Diabetes Mellitus: “Not So Sweet” Prutha Dave, RN, BSN [email protected] MSN 621 Spring 2009 Alverno College

Diabetes Mellitus: “Not So Sweet”

Prutha Dave, RN, [email protected]

MSN 621 Spring 2009Alverno College

Let’s Learn About Type II Diabetes: Home Page

Navigation

Click Below For Instructions On Navigating the Tutorial:

Pre - Test

Click Below To Take The Pre-Test:

Tutorial Objectives

Quick Facts

Patho & Genetics

Signs & Symptoms

Tests & Diagnosis

Treatment & Medications

Patient Education

Mini QuizMini Quiz

Mini QuizMini Quiz

Mini QuizMini Quiz

Mini QuizMini Quiz

Mini QuizMini Quiz Tutorial

Click Below To Start The Tutorial:

Image retrieved with permission from:http://www.fredscorner.nl/animations.html

Navigation• Click on to go to next slide.• Click on to go back to previous slide.• Click on to go to the home page.• Click on to return back to where you were.• Click on to learn more about the topic.• Role the mouse over or click underlined words to

learn more about them.• Click on to take a quick quiz after each

section. Mini QuizMini Quiz

Note: An incorrect answer page will ONLY allow you to return BACK to the QUESTION.

Objectives of this Tutorial

• After completion of this tutorial the participant will gain a better understanding of Diabetes Mellitus, also known as Type II Diabetes.

• Also the participant will be able to care for a patient with the disease more effectively.

• Topics Covered include:– Pathology & Causes.– Symptoms & Treatment.– Labs/Diagnosis & Patient Education.

Quick Facts• In type 2 diabetes, either the body does not

produce enough insulin or the cells ignore the insulin.

• There are 23.6 million children and adults in the United States, or 7.8% of the population, who have diabetes.

• Significant risk factor for coronary heart disease and stroke.

• Leading cause of blindness and end stage renal disease.

• Major contributor to lower extremity amputations.

• Can be successfully managed with the right patient education.

• Usually affects older adults but becoming common in obese adolescents.

Image retrieved with permission from: http://www.india-shopping.net/india-ayurveda-products/image/diabetes.gif

11. How is Diabetes diagnosed?

a. Two separate fasting glucose measurements of 126 mg/dL or higher

b. Using symptoms such as polydypsia, polyphagia, and polyuria

c. A hemoglobin A1C level of 6.5%

Correct! Yay! Great Job!

Two measurements are required to ensure reproducibility and therefore decrease false positives and increase specificity.

Image retrieved from: Prutha Dave`Family Photos

Oops! Try Again!

Question 2 Question 3Question 1 Question 4 Question 5

Click On The Question To Return To It:


22. A deficiency in which of the following results in hyperglycemia?

a. Glucagon

b. Insulin

c. Ketones

d. Cortisol

Correct! Yay!

INSULIN helps to LOWER blood glucose concentration by MOVING GLUCOSE into BODY TISSUES for energy


33. What is the Metabolic Syndrome?

a. Seen in patients with very slow metabolism

b. Seen in patients who lack growth hormone, insulin, and cortisol

c. Seen in patients with the following cluster of abnormalities: obesity, hyperlipidemia, hypertension, and glucose intolerance

Correct! Yay!

Metabolic syndrome is a combination of abnormalities including high triglycerides, low HDL’s, HTN, and inflammation.


44. Which of the following class of oral hypoglycemic medications can cause

excessive hypoglycemia?

a. Biguanides (Metformin)

d. Statins (Lipitor, Crestor)

c. Sulfonylureas (Glyburide, Glipizide)

b. ACE inhibitors (Lisinopril, Captopril)

Correct! Yay!

Sulfonylureas increase insulin levels and the rate at which glucose is removed from the blood, it is important to know that they can cause hypoglycemic reactions.


