Week 4 Flashcards

Question

Irinotecan-induced diarrhea

Answer 1

can cause acute or delayed diarrhea acute: due to cholinergic stimulation *mean duration of symptoms is 30 min *usually respond rapidly to atropine delayed diarrhea: due to GI mucosal damage secondary to SN-38 *usually occur more than 24 hours after amdinistration *noncumulative and occurs at all dose levels

Answer 2

non phar: Iavoid foods that would aggravate the diarrhea aggresive oral rehydration w. fluids that contain water, salt, and sugar Pharm measures: *loperamide-first line (4mg followed by 2 mg q4h or after every unformed stool . (not to exceed 16mg/d for CTID, MDD in regular circumstances is 8mg/d) *diphenoxylate-atropine *1-2 tabs q6hrs until control achieved (not to exceed 8 tablets/day

Answer 3

octreotide tincture of opium probiotics rule of C. diff and infection collitis

Answer 4

symptom: typically occurs within 5-14 days complications: decreased oral intake (poor nutritional status, grade 3: severe oral pain grade 4: requires parenteral or enteral nutrition increase infection risk(gram+ oral flora, candida or fungal infections) pain (may require opioids and pca administration)

Answer 5

mucositis: erythematous and ulcerative lesions of the mucose observed in pts treated w. chemo can occur anywhere in gi tract stomatitis: mucositis limited to the oral cavity

Answer 6

five stage model of oral mucosisits initiation- cellular damaged induced, reactive oxygen species formulations primary damage resoinse *activiation of p53 and nf-kb sgnal aplifiation ulceration- high risk for bacterial colonization healing cessation from ongoing tissue damage

Answer 7

chemo * melphalan cisplastin+radiation *high dose methotrexae doxorubicin busulfan 5-FU pt factors: smoking poor oral hygeine oral lesions at baseline female sex pretreamtent nutritional status

Answer 8

oral hygeine: *avoid acidic or spicy foods *burhs w. soft toothbrush twice daily; fossin gdaily *swithc tabs to solutions o iv if hospitalized *use nonalcoholic mouthwashes at least 4 times day (ex NS or salt and soda cryotherapy: moa: local vasocinstriction-> less drug delivered to the oral mucose *hold ice chips in their mouth for 30min before and/or during chemo

Answer 9

oral decontamination: bland mouthwash or oncology m outhwash. dexamethasone mouthwash for everolimus induced mucositis pain control: 2% iscous lidocaine swish and spit, systemi opioids palliation of dry mouth: artificial salive products or chewing gum to increase saliva production nutritional supports: liquid or soft diet; tpn oral candidiasis trt: nystatin oral solution or clotrimazole lozenge *flucanozole 200 mg po x1 dose, then 100mg daily x 21 days

Answer 10

neutropenia: absolute neutrophil count (ANC)<500 cells/mm3 or expected to decrease to <500 cells/mm3 in 48 hours proound neutropenia: anc<100 CELLS/MM3 PROLONGED NEUTROPENIA: LASTIN LONGER THan 10 days febrile neutropenia: *single temp:>38.3 C orall or >38C over 1 hours AND ANC<500 cells/mm3 or expected to decrease to <500 cells/mm3 in 48 hours

Answer 11

dose reduction or treatment delayes compromise clinical outcomes longer hospital stays increased treatment costs decreased QOL

Answer 12

prior chemo or radiation persistent neutropenia bone marrow involvement by tumor recent surgery and or open wounds liver dysfunction (bilirubin >2.0 mg/dL) renal dysfunction (Crcl <50 ml/min) age> 64 years recieving ful chemo dos eintensity

Answer 13

overall risk for neutropenia High -->(regardless of pt risk factors) G-CSF recommended intermediate risk (+>/1 risk factor) consider GCSF Low (+>2 risk factors). GCSFs may be considered note: G-CSF=granulocyte colony stimulating factor

Answer 14

short -acting g-csf start the next day or up to 3-4 days after completion of chemo given daily until ANC recovery

