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Hem/critical care/Onco > Cancer Sucks > Flashcards

Cancer Sucks Flashcards

1
Q

What are the negative effects of chemotherapy-induced N/V?

A

-increases morbidity
-negatively effects patients quality of life
-more distressful for the patients compared to other side effects
-non-adherence to chemotherapy and/or dose-reductions
-weakness, dehydration, electrolyte imbalance, esophageal tears, decline in behavioral and mental status

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2
Q

Acute CINV

A

-occurring within the first 24 hours after initiation of chemotherapy

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3
Q

Delayed CINV

A

occurring from 24 hrs to several days (days 2-5) after chemotherapy

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4
Q

Breakthrough CINV

A

occurring despite appropriate prophylactic treatment

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5
Q

Anticipatory CINV

A

occurring before a treatment as a conditioned response to the occurrence of CINV in previous cycles

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6
Q

Refractory CINV

A

recurring in subsequent cycles of therapy, excluding anticipatory CINV

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7
Q

Pathology of CINV

A

-communication between several neurotransmitters and receptors in the CNS & GI tract
-Serotonin and its receptors
-Substance P and NK-1 receptors
-Dopamine and its receptors

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8
Q

Emetic response to chemotherapy: Peripheral pathway

A

-5-HT3-mediated
-originates in the GI tract
-activated in the first 24hr after chemotherapy
-primarily associated with acute emesis

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9
Q

Emetic response to chemotherapy: central pathway

A

-NK-1 receptor mediated (substance P as well)
-occurs primarily in the brain
-through to be predominantly involved in delayed CINV

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10
Q

general principles of emesis control

A

-PREVENTION is key!!
-factors in choosing antiemetic agents: emetic risk of the therapy, prior experience with antiemetics, pt factors
**for chemo regimens with multiple agents, anti-emetic prophylaxis should be based on the agent with the highest emetogenic risk
-lifestyle measures may help to alleviate CINV

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11
Q

Risk factors of CINV

A

-age < 50
-female sex
-emetic potential of chemotherapy
-little or no previous alcohol use
-hx of CINV: prone to motion sickness
-emesis during pregnancy

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12
Q

Emesis Prevention: HIGH emetic risk w/ parenteral anticancer agents

A

Day 1: olanzapine, dexamethasone, NK1 RA, 5-HT3 RA
Day 2-4: olazapine, dexamethasone, aprepitant (PO)

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13
Q

Emesis Prevention: MODERATE risk w/ parenteral anticancer agents

A

A: day 1: dexamethasonse & 5-HT3 RA, Day 2-3: Dexamethasone OR 5-HT3 RA
B: day 1: olazapine, dexamethasone, palonosetron
Day 2-3: olanzapine
C: day 1: NK1 RA, dexamethasone, 5-HT3 RA
Day 2-3: Aprepitant +/- dexamethasone

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14
Q

Emesis prevention for low/minimal emetic risk

A

Options:
-dexamethasone
-metoclopramide
-prochlorperazine
-5-HT3 RA

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15
Q

Emesis prevention with ORAL anticancer agents

A

-high to moderate emetic risk: 5-HT3 RA
-low to minimal emetic risk: PRN recommended

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16
Q

Breakthrough emesis treatment

A

-add one agent from a different frug class to the current regimen
-consider routine, around the clock admin rather than PRN dosing
-consider antacid therapy if pt has dyspepsia
-drug options: olazapine, lorazepam, dronabinol, 5-HT3 RA, prochloperazine, dexamethasone, metoclopramide, scopolamine

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17
Q

Anticipatory emesis treatment

A

-PREVENTION is key!
-avoid strong smells that may precipitate symptoms
-LORAZEPAM is useful in anticipatory, anxiety-related, emesis
-acupunture
-behavioral therapy: guided imagery, relaxation, hypnosis, cognitive distraction, yoga, biofeedback, progressive muscle relaxation

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18
Q

Dexamethasone used in CINV

A

-MOA unknown –> Drug of choice!
-AEs: insomnia (administer in the AM), dyspepsia (take with food, consider adding H2 antagonist or PPI as clinically indicated), hyperglycemia, hypertension

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19
Q

5-HT3 RA used in CINV (ondansetron, palonosetron, granisertron)

A

MOA: blocks serotonin, both peripherally on vagal nerve terminals & centrally in the chemoreceptor trigger zone
AEs: headache, constapation, QTc prolongation

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20
Q

5-HT3 RA used in CINV: Ondansetron & Granisetron

A

-1st generation
-most effective in preventing of acute CINV
-short acting –> can be used in breakthrough nausea

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21
Q

5-HT3 RA used in CINV: palonosetron

A

-2nd generation
-effective in preventing acute & delayed CINV
-long acting ( 1/2 life = 40 hrs)

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22
Q

NK1 RA used in CINV: (aprepitant, fosaprepitant, rolapitant, fosnetupitant, netupitant)

A

MOA: inhibits the substance p/ neurokinin 1 –> augments 5HT3-RA & dexamethasone antiemetic activity
-only used for PREVENTION of CINv, not treatment
-DDIs: inhibition of CYP3A4 and CYP2C9 (dec dexamethasone dose to 8 mg daily on days 2-4)
AEs: fatigue, GI upset, headache, hiccups

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23
Q

Olanzapine used in CINV

A

MOA: blocks dopamine, 5-HT3, muscarinic and histamine receptors
–> useful in both prevention and breakthrough nausea
AE: sedation (administer at bedtime, consider low dose for elderly), hyperglycemia, fatigue, QTc prolongation

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24
Q

Dopamine antagonists used in CINV (Prochloperazine, Metoclopramide, Promethazine)

A

MOA: antagonize dopamine in the chemoreceptor trigger zone, most useful for breakthrough CINV
P&P AEs: phenothiazines, drowsiness, constipation
M AEs: benzamines, drowsiness, diarrhea, QTc prolongation, tardive dyskinesia
*Prochlorperazine used in pts at risk of QTc *

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25
Q

Benzodiazepines used in CINV (lorazepam, alprazolam)

A

MOA: anxiolytic
–> most useful for anticipatory CINV or breakthrough CINV that has an anxiety component
–> administer the night before or the morning of chemotherapy or both
AEs: sedation, dizziness

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26
Q

Cannabinoids used in CINV (dronabinol)

A

MOA: CB1 agonism suppresses vomiting, indirect activation of 5HT1a in raphe nucleus
–> rarely used, only indicated for refractory disease
AEs: sedation, euphoria, hallucinations, palpitations, flushing, cough

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27
Q

Scopolamine used in CINV

A

MOA: anticholinergic
–> rarely used, only used for breakthrough disease
AEs: dry mouth, somnolence, blurred vision

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28
Q

Cancer treatment induced diarrhea (CTID)

A

-can cause depletion of fluids and electrolytes, malnutrition, dehydration, and hospitalization/death
-can also be related to chemotherapy dosing delays or reductions

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29
Q

Assessment of CTID

A

-hx, volume and duration of diarrhea, hydration status
added risk factors: fever, orthostatic symptoms, abdominal pain.cramping, weakness

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30
Q

Diarrhea grading: grades 1 & 2

A

1: < 4 stools/day, mild increase in ostomy output
2: 4-6 stools/day, moderate increase in ostomy output, limiting instrumental ADL

