Shared Flashcard Set


Hematology/Oncology Exam 2
Hem/Oc Exam 2

Additional Pharmacology Flashcards





Hospice care - Pain Management:


What's regimen is recommended? Most common agent?


IR doses should be ____ of total daily opioid dose


How do you calculate opioid dose increases?


When switching opioid doses, how does the dose change?


What opioid is avoided in elderly patients and why?


Recommended: Use ATC dosing - Morphine ER q12hr

- Try using same ER and IR medicine (Morphine = gold standard)


IR doses should be 10-15% of total daily opioid dose


Dose increases: Add total daily dose of ER + IR / 2

- That calculated # = new ER dose (Must recalc IR dose)


Switching: reduce dose by 25% to account for cross tolerance


Meperidine = avoided due to active metabolites in elderly


Hospice - Methadone:Morphine comparison


Characteristics which differentiate these two agents


What doses are equal potency between these two?


Methadone = higher bioavailability, longer t 1/2 (30h), takes longer to reach ss (3-7 days), NO active metabolites and fecally eliminated


Morphine = lower bioavailability, shorter 1/2 (3-4h), shorter time to reach ss (12-20hr), active metabolites and renal elimination


**Both are hepatically eliminated


3-5 mg of methadone = 30 mg morphine


Hospice - Methadone:


How often is it usually dosed?  Elderly patients dose?


What is the MOA?


How is it eliminated?


Usually dosed every 8-12 hrs --> long t 1/2 (3-7d for ss)

- Elderly patients may require 24h dosing (active metabolites)


Combined with breakthrough-pain med


MOA: NDMA receptor antagonist and 5-HT3/NE reuptake (x)or


Fecal elimination


Hospice - Treatment of N/V


What are the four drug classes used?


Examples of each and AEs with each


Dopamine antags - Haloperidol, prochlorperazine, metoclopramide

- AEs = sedation and EPS


5-HT3 antags - ondansetron (-setron suffix for all)

- AEs = HA and N


Antihistamines - promethazine, benadryl, hydroxyzine

- AE = sedation


Anticholinergics - transderm scopolamine patches

-AEs = xerostomia, constipation, confusion and blurred vision


Hospice - Dyspnea (subjective symptom):


What is the first line therapy for dyspnea?  How does it work?


What are other possible options (not as commonly used)?


Opioids = first line for treatment of dyspnea (safe/effective)

- has effects on cardiopulmonary system, reduce pain/ax, decreases brain stem responsiveness to CO2 (mechanism in resp. depression) and **proposed to act locally on opioid receptors on alveolar walls


Can be given either po or via nebulizer

- Neb morphine (in NS) - low AEs;

          -  can cause histamine release (problematic for asthma pts)


Other options: CS, benzos and phenothiazines (chlorpromazine)


Hospice - Constipation:


What is the goal of bowel movements in terminally ill patients?


What are the common causes?


What type of treatment should every patient recieve?


What other classes can be used to help relieve constipation?


Goal: 1 bowel movement every 3 days


Causes = low fiber, dehydrated, disease state (e.g. colon cancer) and medications (opioids and TCA's)


Every patient should recieve stimulant laxatives prophylactically**

Ex: Senna or bisacodyl always given at bedtime


Other classes: Stool softener (docusate), bulk forming (well hydrated), osmotic laxatives (lactulose, sorbitol), prokinetics (metoclopramide) and methylnaltrexone (sq; mu-R antag)


Hospice - Delerium:


What are the two distinct types of delirium and Sxs of each?


What are the common causes?


Treament goal? Options?


Hyperactive - agitated, aggresive and combative

Hypoactive - mistaken for depression; sluggish and lethargic

(Can have mixed delirium (combo) --> difficult to treat)


Causes: hypoxia, infxns, fever, dehydrated, stroke and abrupt medication withdrawal (opioids, benzos; should be titrated down)


Symptomatic treatment goal = comfort and safety

-- Can use antipsychotics (haloperidol; lower dose for elderly); atypicals (risperidone) and benzos (lorazepam)


Hospice - Anorexia/Cachexia:


What non-pharm treatment is used?