Answer 15

long acting g-csf admin up to 3-4 days AFTER completion of chemo singe administration!! allow >/12 days between the dose of pegfilgastrim and the next cycle of chemotherapy

Answer 16

long acting c-csf admin ~24hr after completion of chemo single administration do not admin 14 days before and 24 hrs after admin of chemo

Answer 17

did pt recieve ppx g-csf? and which? recieved filgastrim: continue filgastrim recieved pegfilgastrim or eflapegfilgrastrim ppx: no additional g-csfs needed if did not recieve ppx g-csf-> assess risk factors for infection-associated complication

Answer 18

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

Answer 19

(pt has hx of febrile neutropenia or dose limiting neutropenic event) if pt has hz of prior use of g-csf-> consider chemo dose reduction or change in treatment regimen if pt has no prior use of g-csf-> consider gcsf

Answer 20

Disease of bon marrow-> cancer of blood cells

Answer 21

acute rapid onser symptomatic (bleeding) rapidly fatal if untreated immature cells (blasts) usually leukemia chornic *slowly progressive *mos asymptomatic *some survive years without trtment *immature and matue cells leukocystosis can occur in both phases

Answer 22

Cancer can occur in the myeloid or the lymphoid white blood cells when it occurs in the myeloid cells , it is called myelogenous leukemia when it occurs in the lymphocytes , it is called lymphocytic leukemia myeloid cells include granulocytes ( basophils, neutrophils, eosinophils), also platelets, and erythrocytes

Answer 23

most common in adults aged 65-74. average age 68 most deadly leukemia in the US

Answer 24

increasing age prior chemo= therapy related AML (t-AML) ex: anthracyclines, alkylators (ex: cyclophosphamide, melhalan), topoisomerase inhibitors (etoposide) prior pelvic radiation cigarette smoking radiation exposure benzene exposure pesticide exposure

Answer 25

Anemia (fatigue and sob) THOMBOCYTOPENIA (BLEEDING RISK) NEUTROPENIA ANC <500 or <1000 w. anticipated decrease to <500 w.in 48 hr spontanous tumor lysis syndrome (TLS) cns involvement rre(<3%) (somnolecense, headaches, consfusion WBC count: 1/3 pts present w. pancytopenia, 1/3 w. wbc in normal limits, 1/3 w. elevated wbc hyperleukocytosis: elevated wbc >/100,000/mcl *poor prognosis *increases risk of cns involvement *very high risk of Tumor lysis syndrome

Answer 26

hypercellular bone marrow *immature blasts "outgrow" all other cells *crowding results in cytopenias * does not allow room for other cell lineages to grow normal cellularity in marrow: 30-40% sometimes these pts ca have 90-95% cellularity

Answer 27

oncologic emergency 8hyperviscosity syndrome (blood sludging) *stumor, sob, vision changes *can cause stroke, respiratory failure, cardiac ischemia, renal failure, retinal hemorrhage management: hyroxyurea (hydrea) *oral ribonucleitide reductase inhibitor *used for count control *used until clinically stable and ready to start induction chemo *leukopheresis dosing: package insert 50-100mg/kg/day dosing heavily physician/pt specific AE: nvd, risk for tumor lysis syndrome LONG TERM: CUTANEOUS VASCULITIC ULCERATIONS MUCOSITIS ALOPECIA, HYPERIGMENTATION

Answer 28

WHO definition >/20% blasts isolated on bone marrow biopsy (bmbx) or peripheral blood cytogenitically definition: detection of cytogenetic abnormalities known to indicate AML, regardless of blast % on bmbx

Answer 29

cytogenetics!!!; predicts abilility to obtain remission w. induction chemo with persons chromosomal make up aka karyotype, risk of relapse, and overall survivial moelcular abnormalities age primary vs secondary aml performance status availability of stem donor wbc at diagnosis extramedullary disease (disease not in marrow)

Answer 30

two types *internal tandem duplication (ITD) *Tyrosine kinase domain(TKD) point mutations promotes proliferation and blocks differentiation associated w. worse prognosis, increased relapse rate and lower OS associate w. leukocyosis and high percentage of blasts in bone marrow de novo AML (ITD mutations associated w. worse survival/worse prognosis compared to tkd mutation)