55. What are the most common signs of Type II Diabetes?

d. Weight gain, blurred vision, and excessive thirst

a. Palpitations, restlessness, and diarrhea

c. Excessive laughter, bad body odor, and hair loss

b. Dehydration, hypotension, and fatigue

Correct! Yay!


http://www.facebook.com/photo.php?pid=30062411&id=1384885445

Pathophysiology

• Can be due to absolute insulin deficiency or insulin resistance

• A metabolic disorder which is characterized by disturbances in carbohydrate, lipid, and protein metabolism caused by an imbalance between insulin availability and insulin need

• Results in an inability to transport glucose into the cells of the body, thus causing a breakdown of fat and muscle protein

Image retrieved with permission from:http://professional.diabetes.org/Multimedia_Display.aspx?TYP=8&CID=53310

(Porth, 2005)

Video: What Happens in Type II Diabetes?

Video retrieved from with permission from: http://professional.diabetes.org/ResourcesForProfessionals.aspx?typ=17&cid=60425

Click On Video To

View

Insulin

• A polypeptide which has a direct effect in lowering blood glucose level

• Three actions:– Promotes glucose uptake by target cells and

provides for storage as glycogen– Prevents fat and glycogen breakdown– Increases protein synthesis by inhibiting

gluconeogenesis

Insulin Production

• Made by the beta cells of the pancreas (islets of Langerhans)

• Composed of two polypeptide chains: A and B

• Initially made as a larger molecule: proinsulin and then cleaved to the active form of insulin

• Other cleavage product is the inactive C-peptide

Insulin Release1. Glucose enters cell

2. Glycolysis makes ATP

3. ATP production causes K+ channel to close and depolarize the cell

4. Depolarization opens voltage sensitive Ca2+ channels (Ca2+ enters cell)

5. Ca2+ influx causes insulin release by exocytosis

Image retrieved with permission from http://professional.diabetes.org/Multimedia_Display.aspx?TYP=8&CID=53313

Insulin Action

• Travels through the portal circulation to the liver

• Binds to membrane receptor

• Activates intracellular enzymes to increase protein, glycogen, and fat synthesis, as well as increasing glucose transporters

Image received with permission from: http://upload.wikimedia.org/wikipedia/commons/thumb/8/8c/Insulin_glucose_metabolism.jpg/400px-Insulin_glucose_metabolism.jpg

Glucagon: Another Polypeptide

• Antagonist of Insulin• Released during periods of fasting

to maintain blood glucose• Released by pancreatic alpha cells• Causes glycogen breakdown,

gluconeogenesis, protein degradation, all resulting in elevation of blood glucose

• In diabetes, can have a negative effect as glucagon production goes unchecked as cells are starved of glucose resulting in exacerbation of hyperglycemia

Image retrieved with permission from: http://www.endocrineweb.com/insulin.html

http://www.endocrineweb.com/insulin.html

http://www.endocrineweb.com/insulin.html

Pathogenesis

• Genetic and Environmental factors can lead to insulin resistance & decreased release.

• This causes decreased glucose uptake and increased glucose output resulting in hyperglycemia and Type II Diabetes.

Image received with permission from:http://professional.diabetes.org/Multimedia_Display.aspx?TYP=8&CID=53319

Beta Cell Dysfuntion: Another Sign

• Initial decrease in beta cell mass.

• Increased apoptosis of cell and decreased regeneration.

• Long standing insulin resistance – causing the beta cells to get TIRED.

• Glucotoxicity, Lipotoxicity.

• Amyloid disposition causing dysfuction.

Image retrieved with permission from: http://www.bodyclinicindonesia.com/library/beta_cell.jpg

(Porth, 2005)

Genetics and Diabetes Mellitus

• There is a strong inheritance pattern for Type II Diabetes and it is a heterogeneous condition.

• Two major sets of factors play a role in the development of Diabetes Mellitus:

Genetic Factors Environmental Factors

Genetic Factors

(Radha et al, 2003)

•Research shows that Diabetes Mellitus is polygenic Meaning that it has different combinations of gene defects.

