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Review / Wrong Answers > DIT review - Oncology 2 > Flashcards

DIT review - Oncology 2 Flashcards

1
Q

MOA of Cisplatin, Carboplatin, and Oxaliplatin

A

Platinum analog

  • Bind DNA through the formation of intra- and inter-strand cross links with Platinum
  • Leads to inhibition of DNA synthesis and function
  • Primary binding site in N7 position of adjacent guanines
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2
Q

Uses of platinum analogs

A
  • Solid malignancies (e.g. non-small cell lung cancer, small cell lung cancer, testicular cancer, ovarian cancer, bladder cancer)
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3
Q

Adverse effects of platinum analogs

A
  • Neurotoxicity:
    • Ototoxicity, which can lead to sensorineural hearing loss and tinnitus
      • Especially Cisplatin
    • Peripheral neuropathy (numbness, paresthesias, or pain in glove and stocking pattern)
      • Especially Cisplatin
  • Nephrotoxic (e.g. acute kidney injury) – Especially Cisplatin
    • Acute tubular necrosis (ATN – muddy brown casts)
    • Risk decreased with IV fluids given before and after Cisplatin
      • IV saline-induced diuresis prevents cisplatin-induced nephrotoxicity
  • Immunosuppression and increased risk of infection (especially Carboplatin)
  • Myelosuppression (especially Carboplatin)
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4
Q

What drug can be used to protect against Cisplatin-induced nephrotoxicity, and what is it’s MOA?

A
  • Amifostine
    • Sketchy = amethyst
  • Mechanism of action
    • Is an organic thiophosphate
    • Can bind to and detoxify the reactive metabolites (free radicals) of Cisplatin
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5
Q

MOA of Bleomycin

A
  • Sketchy = Beluga whale
  • Mechanism of action
    • Antitumor antibiotic
    • Small peptide with a DNA binding region on one end and an iron binding region on the other end
    • After binding to DNA, it chelates metal ions, producing a pseudo-enzyme that reacts with O2 to produce superoxide and hydroxide free radicals that cleave DNA
    • Free radicals leads to single and double-stranded breaks of DNA
  • Is cell cycle specific – cells become arrested in G2
    • Sketchy = Galleon (GII)
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6
Q

Uses of Bleomycin

A
  • Hematologic and solid malignancies (e.g. Hodgkin and Non-Hodgkin lymphoma, germ cell tumors, squamous cell carcinoma of the skin, cervix, and vulva
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7
Q

Adverse effects of Bleomycin

A
  • Pulmonary toxicity (e.g. pneumonitis, pulmonary infiltrates)
    • Can be fatal in rare cases
  • Skin toxicity (e.g. rash, exfoliation, hyperpigmentation, atrophic striae)
  • Stomatitis and mucositis
  • Alopecia
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8
Q

What are the names of drugs in the Anthracycline family?

A
  • Sketchy = Santa Anthracycline
  • Drugs:
    • “-rubicin**” suffix (e.g. **Doxorubicin, Daunorubicin)
        • rubies
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9
Q

MOA of Anthracycline

A
  • Antitumor antibiotic
  • Promote the generation of oxygen free-radical through an iron-dependent reductive process
  • Also bind to DNA through intercalation – are planar molecules that can fit themselves between base pairs of DNA – leading to blocking of DNA and RNA synthesis
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10
Q

Uses of Anthracycline

A
  • Broad range of solid and hematologic malignancies
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11
Q

Adverse effects of Anthracycline

A
  • Cardiotoxicity secondary to buildup of free radicals in cardiac myocytes
    • Presents as dilated cardiomyopathy with symptoms presenting months after drug is stopped
  • Myelosuppression
  • Stomatitis and mucositis
  • Alopecia
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12
Q

What can be used to prevent Anthracycline-induced cardiotoxicity

A
  • Dexrazoxane is an iron chelator that prevents anthracycline-induced cardiotoxicity
    • = chelating/clinging the heart sack
    • = is on the deck (dex-) with a razor (-razoxane)
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13
Q