Answer 31

ISOCITRATE dehydrogenase(IDH) others being researched: RUNX1, TET2, spliceosome mutations

Answer 32

favorable risk: low risk of relapse if we get them into remission intermediate risk poor risk *intermediate and poor risk pts are taken to transplants once they get to remission

Answer 33

most pts<60 pts >/60 w.o significant co morbidities or end organ dysfunction (adeque renal, hepatic, and cardiac function *adequate performance status pts w. aggressive disease course (hyperleukocytosis, tumor lysis syndrome at presentation) pts who are candidates for an allogenic stem cell transplant

Answer 34

Cytarabine +Anthracycline (7+3) based regimen for pts <60 yo. cytarabine 100mg/m^2 IV daily continuous infusion x7 days +daunorubicin 60 mg/m^2 x 3days OR idarubicin 12mg/m2/dx 3 days for pts >/60 cytarabine 100mg/m^2 IV daily continuous infusion x7 days +daunorubicin 60 mg/m^2 x 3days OR idarubicin 12mg/m2/dx 3 days **note: pts >/65 have <50% complete remission rate (CR)

Answer 35

days 1-7: chemo admin *SE: n/v, GI, fatigue WBC drop significantly Days 8-24: cell count nadir and recovery *side effects: fatigue, fevr/infection, high rbc and platelet transfusion requirmeent days 25+ complete cell count recovery expected. *d/c from hospital once ANC>500 and no longer platlet transfusion dependent

Answer 36

7+3 based regimens *additional chemos and or tyrosine kinase inhibitors added to backbone of 7+3 exs: FLT3-ITD or FLT3TKD positive *Midostaurin *50 mg BID w. food on days 8-21 of each cours of chemo (induction and consolidation) *can cause nausea *favorable/intermediate cytogenetics *gemtuzumab ozogamicin (GO) 3mg/m^2 (max 4.5 mg) on days 1,4, and 7 of induction and day 1 of consolidation courses *antibody drug conjugate. no increase in survival seen in poor risk pts Liposomal Daunorubicin +cytaribine (vyxeos) *indication: 1st line treatment of treatment related/ secondary AML *liposomal formulations

Answer 37

Day 14 bmbx: *Leukemia free state on day 14 Goal: <5-10% blasts, hypocellular (<10-20% cells) complete remission/complete response n(CR) criteria: day 28+ *criteria for CR: <5% blasts and ANC>1000 ANDD platelets>100,000 complete remission w. incomplete count recovery (iCR) *older pts w. prior MDS- residual dysplasia prevents full platelet recovery

Answer 38

complete remission/complete response n(CR) criteria: day 28+ *criteria for CR: <5% blasts and ANC>1000 ANDD platelets>100,000 complete remission w. incomplete count recovery (iCR) *older pts w. prior MDS- residual dysplasia prevents full platelet recovery *repeat bmbx to document complete remission

Answer 39

purpose: to eliminate remaining disease that was not eliminated during induction phase favorable risk pts: A) HiDAC: Hi dose cytarabine *for those who recieved 7+3 based therapies *gold standard consolidation therapy for AML 1.5-3 g/m^2 iv q12hrs x 6 doses q28 days x 3-4 cycles b) other option: Liposomal daunorubicin+ cytarabine Intermediate/poor risk *stem cell transplant *based on cytogenetics, molecular mutations *usually, compete induction and 1+ cycle(s) if consolidation prior to transplant

Answer 40

"low intensity" chemo *reserved for those unfit for intensive chemo or those w. significant comorbidities a) HYpomethylating Agents (hma)+Venetoclax *Azacitidine (Vidoza) 75 mg/m^2/dayx7 days q28 days-> can be subq or iv ****standard of care *Decitabine (Dacogen): 20 mg/m^2/day IVx5 days q28 days b) Low dose cytarabine (LDAC) +venetoclax c)Ivosidenib +Venetoclax *both agents given continuously *only in IDH1 mutated pts d) LDAC+ Glasdegib

