Podcasts about splenomegaly

In this episode, listen to Dr Brady L. Stein share his clinical insights and takeaways on new data for myeloproliferative neoplasms (MPNs) presented at the 2024 ASCO Annual Meeting and the EHA 2024 Congress including:Long-term survival adjusted for treatment crossover in patients with myelofibrosis (MF) treated with momelotinib vs danazol in the MOMENTUM trialEfficacy of pacritinib in patients with MF who have both thrombocytopenia and anemiaUpdated safety and efficacy data from the phase III MANIFEST-2 study of pelabresib in combination with ruxolitinib for JAK inhibitor–naive MFImpact of spleen volume on post-allogenic hematopoietic transplant outcomes in patients with MF: utility of 3D volumetrics in splenomegalyProgression to MF in patients with essential thrombocythemia: an analysis from the prospective MOST studyJAK2V617F molecular response correlates with event-free survival in a patient population with early polycythemia veraPhase III TRANSFORM-1 study: efficacy and safety of navitoclax combined with ruxolitinib vs ruxolitinib plus placebo in patients with untreated MFPatient characteristics, treatment patterns, and health outcomes in a real-world population of patients with MF treated with fedratinib Program faculty:Brady L. Stein, MD, MHSProfessor of MedicineDepartment of Hematology/OncologyNorthwestern University Feinberg School of MedicineChicago, Illinois Resources:To download the slides associated with this podcast discussion, please visit the program page.

Sam welcomes back returning guest Dr Suzy Morton, Consultant Haematologist to discuss this ever-popular PACES topic!^_^ SUPPORT THE SHOW ^_^> > Sign up for Pastest HERE! <

Drs. Ghaith Abu‑Zeinah and Raajit K. Rampal share their insights into managing splenomegaly in myelofibrosis and the impact that spleen reduction can have on patients and outcomes.

In this episode, we review the physiology and pathophysiology, etiology, clinical exam, investigations and treatment in patients with splenomegaly. Our medicine minute addresses the COMFORT II trial published in the New England Journal of Medicine in 2012. Written by: Drs. Owen Luo and Jia Li (Lily) Liu (Internal medicine residents)Reviewed by: Dr. Gizelle Popradi (hematologist) and Dr. Samuel Mamane (general internist) Support the show

In this Hepatology Rafael Medina Subspecialty episode, Dr. Christopher Coe presents a case to Dr. Arpan Patel of a woman presenting with fatigue and splenomegaly.  Session facilitator: Maddy Conte The goal of this series is to expand access to subspecialty, primary care, and internal medicine-adjacent specialty education to learners around the world. If you would… Read More »Episode 313: Rafael Medina Subspecialty Series – Splenomegaly

In this episode we are joined by Haematology Specialist Registrar Dr Claire Kelly to discuss splenomegaly and some important haematological disorders as potential stations in the MRCPI Part II clinical exam. We discuss the approach, physical findings, a differential diagnosis, investigations and management. We then go on to briefly talk through some potential follow-up questions including differentiating a large spleen versus a large kidney, management of Chronic Myeloid Leukaemia (CML) and Myelofibrosis, a brief review of Autoimmune Haemolytic Anaemia (AIHA) and Immune Thrombocytopenia (ITP), splenectomy indications and splenectomy precautions. Common causes of splenomegaly in exams are CML and myelofibrosis. A possible way to learn and work through a splenomegaly differential diagnosis (taken from Pastest Splenomegaly case notes): The causes of splenomegaly can be stratified into three main categories: "1 . Infiltration, malignant or benign - (including myeloproliferative and lymphoproliferative disorders), lymphomas, amyloidosis, sarcoidosis, Gaucher's disease (ie lipid storage disease), thyrotoxicosis. 2. Increased function – with increased removal of defective red blood cells with spherocytes, thalassaemia, nutritional anaemias and early sickle cell anaemia. Also there is immune hyperplasia in response to infection (viral, bacterial, fungal or parasitic) including tropical splenomegaly with chronic malaria and visceral leishmaniosis i.e. Kala-azar. Also consider glandular fever, infectious hepatitis, subacute bacterial endocarditis, brucellosis and disordered immunoregulation (rheumatoid arthritis with Felty's syndrome, SLE, sarcoidosis) 3. Abnormal blood flow, either with cirrhosis, or secondary to a vascular problem, such as hepatic or portal vein obstruction. As there are so many causes of splenomegaly, you may find the examiner will give you a clue to guide you to the diagnosis. Listen carefully for this. So, for example, if the examiner asks you to examine this farmer's abdomen, they may be likely to have Brucellosis. If you were only asked to examine the abdomen itself but given an opportunity to examine elsewhere, you may request to examine the throat for glandular fever. If the examiner asks you to examine this man and informs you he is an Ashkenazi Jew, there may be increased likelihood that the patient may have type 1 Gaucher's. If you are informed the patient has recently returned from Africa, then you should consider chronic malaria, although there would likely be other clinical features such as anaemia." Link to Pastest MRCP Clinical revision resource: https://bit.ly/468j0lT Episode external review by Dr Louisa Shackleton, Haematology SpR Consultant supervisor Professor Declan Byrne, consultant physician St James's Hospital, Dublin Show music by Stepping on Lego - email: steppingonlegoband@gmail.com - socials: @steppingonlego Get in touch with us by email mrcpibedside@gmail.com or social media @mrcpibedside Good luck!

