Acupuncture Continuing Education

California Nursing CEUs Online

Nursing Contact Hours

California Board of Registered Nursing CEU Provider #CEP 15110

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High Cholesterol Pt. 1: Western Medicine

 This course covers western medicine diagnosis and treatment for high cholesterol and triglycerides. 

This course is approved by the California Board of Registered Nursing for 7 nursing CEUs for nursing continuing education credit.

Download the course, complete the online quiz, and receive immediate license credit!

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High Cholesterol Pt. 2: Chinese Medicine Theory

This course covers Traditional Chinese Medicine theoretical principles for the diagnosis and treatment of high cholesterol and high triglycerides.  Learn Chinese Medicine differential diagnosis for the treatment of hyperlipidemia.Download the course, complete the online quiz, and receive immediate license credit!

This course is approved by the California Board of Registered Nursing for 4 nursing CEUs for nursing continuing education credit. 

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High Cholesterol Pt. 3: Chinese Medicine Dietetics

 Learn Chinese medicine food treatments to lower cholesterol and triglyceride levels.  Note: Part Two, Chinese Medicine Theory, is prerequisite to taking this course. Download the course, complete the online quiz, and receive immediate license credit!

This course is approved by the California Board of Registered Nursing for 12 nursing CEUs for nursing continuing education credit.   

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Prescription Drug Addiction

The course Prescription Drug Addiction is an important and insightful work covering the mechanisms of addictions, insights on recovery from physicians, family support for addicts, and the relationship of pain management and addiction.  This course covers the nature of addiction as a chronic, progressive disease and details concerning the specific  prescription drugs involved in abuse are presented.  Methods for recovery for the addict and support groups such as friends, family, and medical professionals are presented including treatment options such as medical detox and family interventions.  Also, a special section on personal insights into the process of addiction and recovery from several prominent physicians is included in this course. Simply purchase and download the course material (PDF document), complete the online quiz, and receive 7 contact hours for California nursing continuing education credit.

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Nursing Continuing Education Online

Sample Course Material

High Cholesterol Pt. 1: Western Medicine

Part One of this three part series on high cholesterol and high triglycerides is approved for 7 continuing education hours.  Part One covers western medicine diagnosis and treatment.  Part Two covers Chinese medicine theory for the treatment of hyperlipidemia.  Part Three covers Chinese medicine dietetics food treatment therapy for hyperlipidemia.

Part One:
Learn the statistical prevalence, pathophysiology, signs and symptoms, and serum lipid levels relevant to an understanding of hyperlipidemia.  Learn the role that chylomicrons, very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL) play in high cholesterol and high triglycerides.  Learn about drug treatment options including HMG-CoA reductase inhibitors (statins), bile acid sequestrants, nicotinic acid, and fibric acids.  This course covers in detail the diagnosis and treatment of high cholesterol and triglycerides according to western medicine.

Introduction
1. Dyslipidemia in Western Medicine
1.1 Definition
1.2 Prevalence
1.3 Pathophysiology
1.4 Signs and Symptoms
1.5 Description of Lipoproteins
Lipoprotein Structure
LDL Cholesterol (LDL-C)
HDL Cholesterol (HDL-C)
VLDL Cholesterol (VLDL-C)
Chylomicrons
Characteristics of the Major Lipoprotein Classes
Characteristics of Lipoproteins
1.6 Serum Lipid Levels
Total Cholesterol
LDL Cholesterol
HDL cholesterol
Triglycerides
VLDL Cholesterol
ATPIII Serum Lipid Level Classification (mg/dL)
1.7 Cholesterol Ratios
1.8 Determining Risk
High-risk
Intermediate Risk
Low-risk
1.9 Therapeutic Options
Drug Treatment
Effects of the major dyslipidemia drugs on serum lipid levels
1.9 Non-Mainstream Ideas about Cholesterol and Dyslipidemia


High Cholesterol Pt. 1: Western Medicine

SAMPLE SECTIONS FROM THE COURSE

 