What are the pharm treatment options?


Non-pharm: Educate family (difficult for them to see), eliminate dietary restrictions and reduce portion size (more meals)


**Treat the symptom preventing patients from eating

- pain, GI motility problems, reflux esophagitis and mouth conditions (dryness, candidiasis and mucositis from chemo)


Pharm treament options:

-- Dexamethasone, mirtazipine, megesterol and dronabinol


Hospice - Fatigue


What non-pharm treatment options are used?


What pharm treatment is used? 


Which is specifically used for opioid induced fatigue?


Non-pharm = permission to be tired and rest (MD write rx for sleep and gives to pt), structure activity to conserve energy and eliminate medications that are not needed that cause fatigue


Pharm treamtent = dexamethasone and antidepressants

-- Methylphenidate (BID) is very effective for opioid induced fatigue**


Hospice - Anxiety and Depression


Non-pharm and pharm treatment for anxiety


Depression pharm treatment options


Anxiety: Non-pharm = relaxation techniques, spirituality

- Pharm: benzos (lorazepam used 1st) and haloperidol (neuroleptics)


Depression - pain is a major risk factor for depression and suicide

- Pharm treatment: SSRIs (sertraline, paroxetine and citalopram), TCAs (amitriptyline, nortriptyline), methylphenidate and mirtazipine

  **Methylphenidate not LT treatment (only in pts w/ few days to live)


Pharmacogenomics: 6-MP (purine antimetabolite)


Genetic variations in what gene effect bioavailability and

toxicity of 6-MP? 


How is this deficiency obtained in patients?


What complications arise in individuals with this polymorphism?



Variations in TMPT gene effect bioavailability and toxicity of 6-MP

- TMPT catalyzes S-methylation of 6-MP to form inactive metabs


The TPMT deficiency = inherited autosomal recessive trait


Patients with TPMT polymorphisms are at risk for severe toxicities when treated with 6-MP b/c of decrease rate of 6-MP metabolism


Allele changes = TMPT*2, TPMT*3A and TPMT*3C

- seen in 95% of observed cases


Pharmacogenomics - Irinotecan


Gene variations in what enzyme lead to severe toxicity?


What specific genotype changes are risk factors? What happens?




Irinotecan inactivated by UGT-1A1


Genotypes UGT1A1*28 and UGT1A1*6 are risk factors for severe tox


Pts have larger than expected dose b/c drug not cleared effectively


UGT1A1*28 found in 35% of whites/blacks --> these patients are at higher risk of grade 4 neutropenia (no clinical adjustments yet)


Pharmacogenomics - Tamoxifen


What enzyme breaks down this drug?


What patients are associated with higher cancer recurrence rates?


Tamoxifen = pro-drug


Metabolized to active forms by CYP-2D6


Poor and intermediate metabolizers have been associated with higher cancer recurrence rates

- b/c less exposure to active drug

        (increase dose to achieve proper concentration)


Pharmacogenomics - 5-FU


What enzyme is responsible for 5-FU metabolism?


DPD (dihydropyrimidine dehydrogenase) catalyzes the rate-limiting step in 5-FU metabolism

- Variability in DPD activity = increase incidence of AEs


Deficiency of DPD = severe toxicity and fatal outcomes w/ 5-FU tx

-- Appears to be genetic disorder in DPYD gene resulting in decreased enzyme activity




Difference between 3 types of genetic testing:


Predictive genetic testing

Prognostic genetic testing

Genetic Diagnostic testing


Predictive = predict risk status of an individual for contracting disease or condition based on genetics


Prognostic = predict efficacy of particular drug based on genetics


Diagnostic = diagnosing an exisiting disease state or condition based on genetics


Pharmacogenomics - Predictive tests


Hereditary Breast and Ovarian Cancer (HBOC) syndrome increases risk of ______ , often before ________.


