This document summarizes several alkylating agents used in chemotherapy. Alkylating agents work by alkylating DNA and RNA, which can cause DNA breaks or abnormal sequences and damage cells' ability to replicate. Common side effects include myelosuppression, nausea/vomiting, and alopecia. Specific agents discussed include cyclophosphamide, ifosfamide, melphalan, busulfan, carmustine, lomustine, procarbazine, dacarbazine, streptozocin, bendamustine, altretamine, and chlorambucil. Each has unique indications and toxicity profiles involving bone marrow suppression, gastrointestinal upset, organ toxicity, secondary cancers, and more.
This document summarizes cancer chemotherapy drugs that act as alkylating agents. It describes how these drugs produce reactive carbonium ions that alkylate and cross-link DNA, inhibiting its replication and causing cell death. The major classes of alkylating agents discussed are nitrogen mustards, ethylenimines, alkyl sulfonates, nitrosoureas, and triazines. Specific drugs from these classes are mentioned along with their mechanisms of action, metabolism, uses, and dosages.
Chemotherapy uses anti-cancer drugs to destroy cancer cells. It can be curative for some cancers like leukemias, Wilms tumor, and Hodgkin's lymphoma. The drugs work by interfering with cell division through different mechanisms and can be cell cycle specific or non-specific. Alkylating agents are a common class of chemotherapy drugs that work by transferring alkyl groups to DNA, causing cross-linkages and strand breaks to damage DNA and inhibit cell proliferation. Combination chemotherapy and intermittent dosing regimens are often used to improve outcomes.
Topoisomerases are enzymes that regulate DNA topology during replication and transcription by introducing temporary breaks in DNA strands. Topoisomerase inhibitors can be classified as topoisomerase I or II inhibitors. Camptothecins like irinotecan and topotecan are topoisomerase I inhibitors that stabilize the covalent complex between topoisomerase I and DNA, preventing rejoining of DNA strands. They are used to treat colorectal cancer and other cancers. Anthracyclines like doxorubicin are topoisomerase II inhibitors that stabilize cleavable complexes and cause DNA damage. They are commonly used to treat breast cancer, lymphomas, sarcomas and other cancers. Both classes
This document summarizes key information about alkylating agents, a class of anticancer drugs. It describes their mechanisms of action involving alkylation of DNA, which interferes with its integrity and functions. Specific agents discussed include nitrogen mustards, nitrosoureas, triazines, and others. Toxicities involving bone marrow suppression and effects on other rapidly dividing tissues are also summarized. Pharmacological properties, indications, and dosing schedules are provided for several common alkylating agents including cyclophosphamide, ifosfamide, chlorambucil, melphalan, busulfan, dacarbazine, temozolamide, and procarbazine.
Chemotherapy induced nausea and vomitingswathisravani
This document discusses chemotherapy induced nausea and vomiting (CINV). It defines CINV and notes that 80% of cancer patients experience it. There are different types of CINV including acute, delayed, anticipated, breakthrough and refractory. Risk factors include age, gender, history of motion sickness and type of chemotherapy drugs. The pathogenesis involves the neurotransmitter serotonin and substance P. Treatment involves both non-pharmacological and pharmacological approaches, with drugs that target serotonin and neurokinin-1 receptors, along with corticosteroids.
Alkylating agents and antimetabolites are two classes of chemotherapy drugs. Alkylating agents work by binding to DNA and RNA, causing crosslinking or breaks that prevent replication. The main types are nitrogen mustards, alkyl sulphonates, nitrosoureas, and thiazines. Antimetabolites mimic normal metabolites and inhibit DNA or RNA synthesis by becoming incorporated. Major types are folate antagonists like methotrexate, pyrimidine analogs like 5-fluorouracil, and purine analogs like mercaptopurine. Both classes cause bone marrow suppression and gastrointestinal toxicity, and resistance can develop through drug inactivation or changes to drug targets.
This document discusses tyrosine kinase inhibitors and their role in cancer therapy. It begins by introducing tyrosine kinases and their importance in cellular signaling pathways. Tyrosine kinases are implicated in cancer development and progression. The document then discusses the classification, structure, and mechanisms of tyrosine kinase receptors. It provides examples of FDA-approved tyrosine kinase inhibitors for various cancers. The document discusses strategies for inhibiting EGFR signaling, including monoclonal antibodies and small molecule tyrosine kinase inhibitors. It also provides information on trastuzumab and its role and use for HER2-positive breast cancer.
This document summarizes cancer chemotherapy drugs that act as alkylating agents. It describes how these drugs produce reactive carbonium ions that alkylate and cross-link DNA, inhibiting its replication and causing cell death. The major classes of alkylating agents discussed are nitrogen mustards, ethylenimines, alkyl sulfonates, nitrosoureas, and triazines. Specific drugs from these classes are mentioned along with their mechanisms of action, metabolism, uses, and dosages.
Chemotherapy uses anti-cancer drugs to destroy cancer cells. It can be curative for some cancers like leukemias, Wilms tumor, and Hodgkin's lymphoma. The drugs work by interfering with cell division through different mechanisms and can be cell cycle specific or non-specific. Alkylating agents are a common class of chemotherapy drugs that work by transferring alkyl groups to DNA, causing cross-linkages and strand breaks to damage DNA and inhibit cell proliferation. Combination chemotherapy and intermittent dosing regimens are often used to improve outcomes.
Topoisomerases are enzymes that regulate DNA topology during replication and transcription by introducing temporary breaks in DNA strands. Topoisomerase inhibitors can be classified as topoisomerase I or II inhibitors. Camptothecins like irinotecan and topotecan are topoisomerase I inhibitors that stabilize the covalent complex between topoisomerase I and DNA, preventing rejoining of DNA strands. They are used to treat colorectal cancer and other cancers. Anthracyclines like doxorubicin are topoisomerase II inhibitors that stabilize cleavable complexes and cause DNA damage. They are commonly used to treat breast cancer, lymphomas, sarcomas and other cancers. Both classes
This document summarizes key information about alkylating agents, a class of anticancer drugs. It describes their mechanisms of action involving alkylation of DNA, which interferes with its integrity and functions. Specific agents discussed include nitrogen mustards, nitrosoureas, triazines, and others. Toxicities involving bone marrow suppression and effects on other rapidly dividing tissues are also summarized. Pharmacological properties, indications, and dosing schedules are provided for several common alkylating agents including cyclophosphamide, ifosfamide, chlorambucil, melphalan, busulfan, dacarbazine, temozolamide, and procarbazine.
Chemotherapy induced nausea and vomitingswathisravani
This document discusses chemotherapy induced nausea and vomiting (CINV). It defines CINV and notes that 80% of cancer patients experience it. There are different types of CINV including acute, delayed, anticipated, breakthrough and refractory. Risk factors include age, gender, history of motion sickness and type of chemotherapy drugs. The pathogenesis involves the neurotransmitter serotonin and substance P. Treatment involves both non-pharmacological and pharmacological approaches, with drugs that target serotonin and neurokinin-1 receptors, along with corticosteroids.
Alkylating agents and antimetabolites are two classes of chemotherapy drugs. Alkylating agents work by binding to DNA and RNA, causing crosslinking or breaks that prevent replication. The main types are nitrogen mustards, alkyl sulphonates, nitrosoureas, and thiazines. Antimetabolites mimic normal metabolites and inhibit DNA or RNA synthesis by becoming incorporated. Major types are folate antagonists like methotrexate, pyrimidine analogs like 5-fluorouracil, and purine analogs like mercaptopurine. Both classes cause bone marrow suppression and gastrointestinal toxicity, and resistance can develop through drug inactivation or changes to drug targets.
This document discusses tyrosine kinase inhibitors and their role in cancer therapy. It begins by introducing tyrosine kinases and their importance in cellular signaling pathways. Tyrosine kinases are implicated in cancer development and progression. The document then discusses the classification, structure, and mechanisms of tyrosine kinase receptors. It provides examples of FDA-approved tyrosine kinase inhibitors for various cancers. The document discusses strategies for inhibiting EGFR signaling, including monoclonal antibodies and small molecule tyrosine kinase inhibitors. It also provides information on trastuzumab and its role and use for HER2-positive breast cancer.
This document discusses the classification and mechanisms of action of various anti-cancer drugs. It categorizes drugs according to their cell cycle specificity, biochemical mechanism, and chemical structure. It provides examples of drugs that are cell cycle nonspecific and cell cycle specific. It also describes the mechanisms and examples of alkylating agents, antimetabolites, antimicrotubule agents, anticancer antibiotics, hormonal agents, and topoisomerase inhibitors. Common toxicities of different drug classes are mentioned.
This document describes alkylating agents, a class of chemotherapy drugs that work by alkylating DNA and proteins. It discusses their mechanism of action, including how they crosslink DNA and cause DNA damage, leading to cell death. It also covers resistance mechanisms, adverse effects like bone marrow toxicity and nausea/vomiting, and important alkylating agents like cisplatin, carboplatin, oxaliplatin, cyclophosphamide, and carmustine. For each drug, it provides absorption, indications, dosage ranges, and special considerations.
This document classifies and describes various anticancer drugs, including cytotoxic drugs like alkylating agents, platinum coordination drugs like cisplatin, antimetabolites, microtubule damaging agents like vincristine and vinblastine, topoisomerase inhibitors, antibiotics, targeted drugs, hormonal drugs, and miscellaneous drugs. It provides details on the mechanisms of action, uses, doses, and common side effects of representative drugs from each class, such as how cisplatin causes DNA cross-linking, how vinca alkaloids inhibit microtubule assembly, and how paclitaxel and docetaxel inhibit beta-tubulin.
The document provides guidelines from multiple organizations for preventing chemotherapy-induced nausea and vomiting (CINV). It summarizes that the ESMO guidelines classify combined anthracycline and cyclophosphamide (AC) regimens as moderately emetic, while ASCO and NCCN classify AC as highly emetic. It recommends for highly emetic chemotherapy, using a three-drug combination of a 5-HT3 antagonist, dexamethasone, and NK1 antagonist. For moderately emetic regimens, it preferentially recommends palonosetron with dexamethasone, or substituting other 5-HT3 antagonists, and optionally adding aprepitant.
This document summarizes antimicrotubule agents, which are tubulin-binding drugs that disrupt microtubule dynamics. It describes the mechanisms and clinical uses of several classes - taxanes like paclitaxel and docetaxel that stabilize microtubules, as well as vinca alkaloids like vincristine and vinblastine that destabilize microtubules. Toxicities like neutropenia and neuropathy are discussed for each drug. The document provides details on pharmacokinetics, metabolism, indications and interactions for these important chemotherapy agents.
Chemotherapy drugs work by targeting rapidly dividing cancer cells. Historically, chemotherapy began with accidental discoveries of drug effects. Modern chemotherapy classifications include cell cycle phase-specific and non-specific drugs. Tumor growth models like Skipper's laws and Goldie-Coldman hypothesis informed chemo design and dosing. Combination chemo is now standard, aiming for maximal cell kill within toxicity limits to overcome resistance. Routes include intravenous, oral, intrathecal and others. Toxicities require careful management.