MOA of Actinomycin D

A
  • Sketchy = artifact-inomycin (doll artifact)
  • Mechanism of action:
    • Is an antitumor antibiotic
    • Intercalates into DNA, blocking DNA and RNA synthesis
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14
Q

Uses of Actinomycin D

A

Numerous pediatric malignancies (e.g. Wilms tumor, Ewing sarcoma, rhabdomyosarcoma)

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15
Q

Adverse effects of Actinomycin D

A
  • Alopecia
  • Myelosuppression
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16
Q

MOA of Etoposide and Teniposide

A
  • Sketchy = side of the tower
  • Mechanism of action
    • Topoisomerase II inhibitors (double stranded breaks to relieve supercoiling)
    • Prevent the relegation of double strand breaks induced by topoisomerase II
  • Cycle specific
    • Inhibit DNA synthesis, arresting cells in the S phase
      • = “Stairs out”
    • Also block the G2 phase (double check and repair) of the cell cycle in cells that happen to make it past the S phase
      • = “Gone 2 forest”
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17
Q

Uses of Etoposide and Teniposide

A
  • Solid and hematologic malignancies (e.g. testicular cancer, small cell lung cancer, Hodkgin and NHL)
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18
Q

Adverse effects of Etoposide and Teniposide

A
  • Myelosuppression
  • Immunosuppression and risk for infections
  • Alopecia
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19
Q

MOA of Topotecan and Irinotecan

A
  • Sketchy = toucan
  • Mechanism of action
    • Topoisomerase I inhibitors (single stranded nicks to relieve supercoiling)
  • Cycle specific
    • Inhibit DNA synthesis, arresting cells in the S phase
      • = “Stairs out”
    • Also block the G2 phase (double check and repair) of the cell cycle in cells that happen to make it past the S phase
      • = “Gone 2 forest”
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20
Q

Uses of Topotecan and Irinotecan

A
  • Topotecan
    • Ovarian cancer and small cell lung cancer
  • Irinotecan
    • Colon cancer
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21
Q

Adverse effects of Topotecan and Irinotecan

A
  • Myelosuppression
  • Severe diarrhea
22
Q

MOA of Vincristine and Vinblastine

A
  • Sketchy:
    • = Christine in vines
    • = blasting vines
  • Mechanism of action
    • Cytotoxic vinca alkaloid
    • Inhibit microtubule production and mitotic spindle assembly
    • This arrests the cell in metaphase and cell division is brought to a halt
  • Cell cycle specific
    • Block mitosis – M phase
23
Q

Uses of Vincristine and Vinblastine

A
  • Hematologic and solid malignancies (e.g. leukemias, lymphomas, pediatric tumors, breast cancer, and germ cell cancer
24
Q

Adverse effects of Vincristine and Vinblastine

A
  • Neurotoxicity (e.g. peripheral sensory neuropathy)
  • Autonomic dysfunction (e.g. paralytic ileus, constipation)
  • Alopecia
  • Myelosuppression (especially Vinblastine)
25
Q

MOA of Taxanes

A
  • Drugs:
    • Paclitaxel, Docetaxel, Cabazitaxel
  • Mechanism of action:
    • Cytotoxic plant alkaloids
    • Bind directly to microtubules
    • Hyper-stabilize microtubules and inhibit degradation (paradoxical), leading to improper mitotic spindle function and cell dicion, leading to cell death
  • Cell cycle specific
    • Block mitosis – M phase
26
Q

Adverse effects of Taxanes

A
  • Neurotoxicity (e.g. peripheral sensory neuropathy)
  • Alopecia
  • Myelosuppression
27
Q