What is usually the cause?


HBOC increases risk for developing breast and ovarian cancer, often before the age of 50 (Inc RISK only --> not everyone will get cancer)


Mutation or alteration in BRCA1 or BRCA2 (inherit from either parent)

- Testing reduces risk, pt makes proactive steps and informed choices


If no BRCA1 or BRCA2 mutations are detected then change of ovarian/breast cancer is significantly reduced

- BUT, only looks for mutations in these genes; other causes can lead to cancer


Pharmacogenomics - Prognostic tests


Oncotype DX BC Assay - what are benefits of this test?


What specific patient is this test intended for?


Oncotype DX - examines tumor tissue at molecular level and helps plan or tailor cancer treatment options


Clinical evidence of it's ability to predict the likelihood of chemotherapy benefit and recurrence in early-stage breast cancer


Intended to be used by women with early-stage (Stage 1 or 2), node-negative, estrogen-R positive (ER+) invasive BC who will be treated with hormone therapy


Pharmacogenomics - Prognostic test


Prolaris use?


What does it measure?


Prostate cancer = highly variable/slow growing/nonaggresive


Helps predict cancer aggresiveness w/ other clinical parameter


Test measure the expression level of genes involved with cell cycle progression to predict disease outcome


Pharmacogenomics - Predictive test


Theraguide 5-FU tests for what two genes?


Using this predictive tests helps _____?


Theraguide 5-FU detects variations in two genes, DPYD or TYMS which will inc risk of dose-limiting AEs related to 5-FU therapy


Predictive testing helps:

- Prevent toxicity in high-risk patients

- Individualize treatment for optimal therapeutic response

- Better determine alternate therapies for at-risk patients

- Implement dose reduction and monitoring strategies when appropriate


Adverse Effects:


What are the chemotherapy agents that do not cause myelosuppression?


What two drugs caused prolonged and delayed myelosuppresion?


Vincristine, MTX (only with Leucovorine rescue*), Bleomycin

(also, Corticosteroids, interferons, L-asparaginase and hormones)


Busulfan and carmustine cause prolonged & delayed myelosuppression

- These agents work closer to the stem cell

What is the days of nadir and recovery of Busulfan and Carmustine?
Busulfan day 11 to 30 nadir, 24-54 recovery Carmustine day 26 to 30 nadir, 35-49 recovery
formula for ANC
total WBC x %neutrophils (segs + bands)
Neutropenia is defined as ANC < ___?
500 or also < 1000/mm3 with expected drop less than 500

Adverse Effects:


What factors put a patient at an increased risk for myelosuppression?


List agents that cause impaired drug elimination via

renal/hepatic routes


Risk factors = poor marrow reserve (inc age), type of chemo, prior pelvis radiation, prior chemo and concurrent radiation therapy


Meds w/ impaired drug elimination:

- Renal = cisplatin, carboplatin, MTX and toptecan

- Hepatic = anthracyclines, vincas, taxanes and irinotecan

(Not always b/c of toxicity to region; could be elimination route ex: adriamycin and anthracyclines eliminated hepatic; not toxic to liver)


Adverse Effects:

Febrile neutropenia defined as ___


Antibiotics must cover ____


Examples of antibiotic regimens? What if G+ is suspected?


What class of meds are not recommended to treat neutropenic fever?


Febrile neutropenia accompanied by temp > 101 or 100 for > 1 hr

- neutropenia = ANC < 500 or ANC < 1000 w/ expected drop < 500


Antibiotic regimens must cover Pseudomonas



- Mono = ceftazidime (?), Cefepem, Imipenem and Meropenem

- Dual = Pip/Tazo or Mono agent + aminoglycoside

- If G+ suspected = either of above + Vanc


CSFs not recommended for treatment of neutropenic fever

** Used in prevention


Adverse Effects - Neutropenia Prevention:


Agents for primary prevention?


When are these drugs deemed cost-effective for primary prevention?


