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Heme/Onc Pathoma > Exam Drugs > Flashcards

Exam Drugs Flashcards

1
Q

Cyclophosphamide

A
  • Chemotherapy Agent
  • Mechanism:
    • alkylating agent: forms DNA cross links resulting in inhibition of DNA synthesis and function
    • Require bioactivation by the liver
  • Major toxicities:
    • Acute: (GI): Nausea and vomitting
    • Delayed: moderate depression of peripheral blood count
    • Excessive doses: severe bone marrow depression and hemorrhagic cystitis (hematuria and bladder pain)
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2
Q

Cisplatin

A
  • Chemotherapy Agent
  • Mechanism: alkylating agent
    • “stick” to the DNA strands
    • Cytotoxic in all stages of cell cycle
  • Toxocities
    • Acute: highly emetogenic
      • nausea and vomitting
    • Delayed: nephrotoxicity, ototoxicity, irreversible nerve dysfunction
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3
Q

Nitrosourea: Carmustine

A
  • Chemotherapy Agent
  • Mechanism:
    • Alkylating agent: DNA cross linking
    • Able to enter CNS
  • Toxicity:
    • Acute: GI
    • Delayed: Myelosuppression
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4
Q

Procarbazine

A
  • Chemotherapy Agent
  • Mechanism
    • Non-classic alkylating agent
    • inhibits DNA, RNA and protein synthesis
  • Toxicities:
    • High risk for second malignancy
    • Adverse drug-drug interactions due to MAOI metabolite activity
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5
Q

Methotrexate

A
  • Chemotherapy Agent
  • Mechanism: Anti-metabolite: blocks synthesis of base pairs
    • Folic acid analog: binds and inhibits DHFR and TS
    • Maximum effect in S phase
  • Toxicities
    • Myelosuppression: neutropenia and thrombocytopenia
  • Effects are reveresed by Leucovorin: reduced folate
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6
Q

5-FU

A
  • Mechanism: antimetabolite: pyrimidine analog
    • block synthesis of base pairs
    • works best in S phase
  • Toxicities
    • Toxicity severe in patients with low or absent dihydropyridine dehydrogenase (DPD)
      • DPD is the enzyme that degrades this trug
    • Myelosuppression
    • Nausea, vomitting, diarrhea, mucositis (painful inflammation and ulceration of the mucous membranes lining the digestive tract)
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7
Q

Capecitabine (highly likely to get tested)

A
  • Chemotherapy agent
  • Mechanism: antimetabolite: pyrimidine analog
    • blocks synthesis of base pairs
    • Pro-pro drug of 5-FU
      • 2 attachments so that its not broken down in the GI
      • ORALLY ACTIVE
  • ​​Toxicity: Reflects continuous infusion
    • Hand-foot syndrome
      • redness, swelling, and pain on the palms of the hands and/or the soles of the feet
    • Diarrhea
    • Low risk of alopecia (hair falling out)
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8
Q

Cladribine

A
  • Chemotherapy Agent
  • Mechanism: Purine analog
    • inhibits DNA sythesis and repair by inhibiting ribonucleotide reductase
  • Toxicity:
    • Myelosupression
    • Nausea and vomitting
    • Immunosupression: CD4 and CD8 T cells
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9
Q

6-Meracaptopurine

A
  • Chemotherapy Agent
  • Mechanism: Purine Antagonist
    • inhibits enzyme of purine synthesis
    • Incorporated into both DNA and RNA
  • Toxicities:
    • 6-MP is deactivated by xanthine oxidase
      • Allopurinol is a potent xanthine oxidase inhibitor leading to excessive toxicity if given together
      • Thiopurine methyl transferase (TPMT) deficiency can result in severe toxicities
        • Myelosuppression
        • Diarrhea
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10
Q

Vincristine

A
  • Chemotherapy Agent
  • Mechanism: Natural Product chemotherapeutic
    • Vinca alkaloid: cause microtubule disfunction
      • spindles provide a foundation/matrix so that the two sets of DNA can separate along these tracks and get folded within the cells and then have normal dividing cells
      • when disrupt this, wipes out the cell
  • Toxicity:
    • Neurotoxicity with peripheral neuropathy
    • Autonomic system dysfunction: orthostatic hypotension, urinary retention, paralytic ileus
    • SIADH
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11
Q

Paclitaxel

A
  • Chemotherapeutic Agent
  • Mechanism
    • Taxane: cause microtubule disfunction by enhancing microtubule polymerization
    • spindles provide a foundation/matrix so that the two sets of DNA can separate along these tracks and get folded within the cells and then have normal dividing cells
    • when disrupt this, wipes out the cell
  • Toxicity:
    • Acute: Hypersensitivity
    • Delayed: Neurotoxicity, peripheral sensory neuropathy
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12
Q

Abraxane

A
  • Chemotherapy Agent
  • Mechanism:
    • Taxane: cause microtubule disfunction by enhancing microtubule polymerization
      • when disrupt this, wipes out the cell
      • spindles provide a foundation/matrix so that the two sets of DNA can separate along these tracks and get folded within the cells and then have normal dividing cells
    • Paclitaxel protein bound or albumin bound
      • ​Avoids hypersensitivity
  • Toxicity: decreased toxicity overall
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13
Q

