

Hypersensitivity rxn due to leukotrienes

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8
Q

Identify the risk of NSAID therapy for acute gout:

45 YO male taking warfarin for DVT prophylaxis

A

Increased risk of bleeding

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9
Q

Why is aspirin contraindicated in the treatment of gout?

A
  • Decreases uric acid secretion
  • Increases uric acid
  • Makes gout worse
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10
Q

A patient that can’t take an NSAID for relief to acute gout symptoms has which of the following options?

  • Wait until symptoms subside (few days)
  • Take low dose colchicine (w/i 48 hrs)
  • Intraarticular glucocorticoid injections
  • Celecoxib
  • Low dose oral steroids
A

All except Celecoxib

NSAID = hypersensitivity

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11
Q

What are the non-biologic DMARDs?

A
  • Methotrexate
  • Sulfasalazine
  • Hydroxychloroquine
  • Azathioprine
  • N-penicillamine
  • Mycophenolate mofetil
  • Leflunomide
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12
Q

What are the biologic DMARDs?

A
  • Etanercept
  • Infliximab
  • Adalimumab
  • Rituximab
  • Anakinra
  • Abatacept
  • Tocilixumab
  • Belimumab
  • Apremilast
  • Tofacitinib
  • Secukinamab
  • Ustekinumab
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13
Q

What is a DMARD?

What are biologics?

A
  • Disease Modifying Anti-Rheumatic Drugs
    • Drugs that slow or halt the progression of disease
  • Biologics
    • A class of drugs which includes monoclonal Ab, receptor analogues, & chimeric small molecules designed to bind to or mimic their molecular targets
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14
Q

Match the drug to the site of action:

  • Methotrexate
  • Infliximab
  • Abatacept
  • Anakinra
  • Rituximab
  • Tocilizumab
A
  • Methotrexate - C
  • Infliximab - D
  • Abatacept - B
  • Anakinra - F
  • Rituximab - A
  • Tocilizumab - E
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15
Q

What is the mechanism of Abatacept?

A

Blocks the co-stimulation of T-cells

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16
Q

What is the mechanism of Methotrexate & Leflunomide?

A

Inhibits the proliferation & activity of T-cells & B-cells

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17
Q

What is the mechanism of Etanercept, Infliximab, Adalimumab, Golimumab & Certolizumab?

A

Inactivate TNF-α

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18
Q

What is the mechanism of Anakinra?

What is the mechanism of Tocilizumab?

A

Anakinra blocks the action of IL-1

Tocilizumab inactivates IL-6

19
Q

What is the mechanism of action of glucocorticoids?

A

Inhibit T-cell activation & IL-2 production by regulation of gene transcription

Inhibit the formation of PGs

20
Q

What is the mechanism of NSAIDs?

A

Inhibit formation of PGs

21
Q

What is the mechanism of Methotrexate?

A
  • Irreversibly binds to & inhibits DHFR
  • Results in inhibition of purine & thymidylic acid synthesis
  • Interfering w/ DNA synthesis, repair & cellular replication
22
Q

What is the mechanism of Sulfasalazine?

A
  • Metabolized to sulfapyridine & 5-aminosalicylic acid
  • Mechanism not known but IgA & IgM rheumatoid factor production are decreased
  • In-vitro suppression of T-cell activation & inhibition of B-cell proliferation
  • Inhibits release of inflammatory cytokines
23
Q

What is the mechanism of Hydroxychloroquine?

A
  • Mechanism unclear
  • Suppression of T-lymphocyte responses to mitogens
  • Decreased leukocyte chemotaxis
  • Stabilization of lysosomal enzymes
  • Inhibition of DNA & RNA synthesis
  • Trapping of free radicals
24
Q

What is the mechanism of Azathioprine?

A
  • Cleaved to 6-mercaptopurine
  • Converted to additional metabolites that inhibit de novo purine synthesis
  • Cell proliferation inhibited, impairing a variety of lymphocyte functions
25
Q

What is the mechanism of N-penicillamine?

A
  • Chelates w/ lead, copper, mercury & 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
26
Q

What is the mechanism of Mycophenolate mofetil?

A
  • Converted to active metabolite that inhibits inosine monophosphate dehydrogenase
  • Leading to suppression of T & B-lymphocyte proliferation
27
Q

What is the mechanism of Leflunomide?

A
  • Undergoes rapid conversion to its active metabolite, A77-1726
  • This metabolite inhibits dihydroorotate dehydrogenase
  • Leads to a decrease in ribonucleotide synthesis & arrest of stimulated cells in the G1 phase of cell growth
  • Consequently, leflunomide inhibits T-cell proliferation & production of autoantibodies by B-cells
28
Q

Which of the following drugs are human monoclonal antibodies?

