Sem 1 Final Flashcards
Ferrous sulfate, ferrous gluconate, ferrous fumarate: SE’s?
N/V, *melena
Ferrous sulfate, ferrous gluconate, ferrous fumarate: indications?
Inadequate absorption of Fe; blood loss; (increased Fe requirements for pregnant, children, premies)
Ferous sulfate, ferrous gluconate, ferrous fumarate: how long does it take to work?
Quick response- anemia reversed in 1-3 months
Ferrous sulfate, ferrous gluconate, ferrous fumarate: MoA?
Route?
Fe supplementation
PO
Iron dextran, iron sucrose, iron gluconate: MoA?
Route?
Fe supplementation
IV or IM
Iron dextran, iron sucrose, iron gluconate: indications?
When the oral form (ferrous __) isn’t tollerated, such as post-GI resection; malabsoprtive syndromes
Iron dextran, iron sucrose, iron gluconate: SE’s?
Pain, tissue staining (IM), HA, fever, N/V, back/joint pain, allergic rxns, anaphylaxis (more than oral ferrous forms)
What can acute Fe toxicity cause?
What can chronic Fe toxicity cause?
- Acute Fe toxicity (usually from over-ingestion of tabs) can cause necrotizing gastroenteritis; death in children.
- Chronic toxicity (hemochromatosis, multiple transfusions) can cause organ failure.
What are some techniques drugs for treating acute Fe toxicity? (3)
- Gastric aspiration
- Gastric lavage (phosphate or carbonate solns)
- Deferoxamine
What are some techniques drugs for treating chronic Fe toxicity? (3)
- Deferoxamine
- Deferasirox
- Intermittent phlebotomy
What can be given for B12 supplementation? Folate supplementation?
- B12: Cyanocobalamine, hydroxycobalamine
- Folate: folic acid
What route can Cyanocobalamine and hydroxycobalamine be given besides PO?
What is the response time?
IM
- Quick response (1-2 months). PO might be even better!
If someone is experiencing B12 or folic acid def., if they are given supplemental folic acid, will the CNS sx be reversed?
No
EPO: routes?
IV, SubQ
EPO: indications?
CKD, aplastic anemia, leukemia, HIV/AIDS-associated anemias, cancers, anemia of prematuraty, post-phlebotomy
EPO: toxicity?
HTN, thrombotic complications, allergic rxns, tumor recurrence and progression
Sargamostrim: MoA?
Recombinant GM-CSF. Stimulates proliferation and differentiation of erythroid and megakaryocytic cells (less specific than below).
Sargamostrim, filgastrim, pegfilgastrim: indications?
they have different MoA’s and SE’s
S/p intesive chemo (particularly for AML), congenital neutropenia, cyclic neutropenia, neutropenia a/w myelodysplasia and aplastic anemia, high-dose chemo w/autologous stem cell rescue, autologous transplant (mobilization of peripheral blood cells)
Sargamostrim: SE’s?
Fever, arthralgia, myalgia, peripheral edema, pleural/pericardial effusion, allergic rxns
Filgastrim, pegfilgastrim: MoA?
Recombinant G-CSF. Promotes the release of hematopoietic stem cells from the marrow into the peripheral circulation. Increases PMN count.
Filgastrim, pegfilgastrim: SE’s?
Bone pain, rarely splenic rupture, allergic rxns.
Which drug is better: sarmostrim or filgastrim?
Filgastrim
How does pegfilgastrim differ in T1/2 from filgastrim?
Pegfilgastrim (conjugated to polyethylene glycol) has a longer T1/2
Oprelvekin: MoA?
Recombinant IL-11. Promotes proliferation of megakaryocyte progenitors. Increases peripheral platelet counts.
Oprelvekin: indications?
Chemo pts who become thrombocytopenic
(Platelet transfusions can produce adverse rxns and pts can be refractory to platelet transfusions as well, so use this drug instead to increase platelet counts)
Oprelvekin: SE’s?
Fatigue, HA, dizziness, dyspnea, arrhythmia, hypokalemia
Romiplostim: MoA?
A novel protein known as a “peptibody” with two domains; a peptide domain that binds the TPO (thrombopoietin) receptor (Mpl), and an antibody Fc domain that increases half-life.
(TPO receptors are also on stem cells, so all stages of hematopoiesis are increased, including RBCs, WBCs, and platelets, making this a promising drug to treat aplastic anemia.)
Romiplostim, eltrombopag: indications?
they have different MoA’s
Thrombocytopenia, idiopathic thrombocytopenic purpura (ITP), asplastic anemia, post-chemo
Romiplostim, eltrombopag: SE’s?
They have different MoA’s
HA, myalgia, bone marrow fibrosis (reversible)
Eltrombopag: MoA?
A thrombopoietin-receptor agonist (small molecule)
Prednisone, prednesilone: MoA?
A glucocorticoid; activates the glucocorticoid receptor TS factor; modifies expression of cytokines and other immunomodulatory genes; suppresses active immune response
Prednisone, prednesilone: indications?
Immunosuppression; to prevent graft rejection; to prevent GvHD; tx of cytokine release syndrome; tx of a wide variety of autoimmune and inflammatory dz’s (SLE, RA, asthma, etc)
Prednisone, prednesilone: toxicity?
Hyperglycemia, HTN, HLD, obesity, diabetes, poor wound healing, increased infection risk, mania & psychosis
*Dose should be gradually reduced and not withdrawn abruptly.
Azathioprine: MoA?
Prodrug that’s converted to active 6-mercaptopurine (6-MP) by HGPRT. Inhibits de novo purine synthesis. Incorporated into DNA and causes SSB mispairing –> apoptosis (inhibits lymphocyte proliferation). Inhibits CD28 co-stimulation.
Azathioprine: indications?
Immunosuppression; to prevent graft rejection; to prevent GvHD; tx of autoimmune dz’s
Azathioprine: toxicity?
Leukopenia/thrombocytopenia, hepatotoxicity, ^ risk infections, ^ risk malignancy
Azathioprine: contraindications?
*Interacts w/anti-gout drugs allopurinol and febuxostat –> ^ [azathioprine] –> ^ toxicity.