Free Hematology CME

Target Audience: Hematologists

Sickle cell disease (SCD) is the most common monogenic blood disorder, affecting millions of people worldwide and approximately 100,000 Americans. Although it may be found in various areas of the world, SCD predominantly affects individuals of African or Hispanic heritage. It is caused by the inheritance of b-globin alleles that code for hemoglobin S, resulting in an amino acid substitution in hemoglobin’s b chain and clinical disease. Patients with SCD have impaired circulation, and lysis of the erythrocytes contributes to a chronic inflammatory response, causing severe pain and less efficient oxygen delivery. The hallmark clinical features of SCD are hemolytic anemia and painful vaso-occlusive crises (VOCs), which may lead to emergency department visits, hospitalization, and potentially fatal complications such as acute chest syndrome, stroke, or pneumonia. In one US study, 45% of deaths among people with SCD were related to cardiopulmonary causes, and VOCs alone have been shown to increase the risk of death by 50%. SCD may disrupt employment or school and is associated with a significant reduction in quality of life. This learning activity has been designed to bring HCPs’ knowledge of rationale behind treatment of SCD up to date and to enhance their competence and performance in the condition’s management.

Activity Description / Statement of Need:

In this online, self-learning activity:

Sickle cell disease (SCD) is the most common monogenic blood disorder, affecting millions of people worldwide and approximately 100,000 Americans. Although it may be found in various areas of the world, SCD predominantly affects individuals of African or Hispanic heritage. It is caused by the inheritance of b-globin alleles that code for hemoglobin S, resulting in an amino acid substitution in hemoglobin’s b chain and clinical disease. Patients with SCD have impaired circulation, and lysis of the erythrocytes contributes to a chronic inflammatory response, causing severe pain and less efficient oxygen delivery. The hallmark clinical features of SCD are hemolytic anemia and painful vaso-occlusive crises (VOCs), which may lead to emergency department visits, hospitalization, and potentially fatal complications such as acute chest syndrome, stroke, or pneumonia.

Target Audience:

The following HCPs: hematologists and primary care physicians; physician assistants, nurse practitioners, nurses, and pharmacists who specialize in the aforementioned areas of specialty; and any other HCPs with an interest in or who may clinically encounter patients with SCD.

Activity Description / Statement of Need:

In this online, self-learning activity:

Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin’s lymphoma (NHL), making up just under a third of NHL cases. In the United States, there are roughly 7 cases of DLBCL per 100,000 patients per year. The pathophysiology of DLBCL is complex and not fully understood; but is characterized by a widespread increase of very large, mature B-cells arising from various gene mutations. DLBCL is heterogenous group of tumors and includes many diverse subtypes based on location, presence of other cells within the tumor, and whether the patient has other related illnesses. Advanced age, immunodeficiency, and Epstein-Barr virus are associated risk factors for DLBCL. The disease is considered an AIDS-defining malignancy, marking the point at which an HIV infection is considered AIDS. Diagnosis of DLBCL is made by a tissue biopsy, and morphology and immunophenotyping play a crucial role in determining which subtype of DLBCL a patient has.

This learning activity has been designed to bring HCPs’ knowledge of present and emerging strategies for treatment and management of DLBCL up to date and to improve their competence and performance in treating it.

Target Audience:

Hematologists and oncologists; physician assistants, nurse practitioners,  pharmacists who practice in oncology, and any other HCPs with an interest in or who clinically encounter patients with DLBCL.

In this online, self-learning activity:

Von Willebrand disease (vWD) is the most common congenital bleeding disorder worldwide. Affecting both male and female births in equal number, vWD is caused by a deficiency or defect in the von Willebrand factor (vWF) glycoprotein, which is responsible for mediating platelet and coagulation factor VIII function. vWD types 1 and 3 are caused by quantitative deficiencies in vWF. In contrast, type 2 vWD is caused by a qualitative defect in the production of vWF. Type 1 is the most common type of vWD, accounting for 60% to 70% of cases, followed by type 2, which is diagnosed in 25% to 30% of patients. Type 3 vWD, the rarest form, affects about 1 in 1,000,000 people. There is evidence that the use of factor VIII/vWF concentrates should be individualized, but no recent vWD guidelines address this issue. Although DDAVP is the treatment of choice for most type 1 vWD patients, data do not support the use of DDAVP for type 2B vWD owing in part to an increased risk for thrombocytopenia. Another practice gap is a lack of guidance around the appropriate ages at which patients with severe vWD are optimally initiated on vWF prophylaxis. Furthermore, although DDAVP is not contraindicated in pregnancy, 31% of physicians consider DDAVP a contraindication according to the results of one survey, illustrating a present area of controversy in practice.

