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149 Cards in this Set
- Front
- Back
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What is filgrastim (Neupogen) administered for?
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Recombinant G-CSF - for granulocytopenia
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What would you administer for a granulocytopenia/monocytopenia
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sargramostim (Leukine)
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What is the advantage of using Peg-filgrastim (Neulasta) over filgrastim (Neupogen)?
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Neulasta has a longer half life than recombinant G-CSF for granulocytopenia, so it can be administered once per chemotherapy
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How long is the half-life of filgrastim (Neupogen)?
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2-7 hours
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What can be administered to stimulate platelet synthesis?
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IL-11 oprelvekin (Neumega)
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What is used for the treatment of chronic immune thrombocytopenia purpura?
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romiplostim (Nplate)
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Which is less toxic and more effective for stimulating peripheral stem cells: sargramostim (Leukine) or filgrastim (Neupogen)?
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filgrastim (Neopogen) (G-CSF)
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Which CSF can induce fever?
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sargramostim (Leukine) (GM-CSF)
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How long should you treat with PO iron someone who had iron deficiency anemia?
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For 3-6 months after Hb normalizes to ensure adequate stores
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For what situations is desferrioxamine used?
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Iron chelator, prevents iron overload in patients repeatedly transfused, or taking erythropoietin
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Of these three, which carries the largest risk of anaphylaxis? Iron sucrose, Iron dextran, ferric gluconate
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Iron dextran (1%).
Minimal to no risk of anaphylaxis in iron sucrose or ferric gluconate |
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What anticancer drug inhibits dihydrofolate reductase, leading to folate deficiency?
What other anti-cancer drugs are associated with low folate? |
Methotrexate (dihydrofolate reductase interferance)
also 5-FU, Ara-C |
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Which two anticonvulsants are associated with decreased folate?
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Phenytoin, primidone
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When would you prescribe folinic acid vs. oral folic acid?
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To a patient on methotrexate (Leucovorin) to prevent inhibition of dihydrofolate reductase
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What are first line treatment options for ITP?
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-Prednisone
-IV IgG (coats receptors in spleen, displacing IgG coated platelets -Anti-D antibody (coats RBCs in antibody, overwhelming RES and displacing coated platelets) |
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What are second line treatment options for ITP?
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-splenectomy
-Rituximab (B cell antibody prevents production of antiplatelet IgG) -chemo (azathioprine, vincristine, danazole) -Thrombopoietin receptor agonists: Romiplostim, Eltrombopag |
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What hemotologic effect all these drugs have in common:
Bactrim (TMP/SMX) Vancomycin Penicillins Acyclovir |
Drug-induced thrombocytopenia
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What can tonic water and H2 blockers (pepcid) cause hemotologically?
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Thrombocytopenia
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What is 1st line treatment for HIT?
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STOP heparin
START non heparin anticoag: -Argatroban (in renal failure) OR -Lepirudin (in liver failure) HOLD all coumadin until platelets >100K |
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What is the treatment for TTP?
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PLASMA EXCHANGE!
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What are treatment options for hemophilia?
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Prophylaxis appropriate after joint bleed: give Factor VIII or IX until >1% activity.
Acute: give factor until 30-100% activity (e.g. ICH = 100%) Desmopressin (DDAVP), a synthetic ADH releases Factor VIII from endothelium, can be used for low risk bleeding in Hemophilia A patients |
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How can you treat a hemophiliac who has begun to produce antibodies to recombinant factor replacement and is now refractory to further treatment with factors?
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Immunosuppression, and recombinant Factor VIIa to induce the common pathway in bleeding
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Why is it important to know whether your patient has Type I or Type II von Willibrand disease?
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Type I (quantitative vWF deficiency) should be treated with DDAVP (synthetic ADH) to release vWF from endothelium.
Type II (qualitative vWF defect) vWD will worsen with DDAVP administration |
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How does warfarin (Coumadin) work?
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Blocks the reduction of Vit K epoxide to Vit K, needed for production of clotting factors X, IX, VII, II, Proteins C & S
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What natural anticoagulant does heparin enhance?
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Antithrombin + heparin = Antithrombin function X1000
Heparin induces a conformational change in ATIII, allowing it to more quickly bind to FREE thrombin (IIa), Xa. (ATIII binds to all unbound activated VitK derived factors: Xa, IXa, VIIa, IIa). Heparin disassociates and can be reused. Only PREVENTS coagulation, does not inhibit thrombin bound to fibrin. |
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If your patient relates that as a child, she had purpura fulminans, what drug should you NOT administer?
