By popular demand, our next series that we are excited to share with you is on MDS/AML! As we prepare for the release of the first episode next week, let’s throw it back to Episode 019 in our Heme/Onc Emergencies Series and talk about APL!

Episode contents:

- How do we diagnose APL?

- What are characteristic findings of APL?

- What is the acute management of this disease?

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** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we have an INCREDIBLE episode for you. We welcome Titilope Fasipe, MD, PhD, who not only is the Co-Director of the Sickle Cell and Thalassemia Program at Texas Children’s and an Assistant Professor in the Department of Pediatrics at the Baylor College of Medicine, she herself also has sickle cell disease! Dr. Fasipe takes us through her life story, from childhood to now. Conducting this interview was such an eye-opening experience for us, and we hope that her message resonates with you when you care for your patients with sickle cell disease.

Contents:

- What it is like growing up with sickle cell disease?

- Pearls to ensure that our practice provides excellent care for our patients with SCD

- Important resources when caring for patients

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An exciting new academic year is about to begin. We know this can be daunting, especially for our newest hematology/oncology fellows. Over the next two weeks, we re-boot some of our high yield episodes you need to know to prepare for your first days as a new fellow and your nights on call. 

Next up: Heparin-induced thrombocytopenia! [Originally episode 071]

Contents:

- What is HIT? How is this different than HITT?

- How do we make this diagnosis?

- How do we treat HIT/HITT?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We have now covered the fundamentals of pharmacology. This week, we sit down with Renee McAlister, PharmD, BCOP to learn more about the nuances of pharmacology from an expert that does this day in and day out.

*The products/resources we share are our OWN opinions. Naming of resources are not endorsements. We are not sponsored by any of these entities.

Pharmacology Capstone:

* Irritant vs. Vesicant:

** For extravasation, what to do?

*** Not a great general source; would recommend checking institutional guidelines.

*** Different drugs may require a cold vs. warm compress.

*** Some drugs have antidotes - it is best to just look this up when it happens

* Why is there a “cut off time” to get in chemotherapy orders?

** Many hospital pharmacies are not 24 hours, therefore need prep time.

** Many drugs take a long time to prepare!

** A lot verification goes into ensuring that the drugs are correctly ordered, prepared, and handled. Therefore this requires adequate staff to do this safely.

* What does "ideal body weight” mean?

** Calculated by the patient’s sex, height, and the calculated body weight based on this information

** Helps with drug-dosing to ensure that drugs are not over/under-dosed

* What does “AUC” mean?

** Incorporates renal function and the amount of exposure you want the patient to have to the drug. Based on the Calvert equation.

** It is important to re-calculate each time with a new Cr to ensure that this is updated.

** Example: https://reference.medscape.com/calculator/169/carboplatin-auc-dosing-calvert

* What is the role of granulocyte colony-stimulating factor (GCSF)?

** Helps to prevent the risk of infection, especially from endogenous bacteria.

** GCSF helps to minimize the window of neutropenia related to treatment with chemotherapy

** NCCN guidelines (www.nccn.org) provides guidelines about febrile neutropenia risk. A risk >20% means that we build in GCSF administration into the treatments.

*** If risk 10-20% with certain risk factors, we may consider adding GCSF

*** Always look at the paper that was what the approval of the regimen was based off of - they will comment on if/how GCSF was used during the study.

*** If patient develops neutropenic fever during a cycle, if even the drug is not traditionally one that we consider GCSF for, it would be appropriate to consider GCSF for future cycles to decrease the risk of febrile neutropenia.

* What are the different “types” of GCSF?

** Examples:

*** Filgrastim (“Neupogen”) - daily dosing, short-acting GCSF

*** Pegylated-filgrastim (“Neulasta”) - don’t have to give daily dosing; one time shot because it lasts for longer

*** On-body injector (OBI) - a device put on the arm that delivers pegylated- filgastrim at approximately 26 hours after chemotherapy

** Dosing: Very different dosing for all of these medications; pay attention to the dosing!

* Supportive care:

** How do you decide what anti-emetics to include?

*** NCCN supportive care guidelines is a great place to start

*** Regimens with >90% emetic potential should get at least three agents (for example: ddACT, cisplatin based regimens)

**** Example: 5-HT3 receptor antagonists, dexamethasone, olanzapine, and aprepetant

*** Moderate emetic potential (30-90%), add at least 2 drugs

**** Example: 5-HT3 receptor antagonists and dexamethasone

*** Lower risk (30%): usually one one drug

**** Example:5-HT3 receptor antagonists

** If patients have refractory nausea in a cycle, add another agent. When adding drugs, always ensure you are incorporating the patient’s other medical history AND drug-drug interactions

* Pharmacists are an amazing source of information! Please reach out with questions!

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Picture this: it's day 1 of fellowship and your attending needs you to "get consent for treatment." Huh? How do you educate your patient? We share our tips!

In this episode, we discuss important considerations, including “does my patient need a port?”, “what if drugs extravasate?”, “how do I keep side effects of drug classes straight?!”

*The resources we share are our OWN opinions. Naming of resources are not endorsements. We are not sponsored by any of these entities.

Pharmacology 101:

* Irritant vs. Vesicant:

** Each drug is deemed one of these based on the degree of tissue damage that can result if drug extravasates under skin. 


** Vesicant: needs central access


** Irritant: can be given peripherally 


* Does my patient need a port/picc?

** If vesicant; for continuous infusions over several days (e.g. 5-FU); some patients with difficult access may request. 


*Advantages of ports:

** Easy access for labs


** Easy access for chemotherapy/fluids


* Disadvantages:

** Risk of infection


** Risk of thrombosis 


* General overview of chemotherapy side effects:

** Going to target the fastest growing cells in the body, which includes cells that line the GI tract, skin, hair/nails, and blood cells


** Therefore side effects are related:

*** GI: nausea/vomiting, diarrhea (sometimes constipation), decreased appetite, taste changes


*** Low blood counts

**** WBC nadir ~10-14 days (generally), and recover 21-28 days after chemo


* What about unique side effects of chemotherapy classes? How do we keep them straight?

** We love keeping “Chemoman” from the USMLE study days in mind!


* Anthracycline

*** MOA: Topoisomerase inhibitors


*** Ends in “rubicin”


*** You might hear people call doxorubicin the “red devil”


*** Used in lots of cancers


*** Hair loss occurs with this one


*** Known to cause cytopenias and associated with higher nausea potential 


*** Unique side effects:

**** Heart failure (always get baseline echo!)


**** Development of MDS and leukemia 


* Alkylating agents

** MOA: Drugs add alkyl group to the guanine base of the DNA molecule, preventing linking of strands


** End in “fosfamide”


** fosfamide or cyclophosphamide (AKA cytoxan)


** Used in lots of cancers


** Known to cause cytopenias and hair loss


** Unique side effects:

*** Secondary MDS or leukemia possible 


*** Ifosfamide = neurotoxicity = methylene blue antidote


*** Cyclophosphamide = hemorrhagic cystitis due to acrolein byproduct accumulation = prevent by giving mesna to protect bladder


* Antimetabolites

** MOA: Purine analog, pyrimidine analog, folate antagonists; therefore prevent production of base pairs or binds instead of normal base pairs


** End in “abine” - capecitabine, cytarabine, gemcitabine, cladribine, fludarabine


** Also 5-FU and 6-MP in this category so “number followed by dash”


** Unique side effects:

*** Think bone marrow suppression in this category  


* Platinum agents

** MOA: Believed to cause cross-linking of DNA


** End in “platin”


** Associated with high risk of neuropathy 


** Unique side effects:

*** Cisplatin:

**** Nephrotoxicity 


**** Ototoxicity 


**** High risk of nausea; need special prophylaxis 


*** Carboplatin: cytopenias


*** Oxaliplatin: higher rates GI side effects 


* Microtubule agents

** MOA: Impair microtubule function, therefore impacting cell division


** End in “taxel” or vincristine/vinblastine (“V-stine”)


** Unique side effects: Neuropathy


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Picture this: it's day 1 of fellowship and your attending needs you to "get consent for treatment." Huh? How do you educate your patient? We share our tips!

