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Hematology
FA complete review part 4 Pharmacology
| Question | Answer |
|---|---|
| What is the mechanism of action of Heparin? | Activates antithrombin, which decreases action of IIa (thrombin) and factor Xa |
| Which coagulation factors are affected by Heparin? | Factor IIa (thrombin) and Factor Xa |
| Which drugs activates antithrombin? | Heparin |
| Heparin has a ___________ half-life. | Short |
| Clinical uses of Heparin include: | 1. Immediate anticoagulation for pulmonary embolism (PE), 2. Acute coronary syndrome 3. MI 4. DVT 5. Safe to use during pregnancy |
| Which is anticoagulant is safe to be used by pregnancy woman? | Heparin |
| Why is heparin used in pregnancy? | Does not cross the placenta |
| Heparin follows ________. | PTT |
| Which drug follow PTT for monitoring? | Heparin |
| Adverse effects of Heparin? | 1. Bleeding 2. Thrombocytopenia (HIT) 3. Osteoporosis 4. Drug-Drug interactions |
| What is used for rapid reversal (antidote) of Heparin? | Protamine sulfate |
| How does Protamine sulfate counteracts heparin toxicity? | Positively charged molecule that bins negatively charged heparin |
| What drug's toxicity is reversed by Protamine sulfate? | Heparin |
| Heparin's antidote | Protamine sulfate |
| Positively charged molecule that binds to negatively charged heparin? | Protamine sulfate |
| What are two common Low-molecular-weight heparins? | Enoxaparin and Dalteparin |
| On which factor do LMWH work primarily? | Factor Xa |
| Which heparin derivative works exclusively (only) on Factor Xa? | Fondaparinux |
| What anticoagulant can be used if we only want it to work on Factor Xa? | Fondaparinux |
| What are advantages of LMWHs over Unfractionated heparin? | 1. 2-4x longer half-life 2. Administered subcutaneously 3. No laboratory monitoring |
| Which, LMWH or unfractionated heparin, needs to be monitored with PTT? | Unfractionated heparin |
| What does HIT stand for? | Heparin-induced thrombocytopenia |
| What is HIT? | Development of IgG antibodies against heparin-bound platelet factor 4 (PF4). |
| What does the Ab-Heparin-PF4 complex cause? | Activates platelets leading to thrombosis and thrombocytopenia. |
| Patient with low platelets and DVT shortly after emergency anticoagulation therapy in the hospital? | Heparin-induced thrombocytopenia |
| What are the clinical symptoms of HIT? | Thrombosis and thrombocytopenia |
| Direct thrombin inhibitors include: | 1. Bivalirudin 2. Argatroban 3. Dabigatran |
| Which is the only oral direct thrombin (IIa) inhibitor? | Dabigatran |
| Related to hirudin, the anticoagulant used by leeches. | Bivalirudin |
| MOA of Direct IIa inhibitors | Directly inhibits activity of free and clot-associated thrombin |
| What are the 3 most common used of direct thrombin inhibitors? | 1. Venous thromboembolism 2. Atrial fibrillation 3. May be used for HIT |
| What can be used to reverse adverse effects of Dabigatran? | Idarucizumab |
| What is the main adverse effect of Direct Thrombin inhibitors? | Bleeding |
| What are second line drugs used to reverse bleeding associated with direct IIa inhibitors? | PCC and/or antifibrinolytics (tranexamic acid) |
| What is the mechanism of action of Warfarin? | Interferes with gamma-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X, and protein C and S. |
| Warfarin has an effect on the ______________ pathway and increase ___. | Extrinsic; PT |
| Contrary to Heparin, Warfarin has a ________ half-life. | Long |
| What can affect the metabolism of Warfarin? | Polymorphisms in the gene for vitamin K epoxide reductase complex (VKORC1). |
| Medication used for as chronic anticoagulation | Warfarin |
| Warfarin increases ______. | PT |