Anthracyclines are a class of chemotherapy drugs that act as topoisomerase II inhibitors. Doxorubicin and daunorubicin were the first anthracyclines developed in the 1960s from bacteria. They intercalate DNA, inhibit topoisomerase and DNA synthesis, and generate free radicals causing DNA damage. Chronic cardiotoxicity is the main toxicity, with risk increasing with cumulative dose. Liposomal doxorubicin and mitoxantrone have less cardiotoxicity. Anthracyclines are used to treat many cancers but dose adjustments are needed for hepatic or renal dysfunction.
This document discusses various aspects of anticancer drugs and chemotherapy, including:
1. Types of chemotherapy drugs like alkylating agents, antimetabolites, antibiotics, and their mechanisms of action and cell cycle effects.
2. Goals and principles of cancer therapy like cure, remission, combination chemotherapy, and developing resistance.
3. Toxicities of chemotherapy drugs and methods to counter them, like growth factors and protective agents.
4. Targeted therapies like monoclonal antibodies and tyrosine kinase inhibitors used to treat specific cancers.
Methotrexate is a folate antagonist antimetabolite drug that works by inhibiting the enzyme dihydrofolate reductase, depleting tetrahydrofolate cofactors needed for DNA synthesis. It is used to treat cancers like acute lymphocytic leukemia, breast cancer, and rheumatoid arthritis. 5-Fluorouracil and capecitabine are pyrimidine antagonist antimetabolites that inhibit the enzyme thymidylate synthase, blocking DNA synthesis. They are used for cancers like colon cancer. Cytarabine is also a pyrimidine antagonist that incorporates into DNA, inhibiting its synthesis, and is used for acute leukemias. 6-Mercap
This document discusses tyrosine kinase inhibitors, which are drugs that target tyrosine kinases. It begins by introducing tyrosine kinases and their role in cell signaling pathways. It then describes several important tyrosine kinase inhibitors, including BCR-ABL inhibitors like imatinib, dasatinib, and nilotinib; EGFR inhibitors like gefitinib and erlotinib; and VEGF inhibitors like sunitinib and sorafenib. For each drug, it provides information on mechanisms of action, pharmacokinetics, dosing, toxicity profiles, and FDA-approved indications. The document concludes by discussing mechanisms of resistance to BCR-ABL kinase inhibitors.
The document discusses the mechanism of action, resistance mechanisms, and adverse effects of alkylating agents and anti-metabolites. Alkylating agents work by transferring alkyl groups to biologically important molecules like DNA, RNA, and proteins. This impairs cell function and can cause cross-linking of DNA. Anti-metabolites inhibit key enzymes in folate and purine synthesis pathways, interfering with DNA, RNA, and protein production. Both classes of drugs can cause myelosuppression and gastrointestinal toxicity as main adverse effects. Resistance can develop through increased DNA repair, reduced drug uptake, or alterations in target enzymes.
Antimetabolites are a class of chemotherapy drugs that work by interfering with DNA and RNA synthesis in cancer cells. They include folic acid analogs like methotrexate, purine analogs like mercaptopurine, and pyrimidine analogs like 5-fluorouracil. These drugs are used to treat many types of cancer including leukemias, lymphomas, and solid tumors in organs like breast, lung, and colon. While they can be effective, their use is often limited by bone marrow suppression and other toxicities due to their effects on rapidly dividing normal cells.
This document discusses the use of hormones in cancer treatment. It describes several classes of drugs that work by blocking hormone receptors, including glucocorticoid receptor agonists, selective estrogen receptor modulators (SERMs) like tamoxifen, selective estrogen receptor downregulators (SERDs) like fulvestrant, aromatase inhibitors (AIs), and progesterone receptor agonists. These drugs are used to treat breast, prostate, and other hormone-dependent cancers based on their mechanisms of competing with or degrading hormone receptors. Common side effects include symptoms of hormone deprivation.
This document discusses chemotherapy for cancer treatment. It describes the main types of anticancer drugs as cytotoxic, targeted, and hormonal drugs. Cytotoxic drugs are further broken down into categories like alkylating agents, platinum coordination compounds, antimetabolites, and microtubule damaging agents. The document also covers general principles of chemotherapy like using combination therapy to achieve total tumour cell kill and targeting actively dividing cancer cells. Adverse effects of cytotoxic drugs are explained, like bone marrow depression and immunosuppression. The goal of cancer therapy is outlined as cure, prolonging remission, or palliation depending on the cancer type and stage.
This document summarizes various classes and subclasses of cancer chemotherapy drugs, including their mechanisms of action, toxicities, and therapeutic uses. It discusses cell cycle-specific agents like alkylating agents, antimetabolites, plant alkaloids, and hormones. Alkylating agents like cyclophosphamide can alkylate DNA. Antimetabolites like methotrexate and 5-fluorouracil interfere with DNA synthesis. Plant alkaloids including vinca alkaloids and taxanes affect microtubules. Hormonal therapies include tamoxifen, aromatase inhibitors, and gonadotropin-releasing hormone agonists. The document provides detailed information on numerous chemotherapy drugs.
The document discusses various classes of anticancer drugs including cytotoxic drugs derived from natural sources like plants and microbes. It focuses on the mechanisms of action and classification of antitumor antibiotic drugs derived from Streptomyces bacteria. Specifically, it describes the structures, mechanisms involving DNA intercalation and inhibition of topoisomerases, and clinical uses of important anthracycline antibiotics like doxorubicin, daunorubicin and actinomycin antibiotics like dactinomycin and mitomycin C.
This document summarizes several classes of antimetabolite drugs, including their mechanisms of action and clinical uses. It discusses antifolate drugs like methotrexate and pemetrexed, which inhibit dihydrofolate reductase and other folate-dependent enzymes. It also covers fluoropyrimidines like 5-fluorouracil and capecitabine, which interfere with thymidylate synthase during DNA synthesis. Deoxycytidine analogs such as cytarabine and gemcitabine are described as inhibiting DNA polymerase. The document concludes by discussing purine antagonists including mercaptopurine, fludarabine, and cladribine, which
Antimicrotubule agents such as paclitaxel and docetaxel are microtubule-stabilizing drugs that directly bind to tubulin. They profoundly alter microtubule dynamics and suppress microtubule depolymerization, leading to mitotic arrest. Peripheral neuropathy is a common side effect due to their effects on microtubules in neurons. Paclitaxel and docetaxel are effective in treating several types of cancer but require premedication to reduce hypersensitivity reactions and have dose-limiting toxicities of neutropenia and neuropathy.
Cisplatin and its platinum analogs are important chemotherapy drugs. The document discusses the properties and mechanisms of several platinum analogs including carboplatin, oxaliplatin, and lobaplatin. It describes how their chemical structures differ from cisplatin in ways that impact properties like stability, reactivity, mechanisms of DNA damage, and toxicity profiles. The document also summarizes key mechanisms of resistance to platinum drugs, like reduced accumulation, inactivation by thiols, increased DNA repair, and enhanced damage tolerance.
This document discusses cytotoxic drugs used in chemotherapy. It begins by defining cytotoxic agents as drugs that destroy or inhibit the growth of malignant cells. It then provides details on various classes of cytotoxic drugs including alkylating agents, platinum coordination complexes, antimetabolites, topoisomerase inhibitors, antibiotics, and targeted therapies. For each drug class and individual drugs, it describes mechanisms of action, indications, dosages, administration routes, metabolism, toxicities and resistance mechanisms. The document provides an in-depth review of cytotoxic chemotherapy agents.
The document discusses epilepsy and antiepileptic drugs. It defines epilepsy as a chronic neurological disorder characterized by recurrent seizures. It describes the types of seizures as partial or generalized depending on the location and spread of abnormal neuronal discharge. The main causes of epilepsy include stroke, head trauma, brain tumors, and certain genetic disorders. Antiepileptic drugs work mainly by reducing electrical excitability of cell membranes or enhancing GABA-mediated synaptic inhibition. Several important antiepileptic drugs are discussed in detail including valproic acid, phenytoin, and carbamazepine.
This document discusses the classification and mechanisms of action of various anti-cancer drugs. It categorizes drugs according to their cell cycle specificity, biochemical mechanism, and chemical structure. It provides examples of drugs that are cell cycle nonspecific and cell cycle specific. It also describes the mechanisms and examples of alkylating agents, antimetabolites, antimicrotubule agents, anticancer antibiotics, hormonal agents, and topoisomerase inhibitors. Common toxicities of different drug classes are mentioned.
This document describes alkylating agents, a class of chemotherapy drugs that work by alkylating DNA and proteins. It discusses their mechanism of action, including how they crosslink DNA and cause DNA damage, leading to cell death. It also covers resistance mechanisms, adverse effects like bone marrow toxicity and nausea/vomiting, and important alkylating agents like cisplatin, carboplatin, oxaliplatin, cyclophosphamide, and carmustine. For each drug, it provides absorption, indications, dosage ranges, and special considerations.
This document classifies and describes various anticancer drugs, including cytotoxic drugs like alkylating agents, platinum coordination drugs like cisplatin, antimetabolites, microtubule damaging agents like vincristine and vinblastine, topoisomerase inhibitors, antibiotics, targeted drugs, hormonal drugs, and miscellaneous drugs. It provides details on the mechanisms of action, uses, doses, and common side effects of representative drugs from each class, such as how cisplatin causes DNA cross-linking, how vinca alkaloids inhibit microtubule assembly, and how paclitaxel and docetaxel inhibit beta-tubulin.
The document provides guidelines from multiple organizations for preventing chemotherapy-induced nausea and vomiting (CINV). It summarizes that the ESMO guidelines classify combined anthracycline and cyclophosphamide (AC) regimens as moderately emetic, while ASCO and NCCN classify AC as highly emetic. It recommends for highly emetic chemotherapy, using a three-drug combination of a 5-HT3 antagonist, dexamethasone, and NK1 antagonist. For moderately emetic regimens, it preferentially recommends palonosetron with dexamethasone, or substituting other 5-HT3 antagonists, and optionally adding aprepitant.
This document summarizes antimicrotubule agents, which are tubulin-binding drugs that disrupt microtubule dynamics. It describes the mechanisms and clinical uses of several classes - taxanes like paclitaxel and docetaxel that stabilize microtubules, as well as vinca alkaloids like vincristine and vinblastine that destabilize microtubules. Toxicities like neutropenia and neuropathy are discussed for each drug. The document provides details on pharmacokinetics, metabolism, indications and interactions for these important chemotherapy agents.
Chemotherapy drugs work by targeting rapidly dividing cancer cells. Historically, chemotherapy began with accidental discoveries of drug effects. Modern chemotherapy classifications include cell cycle phase-specific and non-specific drugs. Tumor growth models like Skipper's laws and Goldie-Coldman hypothesis informed chemo design and dosing. Combination chemo is now standard, aiming for maximal cell kill within toxicity limits to overcome resistance. Routes include intravenous, oral, intrathecal and others. Toxicities require careful management.
Anthracyclines are a class of chemotherapy drugs that act as topoisomerase II inhibitors. Doxorubicin and daunorubicin were the first anthracyclines developed in the 1960s from bacteria. They intercalate DNA, inhibit topoisomerase and DNA synthesis, and generate free radicals causing DNA damage. Chronic cardiotoxicity is the main toxicity, with risk increasing with cumulative dose. Liposomal doxorubicin and mitoxantrone have less cardiotoxicity. Anthracyclines are used to treat many cancers but dose adjustments are needed for hepatic or renal dysfunction.