Irinotecan

A
  • Natural Product Chemo
  • Mechanism: Camptothecins:
    • Topoisomerase 1 inhibitor
      • essential for DNA replication as it cuts and relegates single stranded DNA strands
      • inhibition causes DNA arrest
      • results in S phase arrest
    • Prodrug converted in liver
      • prevents breakdown before getting to the cancer cells
  • Toxicity:
    • Serious diarrhea
      • Early: cholinergic event
      • Late: 2-10 d post treatment, can be severe
    • Bone marrow suppression
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14
Q

Doxorubicin

A
  • Antibiotic: Anthracyclines
    • inhibit Topoisomerase II
    • high affinity DNA intercalation
      • blocks both DNA and RNA synthesis
    • Generate semi-quinone free-radicals
      • Major mechanism of cardiotoxicity
    • Binds to cell membranes and alters fluidity and iron transport
  • Toxicity:
    • Cardiotoxicity
      • Acute (2-3 d) arrhythmias, conduction abnormalities
      • Chronic: dose dependent dilated cardiomyopathy
    • Treating patients with Dexrazoxane, an iron-chelator, can reduce events in high risk patients
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15
Q

Bleomycin

A
  • Antibiotic
    • Binds DNA and causes SS and DS breaks
    • inhibits DNA synthesis
    • G2 phase arrest
  • Toxicity:
    • Pulmonary
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16
Q

Mitomycin C

A
  • antibiotic
  • Mechanism:
    • Needs to be reduced (works on tumor cells that create hypoxic environment)
    • Acts during all cell cycle stages
  • Toxicity:
    • Nausea and vomitting
    • Hemolytic Uremic Syndrome
17
Q

Imatinib

A
  • Tyrosine Kinase Inhibitor
  • Hematologic Disease: Chronic Myelongous Leukemia (CML)
    • Has t(9;22) that creates BCR-ABL philadelphia chromsome
    • Blocks out the effect of the Philadelphia chromosome
  • Target:
    • binds to catalytic cleft of ABL to stop BCR-ABL fusion protein from forming
    • Also inhibits PDGF-R and c-KIT
  • Toxicities:
    • Resistance occurs when mutations in the cleft limit ability of Imatinib to bind
18
Q

ATRA/arsenic

A
  • Target: Retinoic Acid Receptor
  • Mechanism: displaces PML-RAR fusion protein preventing acute differential arrest of cells
  • Hematologic disease:
    • Acute Promyelocytic Leukemia (APML)
  • Toxocity:
    • ATRA syndrome
      • Leukocytosis: high neutrophil count
      • Capillary leak syndrome: pulmonary edema, respiratory failure
      • Renal failure
      • Often used togeth with steroids, chemo and supportive care
      • Occurs shortly after initiation of ATRA therapy in APML
19
Q

Rituximab (Rituxan)

A
  • Chimeric monoclonal antibody
  • Target: CD20 on pre-B cells and mature B cells
  • Hematologic Disease:
    • B cell malignancies
    • Autoimmune Diseases
    • Nonhodgkin lymphoma
20
Q

Crizotinib

A
  • Mechanism: Tyrosine Kinase Inhibitor
    • Inhibits ALK, ROS1, HGFR and other Tyrosine Kinases
  • Given to those with Nonsmall cell Lung Cancer
21
Q

Thalidomide

A
  • Mechanism: unclear
  • Hematologic Disease: Multiple Myeloma
  • Toxicity:
    • terratogenic: focomelia (short limbs)
22
Q

Trastuzumab (Herceptin)

A
  • Monocolonal antibody
  • Mechanism: binds to HER2 receptor, not allowing dimerization and thus preventing signaling
  • Toxicity:
    • Cardiac toxicity
23
Q

Cetuximab (Erbitux)

A
  • Engineered chimeric monoclonal antibody to EGF-R
  • Modest clinical activity in head and neck cancers
  • K-RAS and BRAF mutations are associated with lack of response to Cetuximab
24
Q

Erlotinib

A
  • Mechanism: Tyrosine Kinase Inhibitor
  • Targets:
    • EGF-R (human epidermal growth factor receptor)
25
Q

Bevacizumab

A
  • Monoclonal antibody for colonrectal cancer
  • Mechanism: Inhibits VEGFR
    • VEGF is an important growth factor for endothelial cells (angiogenesis)
  • Target: VEGFR
  • Hematologic Disease: Multiple Myeloma
  • Toxicity:
    • Pulmonary hemorrhage: high risk in patients with squamous cell cancers
    • hypertension, pulmonary hemorrhage, proteinuria
    • Financial toxicity (expensive)
26
Q

Vemurafinib

A
  • Mechanism: small molecule RAF inhibitor
  • Target: targets V600E BRAF mutation
  • Hematologic Disease: Melanoma and others
  • Toxicity:
    • Causes other skin cancers
    • Resistance in colon cancer with V600E
27
Q

Bortezomib (Velcade)

A
  • Mechanism: proteosome inhibitor
  • Hematologic Disease: Multiple Myeloma
  • Toxicity:
    • neuropathy and myelosuppression
28
Q

Nivolumab

A
  • Mechanism: PD-L1 inhibitor
    • Binds to programmed death receptor-1 (PD-1) which inhibits programmed T cell death activity
    • Reverses T cell suppression and induces antitumor response
  • Hematologic Disease: Hodgkin Lymphoma
  • Toxicity:
    • Immune mediated pneumonitis, colitis, hepatitis, endorinopathies
    • Fatigue, rash, musculoskeletal pain, pruritis (itchy skin)

Heme/Onc Pathoma (10 decks)

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