| Which anticoagulant must be avoided in pregnant women? | Warfarin |
| Which medication is known to follow PT/INR? | Warfarin |
| What can be given for reversal of Warfarin? | Vitamin K |
| What is used for rapid reversal of Warfarin? | FFP or PCC |
| What are the main adverse effects of Warfarin? | Bleeding, teratogenic, skin/tissue necrosis, and drug-drug interactions. |
| What is the initial risk of hypercoagulation with Warfarin? | Protein C has shorter half-life than factors II and X. |
| What is Heparin "bridging"? | Heparin frequently used when starting warfarin to reduce risk of recurrent venous thromboembolism and skin/tissue necrosis. |
| How does Heparin bridging prevent skin necrosis and/or venous thromboembolism? | Heparin activates antithrombin which enables anticoagulation. |
| What type of drugs increase warfarin effect? | Cytochrome P-450 inhibitors |
| Site of action of Heparin | Blood |
| Site of action of Warfarin | Liver |
| Heparin monitoring? | PTT (intrinsic pathway) |
| Warfarin monitoring? | PT/INR (extrinsic pathway) |
| Teratogenic anticoagulant | Warfarin |
| Examples of Direct Xa inhibitors: | Apixaban and Rivaroxaban |
| Bind to and directly inhibit factor Xa | Mechanism of action of Direct factor Xa inhibitors |
| What is the main use for Direct factor Xa inhibitors? | Treatment and prophylaxis for DVT and PE |
| Examples of Thrombolytics: | ALteplase (tPA), reteplase (rPA), streptokinase, tenecteplase (TNK-tPA) |
| MOA of Thrombolytics: | Directly or indirectly aid conversion of plasminogen to plasmin, which leaves thrombin and fibrin clots |
| What are the PT, PTT, and PC of thrombolytics? | Increased in PT and PTT, and no change in Platelet count (PC). |
| Uses for Thrombolytics | 1. Early MI 2. Early ischemic stroke 3. Direct thrombolysis of severe PE |
| The use of thrombolytic is contraindicated in: | Active bleeding, Hx of Intracranial bleeding, recent surgery, known bleeding diathesis, or severe hypertension. |
| What are methods of nonspecific revelral of thrombolytics? | 1. Antifibrinolytics 2. Platelet transfusions 3. Factor corrections |
| What are compounds used as factor correctors? | Cryoprecipitate, FFP, PCC |
| What are some examples of ADP receptor inhibitors? | Clopidogrel, prasugrel, ticagrelor (reversible), and ticlopidine |
| Which is the only reversible ADP receptor inhibitor? | Ticagrelor |
| MOA of ADP receptor inhibitors? | Inhibit platelet aggregation by irreversible blocking ADP receptor. |
| What is prevented on platelet surface, the use of ADP receptor inhibitors? | Prevent expression of glycoproteins IIb/IIa on platelet surface. |
| Uses of ADP receptor inhibitor: | 1. Acute coronary syndrome 2. Coronary stenting 3. Decreased incidence or recurrence of thrombotic stroke |
| What are the associated adverse effects of ADP receptor inhibitors? | Neutropenia (ticlopine) and TTP |
| Which ADP receptor inhibitor is associated with Neutropenia? | Ticlopidine |
| What is the mode of action of Cilostazol? | Phosphodiesterase inhibitors |
| MOA of Dipyridamole | Phosphodiesterase inhibitor |
| What are common uses of Cilostazol and Dipyridamole? | Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs |
| What is commonly used with Cilostazol to prevent TIAs or strokes? | Aspirin |
| Adverse effects of Cilostazol and Dipyridamole? | Nausea, headache, facial flushing, hypotension, and abdominal pain. |
| Common GpIIb/IIIa inhibitors: | Abciximab, Eptifibatide, and Tirofiban |
| What drug is made from monoclonal antibody Fab fragments? | Abciximab |
| What type of drug is Abciximab? | GpIIb/IIIa inhibitors |
| What is the mechanism of action of GpIIb/IIIa inhibitors? | Bind to the GpIIb/IIIa on activated platelets, preventing aggregation . |