In this episode, we discuss the fundamentals and some of our favorite resources.

*********The resources we share are our OWN opinions. Naming of resources are not endorsements. We are not sponsored by any of these entities. *********

1) How do you know what regimen to use for a disease?

* www.NCCN.org :

** National Comprehensive Cancer Network

** Free resource, but need to make an account!

** Provides stepwise approach to workup, choosing a regimen, and surveillance information, treatment for refractory disease

* www.HemOnc.org :

**Organized by disease type with long lists of treatment options

** Provides a breakdown of regimen, but also provides the primary literature that lead to the regimen’s approval for use!

**We cannot highlight how important it is to remember to check out the primary literature!

2) Patient education: Use these to drive discussion; you still want to walk your patients through these

* www.Oncolink.org : Ronak’s favorite resource

* www.Chemocare.com : Vivek and Dan’s favorite resource

3) Basic Terminology:

* Cycle: The number of days between one round of treatment until the start of the next; abbreviated with “C”

* Days: Counts the actual days within a cycle; abbreviated with “D”

* Example: C1D1: Cycle 1 of a regimen, day 1 of this cycle

4) Dosing:

* Always have updated height and weight for patients

** Many drugs are dosed based on body surface area (BSA)

** Other drugs use area under the curve (AUC)

* Always get a CMP and CBC prior to giving treatment

5) General categories of cancer therapies:

* Cytotoxic: Kills cells in the body

** Analogous to antibiotics killing bacteria

** Relatively non-specific in terms of what cells they target; but they’re often specific for parts of the cell replication cycle

* Immune therapy: Harness the immune system to attack cancer

** More specific than cytotoxic agents

* Targeted therapy: Drugs made specifically for known mutations

** A cancer with a distinct mutation in a protein is then a target for this drug

** In general:

***“Mab”- antibody targeted for phenotypic expression

***“ib”- small molecule for driver mutation

** Targeted cytotoxic chemotherapy: a monoclonal antibody specific for a mutation linked to very potent chemotherapy

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further.

In this episode, we’ll talk about one of the key hematologic malignancies that you’ll encounter as a fellow, one that requires immediate action to reduce mortality: acute promyelocytic leukemia (APL or APML)

- Acute Promyelocytic leukemia (APL or APML):

**Stay tuned for our upcoming “part two” and “chemotherapy basics” episodes for more information on non-acute management of this disease

**APL is a true hematologic emergency! Although this is a very curable form of leukemia, it is associated with high rates of severe DIC and high mortality in the period immediately following diagnosis

***Untreated, can see pulmonary or cerebrovascular hemorrhage in up to 40% of patients

***10-20% incidence of hemorrhage-related mortality in the initial period

***Statistically significant increase in mortality at 30 days with just a 12-hour delay in initial hematologist consultation

- Disease basics:

** Rare subtype of AML( <10% of cases)

** Driven by translocations involving the retinoic acid receptor alpha (RARA) on chromosome 17, classically with the promelocytic leukemia gene (PML) on chromosome 15 [i.e. t(15;17)]

***Other non-classical translocations exist, but nearly all involve RARA

**Because of this driver mutation, treatment with a specific isoform of vitamin A: all-trans retinoic acid (ATRA) forces promyelocytes to differentiate and ultimately apoptose 

- Initial work up:

**Standard CBC with differential, CMP

** Review smear for characteristic features:

** Large nuclei and scant cytoplasm

** “Folded” appearance to nuclei (like a peach emoji 🍑)

** Auer rods (which tells you blasts are myeloid lineage)

** Heavily granulated cytoplasm (hypergranular form - most common)

***Also a “hypogranular variant,” so like always, make sure to discuss any findings with your friendly neighborhood hematopathologist

**Stat DIC labs:

**PT/aPTT

**Fibrinogen

**Stat PML-RARA FISH (see next section) to look for classic driver mutation and clinch diagnosis

** “Tumor lysis syndrome (TLS) labs”

***LDH

*** Uric acid

**Peripheral flow cytometry

***CD33+, CD 117+

***CD34-, HLA-DR-, CD11a/b/c-

*** Increased side scatter (esp in hypergranular type)

- Acute Management

** Start ATRA: immediate treatment is so important in this disease, and side effect profile is minimal enough that empiric treatment when disease is on the differential is standard of care

**Correct coagulopathies as you detect them 

***Keep fibrinogen > 110 mg/dL

*** Keep INR < 2.0

*** Keep plt > 30k/uL

References:

Gulam Abbas Manji, Samira Khan Manji, Sheetal Karne, and Jeff Chao “Time to ATRA in suspected newly diagnosed acute promyelocytic leukemia and association with early death rate at a non-cancer center institution: Are we meeting the target?” Journal of Clinical Oncology 2012 30:15_suppl, 6615-6615 - impact of treatment delay on 30-day mortality

Eytan M. Stein, Neerav Shukla, Jessica K. Altman “Chapter 20: Acute Myeloid Leukemia” section on acute promyelocytic leukemia ASH SAP 7th Ed pp588-590. DOI: 10.1182/ashsap7.chapter20

Warrell RP Jr, de Thé H, Wang ZY, Degos L. Acute promyelocytic leukemia. N Engl J Med. 1993 Jul 15;329(3):177-89. doi: 10.1056/NEJM199307153290307. PMID: 8515790. - Great review of the basics in NEJM from the early 2000s

Sanz MA, Fenaux P, Tallman MS, Estey EH, Löwenberg B, Naoe T, Lengfelder E, Döhner H, Burnett AK, Chen SJ, Mathews V, Iland H, Rego E, Kantarjian H, Adès L, Avvisati G, Montesinos P, Platzbecker U, Ravandi F, Russell NH, Lo-Coco F. Management of acute promyelocytic leukemia: updated recommendations from an expert panel of the European LeukemiaNet. Blood. 2019 Apr 11;133(15):1630-1643. doi: 10.1182/blood-2019-01-894980. Epub 2019 Feb 25. PMID: 30803991. - Updated treatment guidelines (more on this in “Part 2” to come)

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our fourth hematologic emergency: thrombotic thrombocytopenic purpura (TTP).

Thrombotic thrombocytopenic purpura (TTP):

- Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!

- New anemia and thrombocytopenia should raise concerns for TTP!

