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The Endocrine System: Pituitary, Thyroid, Parathyroid, and Adrenal Glands

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The Endocrine System

Overview of Endocrine Glands

The endocrine system is composed of glands that secrete hormones directly into the bloodstream, regulating various physiological processes. Major glands include the pituitary, thyroid, parathyroid, adrenal glands, pancreas, gonads, and pineal gland. Each gland produces specific hormones that target organs and tissues throughout the body.

Major endocrine glands of the human body

Anterior Pituitary Hormones

Gonadotropins: FSH and LH

Follicle-stimulating hormone (FSH) and Luteinizing hormone (LH) are essential for reproductive function. They are absent in prepubertal children and are regulated by gonadotropin-releasing hormone (GnRH) from the hypothalamus. Gonadal hormones provide negative feedback to suppress their release.

  • FSH: Stimulates gamete (egg or sperm) production.

  • LH: Promotes production of gonadal hormones (estrogen, progesterone, testosterone).

  • Regulation: GnRH triggers release; gonadal hormones inhibit via feedback.

Prolactin (PRL)

Prolactin is secreted by the anterior pituitary and primarily stimulates milk production in females. Its release is inhibited by prolactin-inhibiting hormone (PIH), which is dopamine. Estrogen increases PRL levels, explaining breast changes during the menstrual cycle. Suckling stimulates further PRL release for continued lactation.

  • Role in males: Not well understood.

  • Regulation: PIH prevents release until needed; decreased PIH leads to lactation.

Summary Table: Pituitary Hormones

Hormone

Regulation of Release

Target Organ and Effects

Effects of Hypo/Hypersecretion

Growth hormone (GH)

Stimulated by GHRH; inhibited by GHIH

Liver, muscle, bone, cartilage; stimulates growth

↓: Pituitary dwarfism; ↑: Gigantism/acromegaly

Thyroid-stimulating hormone (TSH)

Stimulated by TRH; inhibited by feedback

Thyroid gland; stimulates thyroid hormone release

↓: Cretinism/myxedema; ↑: Hyperthyroidism

Adrenocorticotropic hormone (ACTH)

Stimulated by CRH; inhibited by feedback

Adrenal cortex; stimulates corticosteroid release

↑: Cushing's disease

FSH/LH

Stimulated by GnRH; inhibited by feedback

Ovaries/testes; gamete and hormone production

↓: Failure of sexual maturation

Prolactin (PRL)

Stimulated by decreased PIH

Breast tissue; promotes lactation

↓: Poor milk production; ↑: Inappropriate milk production

Summary table of pituitary hormonesSummary table of pituitary hormones (continued)

The Thyroid Gland

Anatomy and Histology

The thyroid gland is a butterfly-shaped organ located in the anterior neck, overlying the trachea. It consists of two lateral lobes connected by an isthmus. The gland contains follicles filled with colloid, surrounded by follicular cells (which secrete thyroid hormone), and parafollicular cells (which secrete calcitonin).

Gