Section 3, chapter 13

Uploaded on


  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
    Be the first to like this
No Downloads


Total Views
On Slideshare
From Embeds
Number of Embeds



Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

    No notes for slide


  • 1. Section 3, Chapter 13 The Peripheral Endocrine Glands
  • 2. Thyroid Gland Location: The thyroid gland is located just inferior to the larynx. Structure: • It consists of two lateral lobes connected by an isthmus • Contains several follicles.
  • 3. Thyroid Gland Follicles Follicles consists of simple cuboidal epithelium & a colloid center Follicular Cells: produce T3 & T4 Coloid: contains Thyroglobulin, which is a storage form of thyroid hormones. Extrafollicular Cells: produce Calcitonin Follicular Cells take up thyroglobulin by endocytosis, then release the thyroid hormones into the bloodstream.
  • 4. Thyroid Hormones Target Cells: T3 & T4 affect many cells throughout the body. Actions of T3 & T4: Raise Metabolic Rate • Increase rate of carbohydrate catabolism • Enhance protein synthesis • Promotes the breakdown and use of lipids T3 & T4 are major factors in determining the basal metabolic rate (BMR) BMR = calories required to sustain life
  • 5. Thyroid Hormones Follicular cells require iodine salts (iodide) to produce T3 and T4. T3 & T4 are hydrophobic molecules (insoluble in water) • Nearly 75% of thyroid hormones are attached to thyroid binding globulins. • Only the small amounts of the unbound hormones act on target cells.
  • 6. Transport of Thyroid Hormones T4 accounts for 95% of circulating Thyroid Hormone, But… T3 is physiologically more active. • T3 is 5 times as potent as T4 • T3 also has a 50-fold higher “free” concentration in the plasma (see figure below).
  • 7. Thyroid Disorders Hypothyroidism – insufficient T3 & T4 • During infancy – results in intellectual disability, stunted growth, abnormal bone formation (cretinism) • During adulthood – low metabolic weight, sluggishness, poor appetite, and sensitivity to cold Infantile hypothyroidism Hyperthyroidism – excess T3 & T4 • Results in high metabolic rate, hyperactivity, weight loss, sensitivity to heat, and exophthamia (protruding eyes) • Grave’s Disease • Autoimmune Disorder: Antibodies target the thyroid gland and mimic TSH. Thyroid antibodies Grave’s disease may overstimulate thyroid gland, resulting in cause exophthalmia
  • 8. Calcitonin Extrafollicular cells (C-cells) secrete Calcitonin Calcitonin lowers blood calcium concentrations. Actions of Calcitonin • Stimulates Osteoblast activity – increases bone deposition • Inhibits osteoclast activity – reduces bone resorption • Promotes the excreting of calcium from the kidneys Major Source of Control: elevated blood calcium ion concentrat
  • 9. Parathyroid Glands • Location: 4 small parathyroid glands are located on the posterior aspect of the thyroid gland •Hormone: PTH (parathyroid hormone) One parathyroid gland surrounded by thyroid
  • 10. Parathyroid Hormone (PTH) Parathyroid Hormone elevates blood calcium levels. Actions of PTH: • Stimulates Osteoclast activity – increases bone resorption • Inhibits osteoblast activity – reduces bone deposition • Promotes calcium reabsorption from the kidneys. • PTH also promotes the activation of Vitamin D, which enhances calcium absorption from the small intestine. Major Source of Control: Inadequate blood calcium ion concent
  • 11. Figure 13.27 Parathyroid Hormone (PTH) stimulates bone to release Calcium (Ca2+) and the kidneys to conserve calcium. It indirectly stimulates the intestine to absorb calcium. The resulting increase in blood calcium concentration inhibits secretion of PTH by negative feedback.
  • 12. Calcitonin and PTH have opposing effects on the levels of calcium ions in circulation. Both work together to maintain calcium
  • 13. Adrenal Glands Location: The adrenal glands are located on the superior aspect of the kidneys. Structure: • Adrenal glands are pyramid shaped organs that consist of two parts • Adrenal Medulla = secretions controlled by sympathetic nerve fibers Adrenal Cortex = Under hormonal control
  • 14. Hormones of the Adrenal Medulla Nerve fibers control secretions: Hormones of the adrenal medulla are under control by the sympathetic division (fight or flight) of the ANS. Hormones: Norepinephrine (noradrenalin) & Epinephrine (adrenalin) • Both are classified as catecholamines. Actions: Effects are similar to sympathetic nerve fibers, but longer lasting. • Increases heart rate and force of contraction • Increases blood pressure • Increases metabolic rate • Increases blood glucose levels (primarily epinephrine) • Decreases digestion
  • 15. Beta Blockers • Epinephrine & Norepinephrine exert their effects by binding to Beta (ß) adrenergic receptors in heart and walls of the blood vessels. • Beta blockers bind to ß-receptors, thus obstructing the binding of catecholamines. • Hence beta blockers reduce sympathetic influences of the heart and blood vessels. • Therefore, beta blockers decrease heart rate, contractility, and reduce blood pressure.
