Exam 2 Flashcards
What is the mechanism of nausea and vomiting in oncology patients?
Cytotoxic chemotherapy damages the epithelial cells in the lining of the GI tract. Enterochromaffin cells that line the GI tract contain large stores of serotonin, which is then released in massive quantities after chemo. (serotonin, dopamine, acetylcholine, and substance P are all neurotransmitters that are targets)
The chemoreceptor trigger zone (CTZ) stimulates the vomiting center (medulla stimulates the emetic response).
- Nausea: feeling like you have to vomit
- Wretching: labored movement of abdominal/thoracic muscles before vomiting
- Vomiting: ejection or forced expulsion of gastric contents through the mouth
What are the 5 types of N/V associated with cancer patients?
Anticipatory - learned response due to N/V from prior cycles of chemo
Acute - emetic response w/in 24h of chemotherapy
Delayed - emetic following >24h after completion of chemo, mechanism not fully understood, but may involve substance P binding to neurokinin 1 receptor
Breakthrough - N/V occurring even when patient takes antiemetics
Refractory - N/V that persists despite appropriate antiemetics
Who is at risk for CINV?
- Women > Men
- Younger > Older
- Prior history of motion sickness
- Previous history of morning sickness
- Previous CINV
- Anxiety/high pretreatment anticipation of nausea
What is Regimen A for Highly Emetogenic chemotherapies?
4 drug regimen given right before chemo:
1. NK-1 antagonist: aprepitant, fosprepitant, polapitant, netupitant, posnetupitant
2. Steroid: dexamethasone
3. 5-HT3 antagonist: dolasetron, granisetron, ondansetron, palonosetron
4. Atypical antipsychotic: olanzapine
*NK-1 antagonist & steroid are both really good for acute AND delayed, 5-HT3 antagonist is better for acute (not as much delayed)
*can add lorazepam or H2RA/PPI if needed (to any regimen or emetogenicity)
What is Regimen B for Highly Emetogenic chemotherapies?
3 drug regimen given right before chemo:
1. Atypical antipsychotic: Olanzapine
2. 5-HT3 antagonist: Palonosetron
3. Steroid: Dexamethasone
What is Regimen C for Highly Emetogenic chemotherapies?
3 drug regimen given right before chemo:
1. NK-1 antagonist: Aprepitant, fosprepitant, polapitant, netupitant, posnetupitant
2. 5-HT3 antagonist: Dolasetron, granisetron, ondansetron, palonosetron
3. Steroid: Dexamethasone
What is Regimen A for Moderately Emetogenic chemotherapies?
2 drug regimen:
1. Steroid: Dexamethasone
2. 5HT3 antagonist: Dolasetron, granisetron, ondansetron, palonosetron
What is Regimen B for Moderately Emetogenic chemotherapies?
- Atypical antipsychotic: Olanzapine
- 5-HT3 antagonist: Palonosetron
- Steroid: Dexamethasone
What is Regimen C for Moderately Emetogenic chemotherapies?
3 drug regimen given right before chemo:
1. NK-1 antagonist: Aprepitant, fosprepitant, polapitant, netupitant, posnetupitant
2. 5-HT3 antagonist: Dolasetron, granisetron, ondansetron, palonosetron
3. Steroid: Dexamethasone
What is the regimen for Low Emetogenic chemotherapies?
Only need 1 drug:
- Dexamethosone
- Metoclopramide
- Prochlorperazine
- 5HT3 antagonist (dolasetron, granisetron, ondansetron)
*can also add lorazepam or H2RA/PPI if needed (just like the other ones)
What can we give for breakthrough nausea and vomiting for CINV?
To take home in case they have N/V after they leave the clinic.
*Want to chose something different from what they just had in clinic.
