Endocrine

Energy Production and Glucose Homeostasis

  • Five hormones regulate energy production and glucose homeostasis:
    • Insulin
    • Glucagon
    • Epinephrine
    • Cortisol
    • Growth hormone
  • Focus will be on disorders related to insulin and glucagon.

Insulin

  • Anabolic (energy-producing) hormone.
  • Secreted by beta islet cells of the pancreas in response to high serum glucose levels.
  • Increases glucose uptake into cells, thus lowering serum glucose levels.
  • Stimulates:
    • Glycogen formation (glycogenesis).
    • Protein synthesis.
    • Adipose formation.
  • Genesis means to create, opposite of lysis (to break down).

Glucagon

  • Counterregulatory hormone to insulin (opposite effect).
  • Secreted by the pancreas in response to low serum glucose levels.
  • Increases serum glucose levels by:
    • Stimulating glycogen breakdown (glycogenolysis).
    • Increasing production of new glucose molecules (gluconeogenesis).
  • Lysis means to break down.

Hypoglycemia

  • Too much insulin and not enough glucagon.
  • Serum glucose level \le 50 \text{ mg/dL}.
  • Can be caused by:
    • Developing glycogen stores in neonates/young infants.
    • Transient or persistent hyperinsulinism.
    • Hypopituitarism.
    • Adrenal insufficiency.
    • Liver failure.
    • Inborn errors of metabolism.
  • Symptoms:
    • Decreased level of consciousness.
    • Seizures and tremors.
    • Hypotonia.
    • Apnea (especially in neonates/young infants).
    • Tachycardia.
    • Diaphoresis.
    • Anxiety.

Management of Hypoglycemia

  • Be suspicious of symptoms.
  • Check bedside glucose and monitor for improvement after treatment.
  • Mild/moderate hypoglycemia: oral carbohydrate or glucagon.
  • Severe hypoglycemia or inability to take oral medications: IV glucose.
  • Determine and treat the underlying cause.

Diabetic Ketoacidosis (DKA)

  • Diabetes mellitus patients have an underproduction or deficit of insulin.
  • Without insulin, glucose cannot enter the cell for energy, leading to cellular energy debt.
  • The body increases counterregulatory hormones (glucagon, catecholamines, cortisol, growth hormone) to produce more glucose.
  • The body uses fat and muscle proteins as alternative fuel sources, leading to fatty acid oxidation.
  • Fatty acid oxidation produces ketones and causes acidosis.
  • DKA is a state of:
    • Hyperglycemia.
    • Ketonuria and ketonemia.
    • Metabolic acidosis.
    • Dehydration.
    • Electrolyte imbalances.

Pathophysiology

  • Lactate production from alternate metabolic pathways leads to acidosis.
  • Hyperosmolar diuresis leads to dehydration.
  • Electrolyte imbalances due to acidosis and electrolyte losses in urine.

Clinical Presentation

  • Severe hyperglycemia and ketoacidosis.
  • Electrolyte abnormalities (hyperkalemia, hyperphosphatemia, hypernatremia).
  • Hyperosmolar state leading to osmotic diuresis and dehydration, potentially progressing to hypovolemic shock.
  • Altered mental status and possible signs of elevated intracranial pressure.
  • Dehydration signs (tachycardia, hypotension, poor perfusion; hypotension is a late sign).
  • Tachypnea with Kussmaul respirations and sweet-smelling acetone breath.
  • Abdominal tenderness (especially with nausea/vomiting).
  • Possible signs of infection (precipitating event).

Management of DKA

  • Airway and breathing management.
  • Volume resuscitation.
  • Blood sugar control.
  • Electrolyte imbalance correction.
  • Education for patient and family about diabetes management.

Volume Resuscitation

  • Rapid IV access and fluid bolus.
  • Isotonic fluid (20 mL/kg bolus).
  • Reassess response after each intervention and adjust fluid management.
  • Correct 10-20% dehydration over 48 hours, along with maintenance fluids.

Insulin Therapy

  • Essential to normalize blood glucose and suppress lipolysis/ketogenesis.
  • Avoid insulin bolus to prevent rapid glucose drop (no faster than 50-100 mg/dL per hour).
  • Regular insulin IV infusion at 0.05-0.1 unit/kg/hour.
  • Add glucose to infusion (5% dextrose at serum glucose ~300 mg/dL, 10% dextrose at ~200 mg/dL).
  • Use established insulin and dextrose protocols.

Electrolyte Management

  • Patients are often hyperkalemic and hyperphosphatemic initially.
  • Electrolyte levels decrease as acidosis resolves, requiring possible replacement.
  • Add electrolytes to IV bag as needed rather than giving single replacement doses.
  • Frequent electrolyte monitoring is necessary until DKA is corrected.

Cerebral Edema

  • Occurs in about 1% of DKA episodes, with significant morbidity and mortality.
  • Symptoms can be present initially or occur within the first 48 hours of treatment.
Risk Factors for Cerebral Edema
  • First-time DKA (new onset).
  • Younger age at diagnosis.
  • Increased BUN.
  • Decreased CO_2.
  • Poor DKA management (insulin bolus, rapid glucose correction, aggressive fluids, bicarbonate administration).
Response to Cerebral Edema Signs
  • Respond quickly with typical therapies for increased intracranial pressure.