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Warfarin. Protein C is depleted before any of the clotting factors, leading to warfarin skin necrosis
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What is a good prophylactic treatment for children with sickle cell disease?
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Penicillin - reduces mortality in first 5 years of life from 25% to 3%
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What are treatment options for thalassemia?
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Transfusion for thal major
Iron chelators for iron overload (desferrioxamine, deferasirox) |
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What is the only oral iron chelator available for chronic iron overload?
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deferasirox (Exjade)
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What treatment for sickle cell disease can increase levels of HemeF?
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hydroxyurea, which inhibits DNA synthesis
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How do the thienopyridine drugs clopidogrel and ticlopidine work?
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Block the ADP receptor on platelets, preventing activation and therefore aggregation
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Which of the following is less likely to be discontinued because of side effects:
ticlidopine or clopidogrel |
clopidogrel (Plavix) has fewer GI toxicities than ticlidopine (Ticlid)
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What should be checked weekly when initiating a thienopyridine anticoagulant?
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Platelets - both ticlidopine and clopidogrel carry risk of TTP in first month
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Is clopidogrel (Plavix) superior to aspirin for clot prevention?
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Yes, slightly (8% reduction)but it is best to administer both together (20% reduction) to prevent MI/stroke/death following an event.
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What is the purpose of receptors PAR1 and PAR3 on platelets?
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Protease-activated receptors react to thrombin (Factor IIa), the most potent platelet agonist.
PAR inhibitors are in development |
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What are the source and functions of prostacyclin (PGI2) and thromboxane (TXA2)?
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Thromboxane: platelets. decreases cAMP, encouraging platelet aggregation
Prostacyclin: endothelium. increases cAMP, inhibiting aggregation |
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How does aspirin block platelet aggregation?
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Inhibits cyclooxygenase (1>2), blocking the production of TXA2, and irreversibly inhibiting the affected platelet.
7 days to turn over to a new batch of platelets. |
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What is the most abundant receptor on a platelet, and what are its functions?
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GpIIb/IIIa
1) platelet aggregation together with fibrin polymers. 2) activates other platelets when active through release of microparticles |
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Which GpIIb/IIIa inhibitor is not specific for the GpIIb/IIIa receptor?
abciximab eptifibatide tirofiban |
abciximab (ReoPro) - antibody for another platelet receptor and a leukocyte receptor
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What GpIIb/IIIa inhibitor, when administered with heparin, reduced repeat MI / death within 7 days after an MI compared to heparin alone?
abciximab eptifibatide tirofiban |
tirofiban (Aggrastat) - a snake venom
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What GpIIb/IIIa inhibitor is cleared by the kidney?
abciximab eptifibatide tirofiban |
eptifibatide (Integrilin) a snake venom
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What GpIIb/IIIa inhibitor allows for near-normal platelet function within 24 hours?
abciximab eptifibatide tirofiban |
abciximab (ReoStat)
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Which GpIIb/IIIa inhibitor carries the highest risk of thrombocytopenia?
abciximab eptifibatide tirofiban |
abciximab (ReoPro) - 1%, but >10% with repeat exposure
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What is heparin indicated for?
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Submassive PE
DVT |
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What is the most common side effect of heparin use?
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Bleeding - 5%, but increased in elderly, liver disease, cancer, ASA use
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How can you stop bleeding with heparin?
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Protamine inactivates heparin
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What is the advantage of using LMW heparin over UFH?
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LMW carries lower bleeding risk (BUT CAN'T BE REVERSED
-Lower HIT risk (but don't use with prior HIT) -Lower risk of osteoporosis -Greater bioavailability -Longer half life |
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Which of the following has the greatest factor Xa : IIa inhibition? Why does this matter?
ardeparin enoxaparin fondaparinux dalteparin |
ardeparin (Normiflo) - least risk of bleeding
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What indirect thrombin inhibitor is indicated after hip fracture or hip/knee surgery at high risk of clot?
ardeparin enoxaparin fondaparinux dalteparin |
fondaparinux (Arixtra)
selective Factor Xa inhibitor |
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What is the disadvantage of LMW heparin vs. UFH?
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LMW heparin is irreversible, while UFH effects can be reversed with protamine
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What do all the direct thrombin inhibitors have in common?