Workup:

- Peripheral smear - concern for schistocytes. Look at this first! Example of these cells from ASH image bank here

- ADAMTS13 level - always draw ASAP before any intervention

- Repeat CBC

- Reticulocyte count - will have elevated retic count

- Citrated platelet count

- CMP

- PT, PTT, INR

- Fibrinogen

- Haptoglobin

- LDH

- Viral serologies

Clinical manifestations:

- Fever, Anemia, Thrombocytopenia, Renal (AKI), Altered Mental Status

- If you see this - the patient is in bad shape

Mechanism:

- Tiny blood clots form in the body, causing platelet shearing

- Loss of ADAMTS13 - This protein normally is responsible for chopping up von Willebrand’s factor (vWF)

- In the absence of ADAMTS13, vWF multimers are extra long, therefore interacting with platelets/collagen more and causing activation of platelets and clotting system

- This causes red blood cell shearing due to small vessel microthrombi (brain, kidneys, heart)

- Cytokine release causes fevers

Management:

- Do not reflexively transfuse platelets; can make situation worse

- PLASMIC Score: helps to stratify likelihood of TTP; MDCalc link (https://www.mdcalc.com/plasmic-score-ttp)

Treatment:

- Plasma exchange: replacing ADATMS13-deficient plasma with ADAMTS13-rich plasma

- This is different than plasmapheresis, where we replace plasma with albumin

- Steroids: 1mg/kg prednisone daily to stop auto-antibody (against ADAMTS13) production

- Confirm with ADAMTS13 levels; if <10%, this is confirmatory. This is why this is the FIRST step that we just send off as soon as TTP is suspected

- IF YOU DON’T HAVE ACCESS TO PLASMA EXCHANGE: can administer FFP until you can get them to a center than can do plasma exchange

- Caplacizumab: reserved for patients with severe neurological dysfunction, stroke, or myocardial infarction. Check out the NEJM paper on this (below)!

Microangioathic hemolytic anemia (MAHA):

- Umbrella term for red blood cells shearing in the small blood vessels; TTP is one example of a MAHA

References:

https://ashpublications.org/blood/article/129/21/2836/36273/Thrombotic-thrombocytopenic-purpura - great review article from ASH on TTP

https://www.nejm.org/doi/10.1056/NEJMoa1806311 - NEJM paper on caplacizumab

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our third hematologic emergency: heparin-induced thrombocytopenia (HIT)!

Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!

HIT:

- Any time a patient with heparin exposure and now with a new thrombotic event, you need to think about HIT!

What is HIT?

- Type 1: a transient drop in platelets after heparin is started

- Type 2:

**The scary one! Antibody-mediated process

**Heparin molecules bind to platelet-factor 4 (PF4)

**This complex activates platelets, which then further releases more PF4 from the platelets

What is the difference between HIT and HITT?

- HITT is when there is also thrombosis (HIT + Clot)

Why is this more common in the cardiac ICU?

- It is believed that IgM interacts with ultra-long complexes, which heparin is

- Lots of heparin is required for cardiac surgery

- Therefore lots of exposure to heparin increases likelihood, increasing likelihood for IgM to IgG class-switching; HIT is IgG-mediated process

** Remember - since this is antibody-mediated, therefore it takes a few days for the antibodies to form in patient with a new diagnosis of HIT!

How to stratify?

4-T score (MDCalc Link: https://www.mdcalc.com/4ts-score-heparin-induced-thrombocytopenia)

Workup:

- Sent HIT ELISA test in patient with high suspicion

- ELISA just suggests if the HIT antibody is present

- If ELISA positive, then do confirmatory assay, i.e., is this antibody actually doing anything, is the "serotonin-release assay”

- Send 4 extremity dopplers to look for thrombosis

- STOP heparin/heparin-derived products and SWITCH anticoagulant, such as argatroban, fondaparinux, bivalirudin (do not wait for a positive test if your suspicion is high enough!)

If HIT positive:

- Add heparin to their allergy list

- Continue anticoagulation until platelets are recovered (>150K)

- Continue anticoagulation for 3-6 months for patients with HITT

Words of wisdom: If patient comes from outside hospital and starts having decreasing platelets, consider HIT in your differential!

References:

https://ashpublications.org/blood/article/119/10/2209/29530/How-I-treat-heparin-induced-thrombocytopenia- great review article from ASH on HIT

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our second hematologic emergency: disseminated intravascular coagulation (DIC) with an added bonus of an intro to thrombotic microangiopathic anemias (TMAs).

Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!

Disseminated intravascular coagulation (DIC):

Workup:

CBC

CMP

PT, PTT, INR

Fibrinogen

Peripheral smear - concern for schistocytes. Example of these cells from ASH image bank: https://imagebank.hematology.org/image/60306/schistocytes?type=upload#:~:text=A%20schistocyte%20is%20present%20in,angles%20and%2For%20straight%20borders.

Basic mechanism of DIC is consumption of clotting factors leading to coagulopathy

Need to be weary of thrombotic microangiopathy: Small blood clots forming in the small vessels leading to endothelial damage, which cause shear stress on the RBCs, which then break down into a schistocyte (AKA triangulocyte or helmet cell)

Examples: thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)

Management (our opinion!):

- Repeat coags q4-6 hours initially (but base interval based on patient) NOTE: INR Is NOT a good assessment of “clotting status” in these situations

- Repeat fibrinogen q4-6 hours initially (but base interval based on patient); keep fibrinogen >100 with cryoprecipitate in more stable patients; consider higher thresholds for more acutely ill patients (such as >150)

- Repeat CBC q6-8 hours initially; can provide platelets if low, especially if they are bleeding

- Workup and treatment for trigger of DIC (infection, trauma, medications, etc.)

How does cirrhosis affect data interpretation?

- Use clinical context to determine if labs are acutely abnormal or if they have signs/symptoms to suggest underlying liver dysfunction

- In the acute setting, always just replace what is missing!

How can you tell the difference between nutritional deficiencies vs. consumption (as in with DIC?)

- Factor activity levels! Consider checking: Factor 8 (made in endothelium), Factor 5 (Vit K independent), Factor 7 (vitamin K dependent)

- If all down, then consider DIC

- If Vit K-dependent low, then nutritional deficiency

Reference:

https://ashpublications.org/blood/article/131/8/845/104418/How-I-treat-disseminated-intravascular-coagulation - Great How I Treat article from Blood

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our first hematologic emergency: immune thrombocytopenic purpura (ITP).

Immune thrombocytopenic purpura (ITP):

Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!

Specific instances where there may be close to undetectable platelet count:

* Lab artifact (clumping)

* Very severe DIC

* Thrombotic thrombocytopenic purpura - though usually higher platelets in these cases

* Heparin induced thrombocytopenia (in very severe cases) - though usually higher platelets in these cases

* ITP

ITP: Diagnosis of exclusion

How to confirm it is ITP?

* Post-transfusion CBC - a repeat CBC 30-60 mins after a platelet transfusion. In ITP, the platelet count will likely not budge. (Not perfect test!)

* Immature platelet fraction (if available) - this will be elevated if mature platelets are being destroyed. (Again - not a perfect test)

Treatment in acute cases:

IVIG 1g/kg daily x2 days + Dexamethasone 40mg daily x4 days

Reference:

https://ashpublications.org/blood/article/106/7/2244/21649/How-I-treat-idiopathic-thrombocytopenic-purpura - Great How I Treat article from Blood

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our third oncologic emergency: new brain mets.

Cord compression:

- If someone has a pathologic fracture, think about the following differential as underlying etiologies:

- Females: rule out breast cancer

- Males: Prostate cancer

- Others: multiple myeloma, lymphoma, lung cancer, renal cell carcinoma, bladder

- If cord compression, administer steroids; may require radiation to help with shrinking; also may need involvement of neurosurgery if there is lack of spine stability.