Answer 41

immediatly when pt is on venetoclax, must consider other drugs pt is on to identify any DDI HMA backbone dose: 400mg PO once daily *strong cyp3a4 inhibitors (posiconazole/voriconazole): 100 mg once daily *mod cyp3a4 inhibitors: isavuconazole, diltiazem, verapamil ) or pgp inhibiors (amiodarone, carvedilol) 200 mg once daily LDAC backbone: *strong cyp3a4 inhibitors (posiconazole/voriconazole): 150 mg once daily *mod cyp3a4 inhibitors: isavuconazole, diltiazem, verapamil ) or pgp inhibiors (amiodarone, carvedilol) 300 mg once daily

Answer 42

clinical trial can repeat intial induction regimen if response lasted >12 months etc.

Answer 43

FLT3 mutations (FLT3 ITD, FLT3 TKD) A)FDA approved *Midostaurin (Rydapt)->only used frontline. not used in refractory disease/relapse *Gliteritinib-> only fda approved for relapsed/refractory flt3+ AML IDH inhibitors: a)FDA approved *IVOSIDENIB-targets idh1- approved for newly diagnosed and relapsed/refractory disease *ENASIDENIB- TARGETS idh2->approved for refractory/relapsed disease

Answer 44

A)transfusions *rbc transfusion if hgb<8g/dL *plt transfusion if plt<10,000 mcL b)infection ppx while neutropenic I. Antiviral: HSV/VZV-acyclovir 400mg BID II. antibacterial: ciprofloxacin 500mg BID or levofloxacin 500mg qd III. invasive fungal(Asperigillus & mold (mucomycosis) *posaconazole (covers mucoid) *voriconazole (covers mold as well)

Answer 45

oncologic emergency rapid tumor breakdown following chemotherapy sudden release of intracellular potassium, phosphorous , uric acid onset: 12-72 hrs post chemo risk factors: renal insufficiency elevated uric acid, phosphorous, lactate dehydrogenase dehydration common tumor types: hematologic malignancies associated w. large tumor burden, higher cell turnover, etc.

Answer 46

metabolic disturbances hyperuricemia-> can crystalize and lead to irreversible kidney damage hyperphosphatemia:calcium phophate precipitate inkidneys hyperkalemia hypocalceima clinical manifestations: **acute renal failure *NVD *hematuria *CHF, cardiac dysrhtmias syncope seizures death

Answer 47

A)allopurinol inhibits formulation of uric acid dose: 300-600 mg/day renal adjustment: crcl 10-30: 200 mg/day crcl: <10: 100 mg/dau hydration Rasburicase-> breaks down uric acid( usually used for treatment, not for ppx)

Answer 48

Hyperuricemia *IV hydration maintain urine output >2.5L *furosemide if unable to maintain urine output alone *Rasburicase: 1.5-6 mg as single dose. can repeat q12-24hrs on repeat levels *roswell dosing: 1.5 mg if pt<60kg, 3 if pt>60kg *rasburicase can cause anemia in pts w. g6pd deficiency. Hyperkalemia *EKG-rule out active arrythmia Sodium polystyrene sulfonate (kayexalate) *insulin and glucose *dialysis Hyperphosphatemia *phosphate binders (sevelamer, calcium acetate) *dialysis Hypocalcemia *do not treat

Answer 49

Anthracyclines( daunorubicin, idarubicin, mitoxantrone) *red in color: ink-light reddish urine mitoxantrone: blue in color->blue green urine, sclera *AE: myelosupression cardiotoxicity Cytarabine: AE with HiDAC: neurotoxicity *NEURO CHECKS REQUIRED pior to each dose conjunctivitis Gemtuzumab+Otogamicin (GO): *mab-> infusion reactions( premedicate w. APAP, diphenhydramine, and methylprednisolone hepatotoxic BBW: VENO OCCLUSIVE DISEASE-> fatal disease that causes obstruction of blood veseels that lead into liver *monitor LFTs, bilirubin, ascites, weight gain, hepatomegaly, amdominal pain Low Intensity Chemo *HMA backbones (Azacitidine) AE: constipation-> standing bowel meds low-mod emetogenicity, premedicate w. ondansetron *Venetoclaax: AE: myelosupression