(lepirudin, bivalirudin, argatroban, dabigatran) |
-Do not inhibit thrombin through ATIII
-Inhibit thrombin whether it is free or fibrin bound -Do not require cofactors (predictable) -Irreversible -Monitored with PTT (lepirudin, bivalirudin, argatroban, dabigatran) |
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Match up the following statements with the correct antithrombin agent. May be used more than once.
(hirudin, lepirudin, bivalirudin, argatroban, dabigatran) 1) Derived from leech saliva 2) Synthetic 20AA peptide 3) Approved for HIT in renal failure 4) Approved for HIT in liver failure 5) Approved only for clot prevention in AFib |
1) hirudin/lepirudin - leech
2) bivalirudin - 20AAs 3) argatroban - ok in renal fail 4) lepirudin - ok in liver fail 5) dabigatran - Afib VTE prev |
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How long does it take for warfarin (Coumadin) to take effect?
90 minutes 2 days 3 days |
2 days for effects
3 days for factor VII INR = 2 5 days for full anticoagulation |
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What are normal PT and PTT times?
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Normals:
PT = 12 sec PTT = 30 sec |
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What are the only two indications for dosing warfarin higher than INR 2-3?
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Mechanical prosthetic valves
Failure of lower dose |
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What are the 4 common drugs that potentiate warfarin by inhibiting metabolic clearance by CYP450 2C9/1A2?
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Co-trimoxazole (TMP/SMX)
Clofibrate Cimitedine (Tagamet) Metronidazole (Flagyl) also grapefruit juice |
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What are the drugs that potentiate warfarin without increasing plasma levels?
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Anything that is also a anti-coagulant
Heparin NSAIDs: Aspirin, COX-2 |
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What drugs ANTAGONIZE warfarin action?
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Cholestyramine (bile acid sequestrant - impairs absorption)
Increase clearance Barbiturates (i.e. phenobarbital) Rifampin (TB ab) Carbamazepine Chronic EtOH |
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Which variants of CYP2C9 indicate that you should reduce warfarin dosed by at least 20%?
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CYP 2C9*2 and *3
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What enzyme has variants that affect Vitamin K recycling, and therefore has implications for dosing of warfarin?
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VKORC1
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What should be given to reverse the effects of warfarin?
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Vitamin K PO
Acute: Fresh frozen plasma |
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What is the first line treatment for DVT or submassive PE?
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1st time:
Heparin or fondiparinux Warfarin At least 5 days and until INR >2 for at least 24 hours. Not less than 3 months 2nd event or in Cancer: long term anticoagulation |
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What is a better treatment to prevent cancer-related DVT/PE?
LMWH or warfarin? |
LMWH - 1/2 the risk of DVT/PE
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What drugs mimics tPA?
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streptokinase (from Beta-hemolytic strep)
urokinase (from dead baby kidneys) |
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What is the function of alteplase, reteplase, or tenecteplase?
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tPAs (reteplase is recombinant, TNKase has a longer half life allowing for bolus)
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Apart from recent or active bleeding, what conditions are contraindicated for receiving direct plasmin activators?
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Diabetic retinopathy,
Intracranial neoplasm, aneurism |
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What can be given to encourage hemostasis?
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recombinant Factor VII, but high risk of thrombus
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What is aminocaproic acid (Amicar) given for?
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Adjunct tx for hemophilia
IC aneurism at risk of re-bleed |
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What are treatment options for P Vera?
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Phlebotomy
hydroxyurea interferon? Aspirin/anti-platelets BMT if young, HLA match |
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What are the treatment options for Essential thrombocytosis?
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Hydroxyurea
Anegrelide - reduces platelets, but not as good with clots as Hydroxyurea Interferon - if pregnant |
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What are the treatment options for CML, apart from imatinib?
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Hydroxyurea
alphaIFN BMT |
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What treatments are available for CML refractory to imatinib?
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Dasatinib - inhibits SRC-ABL downstream from BCR-ABL
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Which of the following is associated with improved 6 year survival, cytogenetic response, and median time to progression:
- alphaIFN - hydroxyurea |
alpha interferon has impoved OS, TTP, CCR vs. hydrea
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Mrs. H is a 40 year old female with no past medical history who presents to an outside ED with headache, fevers, severe sore throat for three days.