•Multiple “diabetogenic genes” or polymorphisms, each insufficient in themselves, must be present in order to cause

diabetes.

•These genetic polymorphisms can affect the

utilization of blood glucose.

Click to Learn about Specific Candidate

Genes Associated with

DM

Polymorphic Genes : Defects to Diabetes

Genes Related to Insulin Secretion

Genes Related to Obesity

Genes Related to Insulin Resistance

Mutations in the following “candidate” genes are seen in persons with Type II Diabetes and may directly contribute to the onset of the disease:

*Click To Learn About Specific Genes

Insulin Secretion Genes

Pancreatic Duodenal Homedomain Gene (PDX 1) – a transcription factor gene which

regulates pancreatic devleopment and islet cell

function.

Human Insulin Gene (INS) –transcription of the insulin gene is the restricting step for insulin

synthesis and secretion.

Beta Cell Genes (SUR/KIR 6.2) – these genes encode components of the B-Cell K ATP channel which mediate glucose

metabolism and membrane depolaration to cause insulin realease.

(Radha et al, 2003)Images retrieved from: Microsoft Word Clipart 2003

Insulin Resistance Genes

Peroxisome Proliferator Activated Receptor Gene y (PPAR-y) –a transcription factor gene

associated in the regulation of adipocyte gene expression and glucose metabolism.

Insulin Receptor Substrate Gene (IRS) – this gene is shown to be associated with decreased insulin sensitivity.

Glucose Transporter Gene (GLUT) – acts as a sensor to the B-cell

and as a major signaling molecule.

(Radha et al, 2003)Images retrieved from: Microsoft Word Clipart 2003

Obesity Related Genes• Research has shown that variations in obesity genes have

resulted in insulin resistance followed with the onset of Diabetes Mellitus. (Radha et al, 2003)

Single nucleotide polymorphisms within this gene have been associated with a risk for Type II Diabetes.

Studies with these genes have shown to be associated with obesity and DM.

Mutations may also cause interference with glucose homeostasis.

Mutations of this gene have been associated with hyperglycemia.

Adiponectin Genes CLICK TO DISCOVER MORE

Uncoupling Protein 2 GenesCLICK TO DISCOVER MORE

Leptin Receptor GenesCLICK TO DISCOVER MORE

Environmental Factors• The complex interactions between genes and the

environment make it difficult to identify a single factor that leads to Diabetes Mellitus. (Radha et all, 2003)

• Environmental Factors Include:Central Obesity Lack of

ActivityUncontrolled Diet Viruses

Toxins (Smoking)

What is one function of insulin?

a. Promote weight loss

b. Causes glycogen breakdown

c. Increases protein synthesis

d. Elevate blood glucose

MINI QUIZ: TEST YOUR KNOWLEDGE

Correct! Great Job!

INSULIN promotes glucose uptake, prevents fat and glycogen breakdown, and Increases Protein Synthesis! Good Reading!

Oops! Try Again!


The release of Glucagon has a positive effect on patients with Type II Diabetes: True or

False?

TRUE

FALSE


Correct! Great Job!

Glucagon production can have a NEGATIVE effect if it goes unchecked as cells are starved of

glucose resulting in exacerbation of hyperglycemiaImage retrieved from: Prutha Dave`Family Photos

Sorry! Try Again!


Signs & Symptoms• Sneaky onset• Most common signs: The “Polys”

– Polyuria

– Polydipsia

• Blurred Vision• Fatigue• Skin Infections• Paresthesias • Weight loss at first

Image retrieved with permission from: http://en.wikipedia.org/wiki/Diabetes

Which symptom is the patient speaking of when she says she is having an abnormal touch sensation?


Polyuria

Gas

Presyncope

Paresthesias

Correct! Great Job!


Uh-oh! Try Again!