Introduction

Dyslipidemia affects millions of people worldwide, particularly in areas where fat-rich diets and sedentary lifestyles are prevalent, such as the United States, and is cause for concern due to the increased risk it poses for serious diseases such as coronary heart disease (CHD). While pharmaceutical drug-therapies to reduce total and LDL cholesterol may be necessary in some cases, Chinese medicine offers complementary preventative and remedial therapy options which, when appropriate, are safe, effective, and employable with a basic understanding of Chinese medical ideas. This course aims to provide nurses and other biomedical health care providers with the fundamental knowledge needed to apply Chinese medicine dietary and lifestyle practices, as well as simple herbal remedies, in the management of dyslipidemia patients.


1. Dyslipidemia in Western Medicine

1.1 Definition

Dyslipidemia is defined as disorder of lipoprotein metabolism, including lipoprotein overproduction or deficiency. Dyslipidemia may include elevated plasma concentrations of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglyceride, and a decrease in high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein plasma concentrations. Hyperlipidemia refers to higher than normal levels of plasma lipids, including cholesterol, cholesterol esters, phospholipids, and triglycerides. All of these lipids are transported in the plasma bound to proteins, and these larger compound molecules are called lipoproteins. Lipoproteins have been classified on the basis of their densities into five major classes:

• chylomicrons
• very low-density lipoproteins (VLDL)
• intermediate-density lipoproteins (IDL)
• low-density lipoproteins (LDL)
• high-density lipoproteins (HDL)

When hyperlipidemia is defined in terms of elevated serum lipoproteins, the term hyperlipoproteinemia is used. Higher than normal serum cholesterol is termed hypercholesterolemia, and higher than normal serum triglyceride is termed hypertriglyceridemia. The main risk associated with dyslipidemia is atherosclerosis and subsequent increased risk for coronary heart disease (CHD) and other vascular diseases.


1.2 Prevalence

In recent years there are many studies showing direct correlation between incidence of coronary heart disease (CHD) and elevated total and LDL cholesterol levels. According to the third report of the Adult Treatment Panel (ATP III), issued by the National Cholesterol Education Program (NCEP) in May 2001, each year approximately 1.5 million Americans experience an acute myocardial infarction (MI), and one-third of them do not survive. Adoption of NCEP guidelines for the management of dyslipidemia means many more patients are now candidates for intensive lipid-lowering therapy. The NCEP estimated that under its 2001 guidelines, the number of Americans qualifying for dietary treatment would rise from 52 million to 65 million, and the number of candidates for drug therapy would nearly triple—from 13 million to 36 million.


1.3 Pathophysiology

The main risk of dyslipidemia is atherosclerosis (the leading cause of death and disability in the developed world) and the ensuing risk atherosclerosis poses for coronary heart disease (CHD), myocardial infarction (MI), cerebrovasular accident (CVA), peripheral arterial disease, carotid artery disease, abdominal aortic aneurysm (AAA), etc. Atherosclerosis is a subset of arteriosclerosis (hardening of the arteries), and is the formation of atheromas (fibrous fatty intimal plaques) in arterial walls. The exact pathogenesis of atherosclerosis is controversial and complex, but a simplified explanation is as follows:

Atherosclerosis begins when monocytes congregate on arterial walls in response to lipoprotein oxidation, creating a fatty streak (yellow streak of lipid-filled macrophage foam cells) on the arterial wall. The monocytes leave the bloodstream and enter the arterial intima where they become macrophages. The macrophages then phagocytize the oxidized LDL cholesterol and die, thus contributing to the lipid component of the fatty streak. Fatty streaks represent the initial lesion of atherosclerosis, are asymptomatic, and are present in the aorta and coronary arteries of most individuals by age 20.

As the fatty streak evolves into a more complicated atherosclerotic lesion, smooth-muscle cells accumulate within the expanding intima and the amount of extracellular matrix increases. Thus begins the formation of the fibrous cap, which separates a necrotic core of cellular debris, degenerating foam cells, and cholesterol crystals from the arterial lumen. The plaque eventually calcifies, thus stiffening and increasing the fragility of the blood vessel.