Past Medical History: none Meds: none Physical Exam: Obese female, severe tonsilar edema (no airway obstruction), oral ulcers, petechiae on legs WBC: 278K HCT: 23 PLT: 40 BUN/Cr: 30/0.6 K: 2.8 Patient feels mildly dizzy and still has headache A) Call blood bank and tell them to come in for urgent leukopheresis B) Perform an urgent Bone Marrow Biopsy C) Wait for Flow to come back from blood to determine type of leukemia D) Give Hydroxyurea high rate fluids, and allopurinol to decrease counts and prevent tumor lysis syndrome E) Replete Potassium (2.8) |
A) Call blood bank and tell them to come in for urgent leukopheresis
D) Give Hydroxyurea high rate fluids, and allopurinol to decrease counts and prevent tumor lysis syndrome |
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Are AML patients typically old or young?
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Old - Median age is 70
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What chemotherapeutic agents are associated with 10-20% of acute myelogenous leukemias?
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Alkylating agents (cyclophosphamide, melphalan, busulfan, chlorambucil)
Topo II inhibitors (etoposide, topotecan) |
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What non-chemotherapeutic agents are associated with increased risk for AML?
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Chloramphenicol
Phenobutazone Chloroquine Methoxysporalen LSD |
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What is 7+3
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Refers to chemo regiman for all AML (except APML):
7 days AraC continuous IV 3 days anthracycline hydrate aggressively to prevent tumor lysis |
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What is the effect of AML cytogenetics on bone marrow transplant decision making?
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Good: consolidate with chemo
Intermediate: allo or auto BMT Poor: Allo BMT |
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How does the treatment of t(15;17) APML differ from other forms of AML?
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APML treated with high dose all-trans retinoic acid (ATRA), AraC and adriamycin, with consolidation rounds. All others treated with 7+3 (7 days AraC + 3 days anthracycline)
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What are hallmarks of ALL treatment different greatly from AML?
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EVERY ALL patient gets lumbar puncture and prophylactic CNS therapy - 10% have CNS sx
DO NOT need to leukophorese ALL patients - lymphoblasts do not cause stasis |
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What is treatment for ALL?
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Not very good - BMT if poor prognosis, and chemo for 2 years if not, with 6 agents (vincristine, dexamethasone, daunarubicin, 6-Mercaptopurine, 6-thioguanine, cytarabine, methotrexate and L-asparaginase
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How do you treat MDS?
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Depends on age, prognostic factors and performance. If young, healthy, bad prognosis, might try AML induction, or SCT. If older, good prognosis, watchful waiting/supportive care.
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What is "growth factor support" for MDS?
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Epogen/Aranesp, or G-CSF. Stop if no effect after 2 months
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What chemotherapies are used in MDS?
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azacitine, decitabine (both pyramidine nucleoside analogs). Delay onset of leukemia, prolong OS
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What treatment is particularly effective for 5q deletion MDS?
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Lenalidomide (thalidomide derivative)
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For each of the following anti-neoplastics, say whether its mechanism is cell-cycle specific (and if so, what phase), or non-specific
alkylating agents, antimetabolites, topoisomerase I and II inhibitors and platinum-based agents, DNA cross-linking agents, intercalating agents, antimicrotubule agents |
Cell cycle specific:
antimetabolites, topoisomerase I and II inhibitors and intercalating agents (S-phase), antimicrotubule agents (M-phase) Non-specific: alkylating agents, platinum-based agents, DNA cross-linking and intercalating agents (also specific, but in this case, breaks up DNA) |
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How do alkylating agents work?
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Attach alkyl group to 7Nitrogen of Guanine, causing DNA fragmentation during repair, cross links preventing transcription, and aberrent G-T bonds, causing mutations
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What class of drugs are are nitrogen mustards, nitrosureas and alkyl sulfonates?
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alkylating agents
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What class of drugs are the following: mechlorethamine, cyclophosphamide, ifosfamide, chlorambucil, melphalan, bendamustine
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Nitrogen mustards:
I'm bandera, color me mexico. Remember mustard because of gold eagle on Mexican flag. IfosfaMide (I'm) BENDamustine (Bandera) Ch(o)LORAMabucil (Coloran) MElphalan (Me) MECHlorethamine (Mex) CYClOphosphamide (Ico) |
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What side effects do the nitrogen mustards cyclophosphamide and ifosfamide have in common that require mesna administration to prevent?
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Toxic byproduct causes bladder irritation, hemorrhagic cystitis
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What PO nitrogen mustard is used primarily in multiple myeloma when BMT not planned?