Tests and Diagnosis TESTS TO KNOW:

• Fasting Plasma Glucose: – A blood test that measure the blood glucose level after a person has

been fasting for at least eight hours. This is the fastest, most reproducible, and cheapest method to make the diagnosis.

• Oral Glucose Tolerance Test: – A test in which a 75g dose of a sugary solution is given and then 2

hours later the blood glucose level is measured. This test is slightly more sensitive than the plasma glucose.

• Glycosylated Hemoglobin (HbA1c): – Measures the percentage of red blood cells that have glucose bound to

them and is useful in monitoring glycemic control. Not recommended for routine diagnosis.

FASTING PLASMA GLUCOSE : CLICK TO LEARN MORE

ORAL GLUCOSE TOLERANCE TEST : CLICK TO LEARN MORE

HbA1c : CLICK TO LEARN MORE

How The Diagnosis is MadeNormal Response

Fasting Plasma Glucose (FPG)• A fasting blood glucose level less than or equal to 110

mg/dl. This must be confirmed on a separate occasion.

Oral Glucose Tolerance Test (OGTT)• 2 hour postload glucose level of less than 140 mg/dl.

Impaired Fasting Glucose &

Impaired Glucose Tolerance

In essence, impaired fasting glucose and impaired glucose tolerance are the same thing, just measured differently.

Impaired Fasting Glucose:– A fasting glucose > 110 and < 126 mg/dl. This is considered a risk

factor diabetes, but by itself, does not make the diagnosis of diabetes. The patient will require close monitoring.

Impaired Glucose Tolerance:– 2-hour glucose results from the OGTT that are > 140 and < 200 mg/dl.

This is also considered a risk factor for future diabetes.

Diabetes A DIAGNOSIS OF DIABETES IS MADE WHEN:

1. Fasting Plasma Glucose level greater than 126 mg/dl on separate occasions.

2. Random blood glucose > 200 with classic symptoms.

3. Oral glucose tolerance tests show that the blood glucose level at 2 hours is > 200 mg/dl. This must be confirmed by a second test on another day.

Which of the following tests is not used for a routine diagnosis of Type 2 Diabetes?


Fasting Glucose Oral Glucose

HbA1c Finger Stick

Correct! Great Job!


Good Job. The HbA1C test is a measurement of glycosylated hemoglobin and is a useful tool for monitoring glycemic control but is not recommended for diagnostic purposes.

Almost! Try Again!


True or False: For a diagnosis for Diabetes to be made a person must have a Fasting Plasma Glucose level greater than 126 mg/dl on only one occasion.

True False

Correct! Yaayy!


Must have a Fasting Plasma Glucose of 126 mg/dl or higher on TWO occasions. Great Job!


Oops! Try Again!


Treatments• Aim to control blood glucose levels

Oral medications which lower blood glucose by a variety of mechanisms

Injectable Insulin which directly lowers blood glucose

• Prevention and reversal of diabetes can be achieved by a strict diet, exercise, and weight loss.

Images retrieved from: Microsoft Word Clipart 2003

http://www.clipartguide.com/_pages/0511-0811-1717-0454.html

http://www.clipartguide.com/_pages/0511-0811-1717-0452.html

Oral Medications• Drugs that cause increased insulin release

– Sulfonylureas (Glyburide, Glipizide)– Sitagliptin (Januvia) *newer drug– Exanatide (Byetta) *newer drug

• Drugs that sensitize cells to insulin– Biguanides (Metformin)– Thiazolidinediones (Rosiglitazone, Pioglitazone)

• Drugs that block carbohydrate absorption– Acarbose

CLICK TO REVEAL MEDICATIONS



Sulfonylureas

• Drugs such as Glipizide and Glyburide• Mechanism: Stimulate insulin secretion by closing

the Beta cell’s K+ channel causing depolarization and calcium influx. See prior slide

