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Hematology / Oncology > Pharm 25 - Quick & Easy > Flashcards

Pharm 25 - Quick & Easy Flashcards

1
Q

-famide & -phamide

A

alkylating agents: nitrogen mustards

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2
Q

-platin

A

alkylating agents: platinum analogs

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3
Q

-tecan & -rubicin

A

topoisomerase enzyme inhibitors

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4
Q

-taxel & -istine

A

antimicrotubules

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5
Q

-abine & 5-FU

A

antimetabolites

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6
Q

-mab

A

monoclonal antibodies

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7
Q

-nib

A

tyrosine kinase inhibitors

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8
Q

(nitrogen mustard class)
Mesna:
MOA
S/E

A

○ Binds up acrolein to prevent hemorrhagic cystitis

○ Ifosfamide: has a build-up of acrolein that causes:
§ Hematuria, dysuria, increased urinary frequency
□ Requires bladder treatment to remove clots and continuous bladder irrigation

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9
Q

Nitrogen mustards MOA

A

prevents cell division by cross-linking DNA strands

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10
Q

ADE of nitrogen mustards

A

○ Hemorrhagic cystitis
§ Due to build up of a toxic metabolite (acrolein)
§ Aggressive hydration (IV/PO) essential
§ Adjust for renal dose
□ Causes acute tubular necrosis
○ Alopecia
○ CNS toxic

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11
Q

Mesna is dosed with…

A

○ Given with ifosfamide

§ Not given with cyclophosphamide

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12
Q

Which is less toxic: cyclophosphamide or ifosfamide? (nitrogen mustards)

A

Cyclophosphamide: Less toxic, and thus does not require Mesna

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13
Q

CNS effects of ifosfamide (nitrogen mustard)

A

See confusion, drowsiness, hallucinations, depressive psychosis, seizures

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14
Q

cold sensitivity drug

A

Oxaliplatin

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15
Q

MOA of platinum analogs

A

prevents cell division by cross-linking DNA strands

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16
Q

Nephrotoxicity order for the platinum analogs: place the following in order of greatest toxicity to least

carboplatin, cisplatin, oxaliplatin

A

Cisplatin > Carboplatin > Oxaliplatin

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17
Q

Peripheral neuropathy order for the platinum analogs: place the following in order of greatest neuropathy to least

carboplatin, cisplatin, oxaliplatin

A

Cisplatin & Oxaliplatin > Carboplatin

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18
Q

Highest emetic drug of the platinum analogs

A

Cisplatin: has two phases of acute and delayed

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19
Q

Myelosuppression of carboplatin

A

thrombocytopenia

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20
Q

Myelosuppression of cisplatin

A

anemia

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21
Q

Ototoxic drug of the platnium analogs

A

cisplatin

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22
Q

common reaction of the platinum analogs

A

hypersensitive infusion reactions

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23
Q

nephrotoxic effects of cisplatin

A

Na and Mg wasting –> must be given with fluids that have NaCl and Mg

24
Q

Odd ADE of oxaliplatin

A

Pharyngolaryngeal dysethesia - “tingling,”“burning,”“constriction,” or unpleasant sensation felt in the mouth

25
Q

MOA of topoisomerase enzyme inhibitors

A

Inhibit topoisomerases
○ Topoisomerases are used to catalyze the breaking and rejoining of DNA strands during replication to relieve the strain that is placed on the double helix during unwinding
○ Inhibiting this action allows the drug to stop the replication of the individual cancer cell and thus the subsequent growth of the cancer

26
Q

Irinotecan ADE

A

○ Severe diarrhea
§ Some patients have a mutated allele that causes an increased risk for neutropenia and life threatening diarrhea
§ Pre-medicate patients with atropine if develop acute diarrhea
§ Delayed diarrhea: treat with oral and IV hydration, electrolyte replacement
□ Use loperamide (antidiarrheal that is opioid based and acts on circular/longitudinal muscles of the intestines to slow peristalsis and inhibit fluid/electrolyte secretion to reduce fecal volume)