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Melphalan
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What novel nitrogen mustard is specifically noted not to cause alopecia?
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Bendamustine
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What alkylating agent rarely (but seriously) is associated with pulmonary fibrosis?
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Busulfan - alkylsulfonate
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What are the alkylating agents used to treat brain tumors?
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Nitrosureas:
lomustine, carmustine |
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What foods can cause someone taking the atypical alkylating agent procarbazine to experience a hypertensive crisis?
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Aged meets and cheeses - rich in tyramine
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What is the mechanism of action of antimetabolites?
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Compete with something in the cell cycle, which they resemble
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In what class are methotrexate and pemetrexed?
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Both are antifolate anti-metabolites. Folate is required for thymidine and purine (A/G) synthesis
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What is typically given to patients 24 hours after methotrexate to "rescue" folate for bone marrow?
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Leucovorin
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What antimetabolite is used in cancers of H/N, upper GI, NHL, ALL, breast, and sarcomas?
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methotrexate
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What class are 6MP and 6TG?
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Purine analogues (remember that guanine and adenosine are purines):
6MP: mercaptopurine 6TP: thioguanine |
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Which is indicated for ALL, and which is indicated for AML?
6MP, 6TG |
6MP: ALL
6TG: AML (sometimes CML) |
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What do you usually give for tumor lysis syndrome that you might hold with 6MP?
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Allopurinol. Prevents hyperuricemia in tumor lysis, but may increase 6MP toxicity
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In what class are the following:
5FU capecitabine Cytarabine (AraC) Gemcitabine 5-Azacitidine |
Pyrimidine analogues (C/T)
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What enzyne does 5FU bind to in activated form, causing a "thymidineless death"?
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thymidylate synthetase
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What pyrimidine analogue, isolated from a sponge, is indicated in AML, ALL, CML, NHL? In high doses, it can cause cerebellar damage.
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Cytarabine (AraC)
High doses = HiDAC |
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In addition to mimicking a pyrimidine and being incorporated into DNA, what benefit does 5-azacitidine do for patients with MDS by demethylating gene promoter regions?
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Potentially restores tumor supressor function
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What class are fludarabine, cladribine, anti-neoplastics?
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Nucleoside analogues - antimetabolites. Mimic adenosine
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When administering fludarabine for CLL, NHL or AML, what is your major side effect concern?
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Immunosuppression - PCP, fungi, reactivated herpes
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What is hydroxyurea indicated for?
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hydroxyurea brings down blood counts in several heme malignancies, P Vera and other myeloproliferative disorders
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What drugs, indicated for 5q MDS and multiple myeloma, carry severe risk of birth defects?
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thalildomide, lenalidomide
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What agents are the mainstays of solid tumor chemotherapy?
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Platinum-based agents, which alkylate but also form cross-links with dsDNA and prevent transcription
cisplatin carboplatin oxaliplatin |
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Which platinum based alkylating agent carries the highest risk of nausea/vomiting, renal dysfxn, hearing loss, neuropathy:
cisplatin carboplatin oxaliplatin |
Cisplatin
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What is the mechanism of action of daunorubicin and doxorubicin?
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They are both anthracycline topoisomerase II inhibitors. Produced by streptomyces (soil fungus), TopoII inhibitors prevent DNA uncoiling and therefore replication.
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Which is only indicated for acute leukemias (while the other is indicated for many solid and non solid tumors)
Doxorubicin, Daunorubicin |
Daunorubicin - acute leukemia only
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What are the two most feared side effects of using the Topoisomerase II inhibitors doxorubicin or daunorubicin?
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Cardiac - dysfxn increases with cumulative doses
Skin ulceration with extravasation - admin through central line |
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What prototypic intercalating agent, used primarily in pediatric tumors, was the first natural product isolated for anti-cancer activity?
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Actinomycin
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What is bleomycin's MOA, important to understand because of its link with its potentially fatal long-term side effect?
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Bleomycin, isolated from streptomyces products, complexes with Fe and O2 to form free radicals. Because of the high O2 content in lungs, it can cause life-threatening pulmonary fibrosis with repeated exposure.
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Which natural product and topoisomerase II inhibitor causes fevers and hyperpigmentation, but not myelosuppression?
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bleomycin
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What is the MOA of the camptothecins, or derivatives of the Asian "Happy Tree"?
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Topoisomerase I inhibitors (irinotecan and topotecan)
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What is the mechanism of action of etoposide, from the May apple plant?