Role of radiation in cord compression:

-MRI is beneficial to help with radiation planning

-Where is the disease in proximity to the spinal cord? In the bone? In the epidural space? Or pushing against the spinal cord +/- blocking CSF?

-Is the spine stable? Use SINS scoring (https://radiopaedia.org/articles/spinal-instability-neoplastic-score-sins-2?lang=us)

-If good spine stability (low SINS) or is not surgical candidate or radio-sensitive tumor: radiation up front

-If poor spine stability (high SINS) then may need surgery up front

Radiosensitive tumors examples:

Lymphoma

Germ cell tumors

Small cell lung cancer

Radio-resistant tumor examples (resistant does not mean that radiation cannot be used, however):

Melanoma

Colorectal

Renal cell

Continue steroids as they are undergoing radiation to prevent flare up from inflammation and acute worsening from the mass on the spinal cord

Role of neurosurgery:

- What is a reasonable time that we can wait before operating for a new cord compression?

- As noted above, cord compression has various degrees

- Questions to ask: What neurologic symptoms? Over what time period?

- Asymptomatic: You have time! Perhaps investigate why mass may be there.

- Progressive over a couple of weeks: You have a little bit of time (a few days to get them to surgery)

- Acutely having symptoms: You should intervene.

- Spinal stability: are the weight-bearing components (ligaments) intact? Assessed via upright X-rays

- If the tumor is radio-sensitive, may opt for radiation first (if diagnosis is known)

A HUGE thank you to our special guests:

Ryan Miller, MD, MS: PGY5 in Radiation Oncology at Thomas Jefferson University Hospital, Philadelphia, PA

Joshua Lowenstein, MD, MBA: Neurosurgery Attending, REX Neurosurgery and Spine Specialists, Raleigh, NC

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our second oncologic emergency: new brain mets.

Brain mets:

Strongly consider steroids, particularly with the presence of vasogenic edema associated with brain mets

Stereotactic radiosurgery (SRS): use of high dose radiation delivered in a single treatment (“fraction”) that is delivered focally to the area of disease seen on imaging (typically MRI); great option for brain mets; can be performed by radiation oncology

What to do to expedite Rad Onc planning:

Thin-cut MRI

Start patient on steroids

Interpreting MRI imaging:

T1 post-contrast sequence: to look for brain mass

T2 sequence: looking for vasogenic edema surrounding brain mass

Midline shift is an issue more so when it is acute; this is very different than slow changes over time

Who to operate on? Functional status prior to surgery; not in an area that can cause other harm; no other good alternative treatment options

What to tell your NSGY colleague during a consult:

A quick neuro exam (consciousness, strength, sensation, focal neurologic issues)

Brief cancer history

Underlying organ dysfunction

Antiplatelet/anticoagulants

A HUGE thank you to our special guests:

Ryan Miller, MD, MS: PGY5 in Radiation Oncology at Thomas Jefferson University Hospital, Philadelphia, PA

Joshua Lowenstein, MD, MBA: Neurosurgery Attending, REX Neurosurgery and Spine Specialists, Raleigh, NC

Please visit our website (TheFellowOnCall.com) for more information

Twitter: @TheFellowOnCall

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An exciting new academic year is about to begin. We know this can be daunting, especially for our newest hematology/oncology fellows. Over the next two weeks, we re-boot some of our high yield episodes you need to know to prepare for your first days as a new fellow and your nights on call. 

Next up: Cord compression! [Originally episode 014]

Contents:

- Differential diagnosis

- What is the acute management?

- What other consultants need to be involved in decision-making?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

Love what you hear? Tell a friend and leave a review on our podcast streaming platforms!

Twitter: @TheFellowOnCall

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about first oncologic emergencies: superior vena cava (SVC) syndrome.

Superior vena cava syndrome:

Important: although we focus on a possible malignant mass in this discussion about SVC, other things can also cause SVC syndrome.

How do you know about the chronicity of someone’s possible SVC syndrome? Compare to a recent picture!

Image of patient with collateralization with SVC syndrome: DOI: 10.1056/NEJMicm1311911

Workup:

Need to determine the etiology; imaging is important:

CT of chest (CT venogram)

Consider ultrasound to rule out thrombosis

Get biopsy (eventually) if this is malignancy

DDx of mediastinal masses:

5Ts:

Thymoma

Terrible lymphoma (B or T-cell)

Testicular cancer

Teratoma

Thyroid malignancies

Central line (causing occlusion) +/- clot

So now what?

Yes, an answer to what is causing the issue is important, but we need to ensure that patient has a stable airway and temporize the situation

Often requires input of specialists, such as Interventional Radiology or Radiation Oncology

How to treat patients with SVC syndrome?

- Chemotherapy: Important in chemo-responsive tumors (ex. germ cell tumors, lymphomas, small cell lung cancer); This can take a while to work

-Placement of stents: Provides more immediate relief, but more invasive

-Radiation treatment: Not always possible

- Laryngeal edema/cerebral edema: steroids for life-threatening complications; Can affect diagnostic yield of sample and affect diagnosis, but may be required in emergent situations

When is more emergent treatment indicated and consultants definitely need to be called (TELL YOUR CONSULTANT IF ANY OF THESE ARE SEEN!):

Hemodynamic instability

Worsening respiratory status

Worsening neurological status

Final decision for what to do is often a multi-disciplinary discussion

Stents:

Provides quick relief

Does not prohibit a diagnosis and curative treatment for the underlying malignancy

Radiation:

Takes several days or weeks; depending on underling histology

If they have received prior radiation, they may not be eligible for more radiation

A HUGE thank you to our special guests:

Ryan Miller, MD, MS: PGY5 in Radiation Oncology at Thomas Jefferson University Hospital, Philadelphia, PA (https://www.jefferson.edu/university/jmc/departments/radiation_oncology/education/residency/residents/miller.html)

Rupal Parikh, MD: PGY6 in Diagnostic/Interventional Radiology at the Hospital of the University of Pennsylvania, Philadelphia, PA (https://www.pennmedicine.org/departments-and-centers/department-of-radiology/education-and-training/residency-programs/current-residents/ir-integrated-residents/ir-dr-fifth-year/rupal-parikh-md)

Please visit our website (TheFellowOnCall.com) for more information

Twitter: @TheFellowOnCall

Instagram: @TheFellowOnCall

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In our final stop in our Cytopenias series, we discuss the ins and outs of neutropenia. This is another very commonly seen issue in the clinic and in the hospital so most definitely high yield!

Why is neutropenia dangerous?

Prone to infections, especially gut translocation of bacteria

Definition of neutropenia:

NORMAL: WBC 4400-11000 cells/microL; neutrophils make up 40-70% of that

Neutropenia defined by ANC: WBC (cells/microL) x percent (PMNs  +  bands) ÷ 100 

Breakdown:

Neutropenia: ANC <1500 cells/microL

Mild: ANC ≥1000 and <1500 cells/microL

Moderate: ANC ≥500 and <1000 cells/microL

Severe: ANC <500 cells/microL

Agranulocytosis: ANC <200 cells/microL

Approach to workup: HISTORY IS KEY!