- Dopamine receptor antagonists (haloperidol, metoclopramide)
- Phenothiazines (prochlorperazine, promethazine)
- Antypsychotic (olanzapine)
- Benzodiazepine (lorazepam)
- Cannabinoids (dronabinol, nabilone)
- Serotonin antagonists (dolastreon, ondansetron, granisetron)
- Steroids (dexamethasone)
- Anticholinergic (scopolamine)
What can we give for delayed CINV?
Typically involves use of one of the following: dexamethasone, NK-1 antagonist, olanzapine
What can we give for anticipatory nausea and vomiting (CINV)?
- Prevent it (use antiemetic therapy during every cycle of treatment)
- Behavioral interventions (hypnosis, exercise, etc.)
- Acupuncture
- Lorazepam
What are the common toxicities of the agents we use to prevent CINV?
5HT3 antagonists - headache, constipation, QTc prolongation
Corticosteroids - anxiety, insomnia, hyperglycemia
Substance P antagonists (NK1 antagonists) - hiccups, drug interactions
Dopamine antagonists - extrapyramidal side effects, diarrhea, sedation
What is the pathophysiology of mucositis and how do you treat/prevent it?
Muscositis can range from mild inflammation to bleeding ulcerations. It can be described as initiation, upregulation with generation of messengers, signaling and amplification, ulceration, then healing. It normally progresses in a step wise fashion in parallel with the patient’s nadir (lowest point the pt’s WBC count goes after chemo).
Prevention: avoid rough foods, salty/acidic foods; eat soft or liquid foods; avoid smoking and alcohol
Pain management: Topical anesthetics (lidocaine, diphenhydramine, etc.); oral cryotherapy (ice), oral and parenteral opioid analgesics
How do you prevent and treat neutropenia associated with chemotherapy use?
*always check blood counts before chemo (WBC, platelets, RBC)
- low WBC -> infections, low platelets -> bleeding, low RBC -> fatigue
- Generally, nadir occurs 10-14 days after chemo then the counts recover by 3-4 days
Prophylaxis: Use colony stimulating factors (CSFs)! Given after chemo
- filgrastim, pefligrastim (more expensive and longer 1/2 life), biosimilars
Primary Prophylaxis:
- given to pts who have a chemotherapy regimen that is expected to cause ≥20% incidence of febrile neutropenia
- high risk patients that had/have pre-existing neutropenia, extensive prior chemotherapy, or previous irradiation or the pelvis or other areas containing large amounts of bone marrow
Secondary prophylaxis:
- given to patients who have experienced neutropenic episode previously
How do we approach thrombocytopenia and anemia in chemotherapy patients?
Thrombocytopenia:
Always looks at platelet count. A lot of times, people can live with low platelets, but if the pt needs platelets, we will give them platelets.
Anemia:
When the Hgb drops under 11, evaluate the causes of anemia. Should transfuse the patient if symptomatic (ex. SOB, heard time moving around). We can use iron and consider use of erythropoietic stimulating agents (ESA - don’t use these much anymore).
- ESAs not recommended if pt is receiving myelosuppressive chemo w/ curative intent, if they are not receiving chemo, if they are receiving non-myelosuppressive chemo.
- Consider ESA use in pts with cancer and CKD, pts undergoing palliative chemotherapy, pts without other identifiable causes.
What are the common toxicities that are associated with chemotherapeutic agents and how do we manage them? (5 toxicites)
Myalgias/Arthralgias: (taxanes, aromatase inhibitors, exemestane)
- Treat with NSAIDS (maybe opioids)
Hemorrhagic cystitis: (cyclophosphamide, ifosfamide)
- Treat with hydration (prevention) and Mesna (prevent)
Heart Failure: (anthracyclines, HER2 therapies (trastuzumab), cyclophosphamide)
- Monitor cumulative dose, assess for risk factors, and use Dexrazoxane
Peripheral neuropathy: (taxanes, vinca alkaloids, platinums)
- Treat by changing infusion rate (paclitaxel) and using adjunctive pain meds (ex. gabapentin, amitriptyline)
Pulmonary toxicities: bleomycin
- Treat with corticosteroids
What are the differences in cardiotoxicity from chemotherapeutic agents? (acute, chronic, vs. late onset)
Caused by the formation of iron-dependent oxygen free radicals due to stable anthracycline-iron complexes, which cause electron transfers
- There are low levels of enzymes in the heart that can break down the free radicals.
