Human Anatomy and Physiology: The Endocrine System

Human Anatomy and Physiology: The Endocrine System - Chapter 16 Study Notes

16.7 Thyroid Gland

  • Location and Structure
    • Butterfly-shaped gland located in the anterior neck on the trachea, just inferior to the larynx.
    • Consists of:
    • Isthmus: Median mass connecting two lateral lobes.
    • Follicles: Hollow sphere of epithelial follicular cells that produce glycoprotein thyroglobulin.
    • Colloid: Fluid of follicle lumen containing thyroglobulin and iodine, which is a precursor to thyroid hormone.
    • Parafollicular cells: Produce the hormone calcitonin.

The Thyroid Gland

  • Thyroid Hormone (TH)
    • Body's major metabolic hormone.
    • Found in two forms:
    • T4 (Thyroxine): Major form, consists of two tyrosine molecules with four bound iodine atoms.
    • T3 (Triiodothyronine): Form that has two tyrosines with three bound iodine atoms.
    • TH must be converted to T3 at the tissue level.
    • Both are iodine-containing amine hormones.
Effects of Thyroid Hormone (TH)
  • General Effects:
    • Affects virtually every cell in the body.
    • Enters target cells and binds to intracellular receptors in the nucleus: triggers transcription of various metabolic genes.
    • Specific Effects of TH:
    • Increases basal metabolic rate and heat production (calorigenic effect).
    • Regulates tissue growth and development (critical for normal skeletal and nervous system development and reproductive capabilities).
    • Maintains blood pressure by increasing adrenergic receptors in blood vessels.
Synthesis of Thyroid Hormone
  • Stored extracellularly in the follicle lumen until triggered by TSH to release.
  • Seven Steps in the Synthesis of TH:
    1. Thyroglobulin is synthesized and discharged into the follicle lumen.
    2. Iodide is trapped: iodide ions (I−) are actively taken into the cell and released into the lumen.
    3. Iodide is oxidized: electrons are removed, converting it to iodine (I2).
    4. Iodine attachment to tyrosine:
    • Mediated by peroxidase enzymes:
      • Monoiodotyrosine (MIT): Formed if one iodine attaches.
      • Diiodotyrosine (DIT): Formed if two iodines attach.
    1. Iodinated tyrosines link together to form T3 and T4:
    • T3 is formed if one MIT and one DIT link together.
    • T4 is formed if two DITs link together.
    1. Colloid is endocytosed by follicular cells: vesicle combines with a lysosome.
    2. Lysosomal enzymes cleave T3 and T4 from thyroglobulin, hormones secreted into the bloodstream (mostly T4, T3 also secreted).
Transport and Regulation of TH
  • T4 and T3 are transported by thyroxine-binding globulins (TBGs).
  • Both bind to target receptors, but T3 is 10 times more active than T4.
  • Peripheral tissues have an enzyme that converts T4 to T3 by removing one iodine.
  • Release Regulation:
    • TH release is regulated by negative feedback:
    • Falling TH levels stimulate the release of thyroid-stimulating hormone (TSH).
    • Rising TH levels provide negative feedback inhibition on TSH.
    • TSH can also be inhibited by GHIH, dopamine, and increased levels of cortisol and iodide.
    • Hypothalamic thyrotropin-releasing hormone (TRH) can overcome negative feedback during pregnancy or exposure to cold, especially in infants.
Clinical Homeostatic Imbalance: Thyroid Disorders
  • Hyposecretion:
    • Can lead to myxedema in adults.
    • Symptoms include low metabolic rate, thick/dry skin, puffy eyes, feeling chilled, constipation, edema, mental sluggishness, and lethargy.
    • If due to lack of iodine, a goiter may develop, as lack of iodine decreases TH levels, triggering increased TSH secretion and resulting in thyroid enlargement.
    • Congenital Hypothyroidism:
    • Poor development of thyroid gland causes it.
    • Symptoms may include weak cry, poor feeding, constipation, and prolonged jaundice.
    • TH replacement is crucial and usually lifelong.
  • Hypersecretion:
    • Most commonly seen in Graves’ disease (autoimmune condition).
    • Body produces abnormal antibodies directed against thyroid follicular cells, mimicking TSH and stimulating TH release.
    • Symptoms include elevated metabolic rate, sweating, rapid and irregular heartbeat, nervousness, and weight loss despite adequate food intake.
    • Exophthalmos may occur, where eyes protrude due to tissue behind eyes becoming edematous and fibrous.
    • Treatments include surgical removal of the thyroid or radioactive iodine to destroy active thyroid cells.
  • Calcitonin:
    • Produced by parafollicular (C) cells in response to high Ca2+ levels.
    • Acts as an antagonist to parathyroid hormone (PTH).
    • No known physiological role in humans at normal levels, but at higher doses:
    • Inhibits osteoclast activity and prevents release of Ca2+ from the bone matrix.
    • Stimulates Ca2+ uptake and incorporation into bone matrix.

16.8 Parathyroid Gland

  • Location and Structure
    • Four to eight tiny yellow-brown glands embedded in the posterior aspect of the thyroid.
    • Contains:
    • Oxyphil cells: Function unclear.
    • Parathyroid cells: Secrete parathyroid hormone (PTH), or parathormone.
  • PTH Functions:
    • Most important hormone in Ca2+ homeostasis.
    • Secreted in response to low blood levels of Ca2+; inhibited by rising Ca2+ levels.
    • Target Organs: Skeleton, kidneys, and intestine.
    • Functions Include:
    • Stimulates osteoclasts to digest bone matrix and release Ca2+ into blood.
    • Enhances reabsorption of Ca2+ and secretion of phosphate (PO43−) by kidneys.
    • Promotes activation of vitamin D by kidneys, increasing the absorption of Ca2+ by intestinal mucosa.
Clinical Homeostatic Imbalance: Parathyroid Disorders
  • Hyperparathyroidism:
    • Caused by parathyroid gland tumor.
    • Muscles and bones soften and deform due to calcium leaching.
    • Elevated Ca2+ depresses the nervous system and contributes to kidney stone formation.
    • Severe form known as osteitis fibrosa cystica causes easily fractured bones.
  • Hypoparathyroidism:
    • Following gland trauma or removal, can cause hypocalcemia.
    • Leads to tetany, respiratory paralysis, and death.

