1. Obesity

2. Cardiovascular

3. Kidneys

4. Vascular disease

- Regulates the rate of carbohydrate, fat and protein metabolism

- Binds with a receptor on cell membrane, is transported into the cell

- Stimulates storage of glucose as glycogen

- Inhibits glucogenesis

- Stimulates protein synthesis

- Glucose is locked out of the cell

- Cells become energy depleted

- Increased Blood suagr exerts a strong osmotic force

- ICF becomes dehydrated

- Glucose eventually spills into the urine (glycosuria), you become very thirsty (polydipsia)

1. Insufficient # of beta cells

2. Delayed or insufficient release of insulin

3. Insulin resistance

4. Decreased # of insulin receptor sites

- Symptoms of diabetes and a casual (random, anytime of day no matter when the last meal was) plasma glucose of 200 mg/dL

OR

- FBG (no caloric intake for at least 8 hours) 126 mg/dL.

OR

- 2 hour plasma glucose 200 mg/dL during OGTT (oral glucose tolerance test, using a glucose load containing the equilvalent of 75 g anhydrous glucose dissolved in water)

OR

- A1C > 6.5% (tells us how much glucose is boung to hemoglobin; percentage)

- Onset is most abrupt and rapid

- Some slow but progressive

- Present at ER with ketoacidosis

- Weight loss

- The 3 P's:

-Polydipsia: increased thirst

- Polyuria: increased urintation

- Polyphagia: increased eating

Diabetic Ketoacidosis

(Type 1- DKA)

- Absence of insulin, hyperglycemia

- Occurs hours to days, starts to sleep a lot

- Breakdown of FFA for energy

- Life-threatening

Diabetic Ketoacidosis (DKA)

Type 1 DM

- Severe hyperglycemia ( > 300 - 400 mg/dL)

- Metabolic Acidosis

- Electrolyte imbalance: Na, K, PO4

- Dehydration

- Mental Status changes: lethargy, coma

- Acetone breath

- Kussmauls Respirations- deep and rapid

- N/V

- Arrhythmias

- Hypotension

- Weakness, muscle flaccidity

A1C level < 7%

(Less problems with neuropathy, less problems with eyes and kidneys)

- Insulin

- Diet

- Exercise

- Persistant hyperglycemia associated wtiih relative insulin deficiency

- Developed antibodies

- Accounts for 90-95% of DM in US

- Autosomal dominant gene on chromosome 7 & 20

- No correlation with HLA type found yet

- 2 sub-types (Non-Obese and Obese [80%])

- Beta cell exhaustion

- Increased production of hepatic glucose

- Insulin level may be normal, increased, or decreased

- Insulin resistance problems

- # of insulin receptors may be decreased

- May have decreased tissue response to insulin

- Ketosis resistant- some may present with ketosis

Insulin resistance (metabolic syndrome)

Type 2 DM

-Impaired Glucose Tolerance

- Hyperlipidemia

- Obesity: truncal or central

- Hypertension

- Obesity ( > 20% over ideal body weight)

- HTN

- Hyperlipidemia

- Age > 40 years

- Family history

- Race (Native American, Hispanics, African American)

- Women with hx GDM or delivery of baby > 9 lbs.

- Occasional glucose intolerance

- Insidious

- Gradual

- May be undetected for years

- Marked hyperglycemia (550mg- > 1000 mg/dL)

- Diagnosed when patient seen for another condition

- Fatigue

- Irritability

- Poor healing

- Visual problems

- Polydipsia

- Polyuria

- Nocturia

- physically inactive,

-First degree relative with it

- Member of high risk population (latino, african amer. ect.)

- Are hypertensive

- Have an HDL < 35 mg/dL &/or triglycerides > 250 mg/dL

- Have PCOS

- History of vascular disease

- S/b if > 45 years old especially if BMI > 25 kg/m2

- Achieve maintain near normal BG levels

- Prevent acute complications (hypoglycemia & hyperglycemia)

- Prevent chronic complications (CV disease, nephropathy, retinopathy, peripheral neuropathy)

- Diet

- Exercise

- Medications:

Oran Anti-diabetics (metformin)

Insulin

Other

Medical Nutritional Therapy (MNT)

Emphasis placed on achieving glucose, lipid, B/P goals

- Calorie reduction

- Weight loss

Goals for MNT

Medical Nutrition Therapy

- Use of glycemic index may be an additional benefit

- Low Carb diets not recommended

- Low protein (0.8 g/kg)

- Saturated fats s/b < 7% of total calories

- Intake of trans fat s/b minimized

- Benefit from chromium not proven

- Weight loss recommended for all overweight

- Increase physical activity "(30-45 min/day x 3 days/wk)

- Drug Rx for obesity and surgery for selected pts

- Non-nutritive sweeteners within acceptable levels

- Enhance the effects of insulin

- Increase the sensitivity of muscle tissue to insulin

- lower BG levels

- increase weight loss

- decrease levels of cholesterol and triglycerides

- Monitor BG levels before, during, and after

- Patients must have a functioning pancreas

- Sulfonyureas

- Biguanides

- Alpha-Glucosidase Inhibitors

Sulfonyureas

(Oral Anti-diabetic Agents)

Stimulates beta cells to release insulin

(Glyburide [Diabeta, Micronase])

(Glypizide [Glucotrol])

Biguanides

(Oral Anti-diabetic agents)

increase cell sensitivity to insulin increase gas

(metformin)

Alpha-Glucosidase inhibitors

(Oral Anti-diabetic Agents)

delays CHO breakdown in gut

(acarbose and miglitol)

- Short or rapid acting

- Intermediate acting

- Long acting

Types of insulin...

(3)

- Hypoglycemia

- Lipodystrophy

- Allergies (rare)

- Somogyu Phenomenon

Shaky

weakness

hungry

tremors

pallor

tachycardia

diaphoretic

confused

uncoordinated

loss of consciouness coma

BG < 70 mg/dL

- Paradoxical decreased in BG followed by increase in BG

- Mediated by counterregulatory hormones in response to hypoglycemia

- usually caused by too much insulin

Treatment: Titrate insulin- decreasing dose slowly

- Extremely high BG (500 - >3000 mg/dL)

- Very dehydrated

- Serum Osmolality > 310 mOsm/L

- Insidious

- Mental Status Changes

- Excessive thirst

- Usually brought on by problems with health; MI, Brain attack, MVC, ect.

- IV insulin gtt

- IV fluids

- Correct electrolytes

Glycemic control A1c <7%

-Preprandial (before meal) BG 90-130 mg/dl

- Postprandial (after meal) BG < 140mg/dl

- B/P < 130/80 mm Hg

- Lipids:

LDL < 100 mg/dl

HDL > 40 mg/dl

Triglycerides < 150 mg/dl

> 9% A1C

(RMG > 240 mg/dl)

- Hypoglycemia

- Hyperglycemia

- CV Disease

- Nephropathy

- Neuropathy

- Retinopathy

- Structural damage to basement membranes in vessels

- Interferences with release of oxygen from hemoglobin

- Thickening of vessel walls

CV disease

- CVD major cause of mortality in patients with DM

- DM is a risk factor for CV events, brain attack, PVD

Prevention:

- Blood pressure control

- Lipid Management

- Smoking cessation

- Anti-platelet therapy

- Occurs in 20-40% of patients with DM and is the single leading cause of ESRD

- Microalbuminuria is the earliest sign of kidney dysfunction

- Tight glucose control

- B/P Control

- Optimal glycemic control can substantially reduce the risk and progression of diabetic retinopathy

- Optimal B/P control can reduce the risk and progression of diabetic retinopathy

- Laser treatment

- Regular eye exams - q 6 months

Hypoglycemia unawareness

Gastroparesis

- Impaired sensory function in lower extremeties

- Contributes to injuries to the feet

- Seen in poorly controlled DM

- Several host mechanisms responsible:

-Cell mediated immunity responses decreased

- increased BG leads to decreased A/B properties of leukocytes

- increased BG leads to overgrowth of pathogens