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31
Q

Diarrhea grading: grades 3 & 4

A

3: > 7 stools per day, hospitalization indicated, severe increase in ostomy output, limiting. self care ADL
4: life threatening consequences, urgent intervention indicated

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32
Q

*Irinotecan-induced diarrhea

A

**Irinotecan can cause acute or delayed diarrhea
–> acute: due to cholinergic stimulation, mean duration of symptoms is 30 mins, usually respond rapidly to atropine
–> delayed: due to GI mucosal damage secondary to SN-38, usually occur more than 24 hrs after admin, noncumulative and occurs at all doses

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33
Q

Management of CTID

A

Non-pharm: avoidance of foods that would aggravate the diarrhea, aggressive oral rehydration with fluids that contain water, salt and sugar
Pharm:
-1st line: loperamide ( 4 mg then 2 mg q 4 hrs after MDD 16 mg) –> OTC
-Diphenoxylate-atropine (1-2 tabs q 6 hr until control achieves (MDD 8 tab)

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34
Q

tx of refractory CTID

A

-Octreotide
-tincture of opium
-probiotics
-rule out C. diff and infection colitis

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35
Q

Mucositis

A

-erythematous and ulcerative lesions of the mucosa observed in pts treated with chemotherapy
-can occur anywhere in the GI tract

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36
Q

Stomatitis

A

mucositis limited to the oral cavity

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37
Q

Mucositis complications

A

-symptom onset: typically occurs within 5-14 days
-dec oral intake: poor nutritional status, grade 3 = severe oral pain, grade 4 requires parenteral or enteral nutrition
-inc infection risk: gram _ oral flora, candida or fungal infection
-pain: may require opioids and PCA admin

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38
Q

5 stage model of oral mucositis

A

1) initiation: cellular damage induced, reactive oxygen species formation
2) primary damage response: activation od. p53 & NK-kB
3) signal amplification: release of inflammatory cytokines, tissue damage & cell death
4) ulceration: high risk for bacterial colonization
5) healing: cessation from ongoing tissue damage

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39
Q

risk factors of chemotherapy induced mucositis

A

-chemotherapy: melphalan, cisplatin + radiation, high-dose methotrexate, doxorubicin, busulfan, 5-FU
-patient factors: smoking, poor oral hygiene, oral lesions at baseline, female sex, pretreatment nutritional status

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40
Q

Prevention of chemo-induced mucositis

A

–> oral hygiene: avoid acidic or spicy foods, brushing with a soft toothbrush BID & flossing, switch tablets to solutions or IV, use nonalcohol-based mouthwashes at least QID
–> cryotherapy: local vasoconstriction –> less drug delivered to the oral mucosa, hold ice chips in their mouth for 30 mins before and/or during infusion of chemotherapy

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41
Q

Management of chemotherapy-induced mucositis

A

1- oral decontamination: bland mouthwash or oncology mouthwash –> dexamethasone mouthwash for Everolimus-induced mucositis
2- pain control: 2 % viscous lidocaine swish and spit, systemic opioids
3- palliation of dry mouth: artificial saliva products or chewing gum to increase saliva production
4- nutritional support: liquid or soft diet, TPN
5- oral candidiasis tx: nystatin oral solution or clotrimazole lozange, floconazole 200 mg PO x 1 dose, then 100 mg x 21 days

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42
Q

Neutropenia

A

-absolute neutrophil count < 500 or expected to decrease < 500 in 48 hrs
–> profound neutropenia: ANC < 100
–> prolonged neutropenia: lasting longer than 10 days
–> febrile neutropenia: single temp > 38.3 orally or > 38.0 over 1 h + ANC < 500 or expected to decrease to < 500 cells in 48 hrs

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43
Q

Consequences of neutropenia

A

-dose reduction or treatment delays
-compromise clinical outcomes
-longer hospital stays
-increased treatment costs
-decreased quality of life

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44
Q

Risk assessment for febrile neutropenia

A

-disease
-chemo regimen: high. dose therapy or dose-dense therapy
-patient risk factors: prior chemotherapy or radiation therapy, persistent neutropenia, bone marrow involvement by tumor, recent surgery and/or open wounds, liver dysfunction, renal dysfunction, age > 65 years receiving full chemotherapy dose intensity

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45
Q

Primary prevention for febrile neutropenia

A

–> high risk, regardless of pt risk factors: G-CSFs recommended
–> Intermediate risk + >/- 1 risk factor: consider G-CSFs
–> low risk + >/- 2 risk factors: G-CSFs may be considered

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46
Q

Primary prevention for febrile neutropenia : Filgrastim, tbo-filgrastim (catergory 1) *

A

-short acting G-CSF
-start the next day or up to 3-4 days after completion of chemotherapy
-given daily until ANC recovery

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47
Q

Primary prevention for febrile neutropenia : Pegfilgrastim (catergory 1)*

A

-long acting G-CSF
-adminster up to 3-4 days after completion of chemotherapy
-single adminstration
**allow >12 days between the dose of pegfilgrastrim and the next cycle of chemotherapy

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48
Q

Primary prevention for febrile neutropenia : Eflapegrastim-xnst (catergory 2A) *

A

-long acting G-CSF
-administer ~ 24 hrs after completion of chemotherapy
-single dose admin
*-do not administer 14 days before and 24 hrs after admin of chemotherapy

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49
Q

Treatment of febrile neutropenia

A

-received filgrastim prophylactically: continue filgrastim
-received pegfilgrastim or eflapegrastim-xnst prophylactically: no additional G-CSFs needed
-did not receive prophylactic G-CSFs: assess risk factors for an infection-associated complication

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50
Q

TX of febrile neutropenia: possible indications for G-CSF use in established febrile neutropenia

A

-sepsis syndrome
-age > 65
-ANC < 100
-neutropenia expected to be > 10 days in duration
-pneumonia or other clinically documented infections
-invasive fungal infection
-hospitalization at the time of fever
-prior episodes of febrile neutropenia

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51
Q

Secondary prevention for febrile neutropenia

A

in lue of febrile neutropnia or dose-limiting neutropenic event:
–> prior use of G-CSFs: consider chemo dose reduction or change in tx regimen
–> no prior use of G-CSFs: consider G-CSFs

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52
Q

Acute Leukamias

A

-rapid onset
-symptomatic
-rapidly fatal if untreated
-immature cells (“blasts”)
-usually leukopenia

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53
Q

Chronic Leukemias

A

-slowly progressive
-most asymptomatic
-some survive years without treatment
-immature and mature cells
-

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54
Q

Diagnosis of leukemia

A

-bone marrow responsible for production of circulating blood cells –> includes red blood cells, white blood cells and platelets
-bone marrow aspirate and biopsy required for diagnosis –> allows one to sample space where hematopoiesis occurs

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55
Q

who gets AML?

A

-most common acute leukemia in adults aged 65-74
-most deadly leukemia in the US annually
-median age at diagnosis: 68 y/o

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56
Q

Signs and Symptoms of AML

A

-anemia: fatigue, SOB
-thrombocytopenia: bleeding risk
-neutropenia*: defined as absolute neutrophil count < 500 or < 1000 with anticipated decreased to < 500 within 48 hrs
-spontaneous tumor lysis syndrome
-CNS involvement (rare): somnolence, headaches, confusion

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57
Q

What does AML look like?