This document discusses various aspects of anticancer drugs and chemotherapy, including:
1. Types of chemotherapy drugs like alkylating agents, antimetabolites, antibiotics, and their mechanisms of action and cell cycle effects.
2. Goals and principles of cancer therapy like cure, remission, combination chemotherapy, and developing resistance.
3. Toxicities of chemotherapy drugs and methods to counter them, like growth factors and protective agents.
4. Targeted therapies like monoclonal antibodies and tyrosine kinase inhibitors used to treat specific cancers.
Methotrexate is a folate antagonist antimetabolite drug that works by inhibiting the enzyme dihydrofolate reductase, depleting tetrahydrofolate cofactors needed for DNA synthesis. It is used to treat cancers like acute lymphocytic leukemia, breast cancer, and rheumatoid arthritis. 5-Fluorouracil and capecitabine are pyrimidine antagonist antimetabolites that inhibit the enzyme thymidylate synthase, blocking DNA synthesis. They are used for cancers like colon cancer. Cytarabine is also a pyrimidine antagonist that incorporates into DNA, inhibiting its synthesis, and is used for acute leukemias. 6-Mercap
This document discusses tyrosine kinase inhibitors, which are drugs that target tyrosine kinases. It begins by introducing tyrosine kinases and their role in cell signaling pathways. It then describes several important tyrosine kinase inhibitors, including BCR-ABL inhibitors like imatinib, dasatinib, and nilotinib; EGFR inhibitors like gefitinib and erlotinib; and VEGF inhibitors like sunitinib and sorafenib. For each drug, it provides information on mechanisms of action, pharmacokinetics, dosing, toxicity profiles, and FDA-approved indications. The document concludes by discussing mechanisms of resistance to BCR-ABL kinase inhibitors.
The document discusses the mechanism of action, resistance mechanisms, and adverse effects of alkylating agents and anti-metabolites. Alkylating agents work by transferring alkyl groups to biologically important molecules like DNA, RNA, and proteins. This impairs cell function and can cause cross-linking of DNA. Anti-metabolites inhibit key enzymes in folate and purine synthesis pathways, interfering with DNA, RNA, and protein production. Both classes of drugs can cause myelosuppression and gastrointestinal toxicity as main adverse effects. Resistance can develop through increased DNA repair, reduced drug uptake, or alterations in target enzymes.
Antimetabolites are a class of chemotherapy drugs that work by interfering with DNA and RNA synthesis in cancer cells. They include folic acid analogs like methotrexate, purine analogs like mercaptopurine, and pyrimidine analogs like 5-fluorouracil. These drugs are used to treat many types of cancer including leukemias, lymphomas, and solid tumors in organs like breast, lung, and colon. While they can be effective, their use is often limited by bone marrow suppression and other toxicities due to their effects on rapidly dividing normal cells.
This document discusses the use of hormones in cancer treatment. It describes several classes of drugs that work by blocking hormone receptors, including glucocorticoid receptor agonists, selective estrogen receptor modulators (SERMs) like tamoxifen, selective estrogen receptor downregulators (SERDs) like fulvestrant, aromatase inhibitors (AIs), and progesterone receptor agonists. These drugs are used to treat breast, prostate, and other hormone-dependent cancers based on their mechanisms of competing with or degrading hormone receptors. Common side effects include symptoms of hormone deprivation.
This document discusses chemotherapy for cancer treatment. It describes the main types of anticancer drugs as cytotoxic, targeted, and hormonal drugs. Cytotoxic drugs are further broken down into categories like alkylating agents, platinum coordination compounds, antimetabolites, and microtubule damaging agents. The document also covers general principles of chemotherapy like using combination therapy to achieve total tumour cell kill and targeting actively dividing cancer cells. Adverse effects of cytotoxic drugs are explained, like bone marrow depression and immunosuppression. The goal of cancer therapy is outlined as cure, prolonging remission, or palliation depending on the cancer type and stage.
This document summarizes various classes and subclasses of cancer chemotherapy drugs, including their mechanisms of action, toxicities, and therapeutic uses. It discusses cell cycle-specific agents like alkylating agents, antimetabolites, plant alkaloids, and hormones. Alkylating agents like cyclophosphamide can alkylate DNA. Antimetabolites like methotrexate and 5-fluorouracil interfere with DNA synthesis. Plant alkaloids including vinca alkaloids and taxanes affect microtubules. Hormonal therapies include tamoxifen, aromatase inhibitors, and gonadotropin-releasing hormone agonists. The document provides detailed information on numerous chemotherapy drugs.
The document discusses various classes of anticancer drugs including cytotoxic drugs derived from natural sources like plants and microbes. It focuses on the mechanisms of action and classification of antitumor antibiotic drugs derived from Streptomyces bacteria. Specifically, it describes the structures, mechanisms involving DNA intercalation and inhibition of topoisomerases, and clinical uses of important anthracycline antibiotics like doxorubicin, daunorubicin and actinomycin antibiotics like dactinomycin and mitomycin C.
This document summarizes several classes of antimetabolite drugs, including their mechanisms of action and clinical uses. It discusses antifolate drugs like methotrexate and pemetrexed, which inhibit dihydrofolate reductase and other folate-dependent enzymes. It also covers fluoropyrimidines like 5-fluorouracil and capecitabine, which interfere with thymidylate synthase during DNA synthesis. Deoxycytidine analogs such as cytarabine and gemcitabine are described as inhibiting DNA polymerase. The document concludes by discussing purine antagonists including mercaptopurine, fludarabine, and cladribine, which
Antimicrotubule agents such as paclitaxel and docetaxel are microtubule-stabilizing drugs that directly bind to tubulin. They profoundly alter microtubule dynamics and suppress microtubule depolymerization, leading to mitotic arrest. Peripheral neuropathy is a common side effect due to their effects on microtubules in neurons. Paclitaxel and docetaxel are effective in treating several types of cancer but require premedication to reduce hypersensitivity reactions and have dose-limiting toxicities of neutropenia and neuropathy.
Cisplatin and its platinum analogs are important chemotherapy drugs. The document discusses the properties and mechanisms of several platinum analogs including carboplatin, oxaliplatin, and lobaplatin. It describes how their chemical structures differ from cisplatin in ways that impact properties like stability, reactivity, mechanisms of DNA damage, and toxicity profiles. The document also summarizes key mechanisms of resistance to platinum drugs, like reduced accumulation, inactivation by thiols, increased DNA repair, and enhanced damage tolerance.
This document discusses cytotoxic drugs used in chemotherapy. It begins by defining cytotoxic agents as drugs that destroy or inhibit the growth of malignant cells. It then provides details on various classes of cytotoxic drugs including alkylating agents, platinum coordination complexes, antimetabolites, topoisomerase inhibitors, antibiotics, and targeted therapies. For each drug class and individual drugs, it describes mechanisms of action, indications, dosages, administration routes, metabolism, toxicities and resistance mechanisms. The document provides an in-depth review of cytotoxic chemotherapy agents.
The document discusses epilepsy and antiepileptic drugs. It defines epilepsy as a chronic neurological disorder characterized by recurrent seizures. It describes the types of seizures as partial or generalized depending on the location and spread of abnormal neuronal discharge. The main causes of epilepsy include stroke, head trauma, brain tumors, and certain genetic disorders. Antiepileptic drugs work mainly by reducing electrical excitability of cell membranes or enhancing GABA-mediated synaptic inhibition. Several important antiepileptic drugs are discussed in detail including valproic acid, phenytoin, and carbamazepine.
The document categorizes and describes various classes of drugs used in cancer chemotherapy, including their mechanisms of action, pharmacokinetics, adverse effects, and clinical uses. It discusses cytotoxic drugs that act directly on cells like alkylating agents, antimetabolites, vinca alkaloids, taxanes, and antibiotics. It also covers drugs that alter the hormonal milieu and miscellaneous drugs like hydroxyurea. For each class, it provides one or more examples and describes in detail the example drug's mechanism, pharmacokinetics, adverse effects and clinical applications.
Protozoal infections are caused by eukaryotic, unicellular protozoa and include diseases like malaria, amoebiasis, and giardiasis. They are often caused by unhygienic conditions and can be difficult to treat as anti-protozoal drugs are more toxic than antibiotics for bacterial infections. Malaria is caused by Plasmodium parasites and transmitted between humans and mosquitos. It has an asexual replication phase in humans and a sexual phase in mosquitos. Common antimalarial drugs include chloroquine, primaquine, mefloquine, atovaquone-proguanil, and artemisinin compounds.
This document discusses hepatotoxic drugs and their mechanisms of causing liver damage. It begins by classifying hepatotoxic drugs into intrinsic, idiosyncratic, and chronic categories. It then describes various mechanisms by which drugs can damage the liver, including by forming reactive metabolites, depleting glutathione, and interfering with mitochondrial functions. Specific hepatotoxic drugs are listed for different drug classes. Methods for evaluating hepatotoxicity both in vivo and in vitro are also presented.
Hematologic Malignancies: Approach to Understanding Pathogenesis and Treatmentflasco_org
This document summarizes the pharmacology of various antineoplastic agents used to treat malignant hematology. It discusses the mechanism of action, administration, metabolism, elimination and common toxicities of different classes of drugs including antimetabolites, alkylating agents, vinca alkaloids, anthracyclines, targeted therapies and immunotherapies. Specific attention is given to the pharmacokinetics and toxicity profiles of commonly used drugs like methotrexate, cytarabine, fludarabine, rituximab and imatinib.
1. The document provides an overview of cancer chemotherapy, including targets, classification of drugs, mechanisms of drug resistance, and new approaches.
2. It discusses various classes of chemotherapy drugs like alkylating agents, antimetabolites, plant alkaloids, and antibiotics. Specific drugs like cyclophosphamide, methotrexate, vinblastine, and doxorubicin are described in terms of their mechanisms and toxicities.
3. Newer targeted therapies like imatinib are also mentioned, reflecting the evolution toward more precise inhibition of molecular targets driving cancer growth.
To explain pathogenesis of Bipolar Disorders
To classify drugs used for treatment of Bipolar Disorders
To describe mechanism of action of drugs used for treatment of Bipolar Disorders
To enlist side effects of drugs used for treatment of Bipolar Disorders.
Indications: Bipolar, cyclothymia, schizoaffective, impulse control and intermittent explosive disorders.
Classes: Lithium, anticonvulsants, antipsychotics
Which you select depends on what you are treating and again the side effect profile.
This document provides an overview of drug-induced liver disease (DILD). It defines DILD and discusses its epidemiology and risk factors. Two main mechanisms of hepatotoxicity are described - intrinsic and idiosyncratic. Various types of DILD are outlined including hepatocellular necrosis, steatosis, cholestasis, granulomatous hepatitis, and fibrosis/cirrhosis. Clinical manifestations, investigations, and treatment approaches are summarized. Assessment involves a patient history, liver enzyme levels, biopsy, and nutritional status evaluation. Treatment focuses on diagnosis, drug withdrawal, supportive care, and use of antidotes/corticosteroids if needed.
1. Fatty liver of pregnancy typically occurs late in pregnancy and is associated with preeclampsia. Immediate termination of pregnancy is essential for possible recovery of the patient.
2. Prognosis in fulminant hepatic failure is affected by age, etiology, clinical course, and occurrence of secondary complications such as bleeding and hypoglycemia. Poor prognostic signs include increased prothrombin time and decreased pH.