16.9 Adrenal Gland

  • Location and Structure
    • Paired, pyramid-shaped organs atop kidneys (suprarenal glands).
    • Structurally and functionally two glands:
    • Adrenal Cortex: Three layers of glandular tissue that synthesize and secrete several hormones.
    • Adrenal Medulla: Nervous tissue that is part of the sympathetic nervous system.
Adrenal Cortex
  • Corticosteroids Produced:
    • Over 24 different hormones produced.
    • Layers produce different corticosteroids:
    • Zona Glomerulosa: Mineralocorticoids (e.g., aldosterone).
    • Zona Fasciculata: Glucocorticoids (e.g., cortisol).
    • Zona Reticularis: Gonadocorticoids (e.g., weak androgens).
Mineralocorticoids
  • Function and Regulation:
    • Regulate electrolyte concentrations, primarily Na+ and K+.
    • Aldosterone is the most potent mineralocorticoid.
    • Effects of Aldosterone:
    • Stimulates Na+ reabsorption by kidneys, increasing blood volume and blood pressure.
    • Stimulates K+ elimination by kidneys.
    • Regulators of Aldosterone Secretion:
    • Renin-angiotensin-aldosterone mechanism.
    • Plasma concentration of K+; elevated K+ stimulates release of aldosterone.
    • ACTH can also influence secretion, along with atrial natriuretic peptide (ANP).
Clinical Homeostatic Imbalance: Adrenal Disorders
  • Aldosteronism:
    • Hypersecretion usually due to adrenal tumors.
    • Results in hypertension and edema due to excessive Na+, alongside abnormal neuronal and muscle function due to K+ excretion.
  • Glucocorticoids:
    • Influence metabolism of most cells and help resist stressors while maintaining blood pressure.
    • Cortisol is the main glucocorticoid.
Regulation of Glucocorticoids
  • Released in response to ACTH.
  • Regulation Cycle:
    • Cortisol secretion cycles are influenced by eating and activity patterns.
    • Acute stress can interrupt cortisol rhythm.
Actions of Glucocorticoids
  • Effects Include:
    • Increase blood levels of glucose, fatty acids, and amino acids—primarily gluconeogenesis (formation of glucose from fats and proteins).
    • Prevent inflammation, disrupt normal metabolism, and can be used in treating inflammatory diseases (e.g., arthritis).
Clinical Homeostatic Imbalance: Hyper and Hyposecretion of Glucocorticoids
  • Cushing’s Syndrome:
    • Caused by pituitary/adrenal tumors or overuse of corticosteroids.
    • Symptoms include “moon” face, weight gain, and risk of osteoporosis.
  • Addison’s Disease:
    • Causes hyperpigmentation due to high levels of ACTH; requires corticosteroid replacement therapy.
Gonadocorticoids
  • Weak androgens produced in adrenal cortex.
    • Examples: dehydroepiandrosterone (DHEA) may contribute to onset of puberty and sex characteristics.

Adrenal Medulla

  • Hormonal Production:
    • Synthesizes catecholamines: epinephrine (80%) and norepinephrine (20%).
    • Effects of Catecholamines:
    • Vasoconstriction.
    • Increased heart rate.
    • Raised blood glucose levels.
Stress Response
  • Hormonal responses can affect metabolism; causes quick responses to stressors, unlike long-term effects of adrenal corticosteroids.

Clinical Imbalance

  • Hypersecretion from adrenal medulla can lead to uncontrolled sympathetic nervous system responses, presenting symptoms such as hyperglycemia, rapid heartbeat, and sweating.

16.10 Pineal Gland

  • Location:
    • Small gland hanging from the roof of the third ventricle; produces melatonin.
  • Functions of Melatonin:
    • Regulates sleep/wake cycles, sexual maturation, and production of antioxidant molecules.

16.11 Other Endocrine Organs

  • Pancreas:
    • Triangular gland with exocrine (digestion enzymes) and endocrine (islets of Langerhans) functions.
    • Alpha (α) Cells: Produce glucagon (raises blood glucose).
    • Beta (β) Cells: Produce insulin (lowers blood glucose).
Insulin and Glucagon's Role
  • Glucagon acts as a hyperglycemic agent, while insulin promotes glucose uptake and lowers blood sugar levels.
  • Diabetes Mellitus (DM):
    • Can arise from insulin hyposecretion (Type 1) or hypoactivity (Type 2).
    • Symptoms include polyuria, polydipsia, and polyphagia.
Other Hormonal Functions
  • Adipose Tissue:
    • Releases leptin (appetite control) and resistin (insulin antagonist).
  • Gastrointestinal Tract:
    • Secretes hormones like gastrin, ghrelin, secretin, and CCK to regulate digestion.
  • Kidneys:
    • Secrete erythropoietin (stimulates RBC production) and renin (starts renin-angiotensin-aldosterone mechanism).
Developmental Aspects of the Endocrine System
  • Hormone-producing glands arise from all three germ layers.
  • Aging Effects:
    • Hormone levels (like GH and TH) decline with age, impacting metabolic rates, glucose tolerance, and reproductive functions.

88. Conclusion

  • The endocrine system's function and hormone interactions are critical for maintaining homeostasis and responding to body changes across the lifespan.