A

-pancytopenia, WBC within normal limits, present with elevated WBC
-hyperleukocytosis
-elevated WBC: arbitrarily defined as WBC > 100,000, poor prognosis, increases risk of CNS involvement & very high risk ot TLS

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58
Q

What is hyperleukpcytosis in AML?

A

–> oncologic emergency
-hyperviscosity syndrome - “blood slugging”
-stupor, SOB, vision changes
-stroke, responsibility failure, cardaic ischemia, renal failure, retinal hemorrhage

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59
Q

Management of hyperluekocytosis

A

Hydroxyurea (Hydrea)
-oral ribonucleotide reductase inhibitor
-used for “count control”
-used until clinically stable and ready to start induction chemotherapy
-leukophresis

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60
Q

Hydroxyurea

A

-used for management of hyperluekocytosis
-capsules and suspension
-AEs: N/V/diarrhea, tumer lysis,
–> long term toxicities: cutaneous vasculitic ulcerations, mucositis, alopecia and hyperpigmentation

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61
Q

Diagnostic criteria for AML

A

-WHO: > 20% blasts isolated on bone marrow biopsy or peripheral blood
-detection of cytogenetic abnormalities known to indicate AML regardless of blast % on bmbx

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62
Q

Prognostic Markers of AML

A

**cytogenetics: karyotype (a persons chromosomal make up–> predicts ability to obtain remission with induction chemotherapy, risk of relapse and overall survival
-molecular abnormalities, age, primary vs secondary AML, performance status, availability of a stem cell donor, WBC at diagnosis, extra medullary disease

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63
Q

FMS-like-Tyrosine Kinase (FLT3) mutations

A

-promotes proliferation and blocks differentiation
-associated with worse prognosis, increased relapse rate and lower OS
-associated with leukocytosis and high percentage of blasts in bone marrow in denovo AML –> ITD mutation is associated with worse survival/worse prognosis compared to TDK mutation

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64
Q

Criteria for high-intensity induction chemotherapy for AML

A

-most pts < 60 y/o
-pts > 60 y/o without significant co-morbidities or end organ dysfunction
-pts with aggressive disease course
-pts who are candidates of an allogenic stem cell transplant

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65
Q

Induction chemotherapy: “7+3” for AML

A

-cytarabine 100 mg/m IV daily continuious infuction x 7 d + daunrorubicin 60 mg/m2 x 3d (OR idarubicin 12 mg x 3d)
–> 70% CR for < 60, 50% CR for > 60

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66
Q

When do you use Midostaurin in AML tx?

A

-FLT3-ITD or FLT3-TDK postitive pts
-50 mg BID with food on days 8-21 of each course of chemo

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67
Q

When do you use Gemtuzumab Ozogamicin (GO) in AML tx?

A

-favorable/intermediate cytogenetics
-3 mg.m^2 on days 1, 4 and 7 of induction & day 1 of consolidation courses

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68
Q

When do you use Liposomal Daunorubicin + Cytarabine (Vyxeos) in AML tx?

A

-use with treatment related AML/secondary (past radiation/cancer)
-1:5 fixed molar ratio

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69
Q

Response criteria in AML

A

-“leukemia-free state” - day 14 bmbx (goal is < 5-10% blasts, hypocellular)
-complete remissio/complete response criteria = day 28+ (assessed on repeat bmbx when blood counts recover after chemotherapy

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70
Q

Criteria for complete remission in AML

A

< 5% blasts AND ANC > 1000/mcL AND platelets > 100,000

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71
Q

Criteria for complete remission with incomplete count recovery (CRi) in AML

A

-older pts with prior MDS- residual dysplasia prevents full platelet recovery

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72
Q

AML post-remission therapy (for those who receive intensive chemo ONLY)

A

-high dose Cytarabine (HiDAC)
–> for those who recieve “7+3” based therapies
–> 1.5-3 g/m^2 IV q 12h x 6 doses every 28 days x 3-4 cycles
-addition of Midostaurin for FLT3+ or addition of GO on day 1 for cycles ! & 2 ONLY (for those that received GO in induction)

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73
Q

“low intensity chemo”–> for those unfit for intensive chemo/co-morbidities”

A

-hypomethylating agents + venetoclax
-low dose Cytarabine + Venetoclax
-Ivosidenib + Venetoclax
-LDAC + Glasdegib

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74
Q

AML Therapies: Midostaurin

A

FDA approved for newly-diagnosed FLT3 + AML (not refractory)
-targets FLT3 mutations (FLT3-ITD & TKD)

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75
Q

AML Therapies: Ivosidenib

A

-FDA approved for newly diagnosed AML & relapsed/refractory AML with IDH1 mutation

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76
Q

AML Therapies: Enasidenib

A

-FDA approved for replased/refractory AML with IDH2 mutation

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77
Q

Supportive care in AML*

A

1- transfusions: red blood cell transfusion if Hgb <. 8, platelet tranfusion if platelet < 10,000
2- infection prophylaxis while neutropenic: HSV/VZV (Acyclovir), antibacterial (levofloxacin), invasive fungal & mold (posaconazole ER)

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78
Q

Tumor Lysis Syndrome: Oncologic Emergency

A

-rapid tumor breakdown following chemotherapy (spontaneously may occur prior to start of chemo if high tumor burden
-sudden release of intracellular potassium, phosphorus, uric acid
–> onset = 12-72 hrs post chemo

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79
Q

Tumor Lysis Syndrome Presentation: metabolic disturbances *

A

-hyperuricemia: concentrates & crystalizes in urine –> may lead to irreversible kidney damage
-hyperphosphatemia: calcium phosphate product precipitates in kidney
-hyperkalemia
-hypocalcemia: elevated phosphorus leads to shift of Ca, Ca usually shifts to bone, but can go elsewhere –> may still lead to precipitates

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80
Q

Tumor Lysis Syndrome Prophylaxis

A

allopurinal
-hydration: maintain urine output > 2.5 L/day
-Rasburicase: only used for those at high risk & pre-existing hyperuricemia

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81
Q

Tumor Lysis Syndrome Management

A

-hyperuricemia: IV hydration
-Hyperkalemia: insulin & glucose
-Hyperphosphatemia: sevelamer, calcium acetate
-hypocalcemia: DO NOT treat

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82
Q

AML chemo clinical pearls: Anthracyclines

A

(daunorubicin, Idarubicin, Mitoxantrone)
-pink/red urine (mito = blue urine)
=myelosuppression
-cardiac toxicity –> alwasy do an echo

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83
Q

AML chemo clinical pearls: Cytarabine

A

neurotoxicity
-cerebellar syndrome –> ataxia, nystagmus, dysarthria
-“neuro checks” required prior to each visit
-conjuntivitis (Dez 0.1% eye drops q6h for 3 days after HiDAC is complete

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84
Q

AML chemo clinical pearls: GO

A

(Gemtuzumab)
-infusion-related reactions: pre-medicate with acetaminophin, diphenhydramine and methylprednisolone
-BBW: hepatotoxicity
**dont use in transplant pts

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85
Q

AML chemo clinical pearls: low-intensity chemo

A

-constipation –> standing bowel medications
-low-moderate emetogenicity
-pre-medicate with ondansetron

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86
Q

Myeloid Growth Factors

A

-may be started after 14 bmbx in those who receive intensive chemo
-does NOT prevent neutropenia
-risk of potentiating leukemic cells
AEs: bone pain (used loratadine)

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87
Q

What does CML look like?