  • 16. Hormones of the Adrenal Cortex 3 Layers of the adrenal cortex secrete over 30 types of steroid hormones. Hormones Aldosterone – produced in zona glomerulosa Cortisol – produced in zona fasciculata Androgens – produced in zona reticularis
  • 17. Hormones of the Adrenal Cortex 1. Aldosterone (mineralocorticoid) • regulates Na+ and K+ concentrations • regulates blood pressure Actions • Aldosterone causes the kidneys to reabsorb Na+ and to excrete K+ • Aldosterone indirectly raises blood pressure: Increased Na+ reabsorption increases water reabsorption by osmosis. Controls of Aldosterone Secretion • Low blood pressure stimulates aldosterone secretion (renin-angiotensin-aldosterone pathway) • Elevated blood K+ concentration promotes aldosterone secretion • Low Na+ has only a slight effect on aldosterone secretion.
  • 18. Renin-Angiontensin-Aldosterone System ACE Inhibitors block the actions of ACE, and thus lower blood pressure.
  • 19. Hormones of the Adrenal Cortex 2. Cortisol (glucocorticoid) • Its primary effect is to build up and conserve blood glucose supplies • Its actions keep blood glucose levels constant between meals. Actions • Promotes gluconeogenesis in the liver gluconeogenesis = glucose synthesis from non-carbohydrates • Promotes the release and used of fatty acids from adipose for energy. Using fatty acids for energy allows glucose to be conserved. • Inhibits protein synthesis: amino acids used in gluconeogenesis
  • 20. Hormones of the Adrenal Cortex 3. Androgens • Supplement the sex hormones secreted from the gonads. • Androgens may be converted into testosterone and estrogens.
  • 21. The Pancreas Structure & Location: The pancreas is located posterior to the stomach, attached to the duodenum. The pancreas has both digestive and endocrine functions. • Pancreatic Islets (Islets of Langerhans) = endocrine cells • Digestion cells (we’ll discuss these with the digestive system)
  • 22. Cells of the Pancreatic Islets 3 distinct type of cells secrete 3 hormones: • Alpha Cells – secrete glucagon • Beta Cells – secrete insulin • Delta Cells – secrete somatostatin Pancreatic hormones regulate the storage, use, and release of fuels (glucose).
  • 23. Pancreatic Hormones 1. Glucagon Overall Effect: During fasting, when blood glucose levels drop, glucagon elevates blood glucose levels Actions of Glucagon: • Stimulates glycogenolysis in the liver (breakdown of glycogen into glucose) • Glucagon also promotes gluconeogenesis • Glucagon also stimulates the breakdown of fats into glycerol and fatty acids. • Glycerol is used in gluconeogenesis • Fatty Acids are metabolized for energy
  • 24. Liver Amino acids glycerol Gluconeogenesis glycogen Glycogenolysis glucose glucose Glucagon secretions elevates blood glucose concentrations. • Gluconeogenesis converts noncarbohydrates, such as amino acids and glycerol, into glucose. • Glycogenolysis breaks down large glycogen molecules into glucose.
  • 25. Pancreatic Hormones 2. Insulin Overall Effect: Following a meal, when blood carbohydrate levels are high, insulin removes excess glucose from the blood. Actions of Insulin: • Stimulates glycogenesis in the liver (formation of glycogen from glucose). • It inhibits gluconeogenesis. • Insulin promotes glucose uptake in adipose tissue, skeletal muscles, and cardiac muscle. 3. Somatostatin Overall Effect: Helps regulate glucose metabolism by inhibiting the secretion of glucagon and insulin.
  • 26. Hormonal Control of Glucose Insulin and glucagon function together to stabilize blood glucose concentration. Negative feedback responding to blood glucose concentration controls the levels of both hormones.
  • 27. Diabetes Mellitus Type I Diabetes Mellitus (juvenile) • Autoimmune disease – immune system destroys beta cells, resulting in the loss of insulin production. • Without insulin, blood glucose cannot be taken up and used for energy. • Glucose accumulates in the blood and urine = hyperglycemia. Type II Diabetes Mellitus (adult onset) • Receptors on target cells wear down and become insensitive to insulin. • Target cells resist glucose uptake, even in the presence of insulin. • Insulin levels must be higher than normal just to maintain normal glucose concentrations.
  • 28. Other Endocrine Glands Pineal Gland • Located posterior to thalamus. • The pineal gland secretes melatonin, which regulates circadian rhythms (sleep/wake cycle) • Melatonin secretions are greatest in dark. Light inhibits secretions. Thymus Gland • Secretes thymosins • Promotes development of certain lymphocytes • Important in role of immunity
  • 29. Other Endocrine Glands Reproductive Organs • Ovaries produce estrogens and progesterone • Testes produce testosterone • Placenta produces estrogens, progesterone, and gonadotropin Other organs: digestive glands, heart, and kidney End of Section 3, Chapter 13