What agents are used in secondary prevention?


Primary prevention - prophylactic CSFs or treatment at reduced dose


**CSFs deemed cost-effective if neutropenia incidence > 17%


Secondary prevention = either dose reduction of chemo or CSFs

- CSFs are commonly used when dose intensity is correlated with response


Adverse Effects - CSFs:


What is the dose for G-CSF?


Common AE between all CSFs?


When should you stop: G-CSF and pegfilgrastim?


Clinical trial data supports the use of CSF when _____


In what specific cancer is CSF prophylaxis very imp?


G-CSF dose = 5 mg/kg/d sq until ANC > 10,000/mm3

- Start > 24 hrs but < 72 hrs after start of chemo


AE among CSFs = Medullary bone pain


Stop G-CSF w/n 1-2 days of chemo; Pegfilgrastim stop w/in 14 days


Data supports use of CSFs when FN risk > 20%

- < 20% weigh risk vs benefit (complete cure or palliative care)


CSF prophylaxis is very important breast cancer patients


Adverse Effects - Pegfilgrastim:


Prophylactic use of pegfilgrastim results in what?


What is the dose of pegfilgrastim?


When pegfilgrastim be administered and stopped before next chemo?


How is pegfilgrastim cleared in the body?


Pegfilgrastim prophylaxis results in reduced neutropenia duration, fewer hospital days and fewer days of IV antibiotics


Dose: 6 mg subcutaneously every 21 days

- Administered 24hr after cytotoxic chemo and must be > 14 days till next chemo dose (< 14 days do not use)


Pegfilgrastim - slow clearance of protein portion (extended t 1/2) and is primarily cleared by neutrophils

-- Neutrophil count low then drug conc stay high; once neutrophil counts return to normal drug is eliminated more effectively


Adverse Effects - Thrombocytopenia:


What are the four meds commonly associated with thrombocytopenia?


Broad treatment strategy used ______


What agent is used for prevention?  When is it used?


Topotecan, carboplatin (not cisplatin), gemcitabine and bortezomib


Treatment: platelet infusions when counts < 10-20,000 or

                    < 50,000 with active bleeding


Prevention: IL-11 (Oprevelkin)

- Used in high risk patients where dose reduction may compromise outcomes


Adverse Effects - Oprevelkin (IL-11)


MOA, Dose




When should this agent be initiated and d/c?


This med should be continued until platelet count is _____ for ____


IL-11 stimulates platelet production through stimulation of megakaryocytpoeisis and thrombopoiesis (used to prevent; not tx)


- Dose = 50 ug/kg SC qd

- AEs: fluid retention, pleural effusion, tachy, Afib, Aflutter, **conjunctival redness w/ injection

- Caution in pts with: CHF, cardiac arrhythmias, preexisting visual disturbances, leukemia or multiple myeloma


Dose initiated w/in 6-24hr after completion of chemo; continued until post-nadir platelets is 100,000 for 21 days; treatment should be d/c at least two days before start of next chemo cycle


Adverse Effects - Anemia:


Can occur with any marrow toxic agent.  What agents are common?


When are transfusions of packed RBCs used?


What is the RBC count decreased to in cancer patients?


Common agents = cisplatin and carboplatin

-- most common AE; but Hgb counts not as important w/ chemo tx


Transfusions of pack RBCs for Hgb < 8 or higher if severe symptoms


RBC count decreased to ~ 90 days with cancer

- Anemia inducing substance (AIS) causes reduced EPO production, suppressed BFU-e and CFU-e and impaired iron utilization

- Cancer patients kidneys cannot compensate enough to make up diff



Adverse Effects - EPO and Darbepoetin alfa


Differences between these agents


Dose schedule, structure differences and when to add these agents?