A

main mutation = Philadelphia chromosome (Ph+)
-risk factors: ionizing radiation
-symptoms: up to 50% of pts are asymptomatic, splenomegaly, anorexia, bone pain, purpura, unexplained weight loss, fatigue

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88
Q

CML classifications: chronic phase

A

-want to keep pts here
Goal: delay progression to AP/BP, eradicate philadelphia chromosome

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89
Q

CML classifications: accelerated phase

A

-10-19% blasts in peripheral and/or bone marrow
-goal: control WBC count, bring back to CP and avoid progression to BP

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90
Q

CML classifications: blast phase

A

> 20% blasts
Goal: survive induction, bridge to allogenic stem cell transplant

91
Q

CML: Pre-tyrosine kinase ERA

A

-universally fatal
-temp control with
–> hydroxurea
–> busulfan
–> interferon-alpha (use for pregos)

92
Q

CML TKI low risk score tx

A

1) Imatinib OR
-Bosutinib OR
-Dasatinib OR
-Nilotinib

93
Q

CML TKI intermediate or high risk score

A

1) Bosutinib OR
-Dasatinib OR
-Nilotinib

94
Q

T3151 mutation in CML treatment choices:

A

Asiminib
Ponatinib

95
Q

Ponatinib AE (CML tx)

A

-elevated pancreatic enzymes
-hypertension
-skin toxicity
-thrombotic events

96
Q

Imatinib AE (CML tx)

A

-edema/fluid retentoin
-myalgias
-hypophosphatemia
-GI (diarrhea, N/V)

97
Q

Bosutinib AEs (TML tx)

A

GI (diarrhea, N/V)
-headache
-rash

98
Q

Dasatinib AEs (TML tx)

A

-pleural/pericardail effusions
-bleeding risk
-pulmonary arterial HTN

99
Q

What is a Gleason Score (in prostate cancer)?

A

-described how cancer cells look under a microscope
-cancers with lower Gleason scores (2-4) tend to be less aggressive, while cancers with higher Gleason scores (7-10) tend to be more aggressive

100
Q

Goals of Prostate Cancer therapy

A

-localized disease: control disease and symptoms, decrease morbidity & mortality
-advanced or metastatic disease: palliation symptom relief, improve quality of life, prolong survival

101
Q

Local disease very low & low recurrence risk (prostate cancer) in relation to expected survival

A

< 10 yrs: observation
10-20 yrs: active surveillance
> 20 yrs: active surveillance, extended beam radiation or radical prostatectomy

102
Q

local disease favorable and unfavorable intermediate Recurrence Risk in prostate cancer

A

Favorable:
–> 5-10 yrs: observation
–> > 10 yrs: AS, EBRT, radical prostatectomy
Unfavorable:
–> 5-10 yrs: observation, or EBRT + ADT
–> > 10 yrs: RP +/- pelvic lymph node dissection

103
Q

LHRH agonists in medical castration

A

-reversible method of androgen ablation
-as effective as surgical orchiectomy
-goal serum testosterone < 50 one month after starting therapy
-no direct comparative trials between agents
–> goserelin and leuprolide

104
Q

LHRH agonist adverse effects*

A

acute: tumor flare, hot flashes, erectile dysfunction, edema, gynecomastia, injection site reaction
Long-term: osteoporosis, clinical fracture, obesity, insulin resistance, increased risk of diabetes, CV events, alteration in lipids (hyperlipidemia)

105
Q

LHRH counseling points

A

-initial tumor flare caused by a surge in LH/FSH release
-increased testosterone production: resolved after 2 weeks
-baseline bone mineral density test before starting long-term ADT: calcium and vitamin D supp

106
Q

LHRH ANTagonists for prostate cancer

A

-Degarelix: given SQ monthly
-Relugolix: PO
advantages: much faster drop in testosterone levels, no tumor flare
disadvantages: less flexibility in dosing schedule, high cost

107
Q

Anti androgens for tx of prostate cancer

A

serve as a competitive inhibitor for the binding of dihydrotestosterone and testosterone
–> use 2nd gen agents: Apalutamide, Enzalutamide, Darolutamide

108
Q

Castration Sensitive Prostate Cancer treatment options

A

-combined modality approach as initial therapy for castration sensitive (or naive) prostate cancer for select high risk and metastatic pts:
–> ADT _ Abiraterone or Alpalutamide or Enzalutamide
–> ADT with Docetaxel x6 cycles _ Abiraterone or Darolutamide: use this for high volume = visceral metastases, and/or 4 bone metastases with at least 1 metastasis beyond the pelvis

109
Q

Castration Sensitive Prostate Cancer

A

-serum testosterone < 50 and disease progression
–> if PSA doubling > 10 months: monitor
–> if PSADT < 10 months: apalutamide, enzalutamide, darolutamide

110
Q

Secondary hormone therapy for (M0 or M1) in CSPC

A

-1st generation antiandrogen (nilutamide, flutamide, or bicalutamide)
-corticosteroids
-antiandrogen withdrawal
-ketoconazole + hydrocortisone

111
Q

First generation antiandrogens used in prostate cancer

A

-Apalutamide: seizure occured in 0.2% of pts –> permanently d/c in pts who develop a seizure during tx
-Darolutamide: no increase in seizure compared to placebo!!
-Enzalutamide: increased risk of seizures

112
Q

Metastatic (M1) CRPC treatment: no prior doxetaxel/no prior novel hormone therpy*

A

Preferred:
-Abiraterone
-Docetaxel
-Enzalutamide
Useful in certain circumstances:
-radium-223 for symptomatic bone metastases
-sipuleucel-T

113
Q

Metastatic (M1) CRPC treatment: prior novel hormone therapy/no prior docetaxel *

A

Preferred: docetaxel
useful in certain circumstances:
-cabazital/carboplatin
-olaparib for HRRm
-rucaparib for BRCA mutation
-radium-223 for symtomatic bone metastases
-Sipuleucel -T

114
Q

Metastatic CRPC 1st line tx options

A

(metastases in the liver, lung, adrenal gland, peritoneum or brain)
-Docetaxel: can cause reversible alopecia
-Abiraterone: given with steroids to minimize signs of mineralacorticoid excess from tx
–> Zytiga: take on empty stomach
–> Yonsa: give with steroids

115
Q

Radium-223 in prostate cancer

A

-used for symptomatic bone metastases and no visceral metastases prior to and after docetaxel therapy
-adminstered IV once a month for 6 months

116
Q

Supportive care with prostate cancer

A

-treatment of androgen deprivation-induced bone loss in prostate cancer: Denoscumab
-Osteroporosis: Zoledronic acid

117
Q

Tumor Lysis Syndrome

A

-TLS is a condition that occurs when a large number of cancer cells die within a short period –> cell contents are released into the blood
-most common disease- related oncologic emergency in hematologic malignancies
-can occur spontaneously or after initiation of chemotherapy
-most frequently occurs in pts with rapid proliferating, bulky, chemo-sensitive tumors