Medications; examples of common culprits-  

Chemotherapy 

Methimazole 

Clozapine 

Infections

Any infections due to bone marrow suppression 

Toxins 

Less common causes: 

Congenital

Severe congenital neutropenia:

Diagnosed in childhood; used to be fatal, but now patients living longer because of G-CSF support

10-30% risk of AML in lifetime

Mutations in neutrophil elastase (ELANE) gene or mitochondrial HAX1 gene 

Cyclic neutropenia:

Self-limiting neutropenia that occurs every 2-5 weeks

Spectrum of symptoms: none or oral ulcers/mild infections

Constitutional/ethnic neutropenia:

Mild neutropenia (ANC >1000)

No history of infections

More common in people of Mediterranean and African descent

Duffy Antigen Receptor Complex (DARC) gene mutations in patients of African origin

Benign Familial:

Mild neutropenia

Not linked to particular ethnic group

Unclear underlying etiology

Autoimmune

Primary autoimmune neutropenia rare in adults

Typically secondary autoimmune neutropenia

Due to underlying autoimmune disorder

Seen with SLE and can worsen with flare of disease

Typically mild, seldom needs treatment unless ANC <500

Felty syndrome:  

Rheumatoid arthritis, splenomegaly, and neutropenia

Neutropenia improves with treatment of RA 

Malignancy

Large granular lymphocyte (LGL) leukemia:

Often associated with RA and shares features of Felty syndrome (RA, splenomegaly)

Caused by monoclonal population of large granular lymphocytes

In contrast, in Felty’s: polyclonal or oligoclonal

T-cell LGL is more commonly associated with neutropenia

Requires treatment with methotrexate or cyclophosphamide

Dietary

B12 and folate rarely cause isolated neutropenia

Copper deficiency (gastric bypass): Zinc excess can cause copper deficiencies – ask about denture creams in your history!  

Workup:

History:

Prior CBCs

History of recurrent infections (pneumonia, sinusitis, skin/soft tissue, dental caries)

Ethnic background

Family history

Social history

Dietary history

Surgical history (gastric bypass)

Physical exam:

Adenopathy

Splenomegaly

Skin findings suggesting recent ulcers

Aphthous ulcers

example: https://en.wikipedia.org/wiki/Aphthous_stomatitis

Testing:

CBC with differential

CMP – assess liver and renal function 

Peripheral smear

HIV, Hepatitis serologies

Special scenarios

ANA – if autoimmune disease expected

RF – if autoimmune disease expected

ESR – if autoimmune disease expected; probably not great for inpatient workup

CRP – if autoimmune disease expected; probably not great for inpatient workup

Flow cytometry for LGL

Bone marrow biopsy – mainly for unexplained neutropenia to rule out neoplastic process, such as leukemia, lymphoma, myeloma; if longstanding, likely negative

Management:

Treat the underlying cause

Autoimmune neutropenia –

When to suspect? Workup is negative, but their counts still continue to worsen

Treatment if they have serious complications

Treat with rituximab

LGL-

Responds to low dose methotrexate or cyclophosphamide

Do you give G-CSF?

For patients with recurrent/severe infections or mucosal erosions

Do not treat based on the number alone

Takes time for the growth factors to work

References:

https://doi.org/10.1182/blood-2014-02-482612 - Great “How I Treat” article from Blood!

https://www.uptodate.com/contents/approach-to-the-adult-with-unexplained-neutropenia - UpToDate article written by same author as Blood article

Please visit our website (TheFellowOnCall.com) for more information

Twitter: @TheFellowOnCall

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We continue on our cytopenias journey, this time talking all about anemia. This is a high yield topic for anyone who sees patients, as this is something we will all see.

Determining the acuity of the anemia is the most important first step.

Acute drop in hemoglobin? Consider active bleeding or hemolysis. Dilutional anemia (a drop in hemoglobin following fluid resuscitation) is also on the differential but should be a diagnosis of exclusion.

Remember that we normally transfuse at a hemoglobin level of 7g/dL. If the patient has active cardiac issues, we transfuse at 8g/dL.

Anemia Severity

> 10g/dL = mild

7g/dL to 10g/dL = moderate

4.5g/dL to 7g/dL = severe, especially if acute

1g/dL to 4.5g/dL = these are almost always chronic if patients are conscious. Think about chronic blood loss or nutritional deficiency.

History: Ask about nutrition, melena, hematochezia. Note that a small amount of blood can change the color of the urine, so beware of contributing rapidly developing anemia to hematuria.

Physical Exam: Check the flanks and thighs for bruising. Feel for an enlarged spleen.

Work Up:

Smear—to evaluate for spherocytes, schistocytes, bite cells, etc.

LDH—will be markedly elevated if blood is actively hemolyzing

DAT/Coombs testing—to screen for AIHA, note that there is a high false positive rate

Type & screen

Haptoglobin—sensitive but non-specific marker for blood breakdown

Reticulocyte count

Macrocytic Anemia: Consider copper, B12, folate deficiency, reticulocytosis. Note that chronic zinc excess can cause copper deficiency.

Microcytic Anemia: Consider iron sequestration or deficiency, lead poisoning, thalassemia.

Normocytic Anemia: Usually multifactorial. Consider low erythropoietin level from chronic kidney disease or early iron deficiency anemia.

Please visit our website (TheFellowOnCall.com) for more information

Twitter: @TheFellowOnCall

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One of our most common consults in hematology is teams seeking guidance for workup and management of thrombocytopenia. In this episode, we cover our approach to this hematologic conundrum.

Major Points Covered:

Thrombocytopenia is defined as a platelet count <150K

- Mild: 100-150K

- Moderate: 50-100K

- Severe: <50K

- We get really worried when <20K (risk of spontaneous bleeding)

What to ask in history and in chart review:

- How quickly did the platelets drop - this is just as important as the absolute number; platelets may still be “normal” but have dropped significantly!

- Mucosal bleeding? Menstrual bleeding?

- Rashes?

- Infections/Meds/Toxins?

- Constitutional symptoms

- Weight loss

Our approach to a differential diagnosis - analogous to everyone’s favorite approach to renal AKI: “pre”, “intra,” and “post”:

Pre: Infections/Meds/Toxins

- 1st: HIV, Hepatits

- 2nd: EBV, CMV, Histoplasmosis

Intra: Primary bone marrow failure

Post: Destructions/consumption/splenomegaly (Cirrhosis, too)

- DIC

- ITP

- TTP

- Platelet clumping

Workup:

- Smear - helps to quickly rule in or rule out a lot of the post-BM issues that are emergencies!

- Citrated platelet count (to rule out platelet clumping)

- Repeat CBC

- Coags (PT/PTT/INR)

- Fibrinogen

- HIV serologies

- Hepatitis B/C serologies

- +/- Haptoglobin (note: in liver disease, you can have low haptoglobin)

- Don't send SPEP/IFE!

- If there is no abdominal imaging, consider abdominal ultrasound to evaluate for cirrhosis and/or splenomegaly

References:

https://www.sciencedirect.com/topics/medicine-and-dentistry/hypersplenism (Textbook of Gastrointestinal Radiology, 3rd edition 2008)- 90% of platelets in spleen at one time

https://pubmed.ncbi.nlm.nih.gov/29978544/ (J Thromb Hemostasis 2018)- Platelet threshold for bleeding risk

https://www.bjanaesthesia.org/article/S0007-0912(18)30753-0/fulltext#fig1 (British Journal of Anesthesia 2019)- Perioperative thrombocytopenia (Look at Figure 1)

https://ashpublications.org/blood/article/131/8/845/104418/How-I-treat-disseminated-intravascular-coagulation (Blood 2018) - DIC with normal fibrinogen (Look at case 1, Table 2 shows good diagnostic criteria)

Please visit our website (TheFellowOnCall.com) for more information

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Not to be confused with “carcinoma of unknown primary,” in this episode of metastatic disease of “origin TBD”, we discuss the workup of a mass noted incidentally on imaging. This is a very high yield topic often faced on solid oncology consults!