- This damage is irreversible
Acute: occurs immediately after single dose or course of therapy with an anthracycline.
- Uncommon, transient
Chronic: onset w/in a year of receiving anthracycline therapy
- Common & life-threatening, related to cumulative dose the pt received
Late-onset: develops several years or decades after therapy
- manifests as ventricular dysfunction, CHF, conduction disturbances, arrhythmias
- more often in childhood/adolescent cancer survivors
What is different between anthracyclines and HER2 inhibitors in regard to cardiotoxicity? Can you use the HER2 inhibitor again if it causes cardiotoxicity?
Trastuzumab: REVERSIBLE
- mechanism involves EGFR pathway, which blunts the effects of stress signaling pathways that are required to maintain cardiac function.
- In the case of toxicity, stop the drug & wait for it to go back to normal, then you can restart
Anthracyclines - IRREVERSIBLE
Why do patients with cancer have pain?
- The cancer itself
- The cancer may invade into nerves, causing neuropathic pain
- Disease can invade into organs, such as liver mets or brain mets
- Surgery
- Treatment related, such as radiation or chemotherapy
How do we assess pain?
OPQRSTU:
- O: onset of pain
- P: what provokes the pain
- Q: quality of pain
- R: does the pain radiate
- S: how severe is the pain (0-10)
- T: time of pain
- U: understanding of what is happening/expectations
- Do you have other symptoms associated with pain
- Regular bowel movements?
- What medications have you used in the past?
- Any medication allergies?
How do we make a treatment plan for pain management based on patient specific factors?
We need to understand the cause of the pain, combine maintenance meds with PRN therapies, recognize pain treatment is based on the individual, monitor therapeutics/adverse effects, use the lowest doses necessary.
Patient specific factors: pain severity, medication access, hepatic/renal function, previous analgesic therapy
- non-opioid +/- adjuvant
- opioid for mild-mod pain +/- non-opioid +/- adjuvant
- opioid for mod-severe pain +/- non-opioid +/- adjuvant
What are the non-opioid, combo/mild opioid, and opioid products we have for pain? What are the important max doses?
non-opioids (pain 1-3): APAP (4g max), ibuprofen (3200mg max), aspirin
combo products/mild opioids (pain 4-6): hydrocodone/APAP, oxycodone/APAP, tramadol, codeine/APAP, etc.
- max dose based on either APAP or ibuprofen
opioid (7-10): morphine (most common), hydromorphone, oxycodone, fentanyl, methadone
- max dose to respiratory depression
What insufficiencies should we be cautious with for morphine, hydromorphone, oxycodone, fentanyl, methadone
Morphine: most common
- metabolized in the liver (caution)
- excreted renally (caution)
Hydromorphone:
- metabolized in the liver (caution)
- excreted renally (caution)
Oxycodone:
- metabolized by CYP2D6 (liver)
- no IV formulation
Fentanyl: most potent
- safe in liver and renal dysfunction
- very toxic
Methadone:
- don’t use in sever liver dysfunction
- no adverse effects in renal failure
- t1/2 is very unpredictable
When should we consider methadone for cancer patients? When should we avoid methadone?