27
Q

Irinotecan acute cholinergic etiology

A

combated with atropine

28
Q

Doxorubicin major ADE

A

Severely cumulative and permanent cardiotoxicity

Administer with dexrazoxane as it’s cardioprotective

29
Q

Doxorubicin complications (not cardiotoxicity)

A

Extravasation risk - use dexrazoxane to limit free radical formation

30
Q

Dexrazoxane

A

○ Gives cardioprotective effects from the cardiotoxicity of antitumor agents
§ Inhibits free radical formation to limit cardiotoxicity
§ Potentially decreases anthracycline antitumor effects

31
Q

Antimicrotubule MOA

A

○ Prevents microtubule assembly or disassembly

○ Microtubules are used to pull chromosomes apart during anaphase of the mitotic cell cycle
§ When this is interrupted, the cell can no longer replicate –> inhibits cellular replication

32
Q

Vincristine ADE

A

Fatal if administered intrathecally

§ Neurotoxic
□ Sensory and motor
® Trigeminal neuralgia: jaw pain, pharyngeal pain
® Constipation due to autonomic dysfunction - bowel regimen
□ Peripheral neuropathy
® Tingling and numbness

33
Q

Docetaxel & Paclitaxel ADE

A

§ Infusion related hypersensitivity
□ Give famotidine or diphenhydramine, steroid like dexamethasone (drug that’s used to treat N/V in chemo after other agents have failed)

§ Neurotoxic: cumulative peripheral neuropathy
§ Myelosuppression - neutropenia and anemia
§ Cardiovascular - peripheral edema, flushing
§ Dose adjusted for hepatic dysfunction

34
Q

Antimetabolites: MOA

A

o Act as false metabolites and are incorporated into DNA and RNA ultimately inhibiting synthesis of DNA to stop cellular reproduction/growth
o Capecitabine, Cytarabine, and Fluorouracil (purine/pyrimidine analogues) incorporate directly into DNA and replace nucleotides in the helix to disrupt DNA replication

35
Q

capecitabine, cytarabine, fluorouracil toxicities

A

§ Myelosuppression (pancytopenia)
□ This can occur for 3-25 days
□ VERY LONG TIME to have myelosuppression
§ Neurotoxicity: peripheral neuropathy, visual disturbance, somnolence
§ Adjust for renal dysfunction
§ Skin rash

36
Q

Fluorouracil (5-FU)

A

® Bolus administration can cause myelosuppression
® Continuous infusion can occur for 24 hours to 7 days
◊ Leads to mucosal damage (mucositis and diarrhea)
◊ Palmar-plantar erythrodysesthesia
§ Patients can have a genetic defect that can cause an increase in toxicity with this drug (dihydropyridine dehydrogenase - DPD)

37
Q

Methotrexate (MXT)

A

o Works quite well
§ Also inhibits folate for the patient, so must supplement with Leucovorin to combat

§ Drug interactions
	□ NSAIDs
	□ PPIs (dose dependent)
§ Adjusted for renal dysfunction 
	□ MTX can crystallize in urine and cause renal tubular damage
38
Q

Leucovorin

A

○ A reduced form of folic acid

§ Added to methotrexate to reduce myelosuppression of methotrexate

39
Q

Leucovorin - chemotherapy rescue agent

A

§ Actively competes with and displaces Methotrexate
□ Restores active folate stores required for DNA/RNA synthesis
□ Given 24-36 hours after the start of the MTX infusion

40
Q

Leucovorin - chemotherapy modulating agent

A

§ Combined with fluorouracil to increase enzyme inhibition and cause DNA damage

41
Q

· Antitumor antibiotics: bleomycin MOA

A

binds to DNA and acts like an alkylating agent, produces DNA cross-linking, ultimately inhibiting DNA and RNA synthesis

42
Q

Bleomycin use and ADE

A

Use: prostate cancer
ADE:
○ Bleomycin: “Bleo-Lung” –> pulmonary fibrosis
○ Infusion reactions - fever and chills
○ Dermatologic - hyperpigmentation, alopecia, palmar-plantar erythrodysesthesia

