Diabetes Mellitus Review: Chapter 51

Overview and General Physiology of Diabetes Mellitus

• Definition: Diabetes mellitus is a metabolic disorder of the pancreas that significantly impacts the metabolism of carbohydrates, fats, and proteins.
• Normal Blood Glucose Levels: The normal range for blood sugar is defined as $70-110\,mg/dL$.
• Associated Metabolic Findings:
  • Obesity, particularly in the abdominal region.
  • Hypertension (high blood pressure).
  • Elevated triglyceride levels.
  • High levels of low-density lipoprotein (LDL).
  • Low levels of high-density lipoprotein (HDL).
  • Elevated blood glucose levels.

Classification of Diabetes and Pre-Diabetes

• Type 1 Diabetes Mellitus: Previously known as insulin-dependent diabetes mellitus (IDDM). It is characterized by a total lack of insulin production by the beta cells located in the islets of Langerhans within the pancreas. It is considered an autoimmune disorder.
• Type 2 Diabetes Mellitus: Previously known as non-insulin-dependent diabetes mellitus (NIDDM). It is characterized by insulin resistance or insufficient insulin production. It often runs in families and is heavily linked to obesity.
• Pre-Diabetes: Individuals in this category exhibit impaired glucose levels that do not yet meet the criteria for a full diabetes diagnosis. It is measured via two primary tests:
  • Fasting Glucose (FG): A fasting blood glucose level of $100-125\,mg/dL$ after an overnight fast.
  • Oral Glucose Tolerance (OGT): A blood glucose level of $140-199\,mg/dL$ measured $2\,\text{hours}$ after a glucose tolerance test.

Insulin Functions and Pathophysiology of Hyperglycemia

• Primary Functions of Insulin:
  1. Facilitates the transport of glucose into body cells to be used as the preferred energy source.
  2. Promotes the storage of glucose in the liver in the form of glycogen.
  3. Inhibits the breakdown of glycogen back into glucose.
• Mechanism of Hyperglycemia: Hyperglycemia refers to an elevated blood glucose level. Beyond primary diabetes, it can be associated with:
  • Drugs such as loop and thiazide diuretics.
  • Levodopa.
  • Oral contraceptives.
  • Administration of total parenteral nutrition (TPN).
• Physiological Response to Insulin Deficiency:
  • In Type 1 diabetes, insulin production ceases entirely. Blood glucose can rise to levels between $300-1000\,mg/dL$.
  • Lipolysis: Because glucose cannot enter the cells, the body breaks down fat and protein for energy. The breakdown of fat leads to the accumulation of fatty acids and ketones (metabolic byproducts).
  • Ketoacidosis: An accumulation of ketones in the blood leads to metabolic acidosis. In Type 1 diabetes, this can develop suddenly due to the total cessation of insulin.
  • Type 2 Progression: In Type 2, peripheral insulin resistance exists. The body may initially produce extra insulin (hyperinsulinemia), but eventually, the beta cells become exhausted, leading to a decline in production and eventual insulin deficiency.

Clinical Manifestations and Diagnostic Testing

• The Three Classic Symptoms (Three Ps):
  1. Polyuria: Excessive urine production. High blood sugar pulls fluid into the bloodstream, leading to increased output.
  2. Polydipsia: Excessive thirst resulting from the loss of water (dehydration).
  3. Polyphagia: Excessive hunger. Since glucose is wasted in the urine, the body requires alternative fuel, stimulating the appetite.
• Additional Symptoms:
  • Glycosuria: Glucose in the urine, occurring when blood glucose exceeds the renal threshold of $180\,mg/dL$.
  • Weight loss (despite increased eating), weakness, fatigue, and dehydration.
  • Blurred vision (changes in visual acuity).
  • Skin, urinary tract, and vaginal infections due to high glucose levels supporting bacterial growth.
• Diagnostic Blood Tests:
  • Random Blood Sugar.
  • Fasting Blood Glucose.
  • Postprandial Glucose (measured after a meal).
  • Oral Glucose Tolerance Test (OGTT).
  • Glycosylated Hemoglobin (Hemoglobin A1c): Reflects the average blood glucose over the life span of a red blood cell ($120\,\text{days}$).
  • Normal: $< 7\%$.
  • Inadequate control: $\ge 8\%$, reflecting poor control over the previous $2-3\,\text{months}$.