Answer 50

Granulocyte-colony stimulating Factor (G-CSF): Filgrastrim (Neupogen), filgastrim-sndz(Zarxio) Granulocyte macrophage colony stimulating factor (GM-CSF): Sargramostim indication in leukemia: may be used for severe infections in setting of neutropenia (i.e severe sepsis) AE: bone pain (up to 50%)-> recommend loratidine ((due to histamine release of bone, causing the pain) or hydroxyzine *feevr

Answer 51

driven by acquired mutation that affects hemotopeitic stem cells *philidlphia chromosome (Ph+) mutation creating MCR-ABL fusion onco gene, contains an active tyrosine kinase region which is responsible for cell proliferation, cell growth and survival

Answer 52

ionizing radiation

Answer 53

up to 50% of pts are asymptomatic *splenomegaly >50% are present due to elevated platelets anorexia bone pain purpura unexplained weightloss fatigue

Answer 54

LEKOCYTOSIS - WBC>25 X 10^9/L bone marrow findings *hypercellularity(74-90%) *increased erythropoeisis *increased megakaryocytes *minimal dysplasia blasts<10% *Ph+ chromosome

Answer 55

chronic blast phase(CP): <10% blasts etc. goal: delay progression to AP/BP, eradicate philidelphia chromosome Accelerated Phase: 10-19% blasts in peripheral blood and/or marrow etc. Goal: control wbs, bring back to CP an avoid progressin to BP blast phase (BP): >.20% blasts in peripheral or in bone marrow Goal : survive induction, bridge to allogeneic stem cell transplant

Answer 56

Targeted therapy-Tyrosine Kinase Inhibitors (TKIs) 1st gn: Imatinib (Gleevec) 2nd gen: Dasatinib (Sprycel), Nilotinib 3rd Gen: Bossutinib, Ponatinib STAMP inhibitor: Asciminib, binds to a different place on TKI oral admin now condiered a chronic disease state managed w. TKI's

Answer 57

hematologic response: looking at peripheral blood counts cytogenic response: bmbx, number of Ph+ metaphases remaining molecular response: how much kinase is in blood *how we currently monitor response

Answer 58

Tyrosine Kinase Inhibitors moa: selective inhibitor of bcr-abl TYROSINE KINASE *also inhibits c-kit and plt derived growth factor receptor dose:400 mg daily AE: edema/ fluid retention, myalgias, hypophosphatemia, NVD AE mgt: diuretics, supportive care. consider checking EF if pleaural/pericardiac. for myalgias, calcium supplementation Pearls/considerations: *high doses >400 mg not recommended as initial therapy * developed resistance, lead to development of later gen TKIs

Answer 59

Tyrosine Kinase Inhibitors Dasatinib moa: dose: 100 mg daily AE: *pleural/ pericardial effusions, bleeding risk, pulmonary arterial HTN AE mgt: *pulmonary htn: d/c *fluid retention, edema, ascites: diuretics, supportive Pearls/considerations: *standard oc care *second gen, *cns penetration

Answer 60

Tyrosine Kinase Inhibitors moa: dose: 300 mg AE: elevated pancreatic enzymes, indirect hyperbilirubinemia, qtc prolongation, cv events AE mgt: *qtc prolongation: ecg@baseline, 7 days after intiation, and periodically. corect for hypokalemia and hypomagnesemia. elevatd lft: consider dose reduction or d/c *peripheral arterial occlusive disease: d/c Pearls/considerations: *qtc prolongation *2nd gen mgt

Answer 61

Tyrosine Kinase Inhibitors moa: dose: AE: *Diarrhea manageable w. loperamide, hepatotoxicity, headache, rash AE mgt: *hepatotoxicity: hold until recovery, then dose reduce or d/c *diarrhea: hold until recover, loperamide Pearls/considerations: *3rd gen