118
Q

Laboratory tumor lysis syndrome

A

> 2 of the listed metabolic abnormalities within 3 days before or 7 days after initiation of treatment:
-hyperkalemia (> 6), hyperuricemia (> 8), hyperphosphatemia (> 4.5), hypocalcemia (< 7) or for all of these: 25% increase from baseline

119
Q

Clinical Presentation of TLS

A

-hyperkalemia: ECG abnormalities, cardiac arrest, fatigue
-hyperuricemia: acute kidney injury, crystal nephropathy
-hyperphosphatemia: acute kidney injury, GI upset, AMS
-Hypocalcemia: AMS, seizures, arrhythmias, tetany & spasms

120
Q

High risk of TLS treatment

A

-hydration
-rasburicase: flat dose on 1.5 or 3 mg
-allopurinol

121
Q

Clinical presentation of febrile neutropenia

A

Febrile: single temp > 38.3 or temp > 38 for over 1 hr
Neutropenia: ANC < 500 cells OR ANC < 1000 and expected to drop to < 500 in 48 hrs
–> febrile neutropenia is often the first and sometimes only sign than an immunocompromised pt has developed an infection

122
Q

oral options for management of infections (low risk)

A

-cipro + augmentin
-levo
-moxi
-cipro + clinda
not appropriate for: pts on flouroquinolone prophylaxis at the time of diagnosis, pts with N/V

123
Q

Inpatient management of infections (intermediate-high risk)

A

-IV therapy
-mono-therapy with a broad spectrum, anti-pseudomonal antibiotic: cefepime, pip/tazo, meropenem, imi/cilas, ceftazidime

124
Q

when do you add MRSA coverage for infections in cancer pts?

A

-catheter related infections
-SSTI
-pneumonia
-hemodynamic insufficiency/sepsis
-mucositis
–> vanco, linezolid, daptomycin

125
Q

Adding fungal coverage for infections in cancer pts

A

-fungal coverage is added later on in the course of febrile neutropenia in pts who:
–> do not respond to initial therapy in 4-7 days
–> have positive fungal markers (Beta-D-Glucan/Galactomannan)
–> have positive fungal cultures
Options: fluconazole, voriconazole, etc

126
Q

Hypercalcemia of malignancy: treatment overview

A

–> goal is to treat underlying malignancy
-hold medications that can potentially worsen hypercalcemia (vit D, calcium, thiazide diuretics)
-HYDRATION: saline +/- furosemide
-IV bisphosphonates, RANK-L inhibitor
(secondary therapy: calcitonin, glucocorticoids)

127
Q

clinical pearl of calcitonin

A

*limited to first 48 hrs due to tachyphylaxis
-max of 4 doses

128
Q

clinical pearls of bisphosphonates

A

-zoledronic acid, pramidronate
-onset is 48-72 hrs, with Nadir taking 4-7 days –> dont add ore doses, may take longer to see effect

129
Q

MASCC score

A

-high risk = < 21 (outpatient management, oral antibiotics)
-low risk = >/ 21 (inpatient management, IV antibiotics)

130
Q

Local NSCLC: stage I-II

A

I: surgery
II: surgery followed by adjuvant therapy
-platinum-based regiment +- novolumab in pts who are medically inoperable
-osimertinib (EGFR+) for up to 3 yrs
-Atezolizumab (PD-L1 > 1%) following completion of platinum-based chemotherapy for 1 yr

131
Q

locally advanced NSCLC: stage III

A

IIIA:
-neoadjuvant chemotherapy +- nivolumab for 4 cycles followed by surgery or RT
-adjuvant osimertinib (EGFR+) or atezolizumab (PD-L1 > 1%)
-concurrent chemoradiotherapy for non-surgical candidates
IIIB-IIIC: considered unresectable disease
-concurrent chemoradiation is the mainstay for up to 6 cycles or until progression or unacceptable toxicity
-Durvalumab maintenance for 1 yr upon response to chemo

132
Q

Cisplatin AEs

A

myelosuppression
N/v
diarrhea/constipation
oral mucositis
alopecia
nephrotoxicity
ototoxicity
peripheral neuropathy

133
Q

Carboplatin AEs

A

-thrombocytopenia
-diarrhea/constipation
-oral mucositis
-alopecia

134
Q

Calvert equation to dose carboplatin: dose based on renal function*

A

total dose (mg) = AUC x (CrCL + 25)

135
Q

Epidermal Growth Factor Receptor (EGFR) Inhibitors used in lung cancer tx

A

1st line: Osimertinib (improved CNS activity, tolerability is better)
-EGFR mutations most prevalent in adenocarcinomas and non smokers
-not dependent on pH absorption
AEs: skin rash, dry skin, diarrhea, fatigue, nail toxicity, stomatitis, myelosuppression, QTc prolongation, conjunctivitis

136
Q

ALK inhibitors in lung cancer tx

A

-Alectinib is the only ALKi that has demonstrated significant improvement in overall survival
Brigatinib: CYP3A4 substrate, diarrhea, fatigue, interstitial lung disease/penumonitis, myalgia, HTN
Alectinib: CYP3A4 substrate, constipation, fatigue, LFT abnormalities, peripheral edema, myalgia, anemia
Lorlatinib: CYP3A4, P-gp substrate, fatigue,peripheral edema, mood disorders, neuropathy, cognitive effects, arthralgia, weight increase

137
Q

KRAS inhibitors in SCLC tx

A

-more commonly associated with cigarette smoking (confers poor prognosis) –> indicated for advanced or metastatic NSCLC and KRAS G12C mutation after receipt of one prior therapy
–> sotorasib: CYP3A4 and strong P-gp inhibitor, avoid coadminstration with PPIs and H2RAs (4 hours before or 10 hrs after)**, AEs: diarrhea, nausea, fatigue, LFT abnormalities
–> Adagrasib: CYP3A4 substrate, DOES NOT possess pH-dependent aborption, AEs: same as ^ + renal impairment, edema, QT prolongation, interstitial lung disease/pneumonitis

138
Q

1st line therapy for PD-L1 >/ 50%

A

-pembrolizumab
-atezolizumab
-cemiplimab

139
Q

1st ling therapy for PD-L1 1-49% or < 1%

A

-cisplatin/carboplatin + paclitaxel (squamous) + pembrolizumab
-cisplatin/carboplatin + pemetrexed (nonsquamous) + pembrolizumab
-cisplatin/carboplatin + paclitaxel (squamous) + nivolimab + Ipilimumab
-cisplatin/carboplatin + pemetrexed (nonsquamous) + nivolumab + Ipilimumab

140
Q

**Immunotherapy related AEs in lung cancer

A

onset: within first few weeks-months after initiation but can occur anytime
Management:
–> grade 1: continue immunotherapy
–> grade 2: hold immunotherapy and consider corticiteroid administration
–> grade >3: hold immunotherapy and corticosteroid administration
-prednisone 0.5-2 mg/kg/day (refractory cases: add mycophenolate mofetil, infliximab

