15.EndocrinePT2_study_guide

Page 1: Endocrine System and Pathophysiology

Antidiuretic Hormone (ADH/Vasopressin)

• Function:

  • V1 receptors: Binding leads to vasoconstriction (vasopressor effect).

  • V2 receptors: Binding results in water retention (antidiuretic effect).

• Release Triggers:

  • Increased serum osmolality.

  • Decreased blood volume / hypotension.

  • Stress situations.

Pathological Changes and Predisposing Factors (PF)

• Decreased Hormone Levels:

  • Central/Neurogenic (defect in synthesis/release of ADH):

    • Head injury.

    • Surgery near hypothalamus or pituitary.

  • Nephrogenic (impaired kidney response):

    • Genetic defect.

    • Electrolyte disorders.

    • Certain drugs.

• Increased Hormone Levels:

  • Ectopic production of ADH from tumors or cancers (lungs, lymphoid tissue, etc.).

  • Other intrathoracic conditions/pulmonary lesions (e.g., tuberculosis, severe pneumonia).

  • CNS disorders/injury affecting hypothalamus-pituitary feedback.

  • Stressors (pain, temperature changes, certain drugs).

Nursing Problems and Assessment Findings

• Example of Disorder: Diabetes Insipidus.

• Assessment Findings:

  • Polyuria, polydipsia, dehydration signs (thirst, dry skin).

• Example of Disorder: Syndrome of Inappropriate ADH (SIADH).

• Assessment Findings:

  • Hyponatremia, fluid overload, concentrated urine.

Page 2: Glucose Metabolism and Its Regulation

Normal Physiology of Glucose Metabolism

• Energy Utilization:

  • Body tissues extract glucose from blood.

  • Fasting Glucose Levels: 60-100 mg/dL; Random Glucose Levels: 80-120 mg/dL.

  • Excess glucose stored as glycogen in the liver and muscles, or converted to fat.

  • Blood Glucose Regulation:

    • During fasting, glycogen is broken down (glycogenolysis) or glucose is produced from non-carbohydrate sources (gluconeogenesis).

Glucose-Regulating Hormones

• Hormones Decreasing Blood Glucose:

  • Insulin: Released in response to increased blood glucose, promotes cell uptake and storage.

• Hormones Increasing Blood Glucose: (Counter-regulatory hormones)

  • Glucagon: Acts oppositely to insulin.

  • Epinephrine, Glucocorticoids, Growth Hormone: Ensure brain function and survival during hypoglycemia.

Pathological Changes and PF

• Imbalance Between Insulin Availability and Need:

  • Absolute insulin deficiency, impaired release by beta cells, decreased or defective insulin receptors.

• Type 1 Diabetes Mellitus (DM):

  • Autimmune destruction of beta cells.

  • Genetic predisposition, common in youth.

• Type 2 Diabetes Mellitus (DM):

  • Insulin resistance leading to increased blood glucose levels.

  • Compensatory hyperinsulinemia followed by beta cell exhaustion.

  • Associated with aging, sedentary lifestyle, obesity.

Nursing Problems and Assessment Findings

• Example of Disorder: Diabetes Mellitus, Types 1 and 2.

• Assessment Findings: Hyperglycemia signs, polyuria, polydipsia.

Acute Complications

• Diabetic Ketoacidosis (DKA):

  • Common in Type I diabetes; leads to ketosis due to lack of insulin.

• Hyperosmolar Hyperglycemic State (HHS):

  • Occurs in Type 2; insulin resistance leads to severe hyperglycemia and dehydration.

• Hypoglycemia:

  • Caused by excessive medication, inadequate food intake, or increased physical activity.

Long-term Complications

• Microvascular Complications:

  • Neuropathy, nephropathy, retinopathy due to chronic hyperglycemia.

• Macrovascular Complications:

  • Coronary artery disease (CAD), peripheral vascular disease (PVD), stroke due to chronic hyperglycemia and associated risk factors.

Page 3: Diabetic Foot Ulcers

• Pathophysiology:

  • Result from neuropathy and vascular insufficiency, leading to impaired healing and increased risk of infections.