Endocrine Review - Clinical Manifestations

Pathophysiology Etiology Clinical Manifestations Diagnosis 12/5/2023 KG Diabetes Insipidus (DI) • Two classifications o Central DI: insufficient secretion of ADH o Nephrogenic DI: kidney fails to respond to ADH • Central DI: tumors, head trauma, pituitary surgery • Nephrogenic: nephrotoxic drugs (lithium), ischemia of kidney Fluid Volume Deficit • Increased urine output (polyuria) • Highly dilute urine • Dehydration, confusion, disorientation, seizures, coma • Hypovolemia • Hypernatremia • ↓ ADH • ↑ Serum (plasma) osmolality due to dehydration • ↓Urine osmolality due to dilution Syndrome of Inappropriate Antidiuretic Hormone (SIADH) • ADH stimulates reabsorption of water at the collecting duct of the nephron • SIADH causes excess water reabsorption into the bloodstream (Fluid volume excess) • Acute brain injury, lung cancer, pulmonary disease (emphysema and pneumonia) Fluid Volume Overload • Fatigue, confusion, weakness, seizures • Dyspnea, fluid in lungs • • • • Hypervolemia Hyponatremia (dilutional) ↓Serum osmolality due to volume overload) ↑Urine osmolality due to concentrated urine) Pathophysiology Etiology Hypothyroidism • Autoimmune destruction (Hashimoto’s Thyroiditis) of thyroid • TSH receptor antibodies present-> bind to TSH receptor-> absence of normal response of T3 and T4 o Insufficient amount of thyroid hormone, thyroid is not secreting T3 and T4 • Complication: Myxedema Coma • Older age, pregnancy, radiation to neck, radioactive iodine Clinical Manifestations • Diagnosis • 12/5/2023 KG Decreased metabolic rate o Bradycardia o Cold intolerance, weight gain, lethargy/fatigue o Puffy face: accumulation of sodium/water ↑TSH, ↓T3, T4 Hyperthyroidism • Graves’ Disease (autoimmune)/Thyrotoxicosis: excessive secretion of T3 & T4 • Complication: Thyroid Storm • • • • • Excessive Iodine intake Pregnancy Excessive synthetic thyroid hormone medication intake Increased metabolic rate o Tachycardia o Weight loss o Nervousness, insomnia, sensitivity to heat, weight loss ↓ TSH Pathophysiology Etiology Clinical Manifestations Diagnosis 12/5/2023 KG Addison’s Disease (Hypoadrenalism) • Primary: Autoimmune destruction of adrenal gland o ↓cortisol response to stress leads to adrenal crisis • Autoimmune disease • Adrenal hemorrhage • HIV • Absence of aldosterone o Hyponatremia o Hyperkalemia o Dehydration • Increased ACTH triggers melanocyte-stimulating hormone (MSH)-> causes tanned appearance • Weakness, hypotension, lethargy, easy fatigue • Thin • Hyponatremia • Hyperkalemia • Elevated ACTH Cushing’s Syndrome (Hyperadrenalism) Hypercortisolism from any cause • Excess glucocorticoid production • • • • • Secretion of ACTH from tumors of the pituitary Adrenal tumor Administration of exogenous steroids Weight gain/Redistribution of body fat to face, trunk and abdomen “Buffalo hump” Hyperglycemia Decreased response to infection/injury-> immune suppression Moon facies (puffy face) • • • Hyperglycemia Hypokalemia Elevated blood cortisol levels • • • Pathophysiology Etiology Hypoparathyroidism • Insufficient PTH secretion and resultant decrease in calcium (hypocalcemia) and increase in phosphorous levels (hyperphosphatemia) • Primary: Trauma, Damage or removal of parathyroid glands during thyroid surgery Hyperparathyroidism • Excessive secretion of PTH • Hypercalcemia • Hypophosphatemia • Primary: adenoma-> growth in parathyroid gland causes excessive secretion of PTH-> increases calcium level in blood • Muscle weakness, poor concentration, neuropathies, HTN, kidney stones, metabolic acidosis, pathological fractures Clinical Manifestations • • Pathophysiology Type I DM Absolute lack of insulin -> absence of insulin allows for fat breakdown Type II DM Insulin resistance-> decreased ability to act on target tissues Beta cell exhaustion Genetic, idiopathic, antibodies cause destruction of insulin secreting beta cells Polydipsia, polyuria, polyphagia Glucosuria DKA Fat breakdown into free fatty acids-> results in ketones> Ketoacidosis (metabolic acidosis), hyperglycemia • Increased glucose • Decreased Hc03 (know your normal levels) Genetic, obesity Etiology Clinical Manifestations Complications 12/5/2023 KG S/S of hypocalcemia: tetany, carpopedal spasm Trousseau sign, Chvostek’s sign Same as Type I HHS Profound dehydration, neurologic alterations NO ketones/NO Ketonuria, NO metabolic acidosis/ketosis • Increased glucose • Normal Hc03