Free Internal Medicine CME

Activity Description / Statement of Need:

In this online, self-learning activity:

Alpha 1-antitrypsin deficiency (AATD), characterized by misfolded and lower function of the serine protease inhibitor alpha-1 antitrypsin (AAT), is a genetic disorder resulting in the degradation of lung structures. Reduced levels of AAT result in overactivity of neutrophil elastase, which destroys connectivetissue within the lung and causes degradation of alveoli, reduced pulmonary elastic recoil, and airflow. Breakdown of the alveoli eventually manifest as chronic obstructive lung disease (COPD), and otherassociated complications include liver disease, which occurs in about ten percent of patients with AATD.The most common cause of death in patients with severe AATD is respiratory failure, which accounts for45 to 72% of deaths.

Target Audience:

The following HCPs: pulmonologists and primary care physicians; physician assistants, nurse practitioners, nurses, and pharmacists who practice in pulmonology and internal medicine; and any other healthcare professionals with an interest in or who clinically encounter patients with AATD.

In this online, self-learning activity:

Hereditary angioedema (HAE) is a rare, debilitating, and potentially life-threatening disease due to C1-inhibitor (C1-INH) deficiency with an estimated prevalence of 5,000 people in the U.S. and over 116,000 worldwide. HAE is characterized by recurrent edema, and the cutaneous attacks can be disabling, with the skin, gastrointestinal tract, and upper airways are most commonly affected. Patients are also under persistent risk of laryngeal swelling that may prove fatal if not treated in a timely manner. The disease is classified as: HAE with normal functional C1INH protein (previously known as type III HAE) or HAE due to a deficiency of C1INH protein, with the latter further distinguished either by deficiency in both concentrations and function of C1INH (type I) or by normal levels of dysfunctional C1INH (type II). Owing to its rarity and symptomatic overlap with other conditions, patients not uncommonly experience a diagnostic delay of 8 to 10 years, putting them at a higher risk of inappropriate treatment, morbidity, and mortality.

Target Audience:
HCPs including: allergists, immunologists, emergency medicine specialists, and internists; physician assistants, nurse practitioners, and pharmacists specializing in immunology; and any other HCPs who have an interest in or otherwise clinically encounter patients with HAE.

In this online, self-learning activity:

Alpha-mannosidosis (AM) is a rare recessive lysosomal storage disorder characterized by immune deficiency, facial and skeletal abnormalities, hearing impairment, and intellectual disability. It is caused by mutations in the MAN2B1 gene, leading to deficiency in alpha-mannosidase, a lysosomal enzyme involved in the oligosaccharide degradation pathway. While the exact prevalence of AM in the US is unknown, it has an estimated incidence of 1 in 500,000 live births worldwide. Laboratory indicators of AM often appear shortly after birth, followed by progression of clinical manifestations. While symptoms of AM vary considerably in individual presentations, three clinical subtypes have been identified (mild, moderate, and severe) and are used to guide disease prognosis and management. The current diagnostic algorithm for AM focuses on measuring alpha-mannosidase activity in leukocytes using colorimetry or fluorimetry. An alpha-mannosidase activity level of under 5% suggests AM, and a diagnosis is then confirmed with genetic sequencing.