| What are the associated adverse effects of GpIIb/IIIa inhibitors? | Bleeding and thrombocytopenia. |
| List of Topoisomerase inhibitors: | Etoposide Teniposide Irinotecan Topotecan |
| Which cell phases are interrupted by Topoisomerase inhibitors? | G2 and S-phase |
| Which cancer drugs (list) work exclusively on the S-phase of the cell cycle? | Azathioprine Cladribine Cytarabine 5-fluorouracil Hydroxyurea Methotrexate 6-mercaptopurine |
| In which cell cycle is disrupted by Antimetabolite drugs? | S-phase |
| Which common cancer drugs works exclusively on G2-phase of the cell cycle? | Bleomycin |
| Which cell phase has a the following role: "Double check repair"? | G2 phase |
| Which phase of the cell cycle is interrupted by Microtubule inhibitors? | Mitosis |
| Microtubule inhibitors include: | Paclitaxel Vinblastine and Vincristine Eribulin |
| What occurs during the G1 phase of the cell cycle? | Duplicate cellular content |
| During the _______ phase of cell cycle, the cellular content is duplicated. | G1 |
| Which are the two categories of cell cycle- independent cancer drugs? | 1. Platinum agents (cisplatin) 2. Alkylating agents |
| What are examples of important alkylating agents? | Busulfan, Cyclophosphamide Ifosfamide Nitroureas ( carmustine) |
| Which proteins modulate G1 restriction point? | Rb and p53 |
| Common platinum agent that works in undeficed phase of cell cycle? | Cisplatin |
| What type of cancer drug is Busulfan? | Alkylating agent |
| Cyclophosphamide and Ifosfamide are both _______________ agents. | Alkylating |
| Which cancer drugs inhibit Nucleotide synthesis? | MTX, 5-FU; 6-MP; Hydroxyurea |
| How does MTX and 5-FU inhibit nucleotide synthesis? | Decrease thymidine synthesis |
| Which cancer drugs are known to decrease thymidine synthesis which causes an inhibition of nucleotide synthesis? | MTX and 5-FU |
| MOA of 6-MP, which leads to decreased/inhibition of nucleotide synthesis? | Decreases de novo purine synthesis |
| Antimetabolite that decrases de novo purine synthesis? | 6-MP |
| MOA of Hydroxyurea | Inhibits ribonucleotide reductase leading to a inhibition of nucleotide synthesis |
| Cancer drugs that inhibit DNA synthesis by causing cross-linking in DNA? | Alkylating agents and platinum agents |
| How do platinum agents decrease DNA production? | Cross-link DNA |
| Which cancer drugs work in the same way as Cisplatin? | Alkylating agents |
| How does Bleomycin (MOA) inhibit DNA synthesis? | DNA strand breakage |
| Commonly used DNA intercalators: | Dactinomycin and Doxorubicin |
| Dactinomycin and Doxorubicin are known as ___________________. | DNA intercalators |
| Common anticancer drug that intercalates DNA and causes heart problems? | Doxorubicin |
| MOA of Etoposide and Teniposide? | Inhibits topoisomerase II |
| Which anti-cancer drugs work by inhibiting Topoisomerase II? | Etoposide and Teniposide |
| What is inhibited by Irinotecan and Topotecan? | Topoisomerase I |
| In Topoisomerase inhibitors, if they end in --poside, it indicates? | Inhibits topoisomerase II |
| If the Topoisomerase inhibitor nomenclature ends with --tecan, it indicates inhibition of? | Inhibits topoisomerase I |
| What process of cell cycle is inhibited by Vinca alkaloids and Paclitaxel? | Cellular division |
| Vinca alkaloids MOA? | Inhibits microtubule formation |
| Which anticancer therapy works by inhibiting microtubule formation during mitosis? | Vinca alkaloids |
| What drug inhibits microtubule disassembly? | Paclitaxel |
| MOA of Paclitaxel? | Inhibition of microtubule disassembly |
| Purine (thiol) analogs that work by inhibiting de novo purine synthesis. | Azathioprine and 6-MP |
