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Oncology > Oral Chemotherapy > Flashcards

Oral Chemotherapy Flashcards

1
Q

Thalidomide, Lenalidomide, and Pomalidomide are what kind of oral chemo agents?

A

Immunomodulators
Anti-angiogenics
IMiDs

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2
Q

Why would patients prefer oral chemo?

A

Convenience
Less invasive
Ease of administration
Sense of empowerment

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3
Q

Why oral over IV chemo?

A

Less invasive
Convenient
Self-administered
May be payable through Medicare Part D

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4
Q

Advantages of oral chemo from a healthcare professional standpoint

A

oral admin can provide prolonged drug exposure which may be important for drugs with schedule-dependent efficacy

potential to reduce the use of healthcare resources for inpatient and ambulatory patient care services

may provide better QOL

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5
Q

Challenges of oral chemo therapy

A

many drug-drug and drug-food interactions
patients with hx of dysphagia, odynophagia, severe n/v
patient adherence
less opportunity for healthcare professionals for pt interaction (pt edu, tox management, assessment on dz response)
shift of responsibility from provider to pt
drug cost ($$$)

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6
Q

How do IMiDs work?

A

Selectively inhibit secretion of pro-inflammatory cytokines
Stimulates anti-CD3 stimulated Tcells
Inhibits trophic signals to angiogenic factors in cells
Induces cell cycle arrest and cell death in myeloma cells

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7
Q

Which anti-angiogenic does not need renal adjustment?

A

Thalidomide

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8
Q

Which immunomodulator needs hepatic adjustment?

A

Pomalidomide

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9
Q

What are the 3 adverse effects to immunomodulators/anti-angiogenics/IMiDs?

A

Neuropathy, DVT/PE, Myelosuppression (neutropenia)

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10
Q

What is the major warning related to immunomodulators: Thaliodmide, Lenalidomide, Pomalidomide?

A

Pregnancy Category X - REMS needed

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11
Q

Everolimus blocks which important factor?

A

VEGF (vascular endothelial growth factor) and HIF-1 (hypoxia-inducible factor)

mTOR kinase inhibitor with antiproliferative and antiangiogenic properties

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12
Q

Adverse effects related to Everolimus

A

Metabolic Syndrome (hi-cholesterol, glucose, TG), Electrolyte abnormalities (decrease in K, Ca, Phos, Mg, HCO3), fatigue/malaise, edema

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13
Q

Major DDIs with Everolimus

A

CYP3A4 inducers/inhibitors

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14
Q

Which alkylating agent is available IV and PO?

A

Cyclophosphamide and Temozolomide

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15
Q

Cyclophosphamide has what adverse effects?

A

Hemorrhagic cystitis (dose-dependent), alopecia, N/V (dose-dependent), sterility

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16
Q

What patient education pts are important for cyclophosphamide?

A

Do not administer at bedtime to minimize risk of bladder irritation
Take during or after meals
INCREASE fluid INTAKE while on therapy to decrease risk of hemorrhagic cystitis

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17
Q

MOA of Temozolomide

A

A prodrug**: hydrolyzed to active form MTIC which exerts cytotoxic effects

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18
Q

Adverse Effects of Temozolomide

A

Non-specific: fatigue, N/V, constipation, lymphocytopenia

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19
Q

Patient education for Temozolomide

A

Absorption is affected by food, so consistently take with or without food
May take on empty stomach at bedtime to reduce N/V
Anti-emetics** are recommended that prevent N/V (for higher doses > 75 mg/m2/day)
PCP Prophylaxis** (in pts receiving concomitant radiotherapy, longer dosing regimens, or concomitant steroids)

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20
Q

Selective estrogen receptor modulator (SERM) oral chemotherapy agent

A

Tamoxifen

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21
Q

ADRs for Tamoxifen

A

Mood changes, vasodilation, edema, nausea, vasomotor (hot flashes), vaginal discharge - bone and tumor pain
BBW: VTE and increased risk of uterine malignancies

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22
Q

MOA for Abiraterone

A

Blocks CYP17 (involved in androgen synthesis) and inhibits cortisol production

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23
Q

ADRs for Abiraterone

A

(Since cortisol precursor is still available, it causes the following): hypokalemia, fluid retention, hypertension, vasomotor side-effects, increased LFTs, hypertriglyceridemia