3. Causes of death in fulminant hepatic failure include renal failure, respiratory failure, neurological complications such as cerebral edema, gastrointestinal hemorrhage, bacterial infection, and hemodynamic complications.
This document provides information on various anti-tuberculosis drugs including isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin. It discusses the mechanisms of action, pharmacokinetics, interactions, dosing, and adverse effects of each drug. It also provides historical context on the development of anti-tuberculosis treatments and classifications of first and second-line drugs.
ACUTE LIVER FAILURE - APPROACH AND MANAGEMENTNishant Yadav
Acute liver failure is a clinical syndrome resulting from massive necrosis or impairment of hepatocytes, leaving insufficient liver function. It impairs synthetic, excretory, and detoxifying liver functions. Pediatric acute liver failure is defined by evidence of liver dysfunction within 8 weeks, uncorrectable coagulopathy, and no evidence of chronic liver disease. Causes include viral infections, drugs, and metabolic disorders. Management involves transport to a specialized center, intensive care, supportive care, measures for raised intracranial pressure, coagulopathy, sepsis, and potential liver transplantation.
A 50-year-old man undergoing chemotherapy for a malignant tumor develops megaloblastic anemia. This is likely caused by methotrexate inhibiting folate metabolism. Folic acid supplementation could have prevented the toxicity. Anthracyclines like doxorubicin can cause cardiac toxicity through free radical generation, sometimes requiring dexrazoxane treatment. Bleomycin can cause pulmonary fibrosis.
The document discusses various classes of anti-cancer drugs, including their mechanisms of action, pharmacokinetics, clinical uses, and common adverse effects. It covers alkylating agents, antimetabolites, plant alkaloids, antibiotics, hormonal agents, and other miscellaneous anti-cancer drugs. The classes of drugs discussed attack cancer cells through different mechanisms such as alkylation of DNA, inhibition of DNA synthesis, disruption of microtubule formation, and interference with hormone signaling pathways.
The document discusses various classes of anti-cancer drugs, including their mechanisms of action, pharmacokinetics, clinical uses, and common adverse effects. It covers alkylating agents, antimetabolites, plant alkaloids, antibiotics, hormonal agents, and other miscellaneous anti-cancer drugs. The classes of drugs discussed attack cancer cells through DNA and RNA interference, inhibition of cell cycle progression, and hormone manipulation.
This document discusses jaundice, its causes, and approach to postoperative jaundice. It defines jaundice as yellow discoloration from hyperbilirubinemia. Causes of postoperative jaundice include hemolysis, hepatic dysfunction unrelated to surgery, and obstructive causes. The workup involves liver function tests to determine if the jaundice is prehepatic, hepatocellular, or obstructive. Management depends on the identified cause, but generally involves supportive care, discontinuing hepatotoxic drugs, treating sepsis aggressively, and considering surgery for biliary obstruction.
Therapeutic objective (prevention of DVT) Choose drug & dosing regimen (warfarin od) Monitor therapeutic and toxic response (INR and bleeding) PK PD Initiation and management of drug therapy
Drug levels can be monitored to ensure they remain within a therapeutic range. This involves repeated dosing to maintain steady state levels between a lower limit for adequate effect and an upper limit to avoid toxicity for drugs with a narrow therapeutic index or variable pharmacokinetics. Factors like liver or kidney function and drug interactions can impact drug clearance and require dosing adjustments.
The document discusses therapeutic drug monitoring (TDM), including choosing a drug and dosing regimen for a therapeutic objective, monitoring the therapeutic and toxic response, and managing drug therapy. It provides examples of TDM for various drugs, noting their therapeutic ranges, toxicity risks, and factors that influence pharmacokinetics and clearance. Close monitoring of drug levels is especially important for drugs with a low therapeutic index or highly variable pharmacokinetics.
Similar to Chapter 21 alkylating agents,platins,antimetabolites (20)
Chapter 39 role of radiotherapy in benign diseases.pptx [read only]Nilesh Kucha
This document discusses the role of radiotherapy in treating non-malignant diseases. It begins by classifying non-malignant diseases and outlining some common indications for radiotherapy, such as invasive growth, functional impairment, or pain. It then discusses specific disorders like desmoids, keloids, and Peyronie's disease. For each condition, it describes non-radiotherapy treatments, radiotherapy dose and techniques, and expected clinical outcomes. Throughout, it emphasizes the need for a risk-benefit analysis and informed consent when using radiotherapy for benign rather than malignant purposes.
Chapter 39 role of radiotherapy in benign diseasesNilesh Kucha
Surgery is the last resort
RADIOTHERAPEUTIC TREATMENT
Indications:
- Painful degenerative changes with no or minimal joint space narrowing
- Inflammatory synovitis
- Postoperative pain relief
- As an adjunct to conservative measures
Technique:
- Low energy X-rays or electrons
- Small field sizes (2-4 cm)
- Total dose 6-10 Gy in 3-5 fractions over 1-2 weeks
- Joint immobilization
Results:
- Pain relief in 60-80% patients lasting 3-6 months
- No disease modification
- Repeat treatment possible if pain recurs
Chapter 39 role of radiotherapy in benign diseasesNilesh Kucha
Radiotherapy can successfully treat some non-malignant diseases by reducing inflammation, inhibiting fibroblast proliferation, and preventing mitotic cell proliferation. It may be indicated for aggressive growths, functional impairment, or pain when other methods have failed. Risks include potential long-term induction of tumors. Treatment requires a risk-benefit analysis and informed consent. Doses and techniques vary depending on the condition but are typically fractionated over several days to weeks with total doses of 8-65Gy. Outcomes include improved symptoms for some connective tissue disorders and skin conditions.
Chapter 38 role of surgery in cancer preventionNilesh Kucha
The document discusses the role of surgery in preventing cancers caused by hereditary genetic mutations. It focuses on several high-risk cancer syndromes including BRCA1/2 mutations which increase breast and ovarian cancer risk, CDH1 mutations which increase stomach cancer risk, and APC mutations which cause Familial Adenomatous Polyposis (FAP) and increase colon cancer risk. For each, it describes the associated cancer risks, genetic testing recommendations, surveillance guidelines, and risk-reducing surgical options such as prophylactic mastectomies, salpingo-oophorectomies, and gastrectomies. The timing of such surgeries is based on the earliest age of cancer onset in the
Superior vena cava (SVC) syndrome results from obstruction of blood flow through the SVC, which can be caused by external compression or invasion by adjacent tumors or thrombosis within the SVC. The most common causes are lung cancer, lymphoma, and thrombosis related to intravenous devices. Obstruction of the SVC increases venous blood pressure as collateral veins form, potentially causing symptoms like head and neck swelling, dyspnea, and cough. SVC syndrome is diagnosed based on symptoms and imaging evidence of SVC obstruction.
Regulatory T-cells (Tregs) help maintain self-tolerance and prevent autoimmunity by suppressing immune responses. They express FOXP3 and CD25 and function through various mechanisms like secreting inhibitory cytokines or metabolizing IL-2. Tregs are implicated in tumor immune escape by suppressing anti-tumor immunity. While Tregs are normally beneficial, in cancer high levels associate with poor prognosis by hindering immune response. Emerging immunotherapies aim to deplete or modulate Tregs to enhance anti-tumor immunity.
Tumor lysis syndrome is an oncologic emergency caused by massive tumor cell lysis and release of potassium, phosphate, and nucleic acids into circulation. It often occurs after initiation of cytotoxic therapy in patients with high-grade lymphomas or ALL who have a large tumor burden or high proliferative rate. This can result in hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and acute kidney injury due to uric acid precipitation in renal tubules. Aggressive hydration, allopurinol or rasburicase to reduce uric acid, phosphate binders, and renal replacement therapy if needed are used to treat and prevent tumor lysis syndrome.
This document provides an overview of different types of clinical study designs, including observational studies and experimental studies. It discusses the key aspects and objectives of different phases of clinical trials, including:
1. Phase I trials which aim to determine safety and maximum tolerated dose of new therapies.
2. Phase II trials which provide preliminary evidence of efficacy through surrogate endpoints and further evaluate safety.
3. Phase III trials which are comparative effectiveness trials that use clinical outcomes like survival to compare new treatments to standard of care through randomized controlled designs.
ITC, or isolated tumor cells, refer to small clusters of cancer cells that break off from the primary tumor and circulate in the bloodstream. While only 0.05% of circulating tumor cells survive to form metastases, detection of ITC can provide prognostic information. ITC can be detected using morphological or non-morphological methods like immunohistochemistry and PCR, but non-morphological methods have a higher false positive rate. The presence of ITC may have prognostic value and inform more aggressive treatment, but the evidence for their clinical significance is equivocal for many cancer types. ITC detection is most clearly prognostic in breast cancer, while data is mixed for colorectal cancer.
The document summarizes the process of cancer metastasis through the invasion-metastasis cascade. It involves 6 key steps: 1) Localized invasion of primary tumor cells aided by loss of cell adhesion molecules and matrix metalloproteinases. 2) Intravasation of tumor cells into blood vessels assisted by tumor-associated macrophages. 3) Transport of circulating tumor cells protected by platelet emboli. 4) Extravasation of tumor cells from vessels into distant tissues. 5) Formation of dormant micrometastases. 6) Rare colonization of micrometastases into macroscopic tumors limited by the foreign tissue environment. Metastasis suppressor genes and strategies targeting multiple steps simultaneously show promise for preventing cancer spread.
This document discusses the components of a cancer genetic counseling session. It describes the process of obtaining a family history, assessing cancer risks, discussing genetic testing options and implications for family members. Key parts of the session include getting informed consent, choosing an appropriate candidate for testing, determining cancer risks, implications for relatives, and making management recommendations even if testing is declined.
This document provides guidelines for the management of febrile neutropenia in cancer patients. It defines febrile neutropenia and outlines risks for serious infection. Initial assessment involves evaluating risk of complications to determine treatment approach. Empiric broad-spectrum antibacterial therapy should be initiated within 60 minutes of presentation to cover likely pathogens. The regimen may be modified based on infection source or persistence of fever. Early antifungal therapy should also be considered for high-risk patients.
Dendritic cells are bone marrow-derived antigen-presenting cells that initiate adaptive immune responses. They capture antigens through processes like endocytosis and present them on MHC molecules to activate T cells. Dendritic cells exist in immature and mature forms, and upon maturation they migrate from tissues to lymph nodes to activate T cells. As the most potent antigen-presenting cells, dendritic cells play a key role in anti-cancer immunity by presenting tumor antigens, activating T cells, and generating an immune response against cancer cells.
This document provides an overview of clinical trials and their various phases. It discusses how clinical trials are used to test potential interventions in humans to determine if they should be adopted for general use. The different phases of clinical trials are described, including phase I-IV. Key aspects of clinical trial design such as randomization, blinding, and placebos are explained. Hypothesis testing and its role in statistical analysis is also summarized.
Chapter 27 chemotherapy side effects dr lmsNilesh Kucha
The era of modern chemotherapy began in the early 1940s when Goodman and Gilman first administered nitrogen mustard to lymphoma patients. Although nitrogen mustard was originally developed as a chemical weapon, its toxic effects on the lymphatic system led to clinical trials of its use in cancer treatment. This marked the beginning of chemotherapy as an active field of cancer research and therapy development.