43
Q

bortezomib MOA

A

o MOA: inhibits proteasome enzyme complexes which regulate intracellular protein homeostasis
○ In some cases, can lead to increased cell death due to disruption of neoplastic cell cycle required proteins

44
Q

Bortezomib toxicity

A

○ Peripheral neuropathy: IV and SubQ
§ Usually administered SubQ as less neurotoxic (this is the drug that was given SubQ by nurses as they didn’t know what they were doing)
○ May cause herpes reactivation and thus require antiviral prophylaxis during therapy

45
Q

lenalidomide: use and MOA

A

o Use: treats multiple myeloma
o MOA: changes interferons and interleukins of the immune system
○ Inhibits proinflammatory cytokines
○ Stimulates proliferation of T cells to enhance cell mediated immunity
○ Inhibits trophic signals to angiogenic factors in cells
○ Inhibits growth of myeloma cells by inducing cell cycle arrest and cell death

46
Q

lenalidomide: black box warning

A

§ Myelosuppression: thrombocytopenia, neutropenia
§ Arterial/venous thromboembolic events (with dexamethasone)
§ Severe birth defects, embryo-fetal death

47
Q

Monoclonal antibody ADE toxicities

A

○ Infusion related
§ Titrated and commonly see fever/chills, dyspnea, nausea, anaphylaxis, and rigors
○ Myelosuppression (cytotoxic conjugates)
○ Immune mediated - these types of drugs are created through the use of animal immune systems and thus when introduced into the human body, there are MANY immune responses that can happen (also HIGHLY patient dependent on the reaction)
§ Toxic epidermal necrolysis, enterocolitis, hepatitis, progressive multifocal leukoencephalopathy, mucocutaneous reactions

48
Q

Rituximab toxicities

A

§ Hepatitis B virus reactivation - screen patients for HBV infection
§ CLL patients - Pneumocystis jirovecii and antiherpetic viral prophylaxis
§ High lymphocyte count - high infusion reaction potential

49
Q

Trastuzumab toxicites

A

CHF: Cardiotoxicity: heart failure, arrhythmia, cardiomyopathy

These effects ARE reversible

50
Q

Cetuximab toxicites

A

§ Electrolyte abnormalities - hypomagnesemia
§ Dermatologic: acneiform rash, skin rash
□ Rash resolves with the end of treatment
□ Patients like this drug as they feel like they can see it working/know it’s working when they get a rash
□ Rash needs to be treated with corticosteroids, ABX, antihistamines, moisturizing creams/lotions
§ Infusion related reactions

51
Q

Bevacizumab toxicites

A

○ HTN, impaired wound healing, hemorrhage, proteinuria/nephrotic syndrome, thromboembolism

○ Starves the tumor of the nutrients it needs

52
Q

Pembrolizumab toxicites

A

§ Immune-mediated: colitis, dermatitis, endocrinopathies, nephritis, pneumonitis
□ Because of these, check things like renal function, TSH

53
Q

Tyrosine kinase inhibitors purpose

A

○ Shut off a signaling pathway in one of many different ways
○ Catalyze the transfer of a phosphate group from ATP to tyrosine residues in proteins
§ Can bind on the inside or outside of the cell
○ Regulates messenger activity
Important in cellular regulation of proliferation/differentiation, motility, function, survival

54
Q

Tyrosine kinase inhibitors advantages

A

○ Single compound targeting multiple kinases
○ Efficacy in multiple tumor types
○ Oral therapy - convenient, less complex therapy

55
Q

Tyrosine kinase inhibitors disadvantages

A

○ Potential for drug-drug interactions
○ Still have significant toxicities
○ Patient monitoring less frequently - maybe less adherence/follow-up
○ Resistance is developing

56
Q

Hand-Foot syndrome drugs

A

§ Fluorouracil (antimetabolite)
§ Bleomycin (antitumor ABX)
§ Sorafenib (tyrosine kinase inhibitors)

57
Q

Cardiotoxic drugs

A

§ Doxorubicin (irreversible) - topoisomerase enzyme inhibitor
§ Trastuzumab (reversible) - monoclonal antibody

Hematology / Oncology (4 decks)

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