Target Audience:

The following healthcare professionals: Hematologists and primary care physicians; physician assistants, nurse practitioners, and pharmacists who practice in hematology; and any other healthcare professionals with an interest in or who clinically encounter patients with vWD.

Activity Description / Statement of Need:

In this online, self-learning activity:

Beta-thalassemia (BT) is a progressive, hereditary, microcytic, hypochromic form of anemia characterized by the reduced synthesis of hemoglobin subunit beta and the underproduction of hemoglobin A (HbA). Although there are limited data regarding the incidence of BT, historical estimates of BT have been placed at about 1 in 100,000 individuals. BT is most commonly found in patients with Mediterranean, the Middle Eastern, Central Asian, Indian, East Asian, and the North African heritage. BT is caused by a point mutation in the encoding gene for hemoglobin subunit beta (HBB) on chromosome 11, which either results in lower beta-globin production (termed beta-plus [B⁺] or prevent cells from producing any beta-globin at all (termed beta-zero [B⁰]). The clinical severity the disease depends on the extent of β and γ chain imbalance; more than 350 genetic alterations that can cause BT have been identified.

There is a demonstrated variation in treatment between providers who practice at a beta thalassemia center of excellence (CoE) and those who do not, and those practitioners at CoEs demonstrate greater familiarity with beta thalassemia and its therapies, including butyrates, gene therapy, and luspatercept. Additional areas of educational need include transitioning patients from pediatric care, management of complications, and clinical trial updates.

Target Audience:

The following healthcare professionals: hematologists; physician assistants, nurse practitioners, and pharmacists who practice in hematology; and any other healthcare professionals with an interest in or who may clinically encounter patients with BT.

Thrombotic thrombocytopenic purpura (TTP) is a rare blood disorder that impacts three in a million adults per year, with congenital or hereditary TTP (cTTP, also known as Upshaw-Schulman syndrome) accounting for a third of the overall incidence. The incidence of TTP rises with increasing age and the mortality rate of untreated TTP may be as high as 90%.

In recent years molecular mechanisms contributing to TTP have been identified: patients diagnosed with TTP have larger von Willebrand factor molecules (vWF) and a defective protease enzyme of A Disintegrinlike And Metalloprotease with ThromboSpondin type 1 motif 13 (ADAMTS13), which cleaves larger vWF molecules and inhibits platelet adhesion. In congenital or hereditary TTP (cTTP, also known as Upshaw-Schulman syndrome), the gene that codes of ADAMTS13 is defective and cannot properly produce the enzyme, whereas in acquired TTP, antibody production leads to downstream enzymatic deactivation.

Target Audience:
The following healthcare professionals: hematologists; physician assistants, nurse practitioners, nurses, and pharmacists who practice in hematology; and any other healthcare professionals with an interest in or who clinically encounter patients with cTTP.

By the end of the session the participant will be able to:

• Summarize the most impactful findings presented at the ASH 2019 annual meeting relating to congenital TTP
• Recall the pathophysiology of congenital TTP
• Describe the clinical manifestations and methods of establishing a diagnosis of cTTP, and apply that information to a patient case
• List treatment strategies for cTTP, and apply that information to a patient case

Activity Description / Statement of Need: The COVID-19 pandemic has led to unprecedented changes in health care delivery worldwide, affecting the way that nearly every medical specialty can safely practice. As with other fields of medicine, oncology has its own challenges in navigating the pandemic. Based on pre-pandemic estimates, 1.8 million new cancer diagnoses would be expected in 2020, equating to approximately 5,000 new cancer diagnoses per day. Evidence thus far suggests that COVID-19 is associated with significantly more complications and a higher risk of death in patients with cancer or with a history of cancer. Furthermore, patients with cancer have also been shown to have a higher COVID-19 infection rate than the general population, suggesting increased susceptibility, potentially due to immunosuppression, comorbidities, or poor health status related to cancer or its treatment. Based on these data, oncology specialists are said to be fighting “a war on two fronts” by balancing the risks of COVID-19 transmission and acquisition with the risks of delayed cancer diagnosis and treatment. This represents an unmet need among oncology practitioners as they navigate this new health care landscape.