| What enzyme activates Azathioprine and 6-MP? | HGPRT |
| Role of HGPRT in antimetabolites? | Activation of Azathioprine and 6-MP |
| What is the relation/derivation between Azathioprine and 6-MP? | Azathioprine is metabolized into 6-MP |
| What is the most significant adverse effect of 6-MP and Azathiorine? | Myelosuppression |
| Which enzyme metabolizes azathioprine and 6-MP ? | Xanthine oxidase |
| Which antimetabolites are metabolized by XO? | Azathioprine and 6-MP |
| What medications may increase the 6-MP and Azathioprine's toxicity? | Allopurinol or Febuxostat |
| What are the primary clinical uses for azathioprine and 6-MP? | - Preventing organ rejection - Rheumatoid arthritis - IBD -SLE |
| Antimetabolites commonly used to wean off steroids-therapy in patients with chronic use of steroids? | Azathioprine and 6- MP |
| What is the main clinical use of Cladribine? | Hairy cell leukemia |
| Antimetabolite use to treat Hairy cell leukemia? | Cladribine |
| Two forms of MOA of Cladribine: | 1. Inhibition of DNA polymerase 2. DNA strand breaks |
| What are the associated adverse effects of Cladribine? | 1. Myelosuppression 2. Nephrotoxicity 3. Neurotoxicity |
| Besides myelosuppression, what other organs are at risk of adverse effects by treatment with Cladribine? | Kidneys and CNS |
| Azathioprine, 6-MP, and Cladribine are all ------> | Purine analogs |
| Which antimetabolites are Purine analogs? | Azathioprine, 6-MP, and Cladribine |
| Which antimetabolites are Pyrimidine analogs? | Cytarabine and 5-FU |
| Technical name of Cytarabine | Arabinofuranosyl cytidine |
| MOA of Cytarabine: | DNA chain termination. At higher concentrations ---> inhibits DNA polymerase |
| What condition has to be met in order for Cytarabine to inhibit DNA polymerase? | High drug concentration |
| Which malignancies are most commonly treated with Cytarabine? | Leukemias (AML), and lymphomas |
| Which is the most common leukemia treated with Cytarabine? | AML |
| Which antimetabolite may produce Myelosuppression with megaloblastic anemia? | Cytarabine |
| What is a global adverse effect of Cytarabine? | Pancytopenia |
| Similar drug (activity) to 5-FU? | Capecitabine |
| What is Capecitabine? | Prodrug with similar activity to 5-FU |
| Pyridine analog bioactivated to 5-FdUMP, which convenlay complexes with thymidylate synthase and folic acid . | Mechanism of action of 5-FU |
| Mechanism of action of 5-FU | [ 5-FdUMP/thymidylate synthase/folic acid] complex ---> decrease in dTMP which leads to a decrease in DNA synthesis. |
| What is the featured adverse effect of 5-FU? | Palmar-plantar erythrodysesthesia |
| What cancer drug may cause hand-foot syndrome? | 5-FU |
| What can be used to enhance the effects of 5-FU? | Leucovorin |
| What are the uses for 5-FU? | 1. Colon cancer 2. Pancreatic cancer 3. Actinic keratosis 4. Basal cell carcinoma (topical) |
| Which cutaneous conditions are treated with 5-FU? | Actinic keratosis and Basal cell carcinoma |
| Antimetabolite drug that is a Folic acid analog. | Methotrexate |
| Enzyme inhibited by MTX? | Dihydrofolate reductase |
| MOA of MTX? | Competitively inhibits dihydrofolate reductase leading to a decrease in dTMP which produces a decrease in DNA synthesi |
| What cancers are treated with MTX? | 1. Leukemias (ALL) 2. Lymphomas 3. Choriocarcinoma 4. Sarcomas |
| What are non-neoplastic conditions treated with MTX? | - Ectopic pregnancy - Medical abortion (with misoprostol) - Rheumatoid arthritis -Psoriasis - IBD - Vasculitis |
| Main adverse effect of MTX? | Myelosuppression |
| Treatment of myelosuppression caused by MTX? | Coadministered MTX with Leucovorin |
| Which is the "rescue" medication used in a patient on MTX? | Leucovorin |