MOA and uses of Imatinib

A
  • Sketchy = serious guy IMITATING the king
  • Mechanism of action
    • Small molecule tyrosine kinase inhibitor
  • Uses:
    • Chronic myeloid leukemia, CML
      • Imatinib blocks the tyrosine kinase domain in the BCR/ACL fusion protein (mutation in CML)
        • = BREAKABLE sign on the box
    • Also blocks c-kit tyrosine kinase (in GIST – gastrointestinal stromal tumor)
      • = congress kit box
28
Q

Adverse effects of Imatinib

A
  • Fluid retention (ankle and periorbital edema)
29
Q

MOA and uses of Erlotonib

A
  • Sketchy = british Earl Geoffrey
  • Mechanism of action
    • Small molecule tyrosine kinase inhibitor
    • Blocks the epidermal growth factor receptor (EGFR) tyrosine kinase
      • = Earl GeofFRy
  • Uses:
    • EGFR is overexpressed in a number of tumors (e.g. non-small cell lung cancer (NSCLC), pancreatic cancer)
      • = crab badge over lung-shaped lapel = NSCLC
30
Q

Adverse effects of Erlotinib

A
  • Papulopustular acneiform rash
  • Diarrhea
31
Q

MOA and uses of Sunitinib

A
  • Sketchy = rising sun
  • Mechanism of action
    • Small molecule tyrosine kinase inhibitor
    • Inhibits multiple receptor tyrosine kinases, including vascular endothelial growth factor, VEGFR (angiogenic growth factor)
  • Uses:
    • Renal cell carcinoma
    • Gastrointestinal stromal tumor
32
Q

Adverse effects of Sunitinib

A
  • Hyperkeratosis and skin rash
  • Increased risk of hemorrhage
33
Q

MOA and uses of Sorafenib

A
  • Sketchy = soaring eagle
  • Mechanism of action
    • Small molecule tyrosine kinase inhibitor
    • Inhibits multiple receptor tyrosine kinases, including VEGFR (angiogenic growth factor)
  • Uses:
    • Renal cell cancer
    • Hepatocellular cancer
34
Q

Adverse effects of Sorafenib

A
  • Hyperkeratosis and skin rash
  • Increased risk of hemorrhage
35
Q

MOA and uses of Vemurafenib

A
  • Sketchy = venom of snake drawing
  • Mechanism of action
    • Small molecule tyrosine kinase inhibitor
    • Inhibits B-Raf kinase (B-Raf activates singaling pathways drive melanocyte proliferation)
      • = B. Fra (Ben Franklin signature) written on drawing
    • BRAF mutation V600e (valine to glutamic acid) seen in 40-60% of patients with melanoma
      • You can kind of get this from the name of the drug:
        • V600e (Ve) mutated (mu) B-Raf (raf) inhibitor (nib)
  • Uses
    • Malignant melanoma
36
Q

MOA of Rituximab

A
  • Sketchy = coronation RITUal
  • Mechanism of action à B-cell depletion
    • Antitumor monoclonal antibody
    • Is chimeric IgG
      • = chimera sigil (hybrid animal) on cape of guy getting coronated
    • Targets CD20 (found on B-cells) in order to deplete B-cells (by labelling for apoptosis)
      • = antibody archer being pulled to the ground to kneel for the ritual
      • = straps on archer look like two X’s (XX = 20)
37
Q

Uses of Rituximab

A
  • CD20+ Non-Hodgkin lymphoma
  • Chronic lymphocytic leukemia (CLL)
  • Rheumatoid arthritis (disease modifying antirheumatic drugs – DMARD)
  • Immunosuppression therapy (e.g. microscopic polyangiits, Wegener’s granulomatosis)
38
Q

Adverse effects of Rituximab

A
  • Immunosuppression and increased risk of infection
  • Higher risk of progressive multifocal leukoencephalopathy (PML) due to reactivation of JC virus
  • IV infusion reaction:
    • Constellation of symptoms occurring within first hour (e.g. HA, fever, rash, pruritus, dyspnea, hypotension)
    • Occurs due to antibody-antigen interaction, resulting in cytokine release
      • Managed with antihistamines, acetaminophen, or NSAIDs
  • Delayed onset poisoning – only occurs in chimeric drugs
    • Serum sickness occurring in 7-14 days (e.g. fever, rash, arthralgia) – due to Type III hypersensitivity reaction
    • Serum sickness occurs due to patient’s body attacking the non-human parts of the drug since it is chimeric
39
Q