Recombinant EPO - given either 3x/wk or once a week

Darbepoetin - only given every 3 weeks (longer t 1/2)


EPO = 3 N-linked CHO chains w/ 14 sialic acids

Darbo = 5 N-linked CHO chains w/ 22 sialic acids


These agents should be added when Hgb < 10 (D/c if Hgb > 12)

-- No longer indicated for myelosuppresive anticipated treatment


GI Toxicity - Mucositis:


What is mucositis? Direct vs indirect stomatoxicity


Time course of mucositis parallels ____


Risk factors for mucositis


Mucositis = GI tract lining has rapid turnover rate and high tox risk

- Direct stomatotox = due to cytotoxic agents

- Indirect = due to concurrent neutropenia and thrombocytopenia


Time course usually parallels myelosuppression

- Neutropenic = severe mucositis; Improved neutrohils = muco better


RFs: poor oral hygiene; leukemia/lymphoma; young age; radiation; poor nutritional status and high dose therapy


Adverse Effects - Mucositis:


What agents are commonly associated with mucositis?


Prevention strategies?




What is palifermin? Who's it approved for?


Agents: 5-FU, MTX, Doxorubicin, Bleomycin & Cont. infused taxanes


Prevention: hygiene, leucovorin rescue for MTX

**Amifostine for radiation for head/neck cancers = 200 mg/m2 IV over 3 mins once daily starting 15-30 min before radiation tx


All treatments should be given IV (antimicrobials, antifungals, antivirals, antibiotics, hydration and nutritional support)


Palifermin: stims keratinocytes; approved for BMT pts

- Decreased severity of mucositis only NOT incidence


Adverse Effects - Diarrhea:


What agents are common causes?


Irinotecan causes _____ and is treated with?


Important mutation with irinotecan therapy?


Agents: 5-FU, IL-2, irinotecan and EGFR (x)ors (erlotinib, gefitinib and cetuximab)


Irinotecan causes both early and late diarrhea

- Treat early w/ anticholinergics

- Treat late w/ loperamide <-- NO MAX DOSE IN CANCER PATIENTS

Dose = 4 mg stat and then 2 mg q2hr until diarrhea stops

** UGT-1A1 mutation = more diarrhea/neutropenia; do not use if irinotecan mutation is present


- If diarrhea > 1 day while taking loperamide start levoflox after 24h


Adverse Effects - Constipation:


What agents are associated with constipation?


Prevention strategies?




Agents = constipation and pain medications

- consequences: ab cramps, ileus and bowel obstruction


Prevention: stool softeners, stimulant/hyperosmotic laxatives

- stimulant laxatives: 1 bowel movement q48hrs


Treatment: Increased laxatives, fluids and fiber (not w/ pain meds)

- Methylnatrexone (1 time dose - selective opiod antag periph; does not cross the BBB)


Adverse Effects - Renal toxicity:


What agents are known to cause direct renal toxicity?


How do you prevent and treat these agents?


Cisplatin: tubular necrosis and electrolyte wasting (Mg+ and K+)

- Prevent w/ pre and post hydration = 1 L NS + 20 mEq KCl + 8 mEq Mg-SO4 over 1-2hrs to obtain urine flow rate of > 100 mL/hr

         (same for post-hydration)

- Dose adjust for CrCL < 50 mL/min; use mannitol not diarrhea

- Amifostine - modest protection; give 15-30 mins before


High-dose MTX (precipitates in renal tubules); major DI w/ NSAIDs

- Prevent: alkanize urine pH > 7 (12hr prior and cont 24 hrs after)

- Leucovorine doesn't help w/ water solubility (not given to protect against nephrotoxicity)


Adverse Effects - Bladder Toxicity:


Agents known to cause this and why?


What agent is used to prevent this and what dose regimens are used?


Agents: cyclophosphamide and ifosfamide

- inactive metab acrolein binds to and irritates BV --> bleeding

- can result in hemorrhage, loss of fxn and bladder cancer


Prevention = vigorous hydration and MESNA (binds acrolein)

- Mesna IV-IV-IV: IV bolus 20% ifosfamide dose at the time of administration and 4 and 8 hrs after each dose of ifosfamide

(TDD = 60%)

- Mesna IV-oral-oral: IV bolus 20% ifosfamide dose at time of admin; then 40% ifosfamide dose at 2 and 6 hrs after each ifosfamide dose (TDD = 100%


Adverse Effects - Cardiac toxicity:


What agents are known to cause this?




