Endocrine System: Hormones and Homeostasis – Study Notes

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23.2 Adrenal Glucocorticoids

Adrenal Cortex vs. Adrenal Medulla

The adrenal gland consists of two main regions: the adrenal cortex and the adrenal medulla. Each region produces distinct hormones with specific physiological effects.

Adrenal Cortex: Produces steroid hormones (e.g., cortisol, aldosterone).
Adrenal Medulla: Produces catecholamines (e.g., epinephrine, norepinephrine).
Example: The cortex regulates metabolism and stress response, while the medulla mediates fight-or-flight reactions.

The Adrenal Cortex Secretes Steroid Hormones

The adrenal cortex is divided into three layers, each secreting specific steroid hormones.

Zona Glomerulosa: Secretes aldosterone (regulates sodium and potassium balance).
Zona Fasciculata: Secretes cortisol (regulates metabolism, stress response).
Zona Reticularis: Secretes androgens (sex hormones).
Generalized Effects: Cortisol increases blood glucose, suppresses immune function, and aids in metabolism.

Crossover Effects of Steroid Hormones

Crossover effects occur when steroid hormones influence multiple physiological systems due to their widespread receptor distribution.

Example: Cortisol affects both metabolism and immune response.
Reason: Steroid hormones are lipid-soluble and can enter most cells, binding to intracellular receptors.

Cortisol Secretion Is Controlled by ACTH

Cortisol release is regulated by the hypothalamic-pituitary-adrenal (HPA) axis.

Pathway: Hypothalamus releases CRH → Pituitary releases ACTH → Adrenal cortex releases cortisol.
Diagram: HPA pathway (see Fig. 23.2a).
Diurnal Secretion: Cortisol levels peak in the morning and decline throughout the day.
Mechanism: Cortisol acts via intracellular receptors, influencing gene transcription.

Cortisol Is Essential for Life

Cortisol is a vital hormone with primarily catabolic effects.

Metabolic Effects: Increases gluconeogenesis, protein breakdown, and lipolysis; suppresses immune function.
Example: During stress, cortisol mobilizes energy stores.

Cortisol Is a Useful Therapeutic Drug

Immunosuppressant Effects: Used to treat autoimmune diseases and prevent transplant rejection.
Negative Feedback: Exogenous cortisol suppresses endogenous ACTH and CRH production, potentially leading to adrenal insufficiency.

Cortisol Pathologies: Too Much or Too Little Hormone

Hypercortisolism (Cushing's Syndrome)

Effects: Muscle weakness, fat redistribution, hyperglycemia, hypertension.
Causes: Pituitary tumor (Cushing's disease), adrenal tumor, exogenous corticosteroids.

Hypocortisolism (Addison's Disease)

Effects: Fatigue, weight loss, hypotension, hyperpigmentation.
Causes: Autoimmune destruction, pituitary dysfunction.

CRH and ACTH Have Additional Physiological Functions

Stress and Immune Function: The HPA axis links stress response to immune suppression.
Evidence: Increased cortisol during stress reduces immune cell activity.

CRH Family

Members: Includes CRH, urocortin, and related peptides.
Physiological Effects: Regulates stress response, appetite, and immune function.

POMC and Melanocortins

POMC: Pro-opiomelanocortin is a precursor protein for ACTH, MSH, and endorphins.
Physiological Effects: ACTH stimulates cortisol release; MSH affects skin pigmentation; endorphins modulate pain.
Melanocortin Receptors: Five types identified (MC1R–MC5R).

23.3 Thyroid Hormones

Thyroid Gland Cell Types and Hormones

The thyroid gland contains distinct cell types that secrete specific hormones.

Follicular Cells: Secrete thyroxine (T4) and triiodothyronine (T3).
Parafollicular (C) Cells: Secrete calcitonin.

Thyroid Hormones Contain Iodine

Class: Amino acid-derived hormones containing iodine.
Unusual Feature: Iodine is essential for their synthesis.
Process: Iodide is actively transported into follicular cells, incorporated into tyrosine residues, forming T3 and T4.
Active Hormone: T3 is more active than T4.
Transport: Bound to plasma proteins (thyroid-binding globulin) in blood.
Receptors: Located in the nucleus; hormone binding regulates gene expression.

TSH Controls the Thyroid Gland

Pathway: Hypothalamus releases TRH → Pituitary releases TSH → Thyroid releases T3/T4.
Actions in Children: Essential for growth and development.

Thyroid Pathologies Affect Quality of Life

Hyperthyroidism

Effects: Weight loss, heat intolerance, increased heart rate, anxiety.