MOA of Cetuximab

A
  • Sketchy = tusks of elephant
  • Mechanism of action
    • Antitumor monoclonal antibody
    • Is chimeric IgG
    • Targets epidermal growth factor receptor (EGFR)
      • = GiRaFe pattern on elephant blanket
    • EGFR is a tyrosine kinase receptor
      • = tire swing
40
Q

Uses of Cetuximab

A
  • Solid tumors (e.g. Colorectal cancer, Squamous cell head and neck cancer)
41
Q

Adverse effects of Cetuximab

A
  • Papulopustular acneiform rash (due to abundance of EGFR in the skin)
    • = red spots on giraffes
  • IV infusion reaction:
    • Constellation of symptoms occurring within first hour (e.g. HA, fever, rash, pruritus, dyspnea, hypotension)
      • = red angel statue – swollen cherub with ivy
    • Occurs due to antibody-antigen interaction, resulting in cytokine release
      • Managed with antihistamines, acetaminophen, or NSAIDs
  • Delayed onset poisoning – only occurs in chimeric drugs
    • Serum sickness occurring in 7-14 days (e.g. fever, rash, arthralgia) – due to Type III hypersensitivity reaction
      • = delayed onset poisoning
    • Serum sickness occurs due to patient’s body attacking the non-human parts of the drug since it is chimeric
42
Q

MOA of Bevacizumab

A
  • Sketchy = beverage lady
  • Mechanism of action
    • Antitumor monoclonal antibody
    • Directly binds to VEGF and prevents it from interacting with its receptor
      • = chopped vegetables
    • Functions as an anti-angiogenic, inhibiting the growth of blood vessels in tumors
      • = chopping veggies that look like vessels
43
Q

Uses of Bevacizumab

A
  • Metastatic tumors (e.g. colorectal and lung cancer)
  • Wet macular degeneration
    • Wet degeneration is characterized by retinal hypoxia, which stimulates local VEGF production and causes sub-retinal neovascularization with formation of leaky vessels
    • This causes an acute loss of vision over days to weaks
44
Q

Adverse effects of Bevacizumab

A
  • Can inhibit wound healing due to anti-angiogenic action
  • Increased risk of bleeding (e.g. epistaxis)
  • Increased risk for arterial thromboembolic events (e.g. TIA, strokes, angina, MI)
  • Gastrointestinal perforation
45
Q

MOA of Alemtuzumab

A
  • Sketch = alms of the beggar
  • Mechanism of action
    • Antitumor monoclonal antibody
    • Is an IgG antibody that binds to CD52 (found on normal and malignant B- and T-cells)
      • = beggar grabbing on to antibody archer and T-cell knight
      • = 52 pattern on sword sheath on knight
    • Binding to CD52 leads to a direct cytotoxic effect, through complement fixation and antibody dependent cell-mediated cytotoxicity
46
Q

Uses of Alemtuzumab

A
  • Chronic lymphocytic leukemia (CLL)
47
Q

Adverse effects of Alemtuzumab

A
  • Bone marrow suppression
  • Infections
  • Emergence of autoimmune disorders
48
Q

MOA of Trastuzumab

A
  • Sketchy = tapestry weaver
  • Mechanism of action
    • Antitumor monoclonal antibody
    • Binds to epidermal growth factor receptor 2 (e.g. HER2)
      • = her 2 babies
    • HER2 is a receptor tyrosine kinase
      • = her 2 babies in the tire swing
49
Q

Uses of Trastuzumab

A

HER2+ breast cancer

50
Q

Adverse effects of Trastuzumab

A
  • Cardiotoxicity (e.g. decreased LVEF, heart failure)

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