Consider:
- true morphine allergy
- opioid-induced ADRs
- pain refractory to other opioids at high doses
- neuropathic pain
- in need of long-acting oral dosage form at low cost
Avoid:
- numerous drug interactions
- risk for syncope or arrhythmias
- hx of unpredictable adherence
- poor cognition
What toxicities are we worries about in opioid treament and how do we manage? (7)
Constipation - always add a bowel regimen (pts never develop tolerance to constipation
Sedation - tolerance helps, hold sedatives, consider dose reductions
N/V - change opioid, consider adding anti-emetic
Pruritus (itching) - decrease dose, change opioid, add anti-histamine
Hallucinations/confusion/delirium - decrease dose, change opioid, consider adding neuroleptic medication
Myoclonic jerking - consider changing opioid or treating underlying causes
Respiratory Depression - hold opioid, give low dose naloxone (give slowly)
What are other pain treatment modalities aside from traditional pharmaceutical agents? (5)
- PCA: patient can choose when to administer their doses of pain meds to a certain point (IV)
- Celiac plexus block: the celiac plexus is a group of nerves that supply the organs in the abdomen. Here, the pain medications are ineffective. So we deactivate the nerves through a procedure. Used commonly with pancreatic cancer patients.
- Intrathecal pain pump: similar to insulin pump. It’s implanted into pt spine. Used in pts who are refractory to other opioid therapy or increased toxicities. The meds are way more potent through this route (300:1)
- Radiation therapy: Can treat metastases.
- Bisphosphonate therapy
What is the pathophysiology of thrombosis in a cancer patient?
The tumor cells can produce procoagulants and fibrinolytic activity. This directly increases blood clotting through thrombin & fibrin formation. Additionally, adhesion receptors are expressed that release cytokines and angiogenic factors. This activates host cell procoagulant and pro-adhesive cells. Both of these processes together result in a hyper-coagulable state.
What are some risk factors for VTE in cancer (patient and cancer, treatments, modifiable)
Patient and Cancer:
- Active cancer
- Advanced stage cancer
- Cancer type
- Older age
- Poor performance status
- Medical co-morbidities
Treatment:
- Major surgery
- Central venous catheter
- Chemotherapy
- Exogenous hormone therapy
- ESAs
Modifiable Risks:
- Smoking
- Obesity
- Activity level
What are the treatment options for anticoagulation therapy in patients with cancer?
Monotherapy: start pt on monotherapy for a minumum of three months, continue indefinitely while cancer is active, or if other risk factors persist. If catheter related, can stop after 3 months
- DOACs: preferred in pts w/o gastric or gastroesophageal lesions (low VTE recurrence, but these have higher relevant non-major bleeding)
- LMWHs: preferred in pts w/ gastric or gastroesophageal lesions
- Factor XA inhibitors:
- UFH
Combo therapy: minimum of 3 months, stop at 3 months if catheter related
- LMWH -> Edoxaban
- LMWF/UFH/Fondaparinux -> Warfarin
- If cannot have LMWH: LMWH/UFH -> Dabigatran
What are the standard screening guidelines and how do we apply those to specific cancers? (breast, prostate, colon, lung, cervical, melanoma)
Breast: breast self exam once 20 years old, annual mammogram from 45-54 (can start at 40), biennial mammograms at 55 years old
Prostate: Men at least 50yo, so annual screening if PSA is over 2.5 ng/mL, every 2 years if <2.5 ng/mL +/- digital rectal exam (DRE); High risk pts should start discussion at 45 years old
- 1º degree relatives with prostate cancer puts pt at higher risk, AA race, increasing age, abnormal DRE
Colon: screen once 25 years old regardless of male/female, colonoscopy every 10 years
- detect cancer: annual fecal occult blood test (FOBT) shows many false positives; annual fecal immunohistochemical test (FIT) also test Hb w/o the false +; FIT DNA tests Hb and DNA biomarkers
- detect cancer and advanced lesions: endoscopy/colonoscopy every 10 years
Lung: low dose CT scans - consider in pts age 55-74 w/ 30 year pack smoking history, still smoking or have quit w/in last 15 years, and willing to have curative lung surgery if detected
Cervical: No effective screening tool, just do annual physical and pelvic exam. If high risk, can start pelvic exams/ultrasounds every 6-12months starting at age 25-35.
