February 16, 2006
| February Newsletter |
The February 16, 2006 meeting was held at Alta Cucina in Johnson City, Tn. Dr. Stephen R. Grubb, an endocrinologist from Charleston, West Virginia, gave the presentation. The topic of discussion was Diabetes and Byetta. Dr.Grubb was one of the original investigators for this drug. Our meeting was sponsored by Lilly.
PRESENTATION HIGHLIGHTS Dual concept of Type 2 Diabetes:
Insulin resistance Insulin deficiency = hyperglycemia
Alternative view:
Insulin resistance = increased beta cell workload Insulin deficiency = diminished beta cell response
Role of glucagons in type 2 diabetes:
Overnight glucose production by the liver is a function of glucagons. Postprandial glucose is contributed to increased glucagon levels not suppressed by the type 2 diabetic. Increased glucagon increases hepatic glucose synthesis. Fasting sugar is a reflection of hepatic glucose output.
Diminished beta cell response:
Decreased insulin secretion is a response to elevated glucose but is particularly a decrease in first phase insulin. Decreased first phase insulin response = increased glucose load requiring additional insulin response hours later. Normally insulin levels peak approximately 45 minutes into a meal. Increased beta cell response results in decreased glucagon because of beta cell response in association with decreased beta cell workload. Normal postprandial blood sugars are less than 140 in non-diabetic.
Type 2 Diabetes:
Carbohydrate meal = increased beta cell response/ loss of first phase insulin response/ glucagon not suppressed/ continued production of glucose by the liver culminating in increased postprandial blood sugars.
Postprandial blood sugars:
More levels should be done diagnostically and therapeutically.
A1C < 7.9 - 75% of A1C is from PP blood sugars, 25% from fasting BS. Fasting blood sugar plays a bigger role as the A1C increases.
PP blood sugar observation, control and awareness are the most lacking areas in diabetes care.
Retinopathy can be associated with an A1C of ~ 5.2%.
GLP 1 deficiency in type 2 diabetes:
More glucose is made because glucagon is stimulating hepatic production of glucose; GLP1 normalizes this process in the non-diabetic
GLP1 secreted by intestinal L cells is released upon ingestion of food and glucose reaching the ilium. It stimulates beta cell insulin release; it’s a glucose dependant process. There is a better response to a rising BS than occurs in the absence of GLP1.
Increased beta cell response and decreased beta cell workload occur because of suppression of post prandial glucagon.
Byetta:
The first agent that suppresses during meal and after meal glucagon elevation.
Decreased glucagon = decreases hepatic glucose production
GLP1 reduces gastric emptying
Gastroperesis- most diabetics do not truly have this. BS increases = meal = more glucose in the stomach = glucose not absorbed in stomach its absorbed in the intestines. Glucose emptying is delayed in the presence of high blood sugars. Glucose emptying is enhanced when BS are low.
Byetta: available in 5mcg/sq or 10mcq/sq doses. Mimics natural physiology for self-regulation glycemic control
Provides simple, fixed BID dosing before the morning and evening meals
Most common adverse events include hypoglycemia, when used with a sulfonylurea, and nausea, both mild to moderate.
Byetta increases acute beta-cell response by enhancing glucose-dependent insulin secretion from beta cells in the pancreas
Restores first phase insulin response
Decreases beta-cell workload
Suppresses glucagon secretion from alpha cells in the pancreas, which leads to reduction of hepatic glucose output from the liver
Slows gastric emptying, which allows for timely absorption of nutrients
Reduces food intake
Used as adjunctive therapy to improve glycemic control in patients with type 2 diabetes mellitus who are taking metformin, a sulfonylurea, or a combination of both but have not achieved adequate glycemic control.
Business Meeting
Minutes accepted from January 2006 meeting.
Treasurer’s report: N/A
Nomination committee: Report given by Tina Killebrew, voting by paid members in favor of Kathy Sharp for new NETNPA president.
Congratulations to president elect Kathy Sharp
Kay Bone addressed the issue of bi-law changes and request this be tabled until the next meeting.
TNA list serve now active
Member vote to continue current NETNPA.com website and keeper Melissa Shelton. Vote in favor of paying the fee of $ 277.00 for the yearly plan and domain name registration.
Legislative update: Wendy Vogel addressed TNA list serve activation, guidelines for new grads and Medicare part D.
TNA members will now receive legislative update emails to keep members informed of bills impacting the nursing profession and Tennessee healthcare.
Guidelines for new Advance Practice Nurses found at Tennessee.Gov > Board of Nursing > Advance Practice Nursing > New graduates of Advance nursing program guidelines
There is important info about supervision, use of title, and writing prescriptions as a new grad without certification.
Wendy proposed consideration for holding clinics in Tri-Cities area to help enroll patients in the Medicare part D plans.
Will send out info about training sessions and dates of clinics and also post on website
Wendy Vogel suggested bereavement fund for local NP’s and families: Motion passed Gift of $100.00 will be sent to the family of Paige Connell Odum in memory of her professional gifts and talents.
Informational website for Nursing can be found at www.nursingadvocacy.org
Salary survey update:
Kathy reports the survey will be published in the spring edition of the TN Nurse Magazine.
Feb 2006 in the Non-Physician Practitioner News attention was issued to subject of Medicare ruling that NPPs cannot bill Medicare for readmission services in SNF.
Submitted by Tracey Hensley Secretary NETNPA 3/8/2006 Comments/Corrections/Suggestions to Baby2spoil@yahoo.com
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