| List of adverse effects seen with MTX | 1. Myelosuppression 2. Hepatotoxicity 3. Mucositis 4. Pulmonary fibrosis 5. Folate deficiency 6. Nephrotoxicity (rare) |
| MTX + misoprostol = | Medical abortion |
| What drug is used with MTX to cause an abortion? | Misoprostol |
| Teratogenic effect of MTX | Neural tube defects due to Folate deficiency |
| Which are the "antitumor antibiotics"? | 1. Bleomycin 2. Dactinomycin (actinomycin D) 3. Doxorubicin and Daunorubicin |
| MOA Bleomycin | Induces free radical formation which produce breaks in DNA strands |
| What are the most common uses for Bleomycin? | - Testicular cancer - Hodgkin lymphoma |
| Which antitumor antibiotic is often used to treat Testicular cancer? | Bleomycin |
| Most widely tested (USMLE) adverse effect of Bleomycin? | Pulmonary fibrosis |
| What are the key adverse effects of Bleomycin? | 1. Pulmonary fibrosis 2. Skin hyperpigmentation 3. Minimal myelosuppression |
| A person with Hx of testicular cancer, presents with dark skin and a restrictive lung pattern. Dx? | Adverse effects of Bleomycin therapy |
| What is the mode of action of Dactinomycin? | Intercalated into DNA, preventing RNA synthesis |
| What synthesis is prevented with Dactinomycin? | RNA |
| What is another name for Dactinomycin? | Actinomycin D |
| Antitumor antibiotic often used for childhood tumors | Dactinomycin |
| What tumors are treated with Dactinomycin? | 1. Wilms tumor 2. Ewing sarcoma 3. Rhabdomyosarcoma |
| Dactinomycin associated adverse effect? | Myelosuppression |
| MOA(s) of Doxorubicin and Daunorubicin | 1. Generate free radical by intercalation in DNA causing breaks in DNA and a decrease in replication 2. INterferes with topoisomerase II enzyme |
| Dactinomycin prevents _______ synthesis. | RNA |
| Doxorubicin decreases ________________________. | Replication |
| Solid tumors, leukemias, and lymphomas are treated with: | Doxorubicin and Daunorubicin |
| What is the most common adverse effect of Doxorubicin? | Cardiotoxicity (Dilated cardiomyopathy) |
| Which antitumor antibiotic is associated with development of Dilated cardiomyopathy? | Doxorubicin |
| What medication is used to prevent Doxorubicin-induced DCM? | Dexrazoxane |
| What is Dexrazoxane? | Iron chelating agent used to prevent cardiotoxicity |
| What are less important adverse effects of Daunorubicin and Doxorubicin? | Myelosuppression and alopecia |
| MOA Busulfan | Cross-links DNA |
| Clinical use of Busulfan | Ablate patient's bone marrow before bone marrow transplantation |
| What drug is used to obliterate the bone marrow of bone marrow recipient? | Busulfan |
| What are main 3 adverse effects seen with Busulfan? | 1. Severe myelosuppression 2. Pulmonary fibrosis 3. Hyperpigmentation |
| Which alkylating agent is known to work by cross-link DNA at guanine? | Cyclophosphamide and Ifosfamide |
| Nitrogen mustard | Cyclophosphamide and Ifosfamide |
| What is needed by Cyclophosphamide in order to function? | Bioactivation by liver |
| Featured/ unique adverse effect of Cyclophosphamide? | Hemorrhagic cystitis |
| What is co administered with Cyclophosphamide to prevent Hemorrhagic cystitis? | Mesna |
| Associated adverse effects of Cyclophosphamide and Ifosfamide? | 1. Myelosuppression 2. SIADH 3. Hemorrhagic cystitis (prevented with Mesna) |
| What is Mesna? | Medication given with Cyclophosphamide to prevent Hemorrhagic cystitis |
| MOA of Mesna | Thiol group of mesna binds toxic metabolites of Cyclophosphamide |
| Which alkylating agents are know to cross the BBB? | Nitrosoureas |
| Cross-link DNA; Require bioactivation; Cross the BBB. | Nitrosoureas |
| Alkylating agent often used in Brain tumors? | Nitrosoureas |
