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Diabetes mellitus is the leading cause of ____________, ________________, ____________, ___________, and ______________.
- Heart disease
- Cerebral vascular accidents
- Renal failure
- Blindness
- Non-traumatic limb amputation
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Complications of diabetes is reduced by _____________
glycemic control
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Treatment of __________ and ___________ is essential
- hypertension
- hyperlipidemia
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Diabetes Mellitus
- Disorder of glucose metabolism related to absent or insufficient insulin supply, and/or poor utilization of the insulin available.
- Theories: genetic, autoimmune, viral, and environmental
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Serum Glucose
- ... is controlled by the emptying rate of the stomach and delivery of nutrients into the small instestines
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Bloog Glucose Range
70 - 100 mg/dL
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Basal Insulin Secretion
Insulin that is continuously released in small pulsaatile increments during fasting
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Prandial Insulin Secretion
Increased levels of insulin after eating
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Counter Regulatory Hormones
- Glucagon, Epinephrine, Growth Hormone, and Cortisol
- Oppose the effects of insulin
- Increase blood glucose by stimulating glucose production and liver output
- Combination of insulin and above hormones provide a sustained release of glucose energy during food intake and periods of fasting
- Abnormal levels of hormones may produce DM
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Physiology of INSULIN
- Released from pancreatic Beta cells
- Promotes transport of glucose from the bloodstream across the cell membrane to the cytoplasm of the cell
- Impacted by Incretin hormone
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Rise in insulin after a meal
- Stimulates storage of glucose as glycogen in the liver and muscle (glycogenesis)
- Inhibits conversion of proteins to glucose (gluconeogenesis)
- Enhances fat cells to store triglycerides
- Increases protein synthesis
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Incretin Hormone
- Produced in the intestines
- Secreted in response to the presence of food
- INCREASES insulin, DECREASES glucagon, and SLOWS the rate of gastric emptying
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Fall in insulin during normal overnight
- Release stored glucosed from the liver
- Protein from muscle
- Fat from adipose tissue
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Type I Diabetes
- Formely known as "juvenile diabetes", or "insulin dependent"
- Failure of the pancreas
- Maybe be genetic - recessive (possible mutation on chromosome 11)
- Viral (pt with HLA have exposure to viral infection)
- 5 - 10% of all diabetics
- Usually under age 30
- Peaks from ages 11 - 13
- Incidence is higher in whites
- Same incidence in males & females
- Patients are usually thin/lean, but may be obese
- Progressive destruction of Pancreatic B cells
- Require Exogenous Insulin
- Diabetic Ketoacidosis
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Type I DM: Acute Onset 3 P's
- Polydipsia: excessive thirst
- Polyphagia: excessive hunger
- Polyuria: increased frequency of urination
- weight loss
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Prediabetes (Impaired Glucose Tolerance [IGT]) (Impaired Fasting Glucose [IFG])
- Beta cells become fatigued from overproduction
- Beta cell dysfunction is mild - with slight increase in glucose
- Paitents with IGT are at increased risk for DM II, usually within 10 years
- Approximately 20 million Americans (ages 40 - 75 yrs) have IGT
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Prediabetes
- Fasting Plasma Glucose Level above 100
- Studies show that people with pre-diabetes can prevent or delay the development of type 2 diabetes through changes to their lifestyle that include modest weight loss and regular exercise
- Research has shown that long-term damage, especially to the cardiovascular system, already may be occuring during prediabetes
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Type II Diabetes
- Formerly known as "Adult Onset"
- Most prevalent (90% of patients)
- Correlated with obesity
- Over the age of 35
- Also identified in younger people (especially with increased childhood obesity)
- Genetics - dominant and multifactorial (linked to chromosomes 20, 7, 12)
- Insulin resistance
- Highest among Native American and Hispanics followed by African Americans
- Pancreas usually continues to form some insulin
- Insulin amount is usually insufficient to meet the needs of the body, AND/OR insulin is poorly utilized by tissues
- Results in HHNK
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DM Type II: Insulin Resistance
- Body tissues do not respond to insulin
- Insufficent number of receptors or receptors are unresponsive to insulin
- Hyperglycemia and Hyperinsulinemia
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Metabolic Syndrome
Cluster of abnormalities working synergistically to greatly increase the risk for CV disease and diabetes
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Abonormalities of Metabolic Syndrome
- Elevated insulin levels (insulin resistance)
- High triglycerides
- Decreased HDL
- Increased LDL
- Hypertension
- Obesity (esp. central obesity)
- Sedentary lifestyle
- Esitmated that 34% of Americans fit this criteria
- Can be treated with weight loss and exercise
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Nonspecific Manifestations with Type II Diabetes