What is ROSAH syndrome and how does it affect the visual function of patients with it? Dr. Tsui discusses this with Drs. Laryssa A. Huryn and Shilpa Kodati, authors of the Ophthalmology article, “Ophthalmic manifestations of ROSAH Syndrome, an inherited NF-κB mediated autoinflammatory disease with retinal dystrophy.” Ophthalmic Manifestations of ROSAH (Retinal Dystrophy, Optic Nerve Edema, Splenomegaly, Anhidrosis, and Headache) Syndrome, an Inherited NF κB–Mediated Autoinflammatory Disease with Retinal Dystrophy. Huryn, Laryssa A. et al. Ophthalmology, Volume 130, Issue 4, 423 – 432. Please tell us what you think of our show in a brief 2-minute survey: https://forms.office.com/r/B4rYtvpQad

Addressing the Triple Challenge of Myelofibrosis: Symptoms, Splenomegaly, and Cytopenias

Addressing the Triple Challenge of Myelofibrosis: Symptoms, Splenomegaly, and Cytopenias

Addressing the Triple Challenge of Myelofibrosis: Symptoms, Splenomegaly, and Cytopenias

Addressing the Triple Challenge of Myelofibrosis: Symptoms, Splenomegaly, and Cytopenias

Addressing the Triple Challenge of Myelofibrosis: Symptoms, Splenomegaly, and Cytopenias

Addressing the Triple Challenge of Myelofibrosis: Symptoms, Splenomegaly, and Cytopenias

In this episode, we review three hematology cases. One case illustrates the work-up and treatment of immune thrombocytopenia (ITP). Another case demonstrates how to diagnose and manage heparin-induced thrombocytopenia (HIT). And the final case is a patient who presented with anemia, a new mitral valve murmur, and mild splenomegaly. Host David H. Henry, MD, reviews these cases with three residents from Pennsylvania Hospital in Philadelphia – Sheila De Young, DO; Ronak Mistry, DO; and Debika Shinohara, MD, PhD. Case 1: Suspected ITP with Sheila De Young, DO Patient presentation: A 50-year-old female with no past medical history and incidental platelet count of 4,000/microL (normal 150,000-450,000/microL [150-450 x 109/L]). On physical exam, there was no lymphadenopathy, and the spleen was nonpalpable. She had obvious petechiae on her legs. A urine pregnancy test was negative. Her hemoglobin and white blood cell counts were normal via complete blood count. ITP definition: Acquired thrombocytopenia caused by autoantibodies against platelet antigens. One of the most common causes of thrombocytopenia in otherwise asymptomatic adults. To consider: Increased destruction, decreased production, and pseudothrombocytopenia To ensure the platelet count is not falsely low (in the case of pseudothrombocytopenia), looking at a peripheral smear is helpful. If red blood cells and white blood cells appear normal, we can exclude pseudothrombocytopenia. Work-up: We need to rule out secondary causes of thrombocytopenia such as HIV, hepatitis C, chronic lymphocytic leukemia, systemic lupus erythematosus, etc. Management/treatment: In the acute setting, the treatment for ITP is intravenous immunoglobulin and steroids. Long-term management of ITP includes steroids, splenectomy, thrombopoietin receptor agonists (romiplostim/eltrombopag), and rituximab. Case conclusion: This patient was found to have ITP. Shared decision-making led to the patient receiving a thrombopoietin receptor. Case 2: Possible HIT with Ronak Mistry, DO Patient presentation:  A male with ischemic leg and creatinine phosphokinase greater than 4,000 units/L. His platelet count was 101,000/microL on admission, 70,000/microL on the second day, and 60,000/microL on the third day. The patient was on prophylactic subcutaneous heparin for 48 hours, so the surgery team considered HIT to explain the drop in platelets. HIT definition: A life-threatening complication of exposure to heparin. Results from autoantibody directed against endogenous platelet factor 4 (PF4) in complex with heparin. To consider: Determine baseline platelet count, what type of heparin the patient received, and look at when the heparin was administered in relation to when the platelet count dropped. HIT is far less common in patients who receive subcutaneous heparin versus intravenous heparin. Typically, we see a 50% decrease in platelet count 5-10 days following exposure to heparin. Work-up: In the inpatient setting, it is important to consider other causes that predispose patients to thrombocytopenia (i.e., critical illness, medications). Thrombocytopenia can represent a consumptive process of platelets secondary to tissue injury in the setting of elevated creatine phosphokinase. Diagnosis: Enzyme-linked immunosorbent assays (ELISAs) can detect the presence of PF4-heparin antibody. ELISA should be followed by a confirmatory test. The serotonin release assay is preferred among diagnostic tests for HIT. Management/treatment: Stop heparin immediately. Giving more platelets is not the solution. It increases a person’s risk for thrombotic events. The patient needs to be placed on different anticoagulation, such as argatroban or fondaparinux, to carry them through this procoagulant time frame. Case conclusion: HIT was ruled out in this patient. Case 3: Anemia case with Debika Shinohara, MD, PhD Patient presentation: A female, age 45 years, with a 4-month history of intermittent fevers and unintentional weight loss. Her hemoglobin was 8 g/dL, but she had otherwise unremarkable blood work. On physical exam, she was found to have a new mitral valve murmur and mild splenomegaly. To consider: Increased destruction versus decreased production of red blood cells. Low reticulocyte count (