Hypothyroidism

Effects: Weight gain, cold intolerance, fatigue, slowed metabolism.
Goiter Formation: Primary hypothyroidism (iodine deficiency) vs. primary hypersecretion (Graves' disease).

23.4 Growth Hormone

Factors Important for Normal Growth

Genetics
Nutrition
Hormones: GH, thyroid hormones, sex steroids, insulin.

Growth Hormone Is Anabolic

Secretion: GH is secreted throughout life, with peaks during childhood and adolescence; daily peak occurs during sleep.
Control Pathway: Hypothalamus releases GHRH → Pituitary releases GH → Liver releases IGFs.
Binding Protein: GH binds to growth hormone-binding protein in plasma, prolonging its half-life.
IGFs: Insulin-like growth factors mediate many effects of GH, promoting tissue growth.
Metabolic Effects: Stimulates protein synthesis, increases fat breakdown, raises blood glucose.

Growth Hormone Pathologies

Hypersecretion: Gigantism (children), acromegaly (adults).
Hyposecretion: Dwarfism.

23.5 Tissue and Bone Growth

General Areas of Growth

Soft Tissue Growth: Measured by cell number and size.
Bone Growth: Measured by length and density.

Tissue Growth Requires Hormones and Paracrine Signals

Hormones: GH, IGFs, thyroid hormones, insulin.
Paracrine Signals: Local growth factors.
Hypertrophy: Increase in cell size.
Hyperplasia: Increase in cell number.

Bone Growth Requires Adequate Dietary Calcium

Extracellular Matrix: Composed of collagen fibers and hydroxyapatite (calcium phosphate crystals).
Bone Types: Compact and spongy bone.
Bone Growth: Osteoblasts build bone; osteoclasts resorb bone; osteocytes maintain bone tissue.
Factors Influencing Growth: Nutrition, hormones, mechanical stress.

23.6 Calcium Balance

Calcium in the Body

Location: Most calcium is found in bones; remainder in plasma and cells.
Functions: Muscle contraction, nerve transmission, blood clotting, enzyme activity.

Plasma Calcium Is Closely Regulated

Regulation: Intake (diet), output (urine/feces), and exchange with bone.
Extracellular vs. Intracellular: Extracellular Ca2+ is tightly regulated; intracellular Ca2+ is involved in signaling.

Three Hormones Control Calcium Balance

Parathyroid Hormone (PTH): Increases plasma Ca2+ by stimulating bone resorption, kidney reabsorption, and activating vitamin D.
Calcitriol (Vitamin D): Increases intestinal absorption of Ca2+.
Calcitonin: Lowers plasma Ca2+ by inhibiting bone resorption.

Parathyroid Hormone

Stimulus: Low plasma Ca2+ triggers PTH secretion.
Action: Increases bone resorption, kidney reabsorption, and calcitriol activation.
Osteoclasts: Indirectly activated by PTH via osteoblast signaling.

Calcitriol

Production: Synthesized from vitamin D in skin, liver, and kidney.
Regulation: PTH stimulates final activation step in kidney.
Effect: Increases plasma Ca2+ by enhancing intestinal absorption.

Calcitonin

Chemical Nature: Peptide hormone produced by thyroid C cells.
Role: Reduces plasma Ca2+ by inhibiting osteoclast activity.

Calcium and Phosphate Homeostasis Are Linked

Phosphate Functions: Bone mineralization, energy metabolism (ATP), cell signaling.
Locations: Bone, plasma, intracellular fluid.
Hormones: PTH, calcitriol, and FGF23 regulate phosphate balance.

Osteoporosis: A Disease of Bone Loss

Definition: Osteoporosis is characterized by decreased bone mass and increased fracture risk.
Effects: Fragile bones, increased risk of fractures, loss of height.
Risk Groups: Postmenopausal women, elderly individuals.
Risk Factors: Age, gender, genetics, low calcium/vitamin D intake, inactivity.
Treatment: Bisphosphonates, hormone replacement therapy, calcium/vitamin D supplementation.
Prevention: Adequate calcium/vitamin D intake, regular weight-bearing exercise, avoiding smoking/alcohol.

Table: Comparison of Calcium-Regulating Hormones

Hormone	Source	Main Effect	Target Organs
Parathyroid Hormone (PTH)	Parathyroid glands	Increases plasma Ca2+	Bone, kidney, intestine
Calcitriol (Vitamin D)	Skin, liver, kidney	Increases Ca2+ absorption	Intestine, bone, kidney
Calcitonin	Thyroid C cells	Lowers plasma Ca2+	Bone

Key Equations

Additional info: These notes expand upon the reading questions by providing definitions, mechanisms, and clinical context for each hormone and process described. The table and equations are inferred from standard physiology textbooks.