Medical Management and Lifestyle Interventions

• Treatment Modalities: Diet, exercise, insulin therapy, oral antidiabetic agents, and organ/cell transplantation (pancreas or islet cell).
• Dietary Management: This is a major component for every patient. For some with Type 2, dietary modifications and a weight loss of approximately $1500\,\text{calories}$ per day can control the disease and improve insulin use.
• Exercise: Skeletal muscles have receptors that allow glucose uptake independent of insulin during exercise, helping to metabolize carbohydrates and control blood sugar.
• Transplantation:
  • Pancreas Transplantation: Usually performed for Type 1 patients who also have renal failure (combined kidney/pancreas transplant).
  • Islet Cell Transplantation: Insulin-producing cells are harvested from human donors (requiring two pancreases for sufficient cells) or pigs and injected into the peritoneal cavity.

Insulin Therapy Details

• Administration: Insulin cannot be taken orally because gastrointestinal enzymes inactivate it. It is primarily administered subcutaneously, though Regular insulin can be given intravenously (IV).
• Formulations: Derived via genetic engineering using strains of Escherichia coli or chemical modification of pork insulin.
• Dosage and Mixing:
  • Prescribed in units; $U100$ indicates $100\,\text{units}$ per $1\,mL$.
  • When mixing: Withdraw short-acting Regular insulin into the syringe first. Administer within $15\,\text{minutes}$.
  • Warning: Long-acting insulins ($Lantus$ and $Levemir$) cannot be mixed with other types of insulin.
• Injection Sites: The abdomen is the fastest absorption site. Injection sites must be rotated to prevent lipodystrophy (breakdown of fat) or lipohypertrophy (buildup of fat).
• Insulin/Insulin Analog Action (Table 51-3):
  • Rapid-Acting (e.g., Aspart/NovoLog, Lispro/Humalog): Onset $5-15\,min$, Peak $1-3\,hr$, Duration $3-5\,hr$.
  • Short-Acting (Regular/Humulin R): Onset $30-60\,min$, Peak $2-4\,hr$, Duration $5-8\,hr$.
  • Intermediate-Acting (NPH/Humulin N): Onset $1.5\,hr$, Peak $4-10\,hr$, Duration $14\,hr$.
  • Long-Acting (e.g., Glargine/Lantus): Onset $1\,hr$, No Peak (Steady), Duration $24\,hr$.
  • Combination (e.g., Humulin 70/30): Mixes intermediate and short-acting characteristics.

Oral Antidiabetic Medications

• Criteria for Use in Type 2 Diabetes:
  • Fasting blood glucose $< 200\,mg/dL$.
  • Insulin requirement $< 40\,\text{units/day}$.
  • Absence of ketoacidosis, renal disease, or hepatic disease.
• Drug Classes:
  • Sulfonylureas (e.g., Glyburide, Glipizide): Reduce glucose but can cause weight gain and hypoglycemia.
  • Biguanides (Metformin/Glucophage): An insulin sensitizer; helps tissues use insulin more efficiently. Does not cause weight gain. Side effects: upset stomach, diarrhea, and a small risk of lactic acid acidosis.
  • Thiazolidinediones (TZDs - e.g., Rosiglitazone, Pioglitazone): Insulin sensitizers. Can cause weight gain, edema, and liver damage. Requires liver function tests every $2\,\text{months}$ for the first year.
  • Alpha-Glucosidase Inhibitors (e.g., Acarbose, Miglitol): Inhibit the intestinal enzyme that breaks down complex carbs. Must be taken $15\,\text{minutes}$ before meals. Note: If hypoglycemia occurs, it must be treated with glucose tablets/injection, not fruit juice, as the drug blocks carb conversion.