• Side Effects:– Hypoglycemia– Rashes– GI upset– Hyponatremia

CLICK TO LEARN THE MECHANISM

Biguanides

• Major drug in this class is Metformin• Mechanism: Makes liver more sensitive to

insulin– Great at inducing weight loss

• Side Effects:– Diarrhea, abdominal pain– Lactic Acidosis- serious and potentially fatal

• Thus avoid in patients with renal insufficiency, liver dysfunction or CHF

CLICK TO LEARN MECHANISM

Thiazolidinediones

• Major drugs in this class are Rosiglitazone (Avandia) and Pioglitazone (Actos)

• Mechanism: Makes peripheral tissues such as fat and muscle more sensitive to insulin

• Side Effects:– Weight gain– Liver toxicity– Fluid retention and edema– Contradicted in CHF

CLICK TO LEARN MECHANISM

Acarbose• Mechanism: Inhibits enteric enzymes that

break down complex carbohydrates, resulting in partial malabsorption of carbohydrates.

• Side Effects:– Bloating– Abdominal discomfort– Diarrhea– Flatulence

CLICK TO LEARN THE MECHANISM

Insulin Formulations

• Regular Insulin- (Clear solution) Short acting insulin and the only form given IV.

• Lente and Ultralente- (Cloudy solutions) Intermediate and Long acting versions of insulin.

•NPH- (Cloudy solution) Intermediate acting insulin. Usually given Subcutaneously (SubQ).

Synthetic InsulinModified to have either very short or long half

lives.

Insulin Lispro (Humalog) and Insulin Aspart (Novolog) have a quicker onset and shorter duration than Regular Insulin.

Insulin Glargine (Lantus) is a very long acting form of insulin.

All are administered subcutaneously.

Characteristics of Insulin

Type Onset (hr) Peak (hr) Duration (hr)

Regular 0.5 2-5 6-8Lispro/Aspart 0.2 0.7 2

NPH 2-4 6-10 14-18

Lente 1-3 6-15 18-26

Ultralente 4-6 8-30 24-36

Glargine 4-6 None 24-36

(Andreoli, 2004)

Profile of Action

Image retrieved with permission from: http://www.endotext.org/Diabetes/diabetes20/figures/figure7.png

Dosing Regimens

Intermediate and long acting insulin's are given to mimic the body’s natural 24 hour basal insulin secretion.

Short acting insulin's are given pre-prandially to mimic nutrient stimulated insulin secretion.

Sample Regimens

Image retrieved with permission from: http://www.deo.ucsf.edu/images/graphs/graph_intense_type2.gif

Side Effects of Insulin

• Hypoglycemia – too much Insulin can cause an abnormal decrease in blood glucose resulting in hypoglycemia.

• Lipohypertrophy at injection site

• Edema

• Weight Gain

• Promotes atherosclerosis at high doses

Image retrieved with permission from: Microsoft Clipart 2003


Which of the following patients would you want to avoid giving a Biguanide to?

Patients with hypothyroidism

Patients with pneumonia

Patients with renal insufficiency and CHF

Patients with overactive bladders

Correct! Great Job!


Sorry! Try Again!


Fill In The Blank:________ insulin is the only form of

insulin given intravenously.

NPH

Aspart

Regular

Lantus

Correct! Yay!


Almost! Try Again!


Patient Education• Patient education will be the single most

important factor on helping a newly diagnosed patient manage their Diabetes.

• CLICK ON THE STAR to learn about outcomes and guidelines for Registered Nurses who are initiating Diabetes Self management education:

IMPORTANT !!Patient EducationIMPORTANT !!

Patient Education

• Describing the diabetes disease process and treatment options

• Incorporating nutritional management into lifestyle

• Incorporating physical activity into lifestyle

• Using medication(s) safely and for maximum therapeutic effectiveness

Click Here To Learn More!!



Click here to Learn More!!