Major Points Covered:

Mass found incidentally on imaging → we need to stage always

Initial Workup:

Reasonable to get CBC, CMP, UA, PSA (if male)

Low blood counts, maybe marrow involvement

Cr elevated concern for obstruction possibly

LFTs elevated concern for mass in the biliary/pancreas region

UA w/ hematuria → maybe bladder

But bottom line you’re gonna get a scan, which scan to get though?

Recommend referencing NCCN guidelines to determine additional staging scans

Create an account on nccn.org and look at guidelines by tumor type

Not all cancers require a PET/CT scan

There are newer modalities for imaging other than FDG PET including PSMA PET (prostate), Auxumin PET (prostate), and DOTATE PET (neuroendocrine)

Certain cancers can be diagnosed on imaging alone (RCC and HCC)

Some cancers require Brain MRI for staging

What to biopsy?

FNA often adequate for solid tumors but may need core if non diagnostic

Need core or ideally excisional if highly concerned for lymphoma

Always try to biopsy the site that will upstage

Distant lymph nodes or other metastatic sites

What about tumor markers?

We use this for treatment monitoring, not for diagnostic purposes

Important to establish a baseline to follow, special circumstances for diagnostic purposes to consider below:

PSA in male if concerned about prostate cancer

AFP helpful if concerned for HCC → liver masses in a cirrhotic

AFP and b-HCG if concerned for testicular → young or middle aged male with mediastinal mass

Molecular testing not necessarily needed at the time of biopsy 

Please visit our website (TheFellowOnCall.com) for more information

Twitter: @TheFellowOnCall

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Heme Path Capstone Pt. 2 Pearls

In this episode, we continue our conversation with guest, Dr. Emily Mason, hematopathologist at Vanderbilt University Medical Center (Nashville, TN), as we apply all that we have learned in our Heme Path series. This time, we talk about a patient with a new leukocytosis, fevers, and easy bruising; and our approach to workup and management.

Reminder: While these episodes may seem a little more in-depth than the prior Heme Path episodes, simply break down the conversation into the components we have discussed already and you will be amazed at how much you actually know - we promise!

ELN Risk Stratification: https://www.researchgate.net/figure/ELN-2017-risk-stratification-of-AML-by-genetic-abnormalities-Adapted-from-Dohner-et_fig1_334634713

original paper: https://dx.doi.org/10.1182%2Fblood-2016-08-733196

Please visit our website (TheFellowOnCall.com) for more information

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Heme Path Capstone Pt. 1 Pearls

It’s time to put all you have learned in our Heme Path series to the test! Listen in as our guest, Dr. Emily Mason, hematopathologist at Vanderbilt University Medical Center (Nashville, TN) sits down with us to discuss the approach to diagnosis and workup of a new enlarged lymph node.

While these episodes may seem a little more in-depth than the prior Heme Path episodes, simply break down the conversation into the components we have discussed already and you will be amazed at how much you actually know - we promise!

Please visit our website (TheFellowOnCall.com) for more information

Twitter: @TheFellowOnCall

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Molecular Testing Pearls

In Part 4 of our Heme Path series, we thoroughly examine the details of molecular testing and how it relates to hematologic and oncologic malignancies

I. Molecular Testing Basics

A. Provides a means of assessing patient’s genotypes, specifically at smaller changes in the genetic information

B. How is it performed?

1. Polymerase chain reaction (PCR)-based testing, which involves using a specific primer that is complementary to the area of interest on the patient’s DNA

2. PCR can allow for both amplification and quantification of gene of interest

C. Can look for either single gene mutations (faster) or a panel of mutations (slower but more information) also known as NGS

II. Clinical Utility of Molecular Testing

A. Very useful in risk stratification based on the mutations noted (some mutations are unfavorable and some are favorable)

B. Certain genetic mutations have drugs that are effective against them, therefore provides information about targeted therapeutic options

C. In hematologic malignancies, can be used to also assess response to treatment

1. You can determine minimal residual disease or MRD

2. Can look for a gene mutation that was present in the original cancer clone and see if there is any amount of residual cancer left over on the order of 1 in a million cells

D. In solid cancers, used to determine presence of genetic changes that have prognostic and targeted treatment implications

1. BRAF V600E mutation in melanoma → BRAF inhibitor pill treatment

2. EGFR mutation in lung cancer → EGFR inhibitor pill treatment

III. How is molecular testing different than FISH?

A. Both require choosing probes and understanding what you are looking for before running the test

B. FISH (discussed in part 3!) reports out of 200 cells and provides information about only larger kilobase sized genetic changes (translocations, inversions, deletions)

C. Molecular testing analyzes a much larger number of cells and can detect changes at the single base pair level. Much more detailed and microscopic evaluation of genetic changes

IV. Single Gene Molecular Testing

A. Look for a specific gene mutation (i.e. EGFR for lung cancer, BRAF for melanoma, FLT3-ITD for AML)

B. Pros:

1. Faster turnaround time

2. Has a higher resolution and effective for detecting MRD

B. Cons:

1. Only looks for one genetic mutation as opposed to a panel like in NGS

2. Some diseases ideally require understanding of multiple mutations not just one for prognostication and treatment planning

V. Next Generation Sequencing (NGS)

A. Allows to sift through a larger part of the genome to identify a panel of mutations

B. Panel of mutations chosen is based on the clinical context

1. For example: NGS for acute myeloid leukemia is much different than NGS testing for lung cancer as each cancer has a much different genetic mutation profile

C. Overview of technical aspects of running NGS

1. Massively parallel sequencing meaning that many tiny primers are used and the areas that primers encode may be overlapping

2. A computer takes all of the smaller pieces and puts them together to determine the correct sequence

D. Pros:

1. Gives us an understanding of many different mutations present based on the panel chosen

2. Again, this has both prognostic and predictive treatment implications

E. Cons:

1. May find mutations of undetermined significance meaning we currently do not understand how these mutations will affect prognosis and treatment decisions

2. Very time consuming (~2-4 week turnaround time)

3. Costly

References:

1. https://jamanetwork.com/journals/jamaoncology/fullarticle/2734828 - Quick overview of NGS

2. https://ashpublications.org/blood/article/125/26/3996/34323/Minimal-residual-disease-diagnostics-in-acute - Look at table 1 to see the difference in sensitivity for MRD testing

3. https://www.oncotarget.com/article/27602/text/ - Emphasizes prognostic relevance of EGFR mutations in NSCLC

4. https://www.nejm.org/doi/full/10.1056/NEJMoa1612674 - Phase 3 trial showed that targeted treatment for EGFR mutation in NSCLC was superior to chemotherapy

5. https://www.nejm.org/doi/full/10.1056/nejmoa1614359 - Phase 3 trial showed that targeted treatment of FLT3 mutation in AML improved outcomes

Please visit our website (TheFellowOnCall.com) for more information

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In Part 3 of our Heme Path series, we break down the basics of immunohistochemistry (IHC)

Episode contents:

- What is immunohistochemistry?