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24
Q

PK/PD of Capecitabine

A

Prodrug that converted into active metabolite 5-FU**

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25
ADRs of Capecitabine
HFS**, diarrhea**, mucositis/stomatitis
26
Patient education of Capecitabine
Usually administered in 2 divided doses taken 12 hours apart Doses should be taken with water within 30 min after a meal Avoid prolonged sun exposure (use sunscreen)
27
Largest group of oral chemotherapy agents
Tyrosine Kinase Inhibitors
28
What is the ending of Tyrosine Kinase Inhibitors?
"-nibs" small molecule: used in both solid tumors and heme cancers
29
Class side effects of Tyrosine Kinase Inhibitors from all inhibitions (VEGF, EGFR, BCR-ABL)
Diarrhea**, Fatigue, Rash
30
Class side effects with Tyrosine Kinase Inhibitors for VEGF inhibition
HFS**, HTN, hemorrhage
31
Class side effects with Tyrosine Kinase Inhibitors for EGFR inhibition
Acneiform rash**, nail changes, hair changes
32
Class side effects with Tyrosine Kinase Inhibitors for BCR-ABL inhibition
Fluid retention**
33
FLT-3 inhibitors
Midostaurin, Gilteritinib
34
Midostaurin ADR of FLT-3 Inhibitors
Nausea**, Mucositis**, Myelosuppression**, Diarrhea, Hyperglycemia, Edema, Fatigue, Headache
35
Gilteritinib ADR of FLT-3 Inhibitors
Hypertriglyceridemia**, Increased LFTs**, headache, fatigue, edema, hyperglycemia, nausea, mucositis, diarrhea, myelosuppression
36
CDK-4/6 Inhibitors (3): Cyclin-dependent Kinase inhibitors
Palbociclib, Abemaciclib, Ribociclib
37
MOA of CDK-4/6 Inhibitors
Interrupting hormone signals that stimulate proliferation (usually CDK-4/6 are up-regulated: they are associate with uncontrolled cell proliferation)
38
ADRs with Palbociclib, Abemaciclib, Ribociclib (CDK-4/6 Inhibitors)
Diarrhea (Abemaciclib**), Neutropenia (Palbociclib**), Fatigue, Nausea, Increased LFTs
39
PARP Inhibitors
Olaparib, Niraparib, Rucaparib, Talazoparib (-parib)
40
MOA of Olaparib, Niraparib, Rucaparib, Talazoparib (-parib)
PARP Inhibitor (Poly (ADP-ribose) polymerase enzyme inhibitor; PARP-1/2 are involved in detecting DNA damage, and promoting repair; therefore, inhibition results of apoptosis
41
PARP Inhibitors are not super well tolerated, and usually not the most effective dose. What are the ADRs of Olaparib, Niraparib, Rucaparib, Talazoparib (-parib)?
Myelosuppression (Olaparib**), Nausea (Olaparib, Niraparib, Rucaparib**), Headache, Fatigue
42
IDH-1/2 Inhibitors
Ivosidenib, Enasidenib
43
MOA for IDH-1/2 inhibitors: Ivosidenib, Enasidenib
Inhibitor of mutant isocitrate dehydrogenase 1/2 enzymes. Mutated IDH 1/2 leads to increased levels of 2-hydroxyglutarate, which is responsible for impaired hematopoietic differentiation, typically seen in leukemia cells. SO by blocking the mutant IDH-1/2, restore proper bone marrow differentiation
44
ADRs for IDH-1/2 Inhibitors: Ivosidenib, Enasidenib
Hyperbilirubinemia & Myelosuppression (Enasidenib**), Differentiation Syndrome (think MOA), N/D
45
Why is differentiation syndrome a side effect of IDH-1/2 Inhibitors?
MOA is to prevent impaired differentiation, so it restores proper differentiation. This can cause a hyper-proliferation of myeloid cells = excessive inflammatory response. Causes "sepsis looking" response: hypotension, fever, dyspnea, hypoxia, peripheral edema, pleural or pericardial effusion, and multi-organ dysfunction
46
Management of Differentiation syndrome with Ivosidenib, Enasidenib
Hold therapy and initiate glucocorticoid therapy and monitor hemodynamics Can resume when sxs done
47
PI3K inhibitors
Idelalisib, Duvelisib, Copanlisib (-lisib)
48
MOA of PI3K Inhibitors: Idelalisib, Duvelisib, Copanlisib (-lisib)
Inhibition of delta isoform of phosphatidylinositol-3 kinase will lead to apoptosis PI3K-delta is highly expressed in malignant lymphoid B-cells, and when PI3K is activated, it will cause survival + proliferation + angiogenesis --> development of cancer when dysregulated
49
ADRs for Idelalisib, Duvelisib, Copanlisib (-lisib)
Fatigue, Diarrhea, Nausea, Myelosuppression
50
Proteasome inhibitors
Ixazomib
51
MOA for Ixazomib (Proteasome Inhibitors)
Reversible inhibition of chymotrypsin-like activity of beta-5 subunit of the 20s proteasome leading to cell cycle arrest and apoptosis Proteasome are important for protein degradation and expression [----- Blocking proteasome will lead to accumulation of misfolded proteins to promote cell death
52
ADR for Proteasome Inhibitors (Ixazomib)
Peripheral neuropathy**, eye disease, peripheral edema, diarrhea, nausea, myelosuppression (thrombocytopenia, neutropenia)