Answer 62

SoKal score: calculates relative risk calculation intermediate-high risk Category 1 recommendation: *2nd or 3rd gen TKI low risk: *Imatinib or 2nd gen

Answer 63

color chart: red: tki resistance disease *evaluate pt compliance and ddi. *CONSIDER MUTATIONAL ANALYSIS recommendation: switch to alternate tki and evaluate for allogenic hct yellow: possible tki resistance recommendation: switch to alternate tki, continue same tki (other than imatinib) or increase imatinib dose to max of 800mg and ocnsider evaluation for allognic hct light green: tki sensitive disease recommendation: if optimal, continue same tki, if not optimal, share decision making w. pt green: continue same tki

Answer 64

Asciminib and Ponatinib are only tki that cover BCR-ABL T315I mutation T315I mutation is resistant to other TKIs.

Answer 65

Tyrosine Kinase Inhibitors moa: dose: AE: elevated pancreatic enzymes, HTN, skin toxicity, thrombotic events AE mgt: hepatotoxicity: hold until recover, then dose reduce or d/c *ischemic reactions: d/c elevated lft: hold until recovery Pearls/considerations: *3rd gen *reserved for pts who failed atleast 2 tki, or have T315I mutation *BBW: vascular occlusion, hepatotoxicity, HF

Answer 66

Tyrosine Kinase Inhibitors moa: STAMP inhibitor dose: AE: Pearls/considerations: trt of pts who have previously recieved 2+ tkis or have T31FI mutaion

Answer 67

myelosupression transminitis hepatotoxicity electrolyte changes CV events

Answer 68

imatinib-cyp3a4 substrate and inhibitor Dasatinib, bosutinib, poatinib-cyp3a4 substrate nilotinib: cyp3a4 substrate and inhibitor, also 2cb, 2c9, and 2d6

Answer 69

dasitinib- needs acidic environment for absorption (no ppis or h2 blockers) nilotinib and asciminib: admin on empty stomach. 2 hrs before eating or 1 hr after

Answer 70

imatinib: dose adjust for renal and hepatic nilotinib, bosutinib, ponatinib- dose adjust for hepatic

Answer 71

Goal: return pt to chronic phase all tkis have been shown to induce favorable response rates current recommendations: Dasatinib, niltinib, or bosutinib omacetaxine can be considered in cass of disease progression blast crisis: TKI +/- chemo followed by allogenic HSCT *chemo chosen on subtype of the disease

Answer 72

surrounds urethra produces seminal fluid that nourishes and transports sperm composed of acinar secretory calles arranges in a radial shape surrounded by a foundation of supporting tissue 95% of prostate cancer cases are caused by adenocarcinoma

Answer 73

most diagnosed cancer in males 2nd most common diagnosed cancer in US 5 year relative survivial from 2012-2018: 96.8% for most pts. prostate cancer is a slow growing or indolent disease

Answer 74

Race: african amerians more common, less common in asians. incidence higher in US and scandanavian countries Age:most ppl dagnosed 65-74. Median age of diagnosis: 67 Family hx: increase in men w. family hx of prostate cancer *familial predisposition *BRCA-2 mutations a.w 2-6 fold increase in risk *lynch syndrome 2-5.8 fold increase in risk Lifetime risk of prostate cancer *16% of one first degree raltive vs 8% if no family hx

Answer 75

different organizations have different screening protocols usually involves prostate -specific antigen often determined by pts age and life expectancy

Answer 76

localized *asymptomatic generally locally invasisive *urrerteral dysfunction *urinary frequency *urinary hesitancy *dribbling or decreased urinary stream *incomplete bladder emptying advanced disease *back pain cord compression lower-extremeity edema pthologic factors anemia weightloss

Answer 77

A)protate specific antigen *gycoprotein produced by prostate epithelial cells *specific for prostate, not for cancer (if pt ha bph, psa can be high) *can be reduced by 5-alpha reductase inhibitors) normal range