| What is the most significant side effect of Nitrosoureas? | CNS toxicity, which cause convulsions, ataxia, and dizziness. |
| Glioblastoma multiforme may be treated with which kind of alkylating agents? | Nitrosoureas |
| What kind of cancer drug is Procarbazine? | Alkylating agent |
| What are malignancies often treated with Procarbazine? | Hodgkin lymphoma and Brain tumors |
| What are the associated (severe) adverse effects of Procarbazine? | Bone marrow suppression, pulmonary toxicity, and leukemia |
| Hyper-stabilize polymerized microtubules in M phase so that mitotic spindle cannot break down. | Mechanism of action of Paclitaxel |
| Which mitosis phase cannot occur by using Paclitaxel or other taxanes? | Anaphase |
| What are the two malignancies treated with Paclitaxel? | Ovarian and Breast carcinomas |
| Adverse effects seen with Paclitaxel? | Myelosuppression, neuropathy, and hypersensitivity |
| Vinca alkaloids binding to B-tubulin cause: | Inhibition of polymerization into microtubules, which cause, prevention of mitotic spindle formation |
| M-phase afres is seen with: | Vinca alkaloids |
| Protein to which vinca alkaloids bind to: | B-tubulin |
| Vincristine is used in _________________ lymphomas. | Non-Hodgkin |
| Vinblastine is used to treat __________ lymphomas. | Hodgkin |
| Adverse effects seen with Vincristine: | 1. Neurotoxicity, 2. Constipation |
| Which adverse effect seen with Vinblastine? | Bone marrow suppression |
| Cancer patient develops paralytic ileus. Dx? | Treatment with Vincristine |
| What are clinical signs of Vincristine-caused neurotoxicity? | Arreflexia and peripheral neuritis |
| What are the clinical uses for Cisplatin and Carboplatin? | Testicular, bladder, ovary, and lung carcinomas |
| How is nephrotoxicity caused by Cisplatin prevented? | Coadministration with Amifostine and chloride |
| What is Amifostine? | Free radical scavenger that prevents nephrotoxicity caused by Cisplatin. |
| Associated adverse effects of Platinum agents? | #1 - Nephrotoxicity Peripheral neuropathy, and ototoxicity. |
| Inhibit topoisomerase II leading to increased DNA degradation. | Mechanism of action of Etoposide and Teniposide |
| What are the solid tumors treated with Etoposide and Teniposide? | Testicular and small cell lung cancer |
| MOA of Irinotecan and Topotecan: | -Inhibit topoisomerase I and, -Prevent DNA unwinding and replication |
| Which cancer is treated with Irinotecan? | Colon cancer |
| Topotecan is used to treat: | Ovarian and Small Cell lung cancers |
| What is an inconvenient adverse effect of Irinotecan and Topotecan? | Diarrhea |
| Which anticancer medication decraes DNA synthesis in the S-phase by inhibiting ribonucleotide reductase? | Hydroxyurea |
| What are the main uses for Hydroxyurea? | 1. Myeloproliferative disorders (CML, polycythemia vera) 2. Sickle cell |
| Why is Hydroxyurea used in Sickle cell disease? | Increase levels of HbF |
| Worrisome adverse effect of Hydroxyurea? | Severe myelosuppression |
| Monoclonal antibody against VEGF. | Bevacizumab |
| How does Bevacizumab works? | Monoclonal antibody against VEGF that inhibits angiogenesis |
| Which monoclonal antibody works by inhibiting angiogenesis? | Bevacizumab |
| What type of tumors are often treated with Bevacizumab? | Solid tumors, such as Colorectal cancer and RCC |
| What medication is used to treat Wet age-related macular degeneration? | Bevacizumab |
| Associated adverse effects of Bevacizumab: | Hemorrhage, blood clots, and impaired wound healing |
| MOA of Erlotinib | EGFR tyrosine kinase inhibitor |
| What is the clinical use of Erlotinib? | Non-small cell lung carcinoma |
| Adverse effect associated with Erlotinib: | Rash |
| Monoclonal antibody against EGFR? | Cetuximab |