Chemoprevention seeks to use natural, synthetic, or biological agents to prevent cancer development and progression. It can involve blocking cancer initiation through agents that prevent DNA damage from carcinogens. It can also suppress promotion and progression of initiated cells through inhibition of signal transduction pathways. The FDA has approved selective estrogen receptor modulators like tamoxifen and raloxifene for breast cancer chemoprevention and aspirin use has been associated with reduced colorectal cancer risk. However, some agents like beta-carotene and retinoids have been found to increase cancer risk in smokers.
Chapter 25 assessment of clincal responsesNilesh Kucha
The document discusses guidelines for assessing clinical response in cancer patients based on tumor size changes. The RECIST (Response Evaluation Criteria in Solid Tumors) criteria provide a standardized approach for measuring lesions and determining objective tumor responses. Key points include defining measurable vs. non-measurable lesions, methods for measurement and assessment, and criteria for complete response, partial response, stable disease and progressive disease based on tumor burden changes. The guidelines aim to improve consistency in evaluating clinical trial outcomes.
Metronomic chemotherapy involves the chronic administration of chemotherapy drugs at low, minimally toxic doses on a frequent schedule with no prolonged breaks. This strategy aims to control cancer by targeting tumor vasculature and is an attractive option in resource-limited areas due to its low cost, oral administration, and minimal side effects compared to conventional chemotherapy. Combining metronomic chemotherapy with drug repositioning and targeted therapies may lead to improved cancer control through multi-pronged effects on cancer cells, vasculature, and the immune system. However, determining the optimal biological dose and identifying surrogate markers pose challenges to realizing the full potential of this approach.
Chapter 24.2 lmwh in cancer asso thrombosisNilesh Kucha
The document discusses cancer-associated thrombosis (CAT). It notes that cancer increases the risk of venous thromboembolism (VTE) due to alterations in the coagulation system and inflammatory response to cancer that result in a hypercoagulable state. Several risk assessment scores are used to stratify cancer patients' risk of VTE, with the goal of identifying those who could benefit from thromboprophylaxis. The pathophysiology of CAT involves Virchow's triad of stasis, vessel injury, and hypercoagulability due to factors from cancer cells and cytokines that promote coagulation and clot formation.
Chapter 24.1 kinase inhibitors and monoclonal antibodiesNilesh Kucha
Tyrosine kinases are enzymes that help transfer phosphate groups and play a role in cell signaling. There are two types: receptor tyrosine kinases which are transmembrane proteins, and non-receptor tyrosine kinases which act as intracellular signal transducers. When tyrosine kinases are mutated or overexpressed, they can lead to uncontrolled cell growth and survival contributing to cancer. Tyrosine kinase inhibitors are small molecule drugs that target the intracellular tyrosine kinase domain to inhibit phosphorylation and downstream signaling, thereby inhibiting cancer cell growth and survival. Examples of tyrosine kinase inhibitors discussed in the document include imatinib, gefitinib, lapatinib, crizotinib, sorafenib, sunitin
TEST BANK For Accounting Information Systems, 3rd Edition by Vernon Richardso...rightmanforbloodline
TEST BANK For Accounting Information Systems, 3rd Edition by Vernon Richardson, Verified Chapters 1 - 18, Complete Newest Version
TEST BANK For Accounting Information Systems, 3rd Edition by Vernon Richardson, Verified Chapters 1 - 18, Complete Newest Version
TEST BANK For Accounting Information Systems, 3rd Edition by Vernon Richardson, Verified Chapters 1 - 18, Complete Newest Version
At Apollo Hospital, Lucknow, U.P., we provide specialized care for children experiencing dehydration and other symptoms. We also offer NICU & PICU Ambulance Facility Services. Consult our expert today for the best pediatric emergency care.
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Trauma Outpatient Center is a comprehensive facility dedicated to addressing mental health challenges and providing medication-assisted treatment. We offer a diverse range of services aimed at assisting individuals in overcoming addiction, mental health disorders, and related obstacles. Our team consists of seasoned professionals who are both experienced and compassionate, committed to delivering the highest standard of care to our clients. By utilizing evidence-based treatment methods, we strive to help our clients achieve their goals and lead healthier, more fulfilling lives.
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KEY Points of Leicester travel clinic In London doc.docxNX Healthcare
In order to protect visitors' safety and wellbeing, Travel Clinic Leicester offers a wide range of travel-related health treatments, including individualized counseling and vaccines. Our team of medical experts specializes in getting people ready for international travel, with a particular emphasis on vaccines and health consultations to prevent travel-related illnesses. We provide a range of travel-related services, such as health concerns unique to a trip, prevention of malaria, and travel-related medical supplies. Our clinic is dedicated to providing top-notch care, keeping abreast of the most recent recommendations for vaccinations and travel health precautions. The goal of Travel Clinic Leicester is to keep you safe and well-rested no matter what kind of travel you choose—business, pleasure, or adventure.
Healthy Eating Habits:
Understanding Nutrition Labels: Teaches how to read and interpret food labels, focusing on serving sizes, calorie intake, and nutrients to limit or include.
Tips for Healthy Eating: Offers practical advice such as incorporating a variety of foods, practicing moderation, staying hydrated, and eating mindfully.
Benefits of Regular Exercise:
Physical Benefits: Discusses how exercise aids in weight management, muscle and bone health, cardiovascular health, and flexibility.
Mental Benefits: Explains the psychological advantages, including stress reduction, improved mood, and better sleep.
Tips for Staying Active:
Encourages consistency, variety in exercises, setting realistic goals, and finding enjoyable activities to maintain motivation.
Maintaining a Balanced Lifestyle:
Integrating Nutrition and Exercise: Suggests meal planning and incorporating physical activity into daily routines.
Monitoring Progress: Recommends tracking food intake and exercise, regular health check-ups, and provides tips for achieving balance, such as getting sufficient sleep, managing stress, and staying socially active.
Rate Controlled Drug Delivery Systems, Activation Modulated Drug Delivery Systems, Mechanically activated, pH activated, Enzyme activated, Osmotic activated Drug Delivery Systems, Feedback regulated Drug Delivery Systems systems are discussed here.
This particular slides consist of- what is Pneumothorax,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is a summary of Pneumothorax:
Pneumothorax, also known as a collapsed lung, is a condition that occurs when air leaks into the space between the lung and chest wall. This air buildup puts pressure on the lung, preventing it from expanding fully when you breathe. A pneumothorax can cause a complete or partial collapse of the lung.
International Cancer Survivors Day is celebrated during June, placing the spotlight not only on cancer survivors, but also their caregivers.
CANSA has compiled a list of tips and guidelines of support:
https://cansa.org.za/who-cares-for-cancer-patients-caregivers/
Michigan HealthTech Market Map 2024. Includes 7 categories: Policy Makers, Academic Innovation Centers, Digital Health Providers, Healthcare Providers, Payers / Insurance, Device Companies, Life Science Companies, Innovation Accelerators. Developed by the Michigan-Israel Business Accelerator
The best massage spa Ajman is Chandrima Spa Ajman, which was founded in 2023 and is exclusively for men 24 hours a day. As of right now, our parent firm has been providing massage services to over 50,000+ clients in Ajman for the past 10 years. It has about 8+ branches. This demonstrates that Chandrima Spa Ajman is among the most reasonably priced spas in Ajman and the ideal place to unwind and rejuvenate. We provide a wide range of Spa massage treatments, including Indian, Pakistani, Kerala, Malayali, and body-to-body massages. Numerous massage techniques are available, including deep tissue, Swedish, Thai, Russian, and hot stone massages. Our massage therapists produce genuinely unique treatments that generate a revitalized sense of inner serenely by fusing modern techniques, the cleanest natural substances, and traditional holistic therapists.
INFECTION OF THE BRAIN -ENCEPHALITIS ( PPT)blessyjannu21
Neurological system includes brain and spinal cord. It plays an important role in functioning of our body. Encephalitis is the inflammation of the brain. Causes include viral infections, infections from insect bites or an autoimmune reaction that affects the brain. It can be life-threatening or cause long-term complications. Treatment varies, but most people require hospitalization so they can receive intensive treatment, including life support.
Stem Cell Solutions: Dr. David Greene's Path to Non-Surgical Cardiac CareDr. David Greene Arizona
Explore the groundbreaking work of Dr. David Greene, a pioneer in regenerative medicine, who is revolutionizing the field of cardiology through stem cell therapy in Arizona. This ppt delves into how Dr. Greene's innovative approach is providing non-surgical, effective treatments for heart disease, using the body's own cells to repair heart damage and improve patient outcomes. Learn about the science behind stem cell therapy, its benefits over traditional cardiac surgeries, and the promising future it holds for modern medicine. Join us as we uncover how Dr. Greene's commitment to stem cell research and therapy is setting new standards in healthcare and offering new hope to cardiac patients.
Can Allopathy and Homeopathy Be Used Together in India.pdfDharma Homoeopathy
This article explores the potential for combining allopathy and homeopathy in India, examining the benefits, challenges, and the emerging field of integrative medicine.
Empowering ACOs: Leveraging Quality Management Tools for MIPS and BeyondHealth Catalyst
Join us as we delve into the crucial realm of quality reporting for MSSP (Medicare Shared Savings Program) Accountable Care Organizations (ACOs).
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Under Pressure : Kenneth Kruk's StrategyKenneth Kruk
Kenneth Kruk's story of transforming challenges into opportunities by leading successful medical record transitions and bridging scientific knowledge gaps during COVID-19.
2. ALKYLATING AGENTS
• cell cycle–phase nonspecific.
• DNA and RNA and proteins are alkylated (N-7 position of guanine)
the O6 group of guanine is alkylated by nitrosoureas.
• Alkylation abnormal nucleotide sequences, miscoding of messenger
RNA, cross-linked DNA strands that cannot replicate, breakage of DNA
strandsdamage to the transcription and translation of genetic
material.
• cross-linking of DNA strands & breaks in DNA. not able to complete
the replication cyclecytotoxicity.
• Tumor resistance ↑capacity of cells to repair nucleic acid damage and
to inactivate the drugs by conjugation with glutathione.
3. Altretamine
Indication.- Recurrent ca ovary
Pharmacology
a. M/A- unknown.
b. Metabolism. Rapidly demethylated and hydroxylated in the liver by the
microsomal P450 system. Excreted in urine and hepatobiliary tract as
metabolites
Toxicity
a. Dose limiting. Nausea and vomiting,
b. Common.
• Neurotoxicity (25%), hallucinations,hypoesthesia, hyperreflexia, motor
weakness, confusion,lethargy,including paresthesias, agitation,
coma;depression,
• myelosuppression (mild)
• Nausea , vomiting
c. Occasional.
• Abnormal LFTs, flulike syndrome; abdominal cramps, diarrhea
d. Rare.
• Alopecia, skin rashes, cystitis
4. Bendamustine
Indications.CLL, low-grade B-cell NHL that has progressed within 6
mths of t/t with a rituximab-containing regimen
Pharmacology. Bendamustine is a bifunctional mechlorethamine
derivative containing a purine-like benzimidazole ring. About 90% of
the drug is excreted in the feces.
Toxicity
a. Dose limiting. -Hematosuppression
b. Common.