141
Q

Vascular endothelial growth factor (VEGF) inhibitors in lung cancer

A

-cancer cells secrete angiogenic factors –> induce formation of new blood vessels (inc nutrient flow to permit growth and metastasis)
–> Bevacizumab, ramucirumab (cut off nutrient supply)
-Acute AE: HTN
-Delayed AE: thromboembolic events, epistaxis, major bleeds, GI perforation, diarrhea (ramucirumab)
-AVIOD in pts with squamous histology (bevacizumab), recent hemoptysis, in therapeutic anticoagulation for new onset WTE, recent surgical procedure

142
Q

Chemotherapy agents in lung cancer tx: Taxanes

A

(paclitaxel, docetaxel)
-inhibits mytosis
-AEs: alopecia, peripheral neuropathy, hypersensitivity (pre med with dexamethasone, famotidine, diphenhydramine), peripheral edema (pre med with dexamethasone 8 mg BID day before, day of and day after infusion)

143
Q

Chemotherapy agent in lung cancer tx: Pemetrexed

A

-depletes DNA building blocks
-primarily renal elimination –> avoid if CrCl < 45 (inc toxicities)
AEs: myelosuppression, erythematous/pruitic skin rash, fatigue, diarrhea, N/V –> give folic acid and VIt B, dexamethasone 4 mg BID before, of, after markedly diminishes incidence of skin rash

144
Q

Small Cell Lung Cancer summary*

A

-rapidly dividing malignancy that spreads early in disease course
-60-70% present with extensive-stage disease
-tx of choice is chemotherapy +- radiation
-disease recurrence usually occurs within 6-8 months after complete response
-prophylactic cranial radiation (PCI) is offered upon partial response or CR to therapy
-recurrent disease is typically less responsive to chemotherapy

145
Q

*limited and extensive stage SCLC chemotherapy regimens

A

1st line:
-cisplatin + etoposide
-Carboplatin + etoposide
-carboplatin + etoposide + atezolizumab
-carboplatin + etoposide + durvalumab
-Cisplatin + etoposide + durvalumab
2nd line:
-topotecan
-lurbinectedin
-clinical trial

146
Q

**SCLC chemotherapy agents

A

-Etoposide: leads to double-stranded DNA breaks, AEs: myelosuppression, N/V, stomatitis, alopecia
-Topotecan: AEs: myelosuppression (neutropenia), diarrhea, N/V, fatigue, alopecia
-Lurbinectedin: use with pts who have severe renal dysfunction: AEs: fatigue, hepatic enzyme elevations, extravasation, nausea –> pretreat w/ dexamethasone

147
Q

Signs and Symptoms of Lymphoma

A

-“B symptoms” (1 required): fevers, night sweats, weight loss (10% or more over 6 months or less)
-lymphadenopathy

148
Q

DLBCL cytogenetics *

A

-distinction between translocations and amplified expression
-40% with adverse cytogenetics experience failure
–> BCL2 translocation: anti-apoptotic protein, resistance to chemotherapy
–> BCL6 translocation: blocks cycle progression and response to DNA damage
–> MYC: rearrangement within an IgG gene: double/triple-hit: MYC + BCL2 and/or BCL6 (high grade lymphoma)
–> TP53: 30% of all lymphomas

149
Q

Subtypes of DLBCL*

A

-Diffuse large B cell lymphomas: germinal center B-cell types, activated B-cell type
-primary DLBCL of the CNS
-primary mediastinal large B-cell lymphona
-high-grade B-cell lymphoma, with MYC and BCL2 and/or BCL6 rearrangements
-high-grade B-cell lymphomas, NOS

150
Q

Gold standard frontline tx for lymphoma*

A

-goal is to cure ALL stages
-in fit pts, R-CHOP is considered gold standard:
R: rituximab
C: cyclophosphamide
H: Doxorubicin
O: Vincristine
P: prednisone
–> given every 21 days (usually 6 cycles)

151
Q

Rituximab pharmacology in lymphoma tx

A

*MOA: chimeric monoclonal antibody binds to CD20
AEs: TLS, infusion reactions, GI perforation, hepatitis reactivation, progressive multifocal leukoencephalopathy, vaccinations are less effective

152
Q

R-CHOP clinical pearls (R-C)

A

-Rituximab: infusion reactions - higher with bulky disease, LDH renal function, tumor lysis syndrome, hold 1st cycle is disease in GI tract
-cyclophosphamide pearls: contributes to alopecia, N/V (high risk anti-emesis regimen) & hemorrhagic cystitis (drink fluids!)

153
Q

R-CHOP clinical pearls (HOP)*

A

*Doxorubicin: lifetime dose cap 450 mg/m2: monitor for cardiac dysfunction
*Vincristine: dose.cycle capped 2 mg: NO vines in the spine : fatal given intrathecally, give in small IV piggybacks, neuropathy
-Prednisone pearls: 100mg daily, hyperglycemia, steroid induced psychoses, insomnia

154
Q

CHOP supportive care

A

-emetogenic risk = high: olanzapine use is indicated
-febrile neutropenic risk: growth factors (pegfilgrastim, filgrastim) routinely given
-viral reactivation: give PPX antiviral therapy for any patient who has had HBV
-tumor lysis syndrome: aggressive hydration, allopurinol

155
Q

When is DA-R-EPOCH preferred over R-CHOP?

A

-double/triple hit Lymphoma
-primary mediastinal lymphoma
-HIV associated DLBCL

156
Q

Follicular Lymphoma

A

-“indolent” B-cell lymphoma
-2nd most common BCL
-med age: 59
-incurable

157
Q

Follicular Lymphoma 1st line tx clinical pearls

A

-Obinutuzumab: improved progression free survival, more infusion reactions
-rituximab maintenance preferred- improved PFS

158
Q

Classical Hodgkins Lymphoma

A

-expresses CD30+ (CD20-)
-intracellular changes:
–> promotion of NF-kB pathways
–> JAk2 activation/overexpression
–> EVB enhances both
-expressed cytokines form a reactive shell

159
Q

Nodular Lymphocyte-Predominant Hodgkin’s Lymphoma

A

-CD20+, CD30-
-CD15- Ig+
–> can use retoximubab here
“popcorn cells”

160
Q

Nodular Lymphocyte-Predominant Hodgkin’s Lymphoma treatment

A

-CD20+ (CD30-, CD15-)
-ABVD +- rituximab

161
Q

treatment of hodgkins lymphoma: ABVD*

A

-administered every 14 days, 2 doses per cycle:
-Adriamycin
-Bleomycin
-VinBLAStine
-Dacarbazine

162
Q

Bleomycin AEs

A

MOA: binds to DNA, produces SS and DS breaks through generation of oxygen free radicals
-pulmonary fibrosis: PFT–> HIGHER risk when given with pegfilgrastim/folgrastim

163
Q

Survivorship of Hodgkins lymphoma*

A

-high percentage of pts survive HL
-PMH + cancer is not inert or benign
–> secondary cancers: > 10 yrs later: lung and breast
–> cardiovascular disease
–> hypothyroidism
–> fertility
–> psychosocial complications

164
Q

What are the parameters of anemia?