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Topoisomerase II inhibition - interfering with transcription and replication.
(Epipodophyllotoxin class) |
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What is the MOA of periwinkle plant derivative vinca alkaloids: vincristine, vinblastin, vinorelbine?
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Microtubule binders, block polymerization and halt cell cycle in M phase
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What are the major side effects of vinca alkaloids?
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neuropathy, IV site irritation
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What do the following have in common?
Vincristine Paclitaxel |
Both are anti-microtubule agents
Both cause neuropathy |
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What is the mechanism of action of paclitaxel and docetaxel, produced from of pacific yew?
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Inhibit de-polymerization of microtubules
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What class are tamoxifen and raloxifene?
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SERMs selective estrogen receptor modulators
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Why do you ask about increased bleeding in women receiving tamoxifen?
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Higher risk of endometrial cancer
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Aromatase inhibitors are more effective than SERMs in breast cancer treatment. So why do you give premenopausal women SERMs, like tamoxifen instead of aromatase inhibitors, like anastrozole?
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Because giving an aromatase inhibitor to a woman with working ovaries will upregulate HPO axis, causing increased estrogen production
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What are the side effects of anastrazole?
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Joint pain, hot flashes, vaginal dryness, increased risk for osteoporosis
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What can you give to a breast cancer patient who has progressed on a SERM or AI?
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Fulvestrant - binds to ER, preventing dimerization and accelerating destruction
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What are the hormonal agents goserelin and leuprolide used for?
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Used in high risk or advanced breast or prostate cancers.
LHRH analogs - trick pituitary into thinking enough sex hormone is being produced, causing a hormonally castrate state in both men and women. |
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What anti-androgen can be used in prostate cancer?
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flutamide
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What is the only treatment of curative intent for CLL?
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Allogeneic stem cell transplant, of limited use because most CLL patients are elderly
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What is first line therapy for CLL?
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fludarabine - a purine analogue, but should not use with hemolytic anemia, +/- cyclophosphamide
OR bendamustine - alkylating agent + Rituximab (anti CD20) |
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What agent targets CD52, and is used in refractory CLL?
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alemtuzumab (Campath) - but targets monocytes, T cells and macrophages, leading to risk of infection.
Worry about CMV reactivation |
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If you see that a leukemic patient's peripheral smear stains positive for TRAP (tartrate resistant acid phosphatase), what type of leukemia do you suspect? Why does it matter?
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Hairy Cell Leukemia - TRAP positive, and has all B Cell markers: CD19, 20, Ig, kappa/lambda light chains.
Matters because with purine analogues (Cladribine), life expectancy approaches normal. |
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What is ABVD for HL stand for?
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adriamycin
bleomycin vinblastine dacarbazine chemo for Hodgkin's lymphoma |
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The radioimmunoconjugates tositumomab and ibritumomab are approved for which refractory NHL?
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Follicular lymphoma
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What treatment for multiple myeloma causes the proteasome to dysfunction, drowning the malignant cell in its own garbage?
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Bortezomib (Velcade)
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What would you suspect in a person with macroglossia and periorbital purpura (a big tongue and raccoon eyes)?
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amyloidosis with light chains
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What disease causes birefringent (2 colors) microscopy with congo red stain, going from dark red to apple green?
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Amyloidosis-diagnose with aspirated abdominal fat
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What does Waldenstrom's macroglobulinemia involve?
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Overproduction of IgM. Similar course to CLL, and does not cause bone lesions like multiple myeloma
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What are the most common causes of death after blood transfusion?
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1)TRALI
2)TACO (fluid overload) 3)Bacterial infection |
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Do leukemias usually get allogeneic or autologous stem cell transplants?
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Leukemia = allogeneic
Lymphoma = autologous |
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What is sicca syndrome?
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Contraction of lip tissue and tendons = graft vs. host disease
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After a transplant, approximately when can you expect a massive hemolysis?
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Day 50 - new immune system takes over
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When are patients discharged after a bone marrow transplant?
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3 weeks after transplant (4 weeks after admit for chemo)
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When do you try autologous bone marrow transplant in lymphomas?
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1st remission: Mantle cell
2nd remission: lymphomas and good risk AML |
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When do you try allogeneic bone marrow transplant in lymphomas?
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2nd remission leukemias, or chemo-refractory lymphomas (trying for Graft vs. Leukemia effect)
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