Melanoma: examine your skin, high-risk pts can receive yearly clinical exams
What are the standard prevention guidelines across different tumor types? (breast, prostate, colon, lung, cervical, melanoma)
Breast: high risk patients (BRCA mutations) can talk about surgeries (prophylactic mastectomy, bilateral oophorectomy); tamoxifen decreases risk (some bad side effects), raloxifene decreases risk & both FDA approved
Prostate: finasteride decreases risk & is FDA approved
Colon: diet (high fiber, low fat, calcium rich), NSAIDs/ASA/celecoxib may decrease risk, but increased risk for bleeding, so we don’t really use.
Lung: Stop smoking
Cervical: oral contraceptives, prophylactic oophorectomy, have children
Melanoma: sunscreen >SPF 15, avoid tanning beds
What are the risk factors for developing breast cancer?
- Risk increases with age
- family history (& BRCA-1 and 2)
- previous breast cancer
- radiation from prior treatment for environmental radiation exposure
- estrogen exposure endogenously or exogenously
- alcohol
- prior breast biopses with proliferative histology
- last first birth (>30yo) or never having kinds
- elevated BMI
- Diet
*more than 60% of pts will not have any risk factors
How does breast cancer staging dictate our goals for their therapy?
*adjuvant = therapy after surgery; neoadjuvant: therapy before surgery
Stage I, II, IIIA - our goal is to cure. Surgery is involved. Some II and IIIA patients will do neoadjuvant therapy (larger tumors). Most patients will do adjuvant therapy.
Stage IV (metastatic): Goal is no longer to cure. Treatment is palliative and mostly involves chemo, hormonal, +/- biologics, +/- immunotherapy. Surgery only used for symptomatic relief.
What are the therapies we have for breast cancer? (hormonal (3 classes), chemotherapy (3 classes), biological, radiation, surgery)
hormonal therapy:
- tamoxifen: SERM, remember DVT and endometrial cancer adverse effects
- Leuprolide, Goserelin: LHRH analogs, use in premenopausal women (ovarian suppression)
- letrozole, anastrozole, exemestane: use in post-menopausal women (or use ovarian suppression if premenopausal), watch out for osteoporosis
chemotherapy:
- doxorubicin: anthracyclin (cardiotoxicity)
- cyclophosphamide: alkylating agent
- paclitaxel: taxane (microtubule inhibitor)
biological therapy
- trastuzumab (don’t use with doxorubicin due to cardiotoxicity)
- pertuzumab
- CDK4/6i: abemaciclib, palbociclib, ribociclib
radiation
surgery
how do we decide treatment for hormonal therapy in breast cancer?
If tumor is small (≤0.5cm): hormonal therapy
- if HER2 positive, give HER2 targeted therapy
if tumor is bigger than 0.5cm or 1-3 pos nodes, do the oncotype dx test:
- if low risk (<26), pt needs hormonal therapy only
if high risk (≥26), pt needs hormonal and chemo
- if HER2 positive, give HER2 targeted therapy
if pt is premenopausal at diagnosis, we will likely give aromatase inhibitors + ovarian suppression for 5 years. At the 5 year mark, we may do an additional 5 years. (could also do tamoxifen)
if pt is postmenopausal at dx, we will likely give aromatase inhibitor for 5 years, then maybe another 5 years
how do we decide the chemotherapy regimen for breast cancer? (treatment for HER2- disease)?
if tumor is bigger than 0.5cm or 1-3 pos nodes, do the oncotype dx test:
- if low risk (<26), pt needs hormonal therapy only
if high risk (≥26), pt needs hormonal and chemo
- if HER2 positive, give HER2 targeted therapy
adjuvant chemo longer than 3-6 months does not improve survival
in HER 2 negative disease:
- Dose dense AC -> Paclitaxel: doxorubicin, cyclophosphamide, followed by paclitaxel (dose dense gives same amount of chemo in a shorter time, which is good)
- If heart disease - TC: docetaxel, cyclophosphamide
What 3 medications do we need to administer with paclitaxel? What happens if they have had a hypersensitivity reaction to paclitaxel before?
