Overview
This lecture continues the discussion of the endocrine system, focusing on the thyroid gland, adrenal gland, pancreas, and the roles of their hormones in homeostasis, stress response, and metabolism.
Thyroid Gland
- The hypothalamus releases TRH, which stimulates the anterior pituitary to release TSH.
- TSH targets the thyroid gland's follicular cells to release T3 (triiodothyronine) and T4 (thyroxine).
- T3 and T4 increase basal metabolic rate (BMR) and regulate body temperature.
- Follicular cells produce thyroid hormones; parafollicular cells produce calcitonin.
- Calcitonin lowers blood calcium by inhibiting osteoclasts; it is antagonistic to parathyroid hormone (PTH).
- Hyperthyroidism (e.g., Graves’ disease) increases BMR, body temperature, appetite, and causes weight loss.
- Hypothyroidism (e.g., goiter) decreases BMR, body temperature, and appetite, causing weight gain.
Calcium Homeostasis: PTH and Calcitonin
- PTH (from parathyroid glands) is released when blood calcium is low; it increases blood calcium by stimulating osteoclasts.
- Calcitonin is released when blood calcium is high; it decreases blood calcium by promoting calcium uptake in bones.
- Hyperparathyroidism weakens bones and may cause kidney stones and nervous system depression.
Adrenal Gland
- Adrenal cortex has three layers: zona glomerulosa (mineralocorticoids like aldosterone), zona fasciculata (glucocorticoids like cortisol), zona reticularis (androgens).
- Aldosterone increases sodium reabsorption and potassium secretion in kidneys, raising blood volume and pressure.
- Aldosterone release is regulated by the renin-angiotensin system, plasma K+, ACTH, and inhibited by ANP.
- Glucocorticoids (cortisol) are released during stress, raising blood glucose, fatty acid, and amino acid levels.
- Chronic high cortisol = Cushing’s syndrome; low cortisol = Addison’s disease.
- Adrenal medulla releases epinephrine and norepinephrine for short-term (fight-or-flight) stress, increasing heart rate, blood pressure, and blood glucose.
Pancreas & Glucose Homeostasis
- The pancreas' alpha cells release glucagon (raises blood glucose); beta cells release insulin (lowers blood glucose).
- Insulin (fed state) facilitates glucose uptake, glycogen synthesis, and fat storage, lowering blood glucose.
- Glucagon (fasted state) promotes glycogen breakdown (glycogenolysis) and new glucose synthesis (gluconeogenesis), raising blood glucose.
- Insulin and glucagon are antagonistic, maintaining glucose homeostasis.
Diabetes Mellitus
- Type 1: Insulin deficiency; Type 2: Insulin resistance or hypofunction.
- Hyperglycemia (high blood glucose) results, with glucose spilling into urine (glycosuria).
- Three cardinal signs: polyuria (excessive urination), polydipsia (excessive thirst), polyphagia (excessive hunger).
- Fat breakdown produces acidic ketones (ketoacidosis), causing complications.
Additional Endocrine Organs & Hormones
- Ovaries produce estrogen/progesterone; testes produce testosterone.
- Adipose tissue releases leptin (regulates appetite), GI tract releases gastrin, secretin, CCK (digestive regulation).
- Heart releases ANP (lowers blood volume/pressure); kidneys produce erythropoietin and renin.
Key Terms & Definitions
- TRH — Thyrotropin releasing hormone from hypothalamus.
- TSH — Thyroid stimulating hormone from anterior pituitary.
- T3/T4 — Thyroid hormones increasing BMR.
- Calcitonin — Lowers blood calcium.
- PTH (Parathyroid hormone) — Raises blood calcium.
- Aldosterone — Increases Na+ reabsorption, blood volume/pressure.
- Cortisol — Glucocorticoid managing stress and increasing glucose.
- Insulin — Lowers blood glucose.
- Glucagon — Raises blood glucose.
- Glycogenesis — Formation of glycogen from glucose.
- Glycogenolysis — Breakdown of glycogen to glucose.
- Gluconeogenesis — Formation of glucose from non-carbohydrate sources.
Action Items / Next Steps
- Review textbook tables on hormone functions (especially Table 16.4).
- Study histology slides of thyroid, adrenal, and pancreas.
- Memorize antagonistic hormone pairs and their effects.
- Prepare for quiz/homework on endocrine glands, hormone actions, and feedback mechanisms.