Answer 78

prostate specific antigen (PSA) tumor size and extent of primary tumor histologic grade(gleason score)

Answer 79

localized tumore: excellent long term prognosis locally advanced cancer: 5 year survival is very good metastatic disease: not curable, median survival shortened

Answer 80

TNM: tumor, node, metastasis Tumor (T): clinical staging to determine size Node (N): presence and extent of regional lymph node involvement Metastasis: presence and extent of metastasis

Answer 81

gleason score *describes how cancer cells look under a microscope pathologist gets biopsy of tissue and assigns a score to 1st and second most predominnant tissue score ranges 1-5 closest to 1: low grade tumor cells; looks similar to normal cells closest to 5: high grade tumor cells; mutated so much they barely look like normal cells both numbers are added, to give a score. total score between 2-10.

Answer 82

gleason scores 2-4 tend to be less agressive, gleason scores 7-10 tend to be more agressive

Answer 83

localized disease: cure control disease and symptoms decrease morbidity and mortality advanced/ metastatic disease *palliation *improved qol *prolong survival

Answer 84

pt comorbidities pt symptoms recurrence risk pt life expectancy (expected survivial disease stage **** for localized and regional disease, treatment approach is based on RISK STRATIFICATION rther than stage

Answer 85

Recurrance Risk: Very low expected survival 1) <10 years * initial therapy: observation 2) 10-20 years *initial therapy: Active surveillance 3) >/20 years *initial therapy:

Answer 86

gold standard: Androgen Deprivation therapy (ADT) for advanced prostate cancer testosterone is the driving force of prostate cancer surgical castration: bilateral orchiectomy !!!Medical Castration: *LHRH agonists+/- antiandrogen *LHRH antagonist intent is to lower levels of testosterone

Answer 87

moa: mimics endogenous LHRH, causing sustained release of LH and FSH. release of lh and fsh would normally cause production of testosterone. howevere, sustained release causes negative feedback loop, decreasing the amount of testosterone produced. ex: Leuprolide (Trelstar), Goserelin (Zoladex)

Answer 88

acute: tumor flare (due to short term increase in testosterone due to LH an FSH), hot flashes, erectile dysfunction, edema, gynecomastia, injection site reaction Long term: osteoporosis, clinical fracture, insulin resistance, increased risk of diabetes, CV events, alteration in diabetes

Answer 89

cause by a surge in lh/fsh release, causing increased testosterone production. SS: increased bone pain (if metastatic) or increased urinary SS resolves after 2 weeks starting a first gen anti androgen before admin of LHRH agonist and continuing for 2-4 weeks frequently used to mitigate tumor flare. baseline bone mineral density test bfore starting longterm ADT (calcium and vit. D supplementation

Answer 90

moa: binds to GnRH receptors in on cells in pituitary gland, dramatically reducing LH/FSH resulting reduced production of testosterone to castrate levels ex:Degarelix Relugolix advantage: much faster drop in testosterone levels castration levels seen in 7 days or less compared to 28 days w. lhrh agonists. no tumor flare and thus no antiandrogen needed cons: less flexible indosing schedule, high cost

Answer 91

moa: inhibits anrogen uptke and/orbinding in target tissues. specifcally, a competitice inhibitor for the binding of DHT and testtosterone first gen: bicalutamide flutamide nilutamise second gen: apalutamide enzalutimaide darolutamide 2nd gen more potent ade: diarrhea, gynecomastia, elevated lft, hot fashes monitoring: lfts monthly

Answer 92

lhrh agonist or antagonist +anti androgen contraversial associated w. more ADE

Answer 93

ADT+ abiraterone or Apalutamide or Enzalutamide ADT w. docetaxel x6 cycles +abiraterone or darolutmidde *use din high volume castration sensitive metastatic prostate cancer choice of regimen invoes discussion w. pt about potential toxicities of abiraterone and docetaxel as well as cost of treatment

Answer 94

serum testosterone <50 ng and disease progression nccn recommendation: continue adt and maintain castrate levels while adding therapies therapy base don whether pt has non metastatic m0 or metastatic m1 disease