Doxorubicin (anthracyclines in general)


Mitoxantrone (less cardiotoxic b/c no oxygen free radical formation)


5-FU (angina and MI)


High dose Cyclophosphamide




Imatinib, Dasatinib and Nilotinib (TKI of BCR-abl 1 and 2)

Sunitinib and Sorafenib (TK VEGFR); Bevacizumab (VEGF (x)or)


Adverse Effects - Anthracyclines:


What types of cardiac toxicities do anthracyclines cause?


What is the life-time dose of doxorubicin?




Prevention? (Scan/antidote)


Cause any type of cardiotoxicity (acute = arrhytmias, pericarditis)

- Chronic = CHF and Late = ventricular dysfunction


Life-time Doxorubicin dose > 450-550 mg/m2


MOA: metabolize reactive intermediates that gen O2 free radicals


All pts need baseline MUGA scan to evaluate potential cardiotoxicity

- Ejection fraction should be > 50% (< 50% no anthracyclines)

** Dexrazoxane (antidote) - prevent cardiotoxic by stop binding of the reactive intermediate to iron (metal chelator); peds pts high use


Adverse Effects - Pulmonary toxicity:


What agents cause this?


How do you prevent pulmonary toxicity?


What treatment strategies are used?


Bleomycin (need baseline PFTs and mucositis), Busulfan, Carmustine, Mitomycin C, All trans-retinoic acid, cyclophosph and MTX


Prevent by limiting cumulative doses:

- Bleomycin = < 400 units total of bleomycin

- Busulfan = < 500 mg

- Carmustine = < 1000/m2


Treatment = no antidote; steroids for symptomatic relief


Adverse Effects - Neurotoxicity


What agents are associated and type of toxicity of each?


Vinca (esp vincristine): periph, autonomic & cranial NN neuropathy

- progress neuropathy; ask pt 2 or 3 dose about ting/numb feet


Cisplatin: periph neuropathy and ototoxicity


Oxaliplatin: acute and chronic neuropathies (diff swallowing)


Taxanes: peripheral neuropathy


Intrathecal chemo: Direct CNS tox, seizures and coma


Ifosfamide: confusion, somnolence, seizures and coma (cloudy feel)


Adverse Effects:


What medications always cause alopecia?


What medications have photosensitivity risks?


What meds cause Hand-Foot syndrome?


What med class typically causes rash? What does it look like?


Alopecia: Anthracycline and Paclitaxel (grow back when chemo d/c)


Photosensitivity: 5-FU, MTX, ATRA and EGFR (x)ors


Hand-foot syndrome: Capecitabine, continuous IV infusion 5-FU, sunitinib and sorafenib [VEGFR TK (x)ors]; also lapatanib (EGFR-2)


Rash = EGFR (x)ors --> all drugs cause acne-like rash

-- if EGFRs are working then rash shows it's working (no prob till sev)

EGFR ex = cetuximab, erlotinib and gefitinib


Adverse Effects - Vesicants:


What are known vesicants?




Specific antidotes?


Anthracyclines, vincas, N mustards, mitomycin and dactinomycin


Treatment: stop infusion and attempt to withdraw fluid

-- Ice packs used for all drugs except vincas (Heat for vincas)



- N mustard = sodium thiosulfate sq around extravasation site

- Vincas = hyaluronidase sq

- Anthracycilnes = DMSO topical or Dexrazoxane IV (repackaged)

--- Dexrazoxane dose on BSA for 3 days of IV soln

         (Max single dose = 2000 mg)


Adverse Effects - Hypersensitivity Reactions:


Agents known allergic reactions?


Prevention strategies?


What agents always has a premedication cocktail?