A
  • < 13 g/dL in men OR <12 g/dL in women
    causes: hypo proliferation, maturation disorder, maturation disorders, hemorrhage/hemolysis
165
Q

Causes of Macrocytic anemia (> 100 fL)

A

folic acid deficiency, vitamin B12 deficiency, liver disease, alcohol, hypotension, drugs (sulfonamides, antineoplatics)

166
Q

causes of Normocytuc anemia (80-100 fL)

A

-aplastic anemia
-anemia of chronic disease
-CKD
-hemolytic anemia

167
Q

causes of microcytic anemia (< 80 fL)

A

iron deficiency

168
Q

Iron Deficiency Anemia (IDA)

A

-most common form of anemia (children under 2 and pregos are at high risk)
-causes: blood loss via menstruation, GI bleeding, hemorrhoids, medication use (NSAIDs, corticosteroids, anticoagulants), alcohol, iron malabsorption

169
Q

IDA Diagnosis

A

Iron panel:
-serum iron
-total iron-binding capacity
-% transferrin saturation
-serum ferritin –> MOST sensitive indicator of IDA (DECREASES)

170
Q

IDA Treatment

A

Diet: animal liver, fortified ceeal, meat/fish,eggs,spinach, lentils
Supp: with with orange juice and ascorbic acid rish foods to increase absorption (mild and tea reduce iron absorption)

171
Q

IDA tx: oral supplementation

A

-ferrous sulfate (20% elemental iron)
-ferrous sulfate exsiccated (30%)
-ferrous gluconate (12%)
-ferrous fumarate (33%)
dose every other day

172
Q

Drugs that decrease Iron absorption *

A

-Al/Mg/Ca containing antacids
-tetracycline and doxycycline
-Histamine receptor-2 antagonists
-proton-pump inhibitors
-cholestyramine

173
Q

Drugs decreased by iron*

A

-levadopa (decreases absorption)
-methyldopa (decreases efficacy)
-levothyroxine (decrease efficacy)
-penicillamine
-flouroquimolones
-tetracycline and doxycycline
-mycophenolate

174
Q

IV Iron dosing*

A

generally Iron sucrose 200 mg IV x 5 days
-decrease dose if previously received pRBC transfusions: each pRBC contains ~200 mg of iron replacement (so for each transfusion they had, take away a dose - target is 1,000 mg)

175
Q

Megaloblastic Anemia

A

-caused by abnormal DAN metabolism resulting in vitamin B12/folate deficiencies
Causes: hydroxyurea, zidovudine, cytarabine, methotrexate, azathioprine, 6-mercaptopurine

176
Q

Lab finding in vitamin B 12 deficiency & tx

A

Lab results: ince MCV, MMA and serum homocysteine*
-Cyanocobalamin PO daily or IV/IM weekly, x4 weeks, monthly

177
Q

Lab finding for folic deficiency & tx

A

increase MCV & inc serum homocysteine
-folic acid 1 mg daily, 4 mg in pregos

178
Q

Anemia of inflammation (AI)

A

-one of the most common forms: increased incidence among elderly pts, results from chronic inflammation, malignancy or infection & can occur as early as 1-2 months after onset
Diseases causing: chronic infections (TB, HIV), COPD, gout, liver disease, alcoholic cirrhosis, HF

179
Q

Labs supporting anemia of inflammation and tx

A

-DEC TIBC
-want to treat underlying conditions & consider packed red blood cell transfusions if pt is experiencing acute oxygenation complications or hgb < 7

180
Q

when are ESAs used in AI treatment?

A

-approved for use in AI due to HIV, CKD, anemia from malignancy, myelodysplastic Syndrome
-only effective if bone marrow has adequate stores of iron, B12 & folic acid
-monitor hemoglobin: d/c if > 12

181
Q

ESA Products

A

-Eopetin alfa: identical to endogenous human erythropoietin, 9 hrs 1/2 life
-Darbepoetin: slight amino acid difference, 1.2 life is 25 hrs

182
Q

non modifiable risk factors of breast cancer

A

-female gender at birth
-older age
-fam hx
-personal hx
-genetics: BRCA1 and BRCA2
-breast changes found on biopsy
-ionizing radionation
-breast density
-easrly menarche/late menopause

183
Q

modifiable risk factors of breast cancer

A

-nulliparity or older age at first childbirth
-postmenipausal hormonal replacement therapy
-postmenopausal obesity
-physical inactivity
-alcohol consumption

184
Q

invasive breast cancers: common

A

-invasive ductal carcinoma: 75% of all invasive breast cancers, “limp”, metastatic sites: bone, liver, lung, brain
-invasive lobular carcinoma: 5-10% of all invasive breast cancers, ill-defined thickening of the breast, metastatic sites: leptomeninges, peritoneal surfaces, retroperitoneum, GI tract, reproductive organs

185
Q

Inflammatory breast cancer

A

-characterized by skin edema, redness, warmth and induration of underlying tissue
-cancer cells in dermal lymphatics on biopsy
-very rapid onset & poor prognosis

186
Q

Staging of breast cancer

A

uses TNM staging (Tumor size, Nodal status, Metastases to distant site)
-early stage breast cancer (stages 0, I, II) & locally advanced breast cancer –> cure
-metastatic breast cancer (stage IV) –> palliation

187
Q

Treatment options for invasive BC

A

-ER/PR+, HER2+ = chemo+HER2 + endocrine
-ER/PR+, HER2- = chemo + endocrine
-ER/PR-, HER2+ = hemo + HER2
-ER/PR-, HER2- = chemo

188
Q

preferred chemo regiems for ER/PR(+-), HER2 (-) disease

A

-dose dense doxorubicin/cyclophosphamide (AC) x 4 doses –> paclitaxel every 2 weeks x 4 doses
-dose dence AC x 4 doses –> weekly paclitaxel x 12 doses

189
Q

preferred chemo regimen for ER/PR -, HER2- disease (triple therapy)

A

Neoadjuvant
-pembrolizumab every 3 weeks x 4 doses + weekly paclitaxel/carboplatin x 12 doses –> pembrolizumab + doxorubicin/cyclophosphamide every 3 weeks x 4 doses

190
Q

Preferred chemotherapy regimens: HER2+ disease

A

-docetaxel/carboplatin/trastuzumab +- pertuzumab every 3 weeks x 6 doses OR
-Paclitaxel + trastuzumab weekly x 12 weeks

191
Q

Pertuzumab criteria

A

-needs > T2 or >N1, HER2 + tumor
-higher risk of recurrence
-post chemo, continue trastuzumab or pertuzumab/trastuzumab (MUST BE TAKEN TOGETHER) to. complete 1 yr

192
Q

Counseling points for Taxanes (paclitaxel/docetaxel)*

A

-neuropathy (P>D)
-alopecia
-hypersensitivity reactions (infusion related)
-arthralagias/myalgias
-peripheral edema (D)

193
Q

Counseling points for Doxorubicin*

A

**cardiotoxicity (dose related & IRREVERSIBLE!) –> get baseline ECHO or MUGA & q 3 months
-red secretions/urine discoloration
-secondary malignancies
-vesicant-extravasation (skin irritations/lesions- give drug with a port)

194
Q

Counseling points for cyclophosphamide *

A

-hemorrhagic cystitis - significant bladder irritation due to active metabolite (acrolein)
-sterility

195
Q

Counseling points for HER2 targeted therapy (trastuzumab/pertuzumab)*

A

*cardiotoxicity (CHF/ventricular dysfunction, not dose related & reversible) –> can hold drug & retrial
-diarrhea (P): all or nothing
-infusion reactions

196
Q

Endocrine therapy: Tamoxifen*

A

-inhibits growth of tumors by competitively antagonizing estrogen at its receptor site
-prodrug w/ active metabolite being endoxifen
-AVOID strong CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion)

197
Q

Adjuvant endocrine therapy for pre and post menopausal women*

A

Premeno: Tamoxifen, aromatase inhibitor + ovarian suppression
Postmeno: atomatase inhibitor + tamoxifen

198
Q

What is ovarian suppression?

