 Multi-system disease related to abnormal insulin production, impaired insulin

utilization or both
 Referred to as “high sugars” by lay people.
 20.8 Million (7%) people have Diabetes Mellitus in U.S.*
 CDC: Under diagnosed approximately 6 million Americans*
 41 million with Pre-Diabetes*
 90-95% have Type II DM
 American Association of Clinical Endocrinologists – DM guidelines 2007

Incidence by Ethnicity
o Native Americans: highest incidence of diabetes and highest rate of complications
from diabetes
o African Americans and Hispanics have higher incidence of diabetes than
whites.
 Leading cause of heart disease, cerebral vascular accidents, renal failure, blindness, and
non traumatic limb amputation
 Glycemic control reduces complications of diabetes
 Treatment of hypertension and hyperlipidemia is essential

 Disorder of glucose: metabolism related to absent or insufficient insulin supply and or

poor utilization of the insulin available
 Theories – Genetic, Autoimmune, Viral, Environmental

 Insulin metabolism: Hormone produced by the Beta cells in the islets of Langerhans of
pancreas

 Serum glucose is controlled by the emptying rate of the stomach and delivery of
nutrients into the small intestines.
o Food is ingested then broken down into glucose which enters bloodstream.
o Insulin produced in pancreas and released into bloodstream

 Insulin continuously released in small pulstaile increments during fasts (basal

 insulin secretion) and increased levels after eating (prandial)
 Blood Glucose Range: 70-100mg/dl

Counterregulatory Hormones
 Glucagon, growth hormone, epinephrine and corstisol
 Oppose effects of insulin
 Increase BG 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

Physiology: Insulin
 Released from pancreatic beta cells
 Promotes transport of glucose from bloodstream across cell membrane to cytoplasm of
cell
 Impacted by incretin hormone
 o Produced in intestines
o Secreted in response to presence of food
o Increases insulin, decreases glucagon, slows rate of gastric emptying

Rise in Insulin after a meal:

 Stimulates storage of glucose as glycogen in liver and muscle (glycogenesis)
 Inhibits conversion of proteins to glucose (gluconeogensis)
 Enhances fat cells to store triglycerides
 Increase protein synthesis

Fall in insulin overnight:

 Release stored glucose from liver
 Protein from muscle
 Fat from adipose tissue
 Insulin released overnight while sleeping to counteract effects of growth hormone that is
released that elevates blood sugar

Types of Diabetes:
 Type I
 Type II
 Prediabetes (impaired glucose tolerance)
 Secondary diabetes: chemical induced, disease induced, hormonal

Type I Diabetes
 Formerly known as “juvenile diabetes” or “insulin dependent”
 Failure of pancreas: no insulin production
 May be genetic: recessive; possible mutation of chromosome 11
 Viral; HLA – exposure to viral infection
 5-10% of all diabetics
 usually under age 30; peak ages 11-13; higher incidence among whites
o same incidence in males and females
o patients usually thin/lean but can be obese
o progressive destruction of Pancreatic Beta Cells
o requires exogenous insulin
o diabetic ketoacidosis
 acute onset --- 3 P’s:
o polydipsia: excess urination makes patients dehydrated & thirsty
o polyphagia: cellular response to having sugar in blood but not cells
o polyuria: results when kidney starts to excrete sugar after BG levels reach
>250
o weight loss
Prediabetes; Impaired Glucose Tolerance (IGT) or Impaired Fasting Glucose (IFG)
 beta cells become fatigued from overproduction
 beta cells dysfunction is mild – with slight increase in glucose
 patients with impaired glucose tolerance -> inc’d risk for DM II usu within 10 yrs
 approx. 20 million Americans have IGT

Prediabetes
  fasting plasma glucose level 100-126; > 126 = diabetes
 studies show pts with pre-diabetes can prevent/delay development of DM II
through weight loss and regular exercise
 long-term damage esp cardiovascular can happen

Type II – formerly known as “adult onset”

 most prevalent; 90% of patients
 correlated with obesity
 over age of 35; also in young with inc’d childhood obesity
 genetics: dominant and multifactorial
 insulin resistance
 highest among Native Americans and Hispanics followed by African Americans
 pancreas usually continues to form some insulin
 insulin amt is usu insufficient to meet body’s needs and/or poorly utilized by
tissues -> results in Hyperosmolar Hyperglycemic Nonketotic State HHNK