L-asparaginase, Pacitaxel, bleomycin (rare), cisplatin, anthracyclines (hives at site) and mAbs (more w/ mouse antibodies)


Prevention: L-asparginase and bleomycin = give test doses


** Paclitaxel always given as premedication cocktail: Corticosteroids, Diphenhydramine and H2-blockers


mAbs (more w/ -ximab) --> premed cetuximab w/ diphenhydramine


What is the most important risk factor for CINV?


Do males or females have worse N/V?


Emetogenicity of chemo regimen = most imp CINV RF


Females have worse N/V than males


Increased RFs for N/V:

- Prior exposure to chemo and history of N/V (worse)

- Younger people have worse N/V

- People who don't drink alcohol or smoke have worse N/V


CINV - Antineoplastic agents


What are the three highly emetogenic drugs?


What medications are moderate emetognic drugs?


What medications are listed in low-minimal emetogenic drugs?


High emetogenic = cisplatin, mechlorethamine and dacarbaine

(**cisplatin only platinum high; carbo and anthracyclines = mod)


Moderate = carboplatin, cyclophosphamide, anthracylines and oxaliplatin (2 moderate agents = highly emetogenic regimen)


Low-minimal = Paclitaxel, doxetaxel and vincas;

-- oral target agents = chlorambucil, erlotinib, sorafenib and sunitinib


What are the three most important NTs in CINV?


How do these NTs work in the body?


Serotonin, Substance P (binds NK-1 receptors) and Dopamine


5-HT3: released from enterochromaffin cells in GI tract and activates serotonin receptors that stimulate the CTZ

- Chemo cause cytotoxic damage to GI mucosa --> release of 5-HT3

- works in the periph (gut) and centrally (CTZ)


Dopamine: stimulates the CTZ


Substance P (binds to NK cells): GI tract and vomitting center

What drugs are known to cause delayed emesis?

Delayed emesis is common with cisplatin, carboplatin,

doxorubicin and cyclophosphamide


** Cisplatin has biphasic pattern of CINV

- Max intense w/in 24h post dose

- 2nd phase = 2-4d post dose


In CINV, what is always added to a regimen of 5-HT3 antagonists?


5-HT3 antagonists activity is based on ______?


What is ondansetron IV and PO dose?


What are the most prominent AEs?


What is unique about Palonosetron?


Always add corticosteroids to 5-HT3 chemo regimens!! Increases the efficacy by 15-30%


Serotonin antagonist activity is based on receptor binding, not kinetic parameters.  Once 5-HT3 receptors are saturated, higher do not increase effect


Ondansetron IV = 8-16 mg IV bolus infusion 30 min prior to chemo and q4h x 2 dose (16 mg IV is max dose)

Ondansetron PO = 16-24 mg 30 min prior to chemo (24 mg = max and common dose)


Prominent AEs = HA and GI; constipation

(Granisetron not for PONV; dalosetron = QT prolongation caution)


Palonosetron = inc t1/2 (40hrs) and only given IV; no po dose


Aprepitant (Emend)


MOA, IV dose and indication


What is an important change in regimen that must be made?


Drug interactions


Aprepitant - NK-1 receptor antagonist (blocks substance P binding)

- IV dose = 150 mg IV for 1 day only!!


Indicated for acute, highly emetogenic chemo w/ 5-HT3 antags and CS




Drug interactions = 3A4 (x)or (why cut DXM dose by 50%) so need to decrease effectiveness of oral contraceptives, ketoconazole, clarithromycin, diltiazem and verapamil




MOA, important AEs and place in therapy


MOA: Dopamine and 5-HT3 antagonist that increases GI motility


AEs = EPS and diarrhea (dystonic rxns and CNS)


Used in DELAYED N/V and moderate-highly emetogenic chemotherapy

What medication class is used for anticipatory N/V and why?



AEs = sedation --> reason it's used in CINV


Also used as adjuvant treatment in highly emetogenic chemo!

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