  • Adalimumab
  • Belimumab
  • Tocilizumab
  • Rituximab
  • Infliximab
A
  • Adalimumab, Belimumab, Tocilizumab
  • Rituximab & Infliximab are chimeric
29
Q

Pharmacokinetics of MABs

What is the admin & absorption?

What is the distribution?

A
  • Administration & Absorption
    • SubQ = 24-95% bioavailability
    • IM = 24-95% bioavailability
    • IV = 100% bioavailability
  • Distribution
    • Extracellular
    • Does NOT cross BBB
30
Q

What are the half-lives of MABs?

A
  • Therapeutic Ab from human source have longer biological half-life than those from mouse source
    • Human = 20-21 days
    • Murine = 12-48 hrs
  • Varies w/ IgG isotype
    • Human IgG1, IgG2, IgG4 = 20-21 days
    • Human IgG3 = 7 days
  • Long half-life = infrequent admin
31
Q

What is the 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
  • Fab or F(ab)2 antibody fragments lack Fc region - do not bind FcRn
32
Q

Which of the following drugs inhibit TNF-α?

  • Infliximab
  • Adalimumab
  • Etanercept
  • Only infliximab & adalimumab
  • All of the above
A

All of the above

  • Infliximab & adalimumab bind to both m-TNF & s-TNF & induce apoptosis of expressing cells
  • Etanercept neutralizes s-TNF but not m-TNF
33
Q

What are the mechanisms of action of therapeutic antibodies?

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

What is the action of Belimumab?

A
  • BLSP (BLyS) is the co-stimulator for B-cell survival & function
  • Belimumab is a monoclonal Ab against BLyS
  • Specific binding to BLyS prevents the interaction of BLyS with its receptor & decreases the B-cell survival & production of autoantibodies
35
Q

Which of the following best explains the mechanism of action of rituximab?

  • Complement-dependent cytotoxicity (CDC)
  • Antibody-dependent cellular cytotoxicity (ADCC)
  • Both CDC & ADCC
  • None of the above
A

Both CDC & ADCC

36
Q

What is complement-dependent cytotoxicity? (CDC)

A
  • Antibody binds cell surface antigen on target cell
  • Fc region binds complement protein & activates complement system resulting in cell lysis
37
Q

What is antibody-dependent cellular cytotoxicity? (ADCC)

A
  • 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
38
Q

What are the adverse effects of therapeutic antibodies?

A
  • Generally safe & well-tolerated
  • Immunogenicity: generation of endogenous Ab against the therapeutic Ab
    • Concerns:
      • Neutralizes the effect of therapeutic Ab
      • Hypersensitivity rxn: either localized to injection site or systemic
39
Q

For each pair of drugs, predict which would have greater potential for immunogenicity:

  • Infliximab vs. Adalimumab
  • Rituximab vs. Belimumab
  • Tocilizumab vs. Infliximab
  • Ibritumomab vs. Tocilizumab
A
  • Infliximab vs. Adalimumab
  • Rituximab vs. Belimumab
  • Tocilizumab vs. Infliximab
  • Ibritumomab vs. Tocilizumab
40
Q

What is Ibritumomab?

A
  • Monoclonal Ab directed against CD20 antigen found on pre-B & mature B lymphocytes (normal & malignant)
  • Binding induces apoptosis in B lymphocytes
41
Q

Abatacept

  • Mechanism of Action
  • Administration
  • Use
A
  • Fusion protein
  • After T-cell has engaged in APC, a 2nd signal is produced by CD28 on the T-cell that interacts w/ CD80 or CD86 on the APC, leading to T-cell activation
  • Abatacept binds to CD80 & 86, thereby inhibiting the binding to CD28 and preventing the activation of T-cells
  • Parenteral admin, IV infusion
  • RA w/ inadequate response to other drugs
42
Q

Anakinra

  • Mechanism of action
  • Administration
  • Use
A
  • Recombinant protein
  • Competitive antagonist of IL-1 receptor
  • SubQ admin
  • Moderate/severe RA in adult patients who have failed _>_1 DMARDs
  • May be used alone or in combination w/ DMARDs (other than TNF-α inhibitors)
43
Q

Tofacitinib

  • Mechanism of Action
  • Metabolism
  • Use
A
  • Oral, targeted DMARD
  • Synthetic small molecule
  • Inhibition of JAKs prevents cytokine or growth factor mediated gene expression & cellular activity of immune cells
  • CYP450 metabolism (3A4, 2C19)
  • Moderate/severe RA in adults intolerant to methotrexate
44
Q

Apremilast

  • Mechanism of Action
  • Metabolism
  • Use
  • Side Effects
A
  • Oral, small molecule inhibitor of PDE-4
  • CYP450 metabolism (3A4)
  • Adult patients w/ psoriatic arthritis
  • Neuropsych effects
    • Depression. suicidal ideation, mood changes
  • May cause weight loss

Symptoms (17 decks)

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