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 a