(Funnell et al, 2009)

Patient Education• Monitoring blood glucose and other parameters and

interpreting and using the results for self-management decision making

• Preventing, detecting, and treating acute and chronic complications

• Developing personal strategies to address psychosocial issues and concerns

• Developing personal strategies to promote health and behavior change





(Funnell et al, 2009)

How To Educate Self Management

Describing the Disease

Process: before beginning

education about the disease process,

perform a patient

assessment to gain a better

understanding of the Patient’s

background such as cultural beliefs

as well as readiness to learn.

Teaching NutritionalManagement: first

learn about the patients

current diet and any cultural

influences that may affect diet. Not every

patient will eat the

same or like the same food

that is recommended.

Physical Activity: always, always

promote any physical activity.

Help the patients transition

into incorporating

an exercise

regimen which is appropriate

for them. Again, know

that each patient is exercise.

Safe Medication Use:make sure the

patient understandsthe medication and why and how it will

help manage the disease. Speak clearlyand use simple terms.Also, recommending

The use of a medication box maybe of great help for the newly diagnosed

Diabetic.

http://www.barrysclipart.com/barrysclipart.com/showphoto.php?photo=24916&papass=&sort=1&thecat=197

How To Educate Self Management

Blood GlucoseMonitoring:

help the patient understandthe need for blood

glucose monitoring. Make sure they know

how to use theirspecific device

and have them doa repeat

demonstrationfor you.

Preventing Complications:teach patients

to watch out for any changes in

health status, andwhat specific

symptoms to be aware of. Examples

are eye sight changes or

numbness and tingling.

Psychosocial Issues: Promote discussing

any thoughts or feelings associated

with the new Diabetes diagnosis. Provide resources

for patients to use when dealing

with difficult psychosocial issues

or concerns.

Promoting Health:Always promote healthy lifestyle behaviors such

as quitting smoking, eating healthy, exercising, and

using a family orpersonal support

system to incorporate these

behaviors.

What is one of the most important nursing practices before beginning patient education

for new onset Diabetes?


Making sure that the patient

has all their medications in hand.

Assessing the patients background

and readiness tolearn.

Making sure that theyexercise everyday for

2 hours

Correct! Yay!



Sorry! Try Again!


Name a way that patients can remember to safely take their medications?

Keep all their medication in one

bottle.Slide 82

Obtain a medication pill box with the days listed

and with separate compartments for each

day.

Just double up on medications the next day

if they forget.

Correct! Great Job!


Oops! Try Again!


The End : Credits

*Thank you to my dear husband who put up with me through this crazy semester and for all his medical and technical expertise.

*Thank you to my mom who motivated me to pursue my knowledge in Diabetes.


References • American Diabetes Association, www.diabetes.org.

• Andreoli, T.E., & Carpenter, C.J., & Griggs, R.C., & Loscalzo, J. (2004) Cecil Essentials of Medicine. Philadelphia: Saunders.

• Funnell, M. et al. (2009) National Standards for Diabetes Self-Management Education, American Diabetes Association Diabetes Care, 32, S87-S94 DOI: 10.2337/dc09-S087

• Hansen, L. (2003). Candidate genes and late-onset type 2 diabetes mellitus. Susceptibility genes or common polymorphisms? [Electronic Version]. Dan Med Bull, 50(4), 320-46.

• Jochen, A.L. (2005) Pharmacology of Insulin and Oral Sulfonylureas. Medical Pharmacology.

• Porth, C.M. (2005) Pathophysiology: Concepts of Altered Health States. Philadelphia: Lippincott Williams & Wilkins.

• Radha, V., & Vimaleswaran K.S., & Deepa R., & Mohan, V. (2003). The genetics of diabetes mellitus. Indian J Med Res, 117, 225-238.

• Rossini, A.A., & Mordes, J.P., & Handler, E.S. (1988). Perspectives in Diabetes: Speculations on Etiology of Diabetes Mellitus: Tumbler Hypothesis [Electronic Version]. Diabetes, 37, 257-61.

Documents

Diabetes Mellitus: “Not So Sweet” Prutha Dave, RN, BSN [email protected] MSN 621 Spring 2009 Alverno College