- What are the pros and cons?

- How do we use this clinically?

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** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In Part 2 of our Heme Path series, we get into the details of cytogenetics (conventional karyotype and FISH)

Episode contents:

- What is "cytogenetics"?

- How do we use cytoenetic information clinically?

- What is the difference between the conventional karyotype and FISH?

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An exciting new academic year is about to begin. We know this can be daunting, especially for our newest hematology/oncology fellows. Over the next two weeks, we re-boot some of our high yield episodes you need to know to prepare for your first days as a new fellow and your nights on call. 

Next up: Superior vena cava (SVC) syndrome ! [Originally episode 012]

- What is the workup?

- What is the differential diagnosis?

- What do we do once we get the phone call about this emergency?

- Who should we be consulting?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

Love what you hear? Tell a friend and leave a review on our podcast streaming platforms!

Twitter: @TheFellowOnCall

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In Part 1 of our Heme Path series, we break down the logistics and applications of flow cytometry.

Episode contents:

- What is flow cytometry?

- How do we use this to identify cells?

****Have some time and want to make some extra money? Get paid to participate in market research surveys: https://affiliatepanel.members-only.online/FOC_24?utm_campaign=FOC&utm_source=email&utm_medium=email

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Thank you so much for checking out The Fellow on Call: The Heme/Onc Podcast. In this intro episode, learn more about our show and what you can expect.

Please visit our website (TheFellowOnCall.com) for more information 

Twitter: @TheFellowOnCall

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An exciting new academic year is about to begin. We know this can be daunting, especially for our newest hematology/oncology fellows. Over the next two weeks, we re-boot some of our high yield episodes you need to know to prepare for your first days as a new fellow and your nights on call. 

Next up: Metastatic Cancer of “Origin TBD,” a common question that comes up on solid oncology consults! [Originally episode 008]

Points covered:

- Initial workup

- What additional imaging is needed?

- What to biopsy?

- When to send molecular testing?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

Love what you hear? Tell a friend and leave a review on our podcast streaming platforms!

Twitter: @TheFellowOnCall

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Listen in on: Apple Podcast, Spotify, and Google Podcast

An exciting new academic year is about to begin. We know this can be daunting, especially for our newest hematology/oncology fellows. Over the next two weeks, we re-boot some of our high yield episodes you need to know to prepare for your first days as a new fellow and your nights on call.

Next up: immune thrombocytopenic purpura [Originally episode 015]

Episode contents:

- What is the workup for thrombocytopenia?

- What is ITP? Not to be confused with TTP.

- How do you diagnose ITP?

- How do you treat ITP?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

Love what you hear? Tell a friend and leave a review on our podcast streaming platforms!

Twitter: @TheFellowOnCall

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Listen in on: Apple Podcast, Spotify, and Google Podcast

An exciting new academic year is about to begin. We know this can be daunting, especially for our newest hematology/oncology fellows. Over the next two weeks, we re-boot some of our high yield episodes you need to know to prepare for your first days as a new fellow and your nights on call.

First up: thrombotic thrombocytopenic purpura (TTP) [Originally episode 018]

Episode contents:

- What is the workup for thrombocytopenia?

- What is TTP?

- How do we diagnose TTP?

- How do we treat TTP?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

Love what you hear? Tell a friend and leave a review on our podcast streaming platforms!

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In a recent American Cancer Society publication, there are increasing data that rates of colorectal cancer are rising rapidly among people in their 20s, 30s and 40s. This has certainly caught the attention of the lay press, most recently in a widely circulated New York Times article published in March 2024. Today, we welcome Dr. Chris Cann, who is an Assistant Professor of Hematology/Oncology at the Fox Chase Cancer Center in Philadelphia where he focuses on GI oncology and has a particular area of interest in early onset colorectal cancer. In his short career thus far, Dr. Cann is already making a name for himself in this space on a national level and so we are so glad he was able to join us for this special discussion. Dr. Cann sheds light on what we know and what we don’t know about this phenomenon. Definitely an episode to check out!

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we incorporate medical oncology back into our discussion with our Radiation Oncologist, Dr. Sanford, and our Surgical Oncologist, Dr. Bailey. We discuss how we approach the management of localized rectal cancer. Note that we will be heavily building off our discussions with our specialist. We recommend listening to these episodes if you have not done so already.

Content:

- What information do we need upfront for patients with newly diagnosed rectal cancer?

- How did we get to the current treatment paradigm?

- What is the data for long course vs. short course radiation?

- What is total neoadjuvant therapy?

- What are high risk features in rectal cancer?

- Is surgery always needed?

- Is radiation therapy always needed?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We have another guest joining us this week! Dr. Allison Schepers, PharmD, BCOP is a Clinical Pharmacist Specialist at the Rogel Cancer Center at the University of Michigan where she focuses on GI, GU, and Thoracic malignancies! In this episode, Allison discusses the high yield points we need to know about important drugs we use in the colorectal cancer treatment space and how she approaches counseling her patients. Another great episode from our pharmacy colleagues you do NOT want to miss!

Content:

- Important considerations about capecitabine, oxaliplain, and irinotecan, backbones of our colorectal cancer management

- An overview of targeted agents?

- If someone has a reaction, can we retrial any of these drugs in the future?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

Love what you hear? Tell a friend and leave a review on our podcast streaming platforms!

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This week, we are joined by Dr. Christina Bailey, Associate Professor of Surgery and Program Director of the General Surgery Residency at Vanderbilt University Medical Center in Nashville, Tennessee, for a discussion about the role of surgery in the management of patients with colorectal cancer. This is another amazing multidisciplinary colorectal surgery episode you do not want to miss!

Content:

- Why are MRIs important as part of workup for patients with rectal cancer?

- What is an "LAR" vs. "APR" and how do you decide which to use?

- What are long term complications associated with rectal cancer surgery?

- How much colon should be removed in a patient with colon cancer undergoing surgery?

- How to counsel patients about colon resection?

- How long after surgery should we wait for adjuvant chemotherapy in colon cancer?

- Is there a role for neoadjuvant therapy in metastatic colon cancer?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this week’s episode, we discuss the management of sickle cell disease in the chronic setting. This is a follow up to episode 111 where we discussed acute management of SCD. And furthermore, this is also in addition to our prior discussion about long-term chronic complications from SCD in episode 110. We highly recommend checking out these prior episodes if you haven’t done so already!

Contents:

- Use of hydroxyurea in SCD management

- Newer adjunctive therapies for SCD management

- Perioperative management

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** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we are joined by Dr. Nina Sanford, Assistant Professor and Chief of Gastrointestinal Radiation Oncology Service, UT Southwestern Medical Center in Dallas, Texas, for a discussion about the role of radiation in colorectal cancer, with an emphasis on the role of radiation in rectal cancer. Dr. Sanford is a wealth of knowledge so this is an episode you do NOT want to miss.

Of note, rectal cancer episodes will be released in a few weeks so if all of this does not make sense, don’t worry. It nicely sets the stage for what is to come!

Content:

- What is the role of radiation in rectal cancer vs. colon cancer? Why do we use it more in rectal cancer?

