Diabetes Mellitus Overview

Chronic multisystem disease characterized by hyperglycemia.
Related to abnormal insulin production (type 1), impaired insulin utilization (type 2), or both.
8th leading cause of death in the US.
Leading cause of end-stage renal disease, adult blindness, and non-traumatic lower limb amputations.
Risk Factors: Family history, gestational diabetes, minority groups (American Indians, African Americans, Hispanics, Asian Americans), age > 35, obesity (BMI > 30), birth of an infant > 9 lbs, and inactivity.

Produced by beta cells in the islets of Langerhans.
Released continuously into the bloodstream in small increments with larger amounts released after food.
Function: Stabilizes glucose levels between 70 and 120 mg/dL.
Promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell.

Work against the effects of insulin.
Increase glucose levels by stimulating glucose production and release by the liver and decreasing the movement of glucose into the cells.
Examples: Glucagon, epinephrine, growth hormone, and cortisol.
- Glucagon: Opposite of insulin, released from the liver.
  - Increases blood glucose by glycogenolysis (breakdown of stored glucose) and gluconeogenesis (liver converts fats and proteins into glucose).
- Cortisol: Rises with stress and in the morning.

At risk for type 2 diabetes.
Defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both.
IGT Diagnosis: 2-hour oral glucose tolerance test (OGTT) values between 140 and 199.
IFG Diagnosis: Fasting glucose levels between 100 and 125.
Patient Teaching: Have glucose A1c checked regularly, monitor for symptoms of diabetes (fatigue, frequent infections, slow-healing wounds), maintain a healthy weight, exercise regularly, and make healthy food choices.

Insulin dependent (abnormal insulin production).
Results from the destruction of beta cells in the pancreas, the only cells that produce insulin.
Signs/Symptoms: Polydipsia (excessive thirst), polyuria (frequent urination), polyphagia (excessive hunger), fatigue/weakness, nausea/vomiting.
Treatment: Requires both long-acting and short-acting insulin.

Insulin resistant (impaired insulin utilization).
Combination of inadequate insulin secretion and insulin resistance.
The pancreas usually produces some endogenous insulin, but the body may not produce enough or use it effectively.
Signs/Symptoms: Slow onset of manifestations, with undetected hyperglycemia and few symptoms for many years, polyuria and polydipsia may occur.

Fasting Plasma Glucose (FPG):
- Impaired fasting glucose: >100 and <126 mg/dL.
- DM: >126 mg/dL.
- Goal: FPG < 99 mg/dL.
Hemoglobin A1c (HbA1c):
- Provides an average of glucose levels for the past 3 months.
- Reflects glucose “sticking” to red blood cells, which last about 3 months.
- Goal: 6.5%-7%.
- Diabetic: 6.5% or higher.
Estimated Average Glucose (eAG):
- Calculated conversion of HbA1c.
- Reported in mg/dL, the same units as home blood glucose tests.
Urine Glucose, Ketone, and Protein Levels:
- Glucose: Presence indicates hyperglycemia.
- Ketonuria: Occurs with the breakdown of fats.
- Albuminuria: May indicate early onset of nephropathy.
Serum Cholesterol:
- Diabetics are at risk for atherosclerosis.
- Treatment Goal: LDL < 100 mg/dL.

Do not heat or freeze.
In-use vials can be left at room temperature for up to 4 weeks.
Extra insulin should be refrigerated.
Avoid exposure to direct sunlight, extreme heat or cold.
Store prefilled syringes upright for 1 week if two insulin types; 30 days for one type.

Typically given by subcutaneous injection.
Regular insulin can be given IV for immediate onset.
Insulin is NOT taken orally because it is inactivated by gastric fluids.
Absorption is fastest from the abdomen, followed by the arm, thigh, and buttock.
Teach patients to rotate injection sites within and between areas to prevent excess bruising.

After-effect of fat cells being broken down for glucose stores.
Dehydration: Cells are hungry and have no food, leading to severe dehydration.
Overload of Sugar: Excess sugar in the extracellular fluid leads to vomiting in an attempt to excrete excess sugar.
Clinical Manifestations:
- Dehydration, lethargy, sweet fruity breath, Kussmaul respirations (rapid, deep breathing with dyspnea).
Labs: Blood glucose > 250 mg/dL, pH < 7.3.
Interprofessional Care:
- First goal: Establish IV for fluid and electrolyte replacement.
- Assess renal, cardiopulmonary, and level of consciousness (LOC) status.

Due to insulin deficiency.
Blood sugar can be as high as 600 mg/dL, leading to ICU admission and being very life-threatening.
Less common than DKA.
Often occurs in patients over 60 years of age with type 2 diabetes.
Related to impaired thirst sensation or inability to replace fluids.
Lab Values: Blood glucose > 600 mg/dL, marked increase in serum osmolality, absent or minimal ketone bodies in blood and urine.
Nursing Management:
- Medical emergency with high mortality rate.
- Immediately administer IV insulin and either 0.9% or 0.45% NaCl.
- Monitor administration of IV fluids to correct dehydration, insulin therapy to reduce blood glucose and ketone levels, and electrolytes.
- Use ECG monitoring when giving calcium (can cause arrhythmias or cardiac arrest).

Located in the front of the neck.
Primary Function: Produce thyroid hormone, which controls metabolic rate, metabolism, and growth/development.
Thyroid Hormones:
- Calcitonin: Controls body use of calcium, lowering excess calcium in the blood.
- T3: Composed of iodine, regulates metabolism.
- T4: Composed of iodine, regulates metabolism.
- TSH: Released from the pituitary gland, stimulates the thyroid to release T3 and T4.

TSH and T4 levels are measured to determine if a goiter is associated with normal thyroid function, hyperthyroidism, or hypothyroidism.

Condition where the thyroid gland produces insufficient thyroid hormone.
Primary Hypothyroidism: Thyroid gland malfunction, the thyroid fails to produce enough thyroid hormone.
- Causes: Insufficient iodine diet, Hashimoto's disease, surgical removal of the thyroid, therapeutic radiation, atrophy of the thyroid gland, and thyroid gland tumors.
Secondary Hypothyroidism: Cause is related to pituitary tumors and other pituitary disorders, resulting from alterations in the hypothalamic-pituitary axis.
Clinical Manifestations: Fatigue, weight gain, cold intolerance, constipation, dry skin, thinning hair, and periorbital edema.