- dexamethasone
- antihistamine
- famotidine
give albumin bound paclitaxel to mitigate the hypersensitivity reaction
what treatment regimens can we use for HER2 + breast cancer?
want to do 1 full year of HER2 targeted therapy
APT: (adjuvant)
- paclitaxel
- trastuzumab w/ first dose of paclitaxel
- trastuzumab weekly
TCH:
- docetaxel
- carboplatin
- trastuzumab
TCH + pertuzumab:
- docetaxel
- carboplatin
- traztuzumab
- pertuzumab
*if residual disease found after surgery, can switch to ado-trastuzumab, just need HER2 therapy to be 1 year long total
how can we treat triple negative breast cancer?
HER2 -, ER - , PR -
Immunotherapy - pembrolizumab (PD1 inhibitor) added into chemotherapy regimen
AC -> Paclitaxel
- doxorubicin
- cyclophosphamide
- pembrolizumab (for total of 1 year)
how can we treat metastatic breast cancer? (ER/PR+, bone mets, asymptomatic visceral disease VS ER/PR-, symptomatic visceral disease, or hormone refractory) What are the 1st line options for HER2- & post menopausal/premenopausal w/ovarian suppression?
Our goal shifts from cure to palliative care. Survival time can vary based on where the cancer is (bone and soft tissue metastases usually have better prognosis).
ER/PR+, bone mets, asymptomatic visceral disease: Hormone therapy (aromatase inhibitor + CDK-i) (if bone disease, add bisphosphonate or denosumab) OR clinical trials
ER/PR-, symptomatic visceral disease, or hormone refractory:
- If HER2+, use anti-HER2 therapy +/- chemo: docetaxel, trastuzumab, and pertuzumab OR paclitaxel, trastuzumab, and pertuzumab
- If HER2-, do chemo
What are the risk factors for prostate cancer?
*testosterone is a growth signal to the prostate, so if something increases exposure to testosterone, it’ll increase risk of prostate cancer
- age (typically ≥60 yo)
- african-americans
- family hx
- potentially diet, occupation
What are 5 signs/symptoms of advanced prostate cancer?
- alterations in urinary habits
- impotence
- lower extremity edema
- weight loss
- anemia
**early stage will likely be asymptomatic
What is used to grade prostate cancer? What PSA requires evaluation & what PSA is highly suspicious for malignancy?
Gleason score (2-10)
- 2-4 are slow-growing, well differentiated
-8-10 are aggressive, poorly differentiated
PSA:
>4ng/mL requires evaluation
>10ng/mL is highly suspicious for malignancy
*also look at velocity, if increase is >0.75 per year, that’s suspicious
How do we treat localized prostate cancer?
Observation - Watch and wait. If they start developing symptoms, we can treat palliatively.
- Good for an older man (don’t want to be too aggressive for no reason)
Active surveillance - Watch and wait. If PSA starts to go up, we are going to treat with curative intent.
Radiation - external beam (radiation from the outside in) VS. brachytherapy (radiation pellets placed around prostate. This method comes with side effects and complications (ex. rectal symptoms, ED, etc.)
Adrogen Deprivation Therapy - Use with radiation if pt is high risk. Use an LHRH agonist +/- antiadrogen (abiraterone, bicalutamide, etc.)
Prostatectomy - definitive curative therapy. Very effective, but comes with potential complications.
