LG 3.5 Pharmacology DMARDS Flashcards
1
Q
Identify the following from their stem: monoclonal antibody, kinase inhibitor, fusion protein.
“-nib”
“-mab”
“-cept”
A
- Monoclonal antibody = -mab
- Kinase inhibitor = -nib
- Fusion protein = -cept
2
Q
What is the MOA of monoclonal antibodies?
A
- Bind ligand => inhibits ligand binding of receptor and receptor activation
- Bind receptor => inhibits ligand binding of receptor
3
Q
What is the MOA for fusion proteins?
A
- Protein that resembles the receptor
- Ligand binds fusion protein => inhibits ligand binding of receptor and receptor activation
4
Q
What is the MOA of kinase inhibitors?
A
- Molecules (drug) gets into cell and interacts with receptor in order to cease kinase domain activity
5
Q
What are the concerns with use of anti-TNF biologic DMARDs? What is done during a course of treatment with DMARDs to minimize disease states?
A
- DMARDs cause increased risk for TB (tuberculosis) and fungal infections
- TB tests are giving and monitored throughout treatment.
- May cause lymphoma or other malignancies in adolescence or children taking DMARDs
6
Q
Describe MOA of methotrexate. (Type of antagonist? Inhibits what?)
A
- A folic acid antagonist
- Inhibits dihydrofolate reductase -> decreases intracellular tetrahydrofolate -> inhibits DNA and RNA synthesis
- Inhibits T-Cell proliferation -> inhibits transmethylation reactions required for T-Cell cytotoxicity (PROMOTES RELEASE OF ADENOSINE, AN ENDOGENOUS ANTI-INFLAMMATORY MEDIATOR)
- Interferes with glutathione metabolism -> alter recruitment of monocytes to inflamed joint
7
Q
Describe MOA of leflunomide. (suppresses what? how? overall affect?)
A
- Suppresses de novo synthesis of pyrimidine (uridine and cytidine) nucleotide BY inhibiting dihydroorotate dehydrogenase.
- This blocks T-lymphocytes and B-lymphocytes from developing
- Relatively specific for T-lymphocytes because they have no alternate pathway to produce pyrimidine like other cells do (“cytotoxic toward T-lymphocytes”)