- How to evaluate your patients for radiation and how to decide long course vs. short course radiation

- Side effects of radiation therapy for rectal cancer

- Role of radiation for oligmetastatic colorectal cancer

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this week’s episode, we discuss the management of stage II colon adenocarcinoma, which is defined by a lack of nodal involvement and invasion through the muscularis layer of the colon. If you have not done so already, be sure to check out episode 099 (overview of colorectal cancer) and episode 100 for stage III colon cancer, as we will building on concepts discussed already.

Content:

- Is there a role for adjuvant chemotherapy in stage II colon cancer patients?

- What is the impact on MSI/MMR testing in stage II colon cancer patients?

- Is there a role for evaluating circulating tumor DNA (ctDNA) in colon cancer patients?

- Is there a role for immunotherapy in the adjuvant setting?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we kick off our discussion of adjuvant systemic treatment in colon cancer, beginning with Stage III colon cancer. We will review the evidence basis for adjuvant therapy as well as the two main chemotherapy regimens including duration and side effects.

Content:

- Why do we need adjuvant therapy in stage III colon cancer?

- What is FOLFOX? What is CAPOX? When do we use what?

- What is the optimal duration of therapy?

- What are the characteristics deemed high risk?

- Can we discontinue oxaliplatin early?

- What is the role of oxaliplatin in older patients?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Colorectal cancer is one of the most common cancers diagnosed each year worldwide. This highly anticipated series will take an in-depth look at this disease. In this first episode, we discuss the basics, including staging, tumor markers, and microsatellite instability testing, before tackling the management of colorectal cancer in upcoming episodes.

Content:

- What is the incidence of colorectal cancer (CRC) in the US?

- How are CRC patients staged?

- What is the role of CEA?

- What are microsatellites and mismatch repair proteins, and how do they come into play for treatment purposes?

- Who needs germline testing?

- What is the TNM staging for CRC?

- What are some high risk factors we need to pay attention to on the pathology report?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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With multiple options for frontline therapy in CLL, MRD has the potential to emerge as a factor that could be considered in our decision-making algorithm for sequencing treatment options. In this week’s episode, we dive into a deeper understanding of the role of MRD testing in CLL.

Content:

- What is the role of MRD testing in CLL?

- What are the techniques we use to evaluate for MRD?

- What is the prognostic role of MRD testing?

- Is there data to change treatment based on MRD testing?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we continue our discussion of treatment of CLL, this time focusing on the relapsed/refractory CLL. If you have not done so, we recommend checking out our prior episodes since we will be building on these conversations!

Content:

-If you suspect your patient has relapsed, what do you do?

-What is the approach to treatment in the relapsed/refractory setting?

- What is Richter's transformation?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We continue on our journey through chronic lymphocytic lymphoma (CLL), this time focusing our attention to the treatment of CLL. 

Content:

- What are the indications for treatment?

- Can I wait to treat and not impact OS?

- What is our current approach to treatment ?

- Fixed duration vs. indefinite treatment options?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we start a new series, this time all about the ins-and-outs of chronic lymphocytic leukemia (CLL) / small lymphocytic lymphoma (SLL)! Whether practicing general internal medicine, hospital medicine, or hematology/oncology, you will likely come across a patient with CLL. First, we go through initial diagnosis of this disease!

Content:

- What is CLL? How is this different than SLL?

- What is the approach to diagnosis?

- Do you need a bone marrow biopsy? Imaging?

- How do we prognosticate patients?

- Are smudge cells always suggestive of CLL?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this week’s episode, we finish our series on hemolytic anemias with a discussion on cold agglutinin disease along with a few other causes of acquired hemolytic anemia.

Content:

- What is "cold agglutinin disease"?

- Why is it called "cold"?

- How do we diagnose this disease?

- How do we treat?

- BONUS: What are some other examples of hemolysis?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Next in our heme consult series is all about the workup and management of warm autoimmune hemolytic anemia (wAIHA), a very scary situation! These patients can often be very sick and there can be a lot of underlying issues that may be causing this to occur. Rest assured- after this episode, you’ll be a pro at identifying this disorder and know how to manage it should you ever come across this.

If you have not done so already, we recommend you check out our initial episode about hemolytic anemias (Episode 091)

Content:

- How do we work up warm autoimmune hemolytic anemia (wAIHA)?

- Is it safe to transfuse patients with wAIHA? What about DVT prophylaxis?

- What is the approach to initial treatment of wAIHA? How do manage patients once their hemolysis stabilizes?

- How do we approach more refractory or relapsed cases?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this week’s episode, we discuss the management of acute complications of sickle cell disease including acute pain episodes and acute chest syndrome as well as a discussion of hyperhemolytic syndrome.

Contents:

- How to manage patients with sickle cell disease presenting for acute pain crises

- How to approach management of acute chest syndrome

- What is hyperhemolytic crisis?

- What is splenic and hepatic sequestration syndrome?

**This episode is sponsored by our global research partners! Have some time and want to make some extra money? Get paid to participate in market research surveys: https://affiliatepanel.members-only.online/FOC_24?utm_campaign=FOC&utm_source=email&utm_medium=email

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In the next part of this heme consult series, we discuss several congenital causes of hemolytic anemias. These diseases are relatively rare, but in patients presenting with concerns for hemolysis on history and on labs, but with a negative DAT, it is important to have these in your differential diagnosis! We take you through how to think about these disorders, their diagnosis, and management.

If you have not done so already, be sure to check out Episode 091 where we discuss our initial approach to the diagnosis of hemolytic anemias. We also discuss the most common inherited cause of hemolytic anemia, G6PD deficiency, in that episode!

Content:

- When should we suspect inherited causes of hemolytic anemia?

- What are important examples of membranopathies that can cause hemolytic anemia?

- What are important enzyme deficiencies that can cause hemolytic anemia?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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It’s time for another heme consult series, this time focusing on hemolytic anemias. In this multi-part series, we will go through our approach to thinking about concerns for hemolytic anemias. This is super high yield for anyone who cares for patients, especially those in hematology/oncology. It’s not uncommon to get a consult on the heme consult service for assistance with diagnosis and management of suspected hemolytic anemias!

Content:

- What is "hemolytic anemia"?

- When should we suspect hemolytic anemias?

- What is the workup for acquired hemolytic anemias?

- What is G6PD deficiency? When should we suspect this?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We made it to the end of another series. In our FINAL episode of the prostate cancer series, we turn our attention to metastatic castrate-resistant prostate cancer! We discuss treatment options, the data behind why we do what we do, and more targeted agents.

Content:

- Approach to metastatic castrate-resistant prostate cancer

- Refresher on what it means to be castrate-resistant

- Role of bisphosphate therapy and denosumab

- Treatment options and data surrounding sequencing of agents

- Other options for prostate cancer (radium-223 and lutetium-177-PSMA-617)

- Role of PARP inhibitors in BRCA-mutated disease

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we continue our discussion about metastatic castrate sensitive prostate cancer. Spoiler alert: there is not good guidance or biomarkers that help us pick one regimen over another. In this episode, we go through the data, our critical appraisal of the data, and some things to consider when selecting one regimen over another. 

As a refresher, be sure to check out our Pharmacology Episode and our introductory episodes, as we will be building on these concepts. 

Content:

- Approach to metastatic disease

- Who needs germline testing?

- History of prostate cancer therapy

- Selecting doublet vs. triplet therapy

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Twitter: @TheFellowOnCall

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