• Nausea, vomiting, diarrhea, fever, fatigue, headache, stomatitis, rash,
infusion reactions (consider administering an
antihistamine,acetaminophen, prophylactically)
c. Occasional. Anaphylactic reactions, severe skin reactions, acute renal
failure; peripheral edema, dizziness; myelodysplasia; dysgeusia
5. Busulfan
Indications. Part of conditioning regimen for BMT, CML palliation
Pharmacology. Acts directly; catabolized to inactive products that are excreted
in the urine.
Toxicity
a. Dose limiting. Reversible and irreversible myelosuppression with slow
recovery
b. Common. Mild GI upset, sterility
c. Occasional. Skin hyperpigmentation,alopecia, rash,gynecomastia, cataracts,
LFT abnormalities; seizures
d. Rare. Pulmonary fibrosis (“busulfan lung”), retroperitoneal fibrosis,
endocardial fibrosis; addisonian-like asthenia (without biochemical evidence
of adrenal insufficiency); hypotension, impotence, hemorrhagic cystitis,
secondary neoplasms
6. Chlorambucil
Indications. CLL, Waldenström macroglobulinemia, lymphomas
Pharmacology. It acts directly; spontaneously hydrolyzed to inactive
and active products ; also is extensively metabolized by the hepatic
P450 microsomal system. The drug and metabolic products are
excreted in urine.
Toxicity. Least toxic alkylating agent
a. Dose limiting. Myelosuppression
b. Occasional. GI upset , mild LFT alter, sterility, rash
c. Rare. Rash, alopecia, fever; cachexia, pulmonary fibrosis, neurologic
or ocular toxicity, cystitis; acute leukemia
7. Cyclophosphamide
Indications.HL, lymphocytic lymphoma, mixed cell–type lymphoma, histiocytic lymphoma, Burkitt
lymphoma; multiple myeloma, leukemias, mycosis fungoides, neuroblastoma, adenocarcinoma of
ovary, retinoblastoma, breast carcinoma, conditioning regimen for BMT
Pharmacology. drug is inactive activation by liver P450 system acrolein and an alkylating
metabolite (e.g., phosphoramide mustard). Active and inactive metabolites are excreted in the
urine.
Toxicity
a. Dose limiting
(1) Myelosuppression.
(2)hemorrhagic cystitis-
o prevented by maintaining a high UOP.
o more common and can be severe when massive doses are used (e.g.,BMT); under these circumstances, the
use of mesna can be preventative.
o UB fibrosis with telangiectasia of the mucosa can occur without episodes of cystitis.
o Bladder carcinoma.
b. Side effects
(1) Common. Alopecia, stomatitis, aspermia, amenorrhea; headache
Nausea and vomiting.
(2) Occasional. Skin or fingernail hyperpigmentation; metallic taste during injection; sneezing or a
cold sensation in the nose after injection; abnormal LFTs, dizziness; allergy, fever
(3) Rare. Transient SIADH, hypothyroidism, cataracts,jaundice,pulmonary fibrosis; cardiac necrosis
and acute myopericarditis; secondary neoplasms
8.
9. Dacarbazine [dimethyl-triazeno-imidazole-carboxamide (DTIC, DIC)
Indications. HL,MM, sarcomas, Neuroblastoma
Pharmacology
a. Mechanisms. Dacarbazine acts as a purine analog and inhibits DNA
synthesis; it is an alkylating agent and it interacts with SH groups.
b. Metabolism. liveroxidative N methylation by CYP 450activation
Excreted in urine predominantly, minor HB & pulmonary excretion
Toxicity
a. Dose limiting. Myelosuppression
b. Common. Nausea and vomiting (often severe), anorexia; pain along
the injection site
c. Occasional. Alopecia, facial flushing, photosensitivity, abnormal LFTs.
Flulike syndrome
d. Rare. Diarrhea, stomatitis; cerebral dysfunction; hepatic necrosis;
azotemia; anaphylaxis
10. Ifosfamide
Indications. Lymphomas, sarcomas, relapsed testicular tumors, and
various carcinomas
Pharmacology
a. M/A.- produces phosphotriesters as the predominant rexn products. The t/t of
intact cell nuclei may also result in the formation of DNA–DNA cross-links.
b. Metabolism. hepatic activation acrolein and its alkylating metabolite.
Acrolein is highly toxic to urothelial mucosa.
The chloroacetaldehyde neurotoxic effects, particularly in patients with renal
dysfunction.
Drug and metabolites are excreted in urine.
11. Toxicity
a. Dose limiting.
Myelosuppression,
hemorrhagic cystitis,
encephalopathy
b. Common. Alopecia; anorexia, constipation, nausea, and vomiting;
amenorrhea, oligospermia, and infertility
c. Neurotoxicity
d. Occasional. Salivation, stomatitis, diarrhea; urticaria,
hyperpigmentation, nail ridging; abnormal LFTs, phlebitis, fever;
hypotension, hypertension, hypokalemia; renal tubular acidosis (at
high doses); SIADH
e. Rare. Coma; renal tubular acidosis, or Fanconi-like syndrome
12.
13. MESNA
• Inj- 100 mg /ml
• Tablet- 400 mg
• Prevention of ifosfamide HC
240 mg/m2 IV over 15 min before & 4 & 8 hrs after
240 mg/m2 IV 15 min before & 480 mg/m2 of mesna tab 2 & 6 hrs
after
For cyclophosphamide-20% when injected, 4 & 8 hrs after
14. Melphalan
Indications. MM , BMT
Pharmacology
a. M/A.- A phenylalanine derivative of nitrogen mustard, an alkylating
agent
b. Metabolism. Acts directly. Melphalan is excreted in the urine (about
30%) as unchanged drug and metabolites, remainder in feces.
Toxicity
a. Dose limiting. Myelosuppression
b. Occasional. Anorexia, nausea, vomiting, mucositis, sterility
c. Rare. Alopecia, pruritus, rash, hypersensitivity; secondary
malignancies (acute leukemia); pulmonary fibrosis, vasculitis, cataracts
15. Nitrogen mustard (mechlorethamine)
Indication. HL; T-cell lymphoma
Pharmacology
a. M/A -alkylating agents
b. Metabolism. In water or body fluids, mechlorethamine undergoes rapid
chemical transformation ,drug is no longer present in active form a few
minutes after administration. Metabolites are mostly excreted in urine.
Toxicity
a. Dose limiting. Myelosuppression
b. Common. Severe nausea and vomiting; skin necrosis if extravasated;
burning at IV injection site and facial flushing; metallic taste; discoloration of
the infused vein; abnormal LFTs.
c. Occasional. Alopecia, sterility, diarrhea, thrombophlebitis, gynecomastia
d. Rare. Neurotoxicity (including hearing loss), angioedema, 2nd cancers
16. Carmustine [BCNU, bischlorethyl nitrosourea (BiCNU)]
Indications. Brain tumors, myeloma, HL & NHL. In high doses for BMT.
In the form of implantable wafers: GBM
Pharmacology
a. M/A. Forms interstrand cross-links in DNA preventing DNA replication and
transcription.
b. Metabolism. Highly lipid-soluble drug that enters the brain. Rapid spontaneous
decomposition to active and inert product. Most of the intact drug and metabolic
products are excreted in urine.
Toxicity
a. Dose limiting. Myelosuppression ,aggravated by concurrent RT.
b. Common. Nausea and vomiting. Local pain during injection.
c. Occasional. Stomatitis, esophagitis, diarrhea, LFT abnormalities; alopecia, facial
flushing, brown discoloration of skin; interstitial lung disease with pulmonary
fibrosis ,dizziness, optic neuritis, ataxia, organic brain syndrome; renal insufficiency
d. Rare. 2nd cancer
Lomustine [CCNU, cyclohexyl chlorethyl nitrosourea]
Indications. Brain tumors & HL
17. Procarbazine
Indications. HL
Pharmacology
a. M/A- cessation of protein synthesis. Direct DNA damage
b. Metabolism. Hepatic metabolism and activation. Readily enters the CSF.
Toxicity
a. Dose limiting. Myelosuppression
b. Common. Nausea and vomiting; flulike syndrome; sensitizes tissues to radiation;
amenorrhea and azoospermia, sterility
c. Occasional. Dermatitis, hyperpigmentation, photosensitivity; stomatitis, dysphagia,
diarrhea; hypotension, tachycardia; urinary frequency, hematuria; gynecomastia
d. Neurologic. disorders of consciousness or mild peripheral neuropathies (10%) ,sedation,
depression, agitation, psychosis, decreased deep tendon reflexes, paresthesias, myalgias, and
ataxia.
e. Rare. Xerostomia, retinal hemorrhage, photophobia, papilledema; hypersensitivity
pneumonitis, 2nd cancers
18. Streptozocin (streptozotocin)
Indications. Islet cell cancer of the pancreas, carcinoid tumors
Pharmacology
a. M/A. Alkylating agent.
A cell cycle–nonspecific nitrosourea analog.
Inhibits DNA synthesis and the DNA repair enzyme, guanine-O6-methyltransferase; affects
pyrimidine nucleotide metabolism and inhibits enzymes involved in gluconeogenesis.
Selectively targets pancreatic β cells, presumably due to the glucose moiety on the molecule.
b.Metabolism. Hepatic metabolism to active metabolites and has a short plasma half-life (<1
hour). Crosses the BBB. Excreted in urine as metabolites and unchanged drug
Toxicity
a. Dose limiting. Nephrotoxicity proteinuria ,glycosuria, aminoaciduria, proximal
RTA, nephrogenic DI, and renal failure
b. Common. Nausea and vomiting, myelosuppression, hypoglycemia after infusion,
hypoglycemia or hyperglycemia
c. Occasional. Diarrhea, abdominal cramps, LFT abnormalities
d. Rare. CNS toxicity, fever, 2ND cancer.
19. Temozolomide
Indications. Brain tumors; metastatic melanoma
Pharmacology. similar to dacarbazine
a. M/A. Activated to MTIC by nonenzymatic hydrolysis in tumors.
Inhibits DNA, RNA, and protein synthesis but does not cross-link DNA
strands.
b. Metabolism. Renal excretion. Lipophilic crosses the BBB.
Toxicity
a. Dose limiting. Myelosuppression
b. Common. nausea and vomiting, diarrhea, headache, fatigue
c. Occasional. Photosensitivity, myalgias, fever
d. Rare. Prolonged cytopenia, myelodysplastic syndrome (MDS)
20. Thiotepa (triethylenethiophosphoramide)
Indications. Intracavitary for malignant effusions, intravesicular for urinary bladder, and
intrathecal use for meningeal metastasis; severe thrombocytosis. Also can be used for breast
and ovarian cancers and for HSCT
Pharmacology. Ethylenimine analog, chemically related to nitrogen mustard
a. M/A. Alkylates the N-7 position of guanine, which severs the linkage between the purine
base and the sugar and liberates alkylated guanines.
b. Metabolism. Rapidly decomposed in plasma and excreted in urine. Extensively metabolized
by the hepatic P450 microsomal system to active and inactive metabolites
Toxicity
a. Dose limiting. Myelosuppression
b. Common (for intravesicular administration). Chemical cystitis, abdominal pain, hematuria,
dysuria, frequency, urgency, ureteral obstruction; nausea and vomiting 6 hours after
treatment
c. Occasional. GI upset, abnormal LFTs, hypersensitivity
d. Rare. Alopecia, fever, angioedema, secondary malignancies
21. Trabectedin
Indications. LS or LMS after an anthracycline containing regimen
Pharmacology
a. M/A. binds guanine residues in the minor groove of DNAadductsaffects binding of transcription
factors and DNA repair.
b. Metabolism. It is metabolized in the liver, and only negligible amount is excreted in urine. The drug is
delivered as a 24-hour continuous infusion.