53
BCL-2 Inhibitors
Venetoclax
54
MOA of Venetoclax (BCL-2 Inhibitor)
Selective inhibition of anti-apoptotic BCL-2 protein which is over-expressed in leukemic cells --> causes apoptosis of B cells BCL-2 also mediates tumor cell survival and has been associated with tumor resistance to chemotherapy on the mitochondrial membrane
55
ADRs for Venetoclax (BCL-2 Inhibitor)
TLS**, fatigue, edema, diarrhea, AST elevation, myelosuppression, myalgia
56
Describe TLS associated with Venetoclax (BCL-2 Inhibitor)
**Oncologic emergency** characterized by metabolic disturbances that results from the **massive lysis of tumor cells** that release their contents into the bloodstream Sxs: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia Prophylaxis required during venetoclax initiation/ramp-up phase
57
What is the prophylaxis for TLS during venetoclax initiation/ramp-up phase?
AML: If WBC >=25,000, adequate hydration + anti-hyperuricemic CLL: all levels of tumor burden requires hydration (PO/IV) + anti-hyperuricemic
58
HDAC Inhibitors
Vorinostat, Panobinostat (-inostat)
59
MOA of Vorinostat, Panobinostat (-inostat) : HDAC Inhibitors
Histone deacetylase (HDAC) inhibition resulting in increased acetylation of histone proteins Accumulation of acetylated histones and other proteins induces cell cycle arrest and apoptosis Histones are structural support for DNA. Usually you need to deacetylase to remove the groups. But if it is blocked = cell death
60
ADR of HDAC Inhibitors: Vorinostat, Panobinostat (-inostat)
Fatigue, peripheral edema, nausea, diarrhea, muscle weakness, myelosuppression
61
Clinical Pearls to remember for HDAC Inhibitors: Vorinostat, Panobinostat (-inostat)
Obtain EKG prior to therapy initiation to verify that QTc <450 ms (for Panobinostat) For Vorinostat, Panobinostat (-inostat) prior to treatment, start: - baseline ANC >=1500 - platelet >= 100k * *due to myelosuppression ADR**
62
Hedgehog Pathway inhibitors
Vismodegib, Sonidegib, Glasdegib (-degib)
63
MOA of Vismodegib, Sonidegib, Glasdegib (-degib): Hedgehog pathway inhibitors
Hedgehog pathway **regulates cell growth and differentiation in embryogenesis** Mutation in the hedgehog pathway results to **unrestricted proliferation of basal cells of the skin** Hedgehog inhibitors bind to **Smoothened Homologue (SMO)**, which is the transmembrane protein involved in hedgehog-signal transduction --> cell death
64
ADR for Vismodegib, Sonidegib, Glasdegib (-degib): Hedgehog pathway inhibitors
**Increased CPK**, Fatigue, Nausea, Diarrhea, Decrease appetite
65
Which drug class is known for acneiform rash? (Think MOA)
EGFR Inhibitors (TKIs) - highest for all grades Afatinib
66
Describe acneiform rash cause by EGFR inhibitors
on face, back, chest first 2-4 weeks: first presents with acne-like rash peaks at weeks 4-6: post inflammatory effects, dry skin, fissure decreases after 6-8 weeks: paronychia (a skin infection around the fingernails or toenails)
67
How to decrease incidence rate of acneiform rash with EGFR inhibition
Start one of these WITH therapy for total duration 6-8 weeks (also they are associated with treatment for grades of rash): Topical [Grade 1]: Hydrocortisone 1% cream + moisturizing emollients + sunscreen (SPF 15+) Systemic [Grade 2]: Doxycycline 100 mg PO BID or Minocycline 100 mg PO daily [Grade 3/4]: Prednisone 0.5 mg/kg IV
68
Onset and symptoms of HFS from multi-targeted tyrosine kinase inhibitor
Onset: 2-4 weeks of therapy (1st month) Symptoms: erythema, paresthesia, blisters in the palms and soles followed by thick hyperkeratotic, tender, lesions Dose-dependent effect: Resolution if therapy is held
69
Pharmacologic/Non-Pharmacologic Management of HFS
[Grade 0]: avoid hot water and activities to create friction, wear thick cotton gloves or socks to prevent injury [Grade 1]: Low dose steroid cream (Clobetasol 0.05% cream) [Grade 2]: Keratolytics (Urea Cream 20-40%) + NSAIDs/GABA agonists/Narcotics [Grade 3]: Interrupt treatment until severity decreases to grade 0-1; higher dose urea cream
70
Diarrhea is caused by which drugs?
Capecitabine + TKIs
71
Management for Diarrhea with Capecitabine and TKIs
**Hold oral chemotherapy** if increase of >= 4 stools/day over baseline Increase fluid intake Loperamide (Imodium): **cancer treatment-induced** 4mg followed by 2mg q4hrs or **after each loose stool (no maxdose) OR 4mg follow by 2mg every q2hrs Diphenoxylate/Atropine 2.5/0.025 mg (Lomotil): when imodium fails, **adjunct therapy** 2.5-5mg PO QID until symptoms control

Oncology (6 decks)

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