- Can be the 3 P's
- Fatigue
- Recurrent Infections
- Visual Changes
- Prolonged healing times
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Methods of Diagnosis
- Fasting Plasma Glucose
- Random Glucose
- Two Hour Oral Glucose Tolerance Test (OGTT)
- Glycosylated Hemoglobin A1C (HbA1C)
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Fasting Plasma Glucose
- No caloric intake for at least 8 hours
- (>100 - <126) Impaired Fasting Glucose
- Critical Values: < 60 mg/dL or > 500 mg/dL
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Random Glucose
- Can be drawn at anytime
- Meals, drugs, and stress can cause an increase
- > 180 mg/dL on two occasions
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Two Hour Oral Glucose Tolerance Test (OGTT)
- Multiple blood draws over 2 hours after a glucose load of 75 g
- 200 mg/dL or more = Diabetes
- > 140 and < 199 = Pre-Diabetes
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Glycosylated Hemoglobin A1C (HbA1C)
- Glucose attaches to Hgb and remains attached to the RBC for it's lifespan (90 days)
- Indicates overall glucose control for previous 90 days
- Near-normal levels over time have greatly reduced the risk for development of complications
- Normal range = 4 - 7%
- Goal: A1C level of 6.5% or less
- Condtions that effect RBC turnover may alter HbA1C (blood loss, hemolysis, etc.)
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Diagnostic Tests
- Urine: check protein & ketones
- Kidney Function Tests
- BMI - concern with > 25
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Insulin Onset-Peak-Duration
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Insulin Admixture
- 1. wash hands
- 2. gently rotate NPH insulin bottle
- 3. wipe off tops of insulin vials with alcohol sponge
- 4. draw back amount of air into the syringe that equals the TOTAL dose
- 5. inject air equal to NPH dose into NPH vial; remove syringe from vial
- 6. inject air equal to REGULAR dose into regular vial
- 7. invert REGULAR insulin bottle and withdraw REGULAR insulin dose
- 8. without adding more air to NPH vial, carefully withdraw NPH dose
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Insulin Pump
- Glucose monitor which can send wireless glucose value to insulin "smart" pump
- The pump calculates complex math based on measures sent and recommends dosages to patient
- Change site
every two to three days - Check site for redness or other signs of infection
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Insulin Jet
- Delivers insulin in fine pressurized steam through skin without needle
- Peak onset & etc. occur earlier
- Thorough training and monitoring needed
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Intensive Insulin Therapy
- Consists of multiple daily insulin injections together with frequent self-monitoring of blood glucose
- Glucose needs to be checked 4 to 6 times per day
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Oral Agents for Diabetes Treatment
- Sulfonylurea
- Meglitinides
- Biguanidea
- Alpha Glucosidase Inhibitors
- Thiazolidinediones ((TZD's)
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Sulfonylurea
- "Micronase"
- Increase insulin from the pancreas
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Meglitinides
- "Prandin"
- Rapidly absorbed, increase insulin the the pancreas
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Biguanides
- "Metformin"
- Reduce glucose production by the liver
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Alpha Glucosidase Inhibitors
- "Precose"
- Slow down CHO absorption in small intestine
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Thiazolidinediones (TDZ's)
- "Actose"
- "Insulin Sensitizers"; use with caution with cardiac patients
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DDP-4 (Dipetidyl Peptidase) Inhibitors (Oral)
- New class of glucose-lowering drugs
- Galvus (vildagliptin)
- DDP-4 normally inactivates incretin hormone
- Incretin hormone is released from the intestines, it is released throughout the day, and in response to meals
- Incretin increases insulin synthesis and release from the pancreas
- Low risk of hypoglycemia
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Amylin Analog (Smylin)
- Type I and II
- Adjuct to insulin for better control
- Thigh or abdomen SubQ injection
- CANNOT be mixed with insulin
- Slows gastric emptying and reduces post-prandial glucagon secretion
- May cause severe hypoglycemia in Type I
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Incretin Mimetic (Byetta)
- Type II in place of insulin
- Similar to hormone
- Suppression of glucagon, slows gastric emptying
- Reducing intake by decreasing appetite
- SubQ
- Now approved as monotherapy
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Medications that effect blood glucose levels or interact with sulfonylurea drugs -- BE AWARE
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Pancreas, Pancreas-Kidney Transplantation, & Islet Cell Transplant Indications
- Used for some patients with Type I diabetes
- Some recieve kidney with pancreas due to nephropathy present with current kidney
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Complications of Diabetes
- Hypoglycemia
- Hyperglycemia
- Somogyi Effect
- Dawn Effect
- Diabetic Ketoacidosis
- Hyperosmolar Hyperglycemic State (HHS)
- Lipodystrophy
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Somogyi Effect
- Rebound effect in which an overdose of insulin induces morning hyperglycemia
- Results in decreased blood sugar in the middle of the night as a response to increased insulin
- Compensatory mechanisms occur to rain glucose (release of counterregulatory hormones -- lipolysis, gluconeogenesis, glycogenolysis)
- Results in overcompensation
- Leading to rebound hyperglycemia and ketosis noted in the A.M.