Toxicity
a. Dose limiting.
Rhabdomyolysis (monitor the level of CPK before each dose),
severe and fatal cardiomyopathy (ECG f/u),
severe neutropenia (40%), febrile neutropenia (5%)
b. Common. Elevation of liver enzymes, thrombocytopenia, anemia, nausea, fatigue, vomiting,
constipation, decreased appetite, diarrhea, peripheral edema, dyspnea, and headache
c. Rare. Liver failure, peripheral neuropathy
22. PLATINS-
M/A---
• Enters the cells by diffusion and
covalently binds to DNA N-7
position of guanine and adenine.
• Reacts with two different sites on
DNA to produce cross-links, either
intrastrand (>90%) or interstrand
(<5%).
• Formation of DNA adducts results
in inhibition of DNA synthesis and
function as well as inhibition of
transcription
• not cell cycle specific.
M/RESISTANCE---
• alterations in cellular transport.
• Increased inactivation by
glutathione and related enzymes.
• Increased DNA repair enzymes
activity
• Deficiency in mismatch repair
(MMR) enzymes
23. CISPLATIN
• INDICATIONS
• Testicular cancer
• Ovarian cancer
• Bladder cancer
• Head and neck cancer
• Esophageal cancer
• Small cell and non-small cell lung cancer
• Non-Hodgkin’s lymphoma
• Trophoblastic neoplasms
25. DOSAGE RANGE
• Ovarian cancer - 75mg/m2 IV on day 1 every 21 days as part of the cisplatin / paclitaxel regimen,
and 100mg/m2 on day 1 every 21 days as part of cisplatin / cyclophosphamide regimen.
• Testicular cancer - 20 mg/m2 IV on days 1-5 every 21 days as part of the BEP regimen.
• Bladder cancer : administered as a single agent at a dose of 50-70 mg/m2 IV per cycle repeated
every 4 weeks
• Non - small cell lung cancer : 60-100 mg/m2 IV on day 1 every 21 days as part of the cisplatin /
etoposide or cisplatin / gemcitabine regimens.
• Head and neck cancer : 20 mg/m2/day IV continuous infusion * 4 days.
26. Toxicity
a. Dose limiting
1) renal insufficiency- 5% with adequate hydration 25%-45% without
2) Peripheral sensory neuropathy
>200 mg/m2 and can become dose limiting when the cumulative cisplatin dose exceeds 400
mg/m2.
Symptoms may progress after treatment is discontinued and include loss of proprioception and
vibratory senses, hyporeflexia. Symptoms may resolve slowly after many months.
3) Ototoxicity-
tinnitus and high-frequency hearing loss (5%)
>100 mg/m2 by rapid infusion or high cumulative doses.
b. Common. Severe nausea and vomiting; preventative antiemetic regimens are required.
↓K+↓Mg++
mild myelosuppression alopecia;
azoospermia, sterility, impotence.
c. Occasional. Alopecia, loss of taste, vein irritation, transiently abnormal LFTs, SIADH, hypophosphatemia,
myalgia, fever; optic neuritis
d. Rare. Altered color perception and reversible focal encephalopathy that often causes cortical blindness.
Raynaud phenomenon, bradycardia, bundle-branch block, congestive heart failure; anaphylaxis, tetany
27. Prevention of nephrotoxicity
• Pre-hydration
• Cisplatin dose < 50mg/m2 : N/Saline in 1L × 1 hour. If another drug is being given
in the regimen e.g. etoposide then this would be used as prehydration i.e.
etoposide in 1L N/Saline.
• Cisplatin dose 50-75mg/m2 : N/Saline + KCl 20mmol/L in 1L × 1hr+ 100mls 10%
mannitol (or equivalent)
• Cisplatin dose > 75mg/m2 < 100mg/m2 : N/Saline + KCl 20mmol/L in 1L × 1hr +
200mls 10% mannitol (or equivalent)
• Cisplatin should not be given if UOP is < 100ml/hr.
• If urine output is insufficient, give 500ml N/Saline × 30mins. Consider giving
further mannitol. Do not administer cisplatin until urine output is > 100ml/hr.
28. • Post-hydration
• Cisplatin dose < 50mg/m2 : no post-hydration, recommend oral
intake of 8 glasses of water.
• Cisplatin dose > 50mg/m2 < 75mg/m2 : N/Saline + KCl 20mmol/L +
MgSO4 10mmol/L in 1L × 1 hr.
• Cisplatin dose > 75mg/m2 < 100mg/m2 : N/Saline + KCl 20mmol/L +
MgSO4 10mmol/L in 1L × 1 hr x 2. Monitor BP as required
29.
30.
31. contraindications
• History of hypersensitivity to cisplatin or other platinum containing
compounds.
• Pre-existing renal impairment, myelosuppressed patients or patients with
hearing impairment.
• Pregnancy, breastfeeding
32. CARBOPLATIN
• INDICATIONS
• Ovarian cancer
• Germ cell tumors
• Head and neck cancer
• Small cell and non small cell
lung cancer
• Bladder cancer
• Relapsed and refractory acute
leukemia
• Endometrial cancer
Pharmacology
a. M/A. Heavy metal alkylating-
like agent with mechanisms very
similar to cisplatin, but with
different toxicity profile
b. Metabolism. Plasma half-life of
only 2 to 3 hours. Excreted in
urine as unchanged drug (70%)
and metabolites
33. Dosage range
• Dose of carboplatin is usually calculated to a target area under the curve (AUC) based
on the glomerular filtration rate (GFR).
• Calvert formula is used to calculate dose –
Total dose (mg) = ( target AUC ) x ( GFR + 25 )
• Note: dose is in mg, not mg/m2
• Target AUC is usually between 5 and 7 mg/mL/min for previously untreated patients. In
previously treated patients , lower AUCs (between 4 and 6 mg/mL/min) are
recommended .
• AUCs >7 are not associated with improved response rates.
34. • CrCl + 25 =AUC
• FOR WEEKLY DOSING ~2 AUC
• FOR 3 WEEKLY DOSING 5-6 AUC
OUR SET UP PRACTICE
35. Toxicity
a. Dose limiting. Myelosuppressionespecially thrombocytopenia.
b. Common. Nausea, vomiting, myalgias, weakness, and nephrotoxicity pain at injection
site; cation electrolyte imbalance
c. Occasional. Reversible abnormal LFTs, azotemia; peripheral neuropathy (5%), visual
disturbance; hypersensitivity reactions; amenorrhea, azoospermia, impotence, and
sterility
d. Rare. Alopecia, rash, flulike syndrome, hematuria, hyperamylasemia; hearing loss,
optic neuritis; alopecia
C/I—
• History of hypersensitivity to cisplatin or other platinum containing compounds.
• Severe bone marrow depression or significant bleeding
• Pregnancy category D; breastfeeding should be avoided
36. OXALIPLATIN
• It is available as 50 mg/ 100 mg
vials.
• Reconstituted by using 10 ml
(for 50 mg vial) and 20 ml (for
100 mg vial) of Water or 5%
Dextrose injection.
• It is further diluted in 250-500
ml of 5% Dextrose injection.
• Reconstitution of final dilution
must never be performed with
NaCl solution or other chloride
containing solutions.
Indications. Colorectal,
pancreatic, and gastric cancers
Pharmacology
a. Mechanisms. Binds covalently
to DNA -intrastrand and
interstrand cross-links.
b. Metabolism. Undergoes
extensive nonenzymatic
conversion to its active cytotoxic
species; >50% -kidneys. Only 2% -
feces.
37. INDICATIONS
• Metastatic colorectal cancer : FDA - approved in combination with
infusional 5-FU/LV in patients with advanced, metastatic disease.
• Early stage colon cancer : FDA - approved as adjuvant therapy in
combination with infusional 5 –FU/LV in patients with stage III colon
cancer and also effective in patients with high risk stage II disease.
• Metastatic pancreatic cancer
• Metastatic gastric cancer and gastroesophageal cancer
• DOSAGE--
• Recommended dose is 85 mg/m2 IV over 2 hours, on an every 2 weeks
schedule.
• Can also administer 100-130 mg/m2 IV on an every 3 - weeks schedule.
38. Oxaliplatin
Toxicity
a. Dose limiting
(1) Acute dysesthesias in the hands, feet, perioral area, or throat develop
within hrs or up to 2 days after dosing and may be precipitated or exacerbated by
exposure to cold -usually resolves within 2 weeks-ameliorated by prolonging the
infusion to 6 hrs.
(2) Persistent peripheral sensory neuropathy usually characterized by
paresthesias, dysesthesias, and hypesthesia, including deficits in proprioception,
which is usually reversible within 4 mths of discontinuing oxaliplatin.
b. Common. Anorexia, nausea, vomiting, constipation, diarrhea,
• abdominal pain; fever, fatigue; mild to moderate myelosuppression; mild to moderate LFT
abnormalities
c. Occasional. Allergic reactions, mild nephrotoxicity, headache, stomatitis, taste alteration;
back pain, arthralgias
d. Rare. Pulmonary fibrosis
39. contraindications
• Known history of hypersensitivity to oxaliplatin
• Pregnant
• Breast feeding
• Myelosuppression
• Peripheral sensory neuropathy with functional impairment prior to
first course
• Severely impaired renal function
40. Toxicity profiles of platinum analogs in use
TOXICITY CISPLATIN CARBOPLATIN OXALIPLATIN
MYELOSUPPRESSION
+
NEPHROTOXICITY
+
NEUROTOXICITY
+ +
OTOTOXICITY
+
NAUSEA AND VOMITTING
+ + +
42. ANTIMETABOLITES
• General pharmacology of antimetabolites
1. structure resemblance to purine or pyrimidine precursors or because they interfere
with purine or pyrimidine synthesis.
2. Greatest activity in the S phase
3. most effective when cell proliferation is rapid.
Azacitidine
Indication. Myelodysplastic syndromes (MDS)
Pharmacology
a. M/A-cytidine analogincorporated into DNA and RNAinhibiting protein synthesis; also
inhibits pyrimidine synthesis and DNA methylation.
Toxicity
a. Dose limiting. Myelosuppression; nausea and vomiting.
b. Common. Hepatic dysfunction, fatigue, headache, diarrhea, alopecia, fever, injection site
erythema
c. Occasional. Neurotoxicity ,azotemia, arthralgias, hypophosphatemia with myalgia,
stomatitis, phlebitis, rash
d. Rare. Progressive lethargy and coma, renal tubular acidosis, rhabdomyolysis, hypotension
43. Cladribine
Indications. Hairy cell leukemia
Pharmacology.
a. M/A. An analog of the purine deoxyadenosine.
Inhibits ribonucleotide reductase. Depletes ATP. Induces apoptosis.