| What type of colorectal cancer is treated with Cetuximab? | Stage IV colorectal cancer (wild-type KRAS) |
| What are some adverse effects of Cetuximab? | Rash, elevated LFTs, and diarrhea |
| Imatinib is: | Tyrosine kinase inhibitor of BCR-ABL and c-kit. |
| Which monoclonal antibody works on the Philadelphia chromosome fusion gene in CML? | Imatinib |
| What is a common used drug in CML treatment? | Imatinib |
| What cancers are treated with Imatinib? | 1. CML 2. GI stromal tumors (GIST) |
| A person on Imatinib may develop ______________ due to: | Edema due to fluid retention |
| Adverse effect -- Fluid retention | Imatinib |
| What is the monoclonal antibody against CD20? | Rituximab |
| Where is CD20 expressed/found? | Most B-cell neoplasms |
| Clinical uses of Rituximab: | Non-Hodgkin lymphoma, CLL, ITP, and rheumatoid arthritis |
| Which type fo lymphoma is treated with Rituximab? | Non-Hodgkin lymphoma |
| What is a serious and unique adverse effect of Rituximab? | Incrase risk of progressive multifocal leukoencephalopathy |
| Name 2 proteasome inhibitors, wich induce arrest at G2-M phase and apoptosis? | Bortezomib, and carfilzomib |
| What is often treated with Bortezomib? | Multiple myeloma, and Mantle cell lymphoma |
| MM is treated with what proteasome inhibitor? | Bortezomib |
| What are associated adverse effects of Bortezomib and Carfilzomib? | Peripheral neuropathy and Herpes zoster reactivation |
| What infection is often reactivated by the use of Bortezomib? | Herpes zoster |
| Common SERMs | Tamoxifen and Raloxifene |
| MOA of SERMs | Selective estrogen receptor modulators - receptor antagonists in breast and agonist in bone |
| Block the binding of estrogen to ER (+) cells | SERMs mode of action |
| Which SERM is used in Breast cancer treatment and prevention? | Tamoxifene |
| Common use, non-neoplastic, of Raloxifene? | Osteoporosis |
| What are the adverse effects of Tamoxifen? | Partial agonist in endometrium, which increases changes of endometrial cancer; "hot flashes" |
| Contrary to Tamoxifen, Raloxifene does not increase risk of endometrial cancer because: | It is an Estrogen receptor antagonist in endometrial tissue |
| What is a shared adverse effect of SERMs (Tamoxifen and Raloxifene)? | Increased risk of thromboembolic evens (DVT, PE) |
| Monoclonal antibody against HER-2 (c-erbB2), a tyrosine kinase receptor. | Trastuzumab |
| What is another name for Trastuzumab? | Herceptin |
| Anti-cancer mechanism of Trastuzumab? | Helps kill cancer cell that overexpress HER-2 through inhibition of HER-2 initiated cellular signaling and antibody-dependent cytotoxicity |
| Trastuzumab clinical use: | HER-2 (+) breast cancer and gastric cancer |
| What is the most common adverse effect of Trastuzumab? | Cardiotoxicity |
| What is Vemurafenib? | Small molecule inhibitor of BRAF oncogene (+) melanoma |
| What monoclonal antibody is used for V600E- mutated BRAF inhibition? | Vemurafenib |
| Common anticancer drug used for metastatic melanoma | Vemurafenib |
| MOA of Rasburicase | Recombinant uricase that catalyzes metabolism of uric acid to allantoin. |
| Which drug can cause the conversion of uric acid into allantoin? | Rasburicase |
| Use of Rasburicase | Prevention and treatment of Tumor lysis syndrome |
| Most common toxicities of Cisplatin and Carboplatin: | Ototoxicity and Nephrotoxicity |
| Chemotoxicity of Vincristine | Peripheral neuropathy |
| Which chemotherapy treatments are known to cause Pulmonary fibrosis? | Bleomycin and Busulfan |
| Main chemotoxicity of Doxorubicin | Cardiotoxicity |
| Which cancer medications are known to cause Cardiotoxicity? | Doxorubicin and Trastuzumab |
| Cyclophosphamide may produce which adverse effect? | Hemorrhagic cystitis |