Acute Complications: DKA, HHNKS, and Hypoglycemia

Diabetic Ketoacidosis (DKA)

• Profile: Acute insulin deficiency leading to metabolic acidosis. Common in Type 1 or due to infection/noncompliance.
• Clinical Signs: Warm/dry/flushed skin, rapid/deep Kussmaul respirations, acetone (fruity) breath odor, rapid weak pulse, low BP.
• Lab Values: Glucose $300-1000\,mg/dL$, blood pH $6.8-7.3$, bicarbonate $0-15\,mEq/L$.
• Treatment: IV Regular insulin (approx. $5\,U/hour$), high-volume Isotonic saline ($NS$) at $250-500\,mL/hour$, and electrolyte monitoring (especially potassium).

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNKS)

• Profile: Hyperglycemia without ketosis. Common in older Type 2 diabetics or those on TPN/dialysis.
• Clinical Signs: Glucose $> 500\,mg/dL$, pH remains normal ($7.35-7.45$), extreme thirst, dehydration, neurologic signs (lethargy, seizures, coma).
• Treatment: Insulin administration and fluid/electrolyte correction. Monitor hypotension via central venous pressure.

Hypoglycemia

• Profile: Blood glucose $< 60\,mg/dL$. Caused by too much insulin, skipping meals, or excessive exercise.
• Clinical Signs: Confusion, irritability, tremors, hunger, headache, excessive perspiration, progressing to seizures or unconsciousness.
• Treatment:
  • Conscious: $15-20\,g$ simple carbohydrate (juice, candy, honey).
  • Unconscious: Glucose gel in buccal cavity, IV Glucagon, or $20-50\,mL$ of $50\%$ glucose IV.
  • Follow-up: Complex carbohydrates (e.g., graham crackers and milk) once symptoms abate.

Chronic Complications and Nursing Management

Peripheral and Autonomic Neuropathy

• Pathophysiology: Poor glucose control and decreased circulation (linked to low nitric acid levels) damage nerves.
• Impact:
  • Motor: Muscle atrophy, skeletal deformities (feet/ankles), gait changes.
  • Sensory: Paresthesias (tingling/burning), loss of protective sensation.
  • Autonomic: Gastroparesis (delayed stomach emptying), erectile dysfunction (in $50\%$ of men), urinary retention/infections.
• Treatment: Gabapentin or tricyclic antidepressants for pain; Metoclopramide for gastroparesis; elastic stockings and Midodrine for orthostatic hypotension.

Diabetic Nephropathy

• Glomerular deterioration leads to impaired blood filtration. Characterized by albuminuria (protein in urine), swelling of hands/feet, and hypertension. Managed with ACE inhibitors (Captopril) and smoking cessation.

Diabetic Retinopathy

• Vascular changes in the retina. Nonproliferative (microaneurysms) or Proliferative (fragile new vessel growth, potential retinal detachment). Managed with regular ophthalmic exams and ACE inhibitors (Lisinopril) to dilate retinal vessels.

Vascular Changes

• Accelerated atherosclerosis and arteriosclerosis. Thickening of arterial walls increases incidence of CAD and MI. Managed with low-fat diet, vasodilators, and Aspirin to reduce platelet aggregation.

Essential Nursing Education and Care Guidelines

• Foot Care (Crucial):
  • Inspect feet daily with a mirror; wash daily in warm water and dry thoroughly between toes.
  • Cut toenails straight across; apply moisturizer daily (but not between toes).
  • Never go barefoot; wear well-fitting shoes (avoid plastic/vinyl).
  • Never cut corns or calluses; see a podiatrist.
• General Education:
  • Differentiate between "low calorie" and "no sugar."
  • Ensure consistency in the total amount of carbohydrates consumed.
  • Recognize the onset, peak, and duration of the specific insulin being used.
  • In older adults, monitor for cognitive impairments (dementia, Alzheimer's) that may interfere with self-management.