What are the differences between m0HSPC, m0CRPC, m1HSPC low volume, m1HSPC high volume, and m1CRPC?
m1 = metastatic found on scans
m0 = PSA is going up, but we can’t find it on the scans
HSPC = hormone sensitive prostate cancer
CRPC = castrate resistant prostate cancer (failed hormone therapy)
m1HSPC low volume = 1-2 mets
m1HSPC high volume = numerous mets
How do we treat m0HSPC?
first line - palliation of disease. We want to suppress testosterone production and determine the PSA doubling time (if it doubles fast, we have progressing disease)
m0HSPC - consider ADT if the PSA doubling time is less than 6 months. Can use LHRH agonists (these are reversible and as effective as orchiectomy). Also can do orchiectomy (now we no longer need LHRH agonist).
- can do intermittent ADT, where we stop ADT once we lower the PSA, then start again when the PSA rises again. This can decrease side effects & cost, and it’s just as effective. This is only if we have increasing PSA but we can’t find mets on a scan!!
How do we treat m0CRPC?
This is when the PSA is still increasing, but it is not responding to ADT and there’s no distant metastasis found.
- continue ADT (usually LHRH agonist)
- Add anti-androgen
- enzalutamide: unique toxicities like causing falls, decrease seizure threshold, “enzalutamide syndrome” that causes brain fog/confusion
- apalutamide: risk for seizures, falls, etc.
- darolutamide: structurally different, so it has less adverse effects. Less seizures or falls.
**abiraterone is not approved for m0!!!!
What are the LHRH agonist options that we can use for metastatic prostate cancer? What are the acute and long term toxicities associated with these?
Leuprolide, Eligard, Goserelin, Triptorelin, Histerelin
*no one is better than another, just go based off of what gets paid for by insurance
Relugolix - oral agent!! With less cardiovascualr events!
Acute toxicities: tumor flare (give with another med (anti-androgen like bicalutamide) to reduce the flare), gynecomastia, hot flashes, ED, edema, injection site reaction
Long term: osteoporosis, fracture, increase in fat mass, insulin levels, and cholesterol/triglycerides
How do we treat m1HSPC?
Therapy is determined based on the volume of disease.
- Low volume: ~1-2 mets
- High volume: numerous mets
Low volume:
1. ADT
2. Continue ADT and add abiraterone+prednisone, enzalutamide, or apalutamide
- abiraterone relatively well tolerated, considered better than enzalutamide. Not the best in adrenal insufficiency
High volume:
- could do anything that was previousy mentioned (ADT), but now chemo is an option
- ADT + abiraterone + prednisone
- ADT + enzalutamide
- ADT + apalutamide
1. docetaxel + ADT
- can do ADT + docetaxel + abiraterone/darolutamide
How do we treat m1CRPC?
- continue ADT
- want to maintain castrate testosterone concentrations
- Sipuleucel-T (but $$$, so not used a lot)
- docetaxel (alone or in combo w/ abiraterone or darolutamide)
- Cabazitaxel (unlike other taxanes)
- more options
*can do bisphosphonate or radium 223 for bone metastases. causes lots of myelosuppression though. Do radium 223 after trying bisphosphonate
What are the common risk factors and etiology of lung cancer? What are the important mutations?
- Smoking
- Asbestos exposure
- Heavy metals/ionizing radiation
- Genetic predisposition
Etiology: chronic exposure of epithelial cells to carcinogens, which results in chronic inflammation. This induces genetic and cytologic changes, which eventually leads to carcinogenesis.
Mutations:
- EGFR: mutation predicts sensitivity to tyrosine kinase inhibitors
- K-RAS: mutation predicts resistance to our tyrosine kinase inhibitors
- ALK: will likely be less sensitive to EGFR inhibitors and chemo
- ROS-1
- BRAF V600E
*pts with EGFR mutations or ALK/ROS-1 rearrangements typically don’t have PD1 expression
What is the difference between non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC)?
Non-small cell: slower growth fraction. Moderately sensitive to radiation, marginally sensitive to chemo.
- adenocarcinoma: (50%) most common in non-smokers
- squamous: (30%) clearly related to smoking
Small cell: (15%) related to smoking. Fast growing and rapidly progressive. Highly sensitive to radiation and chemotherapy