Target Audience:

Healthcare professionals, including medical oncologists; radiation oncologists; surgical oncologists; surgeons; radiologists; nuclear medicine specialists; nurse practitioners and physician assistants who practice in oncology; and other healthcare providers who manage cancer.

By the end of the session the participant will be able to:

• Recall the symptoms of COVID-19 infection and best practices for screening patients, health care providers, and staff in the oncology setting.
• Develop a plan to provide oncology care in the setting of the COVID-19 pandemic.
• Describe the risks of delaying cancer diagnosis and treatment against the risk of COVID-19 exposure and infection.
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Hemophilia is a genetic disease caused by mutation of one of the genes for coagulation proteins leading to dangerous, uncontrolled bleeding. In hemophilia B, a mutation in the gene for factor IX (FIX) leads to an endogenous deficiency in the clotting factor. The incidence of hemophilia B is the same in all geographic regions, populations, and ethnic groups,affecting approximately 1 out of every 30,000 male births. The condition is diagnosed by measuring FIX activity, and patients with severe hemophilia have levels of 1% or less.

Patients with severe hemophilia B are at risk for spontaneous, life-threatening bleeding episodes. Untreated, the life expectancy is approximately 20 years,and painful or even life-threatening morbidities include intracranial hemorrhage, severe bleeding in other organ systems, musculoskeletal injury, and joint injury. In contrast, in people with moderate or mild hemophilia, abnormal bleeding usually occurs after minor trauma or surgery.

Physical therapy can ease symptoms if internal bleeding has damaged a patient’s joints, and surgery may be necessary if internal bleeding has caused severe damage. However, the current standard of therapy for hemophilia B is intravenous infusion of therapeutic factor concentrates. Through the reduction in the number of bleeding incidences and improvement in quality of life, factor replacement therapy has significantly reduced the morbidity and mortality of hemophilia. Furthermore, prophylactic therapy has the demonstrated benefit of reducing the development of hemophilic arthropathy.

Target Audience:

The following healthcare professionals: hematology, primary care physicians, and pediatricians; physician assistants, nurse practitioners, nurses, and pharmacists who practice in hematology as well as other Hemophilia Treatment Center HCPs; and any other clinicians with an interest in hemophilia B.

By the end of the session the participant will be able to:

• Describe the risk factors and occurrence of hemophilia B.
• Identify available prophylactic and treatment options for hemophilia B and apply them to a patient case.
• Identify the new treatment options for hemophilia B.
• Identify adherence barriers in and deliver effective treatment counseling to patients with hemophilia B.

Hemophilia is a genetic disease caused by mutation of one of the genes for coagulation proteins leading to dangerous, uncontrolled bleeding. In hemophilia A, a mutation in the gene for factor VIII (FVIII) leads to an endogenous deficiency in the clotting factor. The incidence of hemophilia A is the same in all geographic regions, populations, and ethnic groups, affecting approximately 1 out of every 5000 male births. The condition is diagnosed by measuring FVIII activity, and patients with severe hemophilia have FVIII activity of 1% or less. Patients with severe hemophilia A are at risk for spontaneous, life-threatening bleeding episodes. Untreated, the life expectancy is approximately 20 years, and painful or even life-threatening morbidities include intracranial hemorrhage, severe bleeding in other organ systems, musculoskeletal injury, and joint injury. In contrast, in people with moderate or mild hemophilia, abnormal bleeding usually occurs after minor trauma or surgery.

Target Audience:

The following healthcare professionals: hematology, primary care physicians, and pediatricians; physician assistants, nurse practitioners, nurses, and pharmacists who practice in hematology as well as other Hemophilia Treatment Center HCPs; and any other clinicians with an interest in hemophilia A.

By the end of the session the participant will be able to:

• Describe the risk factors and occurrence of hemophilia A.
• Identify available prophylactic and treatment options for hemophilia A and apply them to a patient case.
• Identify the new treatment options for hemophilia A.
• Identify adherence barriers in and deliver effective treatment counseling to patients with hemophilia A.