Steph, Sharmin, Arsalan and Dan share a case of syncope and splenomegaly – let’s practice those schemas together! Download CPSolvers App here Patreon website Splenomegaly Schema Syncope Schema

The TWiP professors solve the case of the Ugandan Child with Splenomegaly, and reveal that mutations in the P. falciparum genome that confer artemisinin resistance interfere with endocytic uptake of hemoglobin. Hosts: Vincent Racaniello, Dickson Despommier, and Daniel Griffin Subscribe (free): iTunes, Google Podcasts, RSS, email Links for this episode PWB social media: Facebook, Instagram, Twitter Endocytosis pathway mediates artemisinin resistance in malaria parasites (Science) Letters read on TWiP 180 Become a patron of TWiP. Case Study for TWiP 180 Uganda with a twist. Meets two people with watery diarrhea, 12 episodes/day, loss of appetite. No fever, no blood in stool. Living for months at staff guest house. One week prior to onset went on weekend trip to area with waterfalls. Were served outdoor meal: meat, salad, fruit. Recommends empiric treatment trimethoprim/sulfamethoxzole for 7 days. Prompt resolution of diarrhea. A few days later, upon drinking coffee with milk gets severe cramps. 20s, long term female volunteers.  Send your case diagnosis, questions and comments to twip@microbe.tv Music by Ronald Jenkees

Reza presents a clinical unknown to Rabih.

Hosts: Vincent Racaniello and Daniel Griffin Guest: Paul Daniel and Vincent solve the case of the Truck Driver from India, discuss why parasites resistant to an antimalarial drug are not transmitted by mosquitoes, and introduce Paul who presents a new case study.   Links for this episode: Atovaquone resistant parasites not transmitted by mosquitoes (Science) Image credit Letters read on TWiP 109 This episode is sponsored by CuriosityStream, a subscription streaming service that offers over 1,400 documentaries and non­fiction series from the world's best filmmakers. Get unlimited access starting at just $2.99 a month, and for our audience, the first two months are completely free if you sign up at curiositystream.com/m​icrobe ​and use the promo code MICROBE​. Send your case diagnosis, questions and comments to twip@microbe.tv

Editor's Audio Summary by Howard Bauchner, MD, Editor in Chief of JAMA, the Journal of the American Medical Association, for the February 17, 2015 issue

Srdan Verstovsek, MD PhD, associate professor of Medicine, department of Leukemia, at the university of texas, MD anderson cancer center, discussing observations and results of a randomised trial using Jak2 inhibitors in Myelofibrosis.

Srdan Verstovsek, MD PhD, associate professor of Medicine, department of Leukemia, at the university of texas, MD anderson cancer center, discussing observations and results of a randomised trial using Jak2 inhibitors in Myelofibrosis.

Joan Stephenson, PhD, discusses Splenomegaly with Dr David Simel.

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