A

-oophorectomy (removal of ovaries)
-luteinizing hormone releasing hormone (LHRH): reversible, continuous stimulation of pituitary
–> decreases FSH and LH secretion, decreases estrogen production from ovaries
-goserelin 3.6 mg SQ q 28 days
-Leuprolide 3.75 mg IM q28 days

199
Q

Endocrine therapy counseling points: Tamoxifen*

A

-menopausal symptoms (hot flashes, night sweats, vaginal. dryness)
-menstrual changes (premenopausal)
-uterine or endometrial cancer
-VTE, stroke
-pregnancy category D

200
Q

Endocrine Therapy counseling points: aromatase inhibitors (anastrazole, letrozole, exemestane) *

A

-menopausal symptoms (hot flashes, night sweats, vaginal dryness)
-musculoskeletal symptoms (arthralgia, joint stiffness, bone pain)
-Inc bone loss (osterporosis/fractures)
-hypercholesterolemia
-cardiovascular risk

201
Q

adjuvant zoledronic acid

A

-give to postmenopausal pts
- 4mg IV 1 6 months, contineu for 3-5 yrs

202
Q

Endocrine therapy for metastatic breast cancer *

A

Palbociclib (Ibrance)
-used for tx of hormone receptor - positive, HER2- MBC
-used in combo with aromatase inhibitor as initial endocrine therapy & flivestrant with disease progression following endocrine therapy
-toxicity: fatigue, neutropenia, anemia, alopecia

203
Q

Alpelisib endocrine therapy for MBC*

A

indication for hormone receptor-postitive HER2-, PIK3CA-MUTATED MBC in combo with fluvestrant
-toxicity: hyperglycemia, skin rash, diarrhea, nausea, fatigue, increased serum creatinine

204
Q

HER2+ - MBC chemotherapy regimens

A

-Pertuzumab + trastuzumab + docetaxel
-Pertuzumab + trastuzumab + paclitaxel

205
Q

MBC: bone metastases

A

-bisphosphonates (zoledronic acid, pamidronate)
-used for prevention of skeletal-related events, fractures, surgeries, radiation, spinal cord compression
-Denosumab: prevention of skeletal-related events

206
Q

colorectal cancer

A

-most being as polyps on the innermost lining of the colon or rectum (mucosa) and can grow outward into blood vessels and nearby lumph nodes or distant organs

207
Q

treatment of colorectal cancer based on stage

A

I: no adjuvant chemo
II: no treatment or adjuvant chemo
III: adjuvant chemo
IV: chemo, targeted therapy & immunotherapy

208
Q

5-FU therapy in colorectal cancer

A

-inhibits thymidylate synthase, inhibiting DNA synthesis
–> folic acid helps to stabilize fdUMP binding to thymidylate synthase & enhances 5-FU cytotoxic effects
-Bolus AEs: myelosuppression
-continuous infusion effects: hand-foot syndrome, diarrhea, mucositis

209
Q

Capecitabine tx of colorectal cancer

A

-pro-drug of 5-FU
-dose limiting toxicities: hyperbilirubinemia, diarrhea, hand-foot syndrome, mucositis
-radio-sensitizer (rectal cancer, potentiates the radiation
**CI in dihydropyrimidine dehydrogenase (DPD) deficiency (even if they are hetero- dont give)

210
Q

Oxaliplatin-Induced Neuropathy vs. cold Sensitivity (acute)

A

Acute: see sensory- cold-induced paresthesias, cold induced pharyngeal dysesthesia alongside motor: cramps, jaw tightness/cracking, dysphonia

211
Q

Oxaliplatin-Induced Neuropathy vs. cold Sensitivity (chronic & TX)

A

-cumulative
-S&S: distal sensory neuropathy, deep tendon reflex suppressed
Treatments: eating/drinking at room temp, GABA analogues, SNRI

212
Q

Irinotecan for the treatment of colorectal cancer

A

-DIARRHEA
Acute onset: within 24 hrs, cholinergic excess (runny nose, increased saliva, watery eyes, shrinking pupils, sweating, flushing, cramps) –> atropine 0.4 mg SQ
Delayed onset: after 24 hrs, metabolism related –> loperamide max 16 mg daily

213
Q

Anti-Angiogenesis Therapy for colorectal cancer

A

-Bevacizumab: approved for metastatic colorectal cancer with infusional 5-FU
-Ziv-aflibercept: approved in mCRC pts who have progressed on an oxaliplatin-based regimen
common toxicities: HTN, delayed wound healing (d/c 4 weeks before surgery & restart 4 weeks after), proteinuria (foamy urine), hemorrhage, arterial thrombosis, diarrhea, neutropenia

214
Q

EGFR innhibitors in colorectal cancer (Cetuximab- chimeric, Panitumumab- recomb)

A

-must be KRAS-wild type!!
C: used 1st line with FOLFIRI
P: used 1st line with FOLFOX
Toxicities: infusion reactions, hypomagnesemia, paronychia, acneiform rash
–> prevention is key: limit sun exposure, avoid over drying skin, moisturize skin, avoid OTC acne products

215
Q

EGFR inhibitors- rash. treatment (4 grades)

A

1: macular/papular eruption–> topical clindamycin 2% +- hydrocortisone 1%
2: eruption –> ^ or minocycline or doxycycline
3: macular, papular or vesicular eruption –> hold tx until grade 2, for 2nd or 3rd occurrence, dose reduce, for 4th occurence D/C
4: generalized exfoliative ulcerative or blistering –> d/c drug

216
Q

Multikinase inhibitor- Regorafenib for colorectal cancer

A

-inhibits VEGFR 2 & 3, RET, KIT, PDGER & Raf kinase
-BBW: hepatotoxicity
-salvage therapy

217
Q

Immunotherapy in colorectal cancer

A

-for MSI-H tumors only, typically in stage IV disease
-Pembrolizumab
-Nivolumab
AEs: colitis, rash, hepatitis, nephritis, pneumonitis

218
Q

Colorectal cancer stage I tx

A

surveillance (no adjuvant therapy)

219
Q

Colorectal cancer stage IIA - no high risk features tx

A

observation or consider capecitabine of 5-FU/Leucivorin (6 months)

220
Q

Colorectal cancer stage IIA (high risk) IIB, IIC tx

A

-FOLFOX
-Capecitabine
-5-FU/leucovorin or capeOX or observation

221
Q

Colorectal cancer stage III (low risk) tx

A

-capeOx preferred
-FOLFOX

222
Q

Colorectal cancer stage III (high risk) tx

A

-CapeOx
-FOLFOX

223
Q

colorectal cancer tx if pts cannot tolerate invasive therapy (old peeps)

A

-infusional 5-FU/Leucovorin +- Bevacizumab
-Capecitabine +- Bevacizumab

Hem/critical care/Onco (2 decks)

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