Onsite CME Information

CME Credits are an essential part of professional development

Physicians 
This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AKH Inc., Advancing Knowledge in Healthcare, Clinical Education, and Doctor’s Data, Inc.  AKH Inc., Advancing Knowledge in Healthcare is accredited by the ACCME to provide continuing medical education for physicians.

AKH Inc., Advancing Knowledge in Healthcare designates this live activity for a maximum of 9.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Physician Assistants
NCCPA accepts AMA PRA Category 1 Credit™ from organizations accredited by ACCME.

 

Needs Assessment and Learning Objectives

Non-alcoholic Fatty Liver Disease: Mechanisms and Assessment of Key Causal Factors

These presentations will address the pandemic juvenile and adult non-alcoholic fatty liver disease (NAFLD) that may progress to end-stage liver disease and hepatocellular carcinoma.   The talks will focus on the mechanisms associated with the array of causative factors, and objective laboratory testing that addresses many of the risk factors and outcomes. The “silent” disease comprises a wide spectrum of liver damage, ranging from simple steatosis, to steatohepatitis, to advanced fibrosis and cirrhosis. The rising prevalence of NAFLD is related to the epidemic of obesity, but not all patients presenting with NAFLD are obese. The primary initiating factor in the disease process is insulin resistance/hyperinsulinemia which drives hepatic lipogenesis. Consequentially hepatic accumulation of triglycerides, mitochondrial dysfunction and inflammation ensue, as well as pro-atherogenic hyperlipidemia / dyslipoproteinemia.  Altered levels of two adipocytokines, adiponectin and leptin, are major players in the disease process. That is due, in part, to the association of visceral fat with the hepatic portal venous system which is a critical regulator of glucose and fat metabolism. The common overconsumption of fructose is both a substrate and inducer of hepatic lipogenesis, and has been implicated in the development of NAFLD and cardiovascular disease.  Patients with NAFLD commonly present with elevated levels of pro-atherogenic small dense LDL and oxidized LDL (ox-LDL). In turn ox-LDL plays a role in in the progression of NAFLD.  Aberrant paracellular permeability of the gastrointestinal endothelial barrier can also be associated with NAFLD. NAFLD is the most common cause of persistent abnormalities in liver enzyme test results in North America; however elevated liver enzymes (e.g. AST) are not clinically sensitive or specific enough for diagnostic purposes. Imaging and palpation exams are helpful in diagnosis of NAFLD, but the earlier the detection and clinical remediation of associated metabolic abnormalities the better the prognosis.  Towards that end a comprehensive cardiometabolomic profile that addresses the most specific risk factors for Metabolic syndrome and CVD provides the clinician with abundance of information relevant to NAFLD.

 

Aberrant Methionine Metabolism: Clinical Implications and Intervention

These presentations will define the clinically relevant aspects of abnormal methionine metabolism, and present case studies with initial assessments and follow up after clinical intervention.  Basic protocols will be provided based upon objective laboratory testing and clinical experience. Methionine, an essential amino acid, is considered by many to be of utmost importance due to its vital roles in methylation, transsulfuration and transmethylation of homocysteine.  On first pass through the liver about 50% of dietary methionine is metabolized to s-adenosyl methionine (SAM) which is the donor of methyl groups to DNA/RNA, proteins, neurotransmitters, and phospholipids. Methylation of DNA is a major mechanism for the regulation of gene expression. After methyl group donation SAM is converted to s-adenosylhomocysteine (SAH).  SAH is a very potent inhibitor of all methylation reactions in the body, and the ratio of SAM to SAH has been described as the methylation index. Subsequently SAH is reversibly converted to homocysteine which is a branch point whereby homocysteine can conditionally be metabolized through the transsulfuration pathway ultimately to form taurine, cysteine, glutathione (GSH) and essential sulfate ions.  Alternatively homocysteine can be metabolized through the transmethylation pathway back to methionine.  SAH is also emerging as a risk factor for cardiovascular disease and has been implicated in NAFLD. There are many genetic (single nucleotide polymorphisms (SNPs) and epigenetic factors (nutrients, oxidative stress and environmental toxicants) that can adversely affect methionine metabolism at a variety of enzymatic steps.  Clinical consequences of aberrant methionine metabolism are common and may result in a plethora of consequences including: aberrant neurotransmitter metabolism, developmental delay, psychiatric disorders, oxidative stress, compromised DNA synthesis and repair, immune dysregulation, carcinogenesis, impaired innate detoxification, and perhaps increased risk for autism spectrum disorder. The most common SNPs and epigenetic disruptors of methionine metabolism will be discussed, and protocols for successful remediation will be provided. The second talk will present case studies. The case studies will provide patient symptoms and comprehensive laboratory testing before and after clinical intervention.

 

Learning objectives

Upon completion of this activity participants will be able to:

  1. Discuss the prevalence of NAFLD and the basic mechanisms involved in the development and progression of the disease process.
  2. Explain the pathophysiological implications of NAFLD and define the key causal factors of the disease.
  3. Describe the metabolic abnormalities in lipid and lipoprotein metabolism associated with NAFLD and apply them to cardiovascular risk assessment in patients.
  4. Justify and apply appropriate laboratory testing to identify the primary risk factors for NAFLD and associated cardiovascular disease.
  5. Recognize when to consider evaluation of methylation and transsulfuration disruption.
  6. Discuss the three primary aspects of methionine metabolism as it relates to pathophysiology.
  7. Describe safe and efficacious protocols for remediation of abnormal methionine metabolism.
  8. Recall the primary SNPs involved in abnormal methionine metabolism.

 

 

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