Type II Insulin Resistance

 body tissues don’t respond to insulin
 insufficient # of receptors or receptors unresponsive to insulin
 hyperglycemia and hyperinsulinemia

Metabolic Syndrome: cluster of abnormalities working synergistically to greatly increase

risk for CV disease and diabetes
 elevated insulin levels due to insulin resistance, high triglycerides, decreased HDL,
increased LDL, HTN, obesity, sedentary lifetstyle, 34% Americans
 treatment: weight loss and exercise

Type II – nonspecific manifestations

 3Ps, fatigue, recurrent infections, visual changes, prolonged healing times

Type II Diagnosis
 urine: check protein, ketones; kidney function tests, BMI > 25
 Fasting Plasma Glucose – no caloric intake for at least 8 hours
o >100 --- <126 Impaired Fasting Glucose
o critical values <60 or > 500
 Random Glucose – not ideal test
o can be drawn any time; > 180 on 2 occasions
o meals, drugs, stress can cause increase
 Two Hours Oral Glucose Tolerance Test
o Multiple blood draws over 2 hours after a glucose load of 75g
o > 200 or more = diabetes
o > 140 and < 199 = pre-diabetes

 Glycosylated Hemoglobin A1C (HbA1C) – becoming standard test

o Glucose attaches to Hgb and remains attached to RBC for lifespan (90 days)
o Indicates overall glucose control for previous 90 days
o Near-normal levels over time have greatly reduced risk for development of
complications
 o Normal range = 4-7%
o Goals: A1C level of 6.5% or less (BG around 120)
o Conditions affecting RBC turnover may alter HbA1C (blood loss, hemolysis)

Type II Treatment
 Drug therapy: exogenous insulin
 Rapid-acting: lispro, aspart, gluisine
o Onset:15 minutes; Peak: 60-90 min; Duration: 3-4 hours
 Short-acting: regular
o Onset: 1/2-1hr; Peak: 2-3 hours; Duration: 3-6 hours
 Intermediate-acting: NPH or Lente
o Onset: 2-4 hours; Peak: 4-10 hours; Duration: 10-16 hours
 Long-acting: glargine, detemir
o Onset: 1-2 hours; no pronounced peak; Duration: 24+ hours

Insulin Admixture
1. rotate NPH bottle, draw back amt of air into syringe that equals total dose
2. inject air equal to NPH dose into NPH vial & remove syringe
3. inject air equal to regular dose into regular vial
4. invert regular vial and withdraw regular dose
5. without adding more air to NPH vial, withdraw NPH dose

Insulin Administration Sites: posterior upper arms, ventrogluteal, upper thighs, abs
 Rotate sites to prevent adipose atrophy and irritation or infection

Insulin Pump: catheter delivers insulin; sensor under skin continuously sends data to
transmitter
 change site every 2-3 days; check site for redness/signs of infection

Insulin Jet: delivers insulin in fine pressurized steam through skin w/o needle
 Peak onset occurs earlier, thorough training/monitoring needed

Intensive Insulin Therapy: multiple daily insulin injections together with frequent self-
monitoring of blood glucoses
 Need to check glucose 4-6 times daily

Treatment: Oral Agents

Sulfonylurea (Micronase) – increase insulin from pancreas
Meglitinides (Prandin) – rapidly absorbed; increase insulin from prancreas
Biguanides (Metformin) – reduce glucose production by liver
Alpha Glucosidase Inhibitors (Precose) – slows small intestine’s CHO absorption
Thiazolidinediones; TZD’s(“Actose”) – use with caution with cardiac patients

DPP-4 (Dipetidyl Peptidase) Inhibitors Oral

 New class of glucose-lowering drugs
 Galvus (vildagliptin)
 DPP-4 normally inactivates incretin hormone
 Incretin is released throughout the day in response to meals
 Incretin increases insulin synthesis and release from the pancreas
  Low risk of hypoglycemia (respond to presence of glucose)

Amylin Analog (Symlin)

 Type I and II
 Adjunct to insulin for better control
 Thigh or abdomen SQ
 Cannot be mixed with insulin
 Slows gastric emptying & reduces post-prandial glucagon secretion
 May cause severe hypoglycemia in Type I

Incretin Mimetic (Byetta)

 Type II in place of insulin; similar to hormone
 Suppression of glucagon, slows gastric emptying
 Reduce intake by decreasing appetite
 SQ
 Now approved as monotherapy

BE AWARE OF MEDICATIONS THAT AFFECT BLOOD GLUCOSE LEVELS OR INTERACT

WITH SULFONYLUREA DRUGS!