Answer 95

M0-> continue AT to maintain castrate tstosterone if PROSTATE DOUBLES >10 MONTHS A) MONITOR or 2) other secondary hormone therapy id prostate doubles <10 months a) apalutamide b)enzalutamide

Answer 96

continue ADT to maintain castarte levels of testosterone and add: 2nd gen antiandrogen *apalutamide for m0 and PSADT

Answer 97

Second generation antiandrogen therapies moa: nonsteroidal androgen receptor inhibitor, binds dirctly to androgen receptor preventing androgen translocation, dna binding, and transcription. causes decreased prolifration of tumor cells and increased apoptosis leading to decreased tumor volume dosing 240 mg once daily w. or w.o food ADE: fatigue, htn considertions/pearls *ci in pts w. seizures

Answer 98

Second generation antiandrogen therapies moa dosing ADE considertions/pearls no increase risk in seizures renal dosing

Answer 99

Second generation antiandrogen therapies moa dosing ADE considertions/pearls *increased risk of seizures

Answer 100

MOST PROSTATE CANCERS ARE ADENOCARCINOMAS. IF HISTOLOGY IS UNKOWN, TREAT AS IF ADENOCARCINMOMA. no prior docetaxel/ no prior hormone therapy preffered regimens *abiraterone docetaxel enzalutamide cirtain circumstances: radium 223 for symptomatic bone metas. sipuleacual

Answer 101

preferred: docetaxel

Answer 102

preferred: abiraterone cabazitaxel enzalutamide

Answer 103

preferred regimend: docetaxel rechallange, cabazitaxel

Answer 104

if pt has viseral metas (liver, lung, adrenal, peritoneum,brain (consider docetaxel if pt has not recieved it and pt is fit for chemo no viseral metas.: treat based on prior therapy symptomatic bone metas: radium 223 asymptomatic or minimally symptomatic, no liver metas, life expectancy> 6 months.. consider sipuleucal-T

Answer 105

chemo therapy agents for prostate cancer moa:microtubule inhibitot dose: dose+prednisone ade: *alopecia, myelosupression, peripheral neuropathy, hypersensitivity reaction (premidcate before) considerations/ pearls: cause hepatic impairment

Answer 106

chemo therapy agents for prostate cancer moa: inhibits CYP17. responsible for androgen biosynthesis in many diff tissues, inhibits formtion of testosterone precursors dose: ade:hypokalemia, diarrhea, edma, htn, hepatotoxicity considerations/ pearls: give w. steroids to prevent hypokalemia due to mineralcorticoid excesscaused by drug long term. prednisone can increase glucose *monitor lft, K+, po4, bp on monthly basis

Answer 107

chemo therapy agents for prostate cancer moa: dose: ade: considerations/ pearls: *pt must always recieve w. steroid

Answer 108

chemo therapy agents for prostate cancer moa: dose: ade: considerations/ pearls only used in pt w. bone metas. ONLY and no visceral metas. not used in combo w. chemo

Answer 109

chemo therapy agents for prostate cancer moa: dendritic cell vaccine designed to enhance t cell immune response to prostatic acid phosphatase cells exposed to PAP fused with GM-CSF). dose: ade:infusion reactions considerations/ pearls $100,000 per dose

Answer 110

if prir chemo, consider hormone therpay *cabazitaxel cabazitxel/ carboplatin LU-177-PSMA-617 other trtments *pembralizumab radium 223 bone metastesis etc.

Answer 111

chemo therapy agents for prostate cancer moa: microtubule inhibitor dose: ade:*febrine neutropenia considerations/ pearls 2nd line if pt still has disease progression *pt must be on prednisone

Answer 112

adt associted w. increase risk of bone fracture *baseline dexa scans *calcium 1000-1200 mg daily and vit. 400-800 iu bone metas.: must give bone modifying agents *Zolendronic acid, denosumab (at doses didfferent than in osteoporosis

Week 4 Flashcards

(136 cards)