The endothelium plays a major role in the pathophysiology of atherosclerosis. Endothelial cells normally provide a permeability barrier, reduce clotting, and regulate vascular tone. In atherosclerosis, the intimal endothelium becomes dysfunctional, loses its ability to produce nitrous oxide (NO), and expresses selectins/integrins for leukocyte recruitment. NO is a vasoprotective gas released by the endothelium which has vasodilatory, anti-thrombotic, and anti-inflammatory effects. NO activates guanylate cyclase to generate cGMP, which causes smooth muscle dilation. NO also blocks vascular inflammation by inhibiting endothelial release of inflammatory granules, and blocks platelet aggregation. Endothelial cells lose their ability to produce NO due to the presence of inflammation, toxins, atherosclerosis, or oxidized LDL.

Atherosclerosis is an inflammatory disease, which is why levels of C Reactive Protein closely correlate with and predict MI. LDL cholesterol, cigarettes and other toxins initiate vascular inflammation, damage the endothelium, and activate macrophages.

Atherosclerosis leads to vascular occlusion when the plaque ruptures or ulcerates, exposing thrombogenic material and leading to the formation of a blood clot, or thrombus.  The thrombus may block the artery, causing MI or CVA, or it may become incorporated into the plaque, enlarging its size. Atherosclerotic dysfunction of the endothelium prevents NO production, inhibiting vasodilation and further aggravating the occlusion. Additionally, embolization may occur if pieces of the plaque, called atheroma, break off and become lodged in distal sites.

In the heart, increased plaque volume causes arterial remodeling, which results in an outward expansion of the coronary arteries. The arteries expand in an effort to overcome the effects of the blockage, allowing blood to flow through the stenosed arterial segment. This expansion continues until the artery reaches its maximum point of flexibility and can no longer accommodate the continued growth of the plaque. This threshold generally occurs when the arterial stenosis reaches 40%. As the plaque ages, an increasing amount of fibrous tissue accumulates, leading to the formation of a fibrous cap, which is vulnerable to rupture. Progressive arterial stenoses eventually lead to ischemic vascular disease, and the rupture of a plaque can cause a myocardial infarction.


1.4 Signs and Symptoms

The primary clinical manifestations of dyslipidemia are ischemic vascular disease, pancreatitis, and xanthomatosis. The major ischemic vascular diseases are atherosclerosis, coronary heart disease, peripheral vascular disease, and cerebrovascular disease. Pancreatitis may be associated with hypertriglyceridemia. Xanthomas are tumor-like collections of lipids (triglycerides and cholesteryl esters) that can arise in the tendons, points of continued trauma, legs, knees and elbows, as well as palms.


1.5 Description of Lipoproteins

Lipoprotein Structure
Lipoproteins are spherical particles made up of hundreds of lipid and protein molecules, yet they are smaller than red blood cells. The major lipids of the lipoproteins are cholesterol, triglycerides, and phospholipids. Triglycerides and cholesterol esters are nonpolar, hydrophobic lipids that make up the core of the lipoproteins. Phosphoplipids and a small amount of unesterified cholesterol cover the surface of the lipoproteins, where they act as the interface between the plasma and core components. A family of proteins, known as apolipoproteins, also occupies the surface of the lipoproteins and plays an important role in the regulation of lipid transport and lipoprotein metabolism.

LDL Cholesterol (LDL-C)
LDL cholesterol typically accounts for 60-70% of total serum cholesterol. LDL is the main atherogenic lipoprotein and is the primary target of cholesterol-lowering therapy. The focus on LDL reduction has been strongly validated in recent years by clinical trials that show the efficacy of LDL-lowering therapy in reducing CHD risk. However, recent studies have also shown the significance of LDL particle size in relation to atherosclerosis and heart disease. Smaller, denser LDL carries more atherogenic potential than larger, less dense LDL particles.

 

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