Active against both dividing and resting cells
Toxicity. Patients are at increased risk for opportunistic infections.
a. Dose limiting. Myelosuppression
b. Common. Immunosuppression with decreases in CD4+ and CD8+ cells; nausea,
skin reactions at injection site; fever , chills, flulike syndrome
c. Occasional. Neurotoxicity, hypersensitivity reactions, fatigue
d. Rare. Severe neurotoxicity, pancreatitis
44. Clofarabine
Indications. Relapsed or refractory ALL
Pharmacology. Purine antimetabolite
Toxicity
a. Dose limiting.
(1) Capillary leak syndrome (CLS)/SIRS –due to cytokine release
(2) Hematosuppression (90%)
(3) Hepatotoxicity and nephrotoxicity
b. Common. Tachycardia, hypotension, flushing; headache, fever, chills, fatigue;
pruritus, rash; nausea, vomiting, diarrhea; abnormal LFTs (80%); increased
creatinine (50%), limb pain
c. Occasional. Hypertension, edema, dyspnea, pleural, or pericardial effusion;
mucositis; myalgia, arthralgia; irritability, somnolence, agitation; cecitis; CLS (4%),
SIRS (2%)
d. Rare. Hepatic venoocclusive disease, Stevens-Johnson syndrome, hallucination
45. Cytarabine
Indications. Acute leukemia, lymphoma, meningeal involvement with tumor
Pharmacology. An analog of deoxycytidine
a. M/A. Antimetabolite.Intracellular activation ara-CTPinhibits DNA
polymerases; some are incorporated into DNA.
Ara-CTP inhibits ribonucleotide reductase DNA synthesis and function.
b. Metabolism. In patients with renal insufficiencyhigh concentrations of ara-
CTP, which may result in CNS toxicity.
Toxicity
a. Dose limiting. Myelosuppression
b. Common. Nausea, vomiting, mucositis, diarrhea; conjunctivitis; hydradenitis,
arachnoiditis with intrathecal administration
c. Neurotoxicity (cerebellar ataxia, lethargy, confusion)
d. Occasional. Alopecia, stomatitis, metallic taste, esophagitis, hepatic dysfunction,
pancreatitis, severe GI ulceration; thrombophlebitis; headache; rash, transient skin
erythema without exfoliation.
46. Decitabine
Indications. MDS
Pharmacology. analogue of 2′-decoxycytidine.
a. M/A- inhibits DNA methyltransferase, causing hypomethylation of
DNA and cellular differentiation or apoptosis.
Toxicity
a. Dose limiting. Hematosuppression
b. Common. Hematosuppression, fatigue, fever; nausea, constipation
(35%), diarrhea; headache, arthralgias, rigors, edema, cough;
hyperglycemia, ↓K+, ↓ Mg++
47. Fludarabine
Indications. CLL, low-grade lymphomas
Pharmacology. analog of ara-A (arabinofuranosyladenosine).
drug is resistant to adenosine deaminase activity(compare with
cytarabine).
high specificity for lymphoid cells.
It has activity against both dividing and resting cells and induces
apoptosis.
Toxicity
a. Dose limiting. Myelosuppression; AIHA
b. Common. Immunosuppression -risk for opportunistic infections;
mild nausea and vomiting; fever; cough, weakness, arthralgia/myalgias
c. Occasional. Alopecia (mild), abnormal LFTs, tumor lysis syndrome
48. 5-Fluorouracil
A fluoropyrimidine analog
M/A- blocking thymidylate synthetase (TS)interfere with DNA syn
Incorporation of another metabolite (FdUTP) into DNA results in inhibition
of DNA synthesis and function.
It is cell–cycle S-phase specific but acts in other cell cycle phases as well.
5-FU rapidly enters all tissues, including spinal fluid and malignant
effusions.
Toxicity is more common and more severe in patients with
dihydropyrimidine dehydrogenase deficiency.
51. TOXICITY
a. Dose limiting. Myelosuppression; mucositis; diarrhea
b. Common. Nasal discharge; eye irritation and excessive lacrimation due to
dacryocystitis and lacrimal duct stenosis; dry skin, photosensitivity, and
pigmentation of the infused vein
c. Neurologic. Reversible cerebellar dysfunction, somnolence, confusion, or
seizures occurs in about 1% of patients.
d. Occasional. Esophagitis; hand–foot syndrome; coronary vasospasm;
thrombophlebitis; nausea, vomiting
e. Rare. Alopecia, dermatitis, loss of nails, dark bands on nails; blurred vision,
“black hairy tongue” (hypertrophy of filiform papillae), anaphylaxis, fever
52. Capecitabine
Indications. breast or colon ca
Pharmacology. Capecitabine is a fluoropyrimidine carbamate that is a systemic
prodrug of 5′-deoxy-5-fluorouridine (5′-DFUR), which is converted in vivo to 5-FU.
M/A & metabolism & toxicity- same as 5-FU.
Toxicity.
a. Dose limiting. Diarrhea (50%), hand–foot syndrome
b. Common. Hand–foot syndrome -15% to 50%; nausea, vomiting,
hematosuppression; fatigue
c. Occasional. Abnormal LFTs, neurotoxicity; cardiac ischemia in patients with a
prior history of coronary artery disease; tear duct stenosis, conjunctivitis,
blepharitis; confusion, cerebellar ataxia
53.
54.
55. Gemcitabine
Indications. Carcinoma of pancreas, bladder, lung, ovary; STS
Pharmacology. A fluorine-substituted deoxycytidine analog
a. M/A. Cell-phase specific-S phase -blocking the progression of cells
through the G1-S-phase also.
Inhibits ribonucleotide reductase; competes with deoxycytidine
triphosphate (dCTP) for incorporation into DNA
Toxicity
a. Dose limiting. Myelosuppression
b. Common. Nausea, vomiting, diarrhea, stomatitis; fever with flulike symptoms (40%);
macular or maculopapular rash; transient LFT elevations; mild proteinuria and hematuria
c. Occasional. Hair loss, rash, edema
d. Rare. Hemolytic–uremic syndrome; pulmonary drug toxicity; hypersensitivity reactions;
alopecia
56.
57. Hydroxyurea
Indications. MPD, refractory ca ovary, sickle cell disease
Pharmacology. An analog of urea
a. M/A. Antimetabolite.
inhibiting nucleotide reductaseinterfere with DNA syn
Inhibits DNA repair and thymidine incorporation into DNA.
Cell cycle S-phase specific but acts in other phases as well
b. Metabolism. Crosses the BBB. Half of the drug is rapidly degraded into
inactive compounds by the liver. Inactive products and unchanged drug (50%)
are excreted in urine.
Toxicity
a. Dose limiting. Myelosuppression
b. Occasional. Nausea, vomiting, diarrhea; skin rash, facial erythema, hyperpigmentation; azotemia,
proteinuria; transient LFT abnormalities;
c. Rare. Alopecia, mucositis, diarrhea, constipation; neurologic events; pulmonary edema; flulike
syndrome; painful perimalleolar ulcers; possible acute leukemia in myeloproliferative disorders
58. 6-Mercaptopurine
Indication. Acute lymphoblastic leukemia (maintenance therapy)
a. M/A- Purine analog
The parent drug is inactive. Requires intracellular phosphorylation –
HGPRTase
b. Metabolism-by xanthine oxidase.
Allopurinol- XO inhibitortoxicity.
Toxicity
a. Dose limiting. Myelosuppression
b. Common. Mild nausea, vomiting, anorexia (25%); usually reversible
cholestasis (30%); dry skin, photosensitivity; immunosuppression
c. Rare. Stomatitis, diarrhea, dermatitis, fever, hematuria, BuddChiari–
like syndrome, hepatic necrosis
59. Methotrexate
Indications. A wide variety of conditions
a.M/A- interfere with DNA syn.
The drug also inhibits RNA and protein
synthesis and prevents cells from entering the S
phase of the cell cycle.
b. Metabolism. Renal dysfunction results in
dangerous blood levels of MTX and possible
further renal damage.
60. Toxicity. Leucovorin can reverse the immediate cytotoxic effects of
MTX; generally, 1 mg of leucovorin is given for each 1 mg of MTX.
a. Dose limiting. Myelosuppression, stomatitis, renal dysfunction
b. High-dose regimens. Nausea, vomiting, renal tubular necrosis,
cortical blindness
c. Skin erythema, pulmonary fibrosis, transverse myelitis, cerebritis
d. Chronic therapy. Liver cirrhosis; osteoporosis
e. Neurotoxicity. acute aseptic meningitis,subacute encephalopathy and myelopathy. irreversible
leukoencephalopathy
f. Occasional. Nausea, vomiting, dermatitis, photosensitivity, altered pigmentation, furunculosis;
conjunctivitis, photophobia, excessive lacrimation, cataracts; fever, reversible oligospermia, flank pain
g. Rare. Alopecia, MTX pneumonitis
61. Pemetrexed
Indications. Mesothelioma (with cisplatin) & NSCLC
a. M/A. antifolate analog
activity in the S phase of the cell cycle.
Inhibition of TS & DHFRase.
b. Metabolism- cleared by the kidneys. About 90% of the drug is
excreted unchanged in the urine within 24 hours.
Toxicity.
a. Dose limiting. Myelosuppression.
All patients are given 350 μg/d PO of folic acid and 1,000 mg of vitamin B12 SC
every 3 weeks to reduce drug toxicity.
b. Common. Skin rash (usually as the hand–foot syndrome), mucositis,
nausea, vomiting, diarrhea; mild dyspnea, fatigue; transient elevation
of LFTs
c. Occasional. Myalgia/arthralgia, fever
62. Pentostatin
Indications. CLL, hairy cell leukemia, and cutaneous T-cell lymphoma
Pharmacology. A fermentation product of Streptomyces antibioticus
a. M/A- Antimetabolite.
Both cell cycle specific and cell cycle nonspecific.
Inhibitor of adenine deaminase., ribonucleotide reductase
b. Metabolism. excreted unchanged in urine.
Toxicity
a. Dose limiting. Myelosuppression
b. Common. Immunosuppression; mild nausea and vomiting, diarrhea,
altered taste; fatigue, fever; erythematous, papular, vesiculobullous
rashes
c. Occasional. Chills, myalgia, arthralgia; abnormal LFTs;
keratoconjunctivitis, photophobia; cough, renal failure
63. Pralatrexate
Indications. Relapsed or refractory peripheral T-cell lymphoma
Pharmacology: An antineoplastic folate analog
a. M/A. Competitively inhibits DHFRase and polyglutamylation by the
enzyme folylpolyglutamyl synthetase
b. Metabolism. Approximately 33% of the drug is excreted unchanged
in the urine.
Toxicity
a. Dose limiting. Thrombocytopenia, neutropenia, and mucositis
b. Common. Anorexia, nausea, vomiting, diarrhea, constipation;
fatigue, fever, edema; rash
d. Rare. Hepatitis; pulmonary infiltrates and insufficiency
64. 6-Thioguanine
Indication. AML
a. M/A. Purine analog with cell cycle–specific activity in the S phase.
The drug requires intracellular phosphorylation by HGPRT
The drug is incorporated extensively into DNA, resulting in miscoding
of transcription and DNA replication, and into RNA.
b. Metabolism.
can be given in full doses with allopurinol.
Clearance of the drug is primarily hepatic, but also renal.
Toxicity
a. Dose limiting. Myelosuppression
b. Common. Stomatitis, diarrhea
c. Occasional. Nausea and vomiting, hepatic dysfunction, hepatic
venoocclusive disease; decreased vibratory sensation, unsteady gait