Pancreas, pancreas-kidney transplantation & Islet Cell Transplant:

 Indications: used for some pts with Type I. Some receive kidney with pancreas due
to nephropathy present with current kidney.

Complications
 Hypoglycemia, hyperglycemia, DKA, Hyperosmolar Hyperglycemic State
 Somogymi Effect: rebound effect of excessive insulin usually at night
 Dawn Effect: hyperglycemia present on awakening impacted by release of GH
during sleep
 Lipodystrophy: hypertrophy or atrophy of s.c. tissue due to frequent use of same
injection site or an immune reaction to impurities in insulin

Hypoglycemia Symptoms: glucose < 70

 Skin: cool & clammy
 Perspiration: profuse
 Mental status: anxious, nervous, irritable, confusion, seizures, coma
 Weakness, diplopia, hunger, tachycardia, palpitations
 Ketones: negative
 Tx: rapid acting sugars (juice, candy), IV dextrose, or glucagon followed by complex
CHO

Hyperglycemia Symptoms: glucose > 250

 Skin: hot & dry, dehydration
 Respirations: rapid, deep with acetone to breath
 Mental status: varies from alert to stuporous, obtunded or frank coma
 Ketones: positive

Somogyi Effect: rebound effect of insulin overdose induced AM hypoglycemia

  Results in dec’d BS in middle of night as response to inc’d insulin
 Compensatory mechanisms occur to raise glucose
o Release of counterregulatory hormones -> lipolysis, gluconeogenesis,
glycogenolysis
o Results in overcompensation -> rebound hyperglycemia & ketosis in AM
 Problem: possible undetected hypoglycemia during the night
 Treatment: check BS between 2 and 4AM
o If AM BS too low, reduce PM dose of insulin or eat substantial bedtime snack

Dawn Phenomenon: hyperglycemia noted on awakening in AM from release of

hormones in predawn hours
 Growth hormone is possible factor
 Affects majority of those with diabetes but most severe in adolescence
 Problem: high BS usually after 3AM
 Treatment: check BS between 2-4AM
o If BS high, increase insulin and eat bedtime snack
o Change timing of PM intermediate acting from dinnertime to bedtime

Diabetic Ketoacidosis (DKA)

 Profound insulin deficiency; hyperglycemia BS > 300
 Ketosis, acidosis, dehydration
 Fruity odor to breath, Kussmaul respirations
 Anorexia, nausea, vomiting
 Lethargy, weakness, altered mental status
 Lead to coma, electrolyte imbalance, death

Hyperglycemic Hyperosmolar State (HHS)

Hyperosmolar Hyperglycemic Nonketotic State (HHNK)
 Produce enough insulin to prevent DKA
 Not enough insulin to prevent osmotic diuresis, hyperglycemia or ECF depletion
 Increase in serum osmolarity from high BG; produces neurological manifestations
(coma, seizures, stroke like sx)
 BS > 400
 Ketones are absent
 Fewer sx seen with HHNS so BS can get high!

Treatment of DKA and HHS

 Medical emergency
 IV administration of NSS or ½ NSS, regular insulin
 When glucose < 250, add IV glucose (D5½)
 Electrolyte replacement
 Bicarbonate for DKA in pH < 7.10
 Treat underlying cause and complications; monitor cardiac ftn

Chronic Complications
 Cataracts, retinopathy/blindness, infections like gangrene
 Neuropathy, arteriosclerosis, MI, kidney disease, valve disease, CVA, ED
Nutritional Therapy: counseling, well-balanced diet, education, decrease alcohol

Nursing Care
 Self monitoring of blood glucose levels
 Stress of acute illness and surgery
 Patient education: medication, follow-up visits to specialists, foot care
o Risk of amputation 15x in diabetics
o Daily foot assessment with mirror, proper footwear, podiatrist visits

Home Care of Diabetic when Ill:

 illness causes increased BS
o eat regular diabetic diet, increase noncaloric fluids
o continue with oral agents/insulin
o monitor BS q4H; if > 240 check urine for ketones & report to MD
 illness may cause decreased PO intake:
o supplement CHO food intake with CHO-containing fluids + oral
agents/insulin
o notify MD immediately if unable to keep any food/fluids down

Exercise
 lowers BG by increasing CHO metabolism
 fosters weight reduction & maintenance
 increases insulin sensitivity
 increases HDL
 decreases triglyceride levels, lowers BP, reduces stress & tension