- Problem: possible undetected hypoglycemia during the night
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Dawn Effect
Hyperglycemia present on awakening impacted by release of growth hormone during sleep
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Lipodystrophy
Hypertrophy or atrophy of s.c. tussie due to frequent use of the same injection site or an immune reaction to impurities in insulin
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HYPOglycemia Symptoms
- Skin: cool & clammy
- Perspiration: profuse
- Mental Status: anxious, nervous, irritable, mental confusion, seizures, coma
- Misc: Weakness, Double or blurred vision, Hunger, Tachycardia, Palpitations
- Glucose: < 70 mg/dL
- Ketones: negative
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Treatment for HYPOglycemia
- Rapid acting sugars (OJ, candy)
- IV Dextrose or Glucagon ... followed by complex CHO snack
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HYPERglycemia Symptoms
- Skin: hot & dry
- Dehydration: present
- Respiration: Rapid, deep, acetone to breath
- Mental Status: varies from alert to stuporous, obtunded, or frank coma
- Glucose: > 250 mg/dL
- Ketones: positive
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Treatment for Somogyi Effect
- Check blood sugar between 2 and 4 AM
- If this AM blood sugar is low ... then reduce PM dose of insulin or eat a more substantial bedtime snack
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Dawn Phenomenon
- Hyperglycemia noted on awakening in AM due to release of hormones in predawn hours
- Growth hormone is a possible factor
- Affects majority of those with diabetes but most severe in adolescence and young adulthood
- Problem: high blood sugar usually after 3 AM
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Treatment for Dawn Phenomenon
- Check blood sugar between 2 and 4 AM
- If high, then increase insulin and eat bedtime snack
- Change timing of evening or intermediate acting insulin from dinnertime to bedtime
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Hyperglycemic Hyperosmolar State (HHS)
Hyperosmolar Hyperglycemis Nonketotic State (HHNK)
- (Formely HHNS)
- Produce enough insulin to prevent DKA
- Not enough insulin to prevent osmotic diuresis, hyperglycemia, or ECF depletion
- Increse in serum osmolarity
- BS > 400 mg/dL
- High BG produces high serum osmolarity thus producing neurological manifestions (coma, seizures, etc.), strokelike symptoms
- *** Fewer symptoms are seen earlier with HHNS so BS can get quite high
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Treatment of DKA and HHS
- Medical emergency
- IV administration of NSS of 1/2 NSS
- Regular Insulin IV
- When glucose falls < 250 ... add IV glucose (D5 1/2)
- Electrolyte replacement
- Bicarbonate for DKA in pH < 7.10
- Treat underlying cause and complications
- Cardiac monitoring
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Chronic Complications
- Cataracts *
- Retinopathy/Blindness *
- Infections such as Gangrene *
- Neuropathy
- Arteriosclerosis
- Myocardial Infarctions
- Kidney disease
- Valve disease
- Cerebral Vascular Accidents
- Erectile dysfunction
* most common
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Exercise
- Lowers blood glucose by increasing CHO
- ** On occasion, exercise may be a stressor especially in Type I and may raise BS
- Fosters weight reduction and maintenance
- Increases insulin sensitivity
- Increases LDL levels
- Decreases triglceride levels
- Lowers BP
- Reduces stress & tension
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Patient Education
- Medication
- Follow-up visits to specialists
- Foot care - risk of amputation 15x greater in diabetics; foot assessment; podiatrist
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Home care when illness cuases increased BS
- Eat a regular diabetic diet
- Increase noncaloric fluids
- Continue with oral agents and/or insulin
- Monitor BS every 4 hours ... if > 240 check urine for ketones, report + ketones to physician
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Home care if illness leads to decreased PO intake
- Supplement CHO food intake with CHO-containing fluids while continuing with oral agents and/or insulin
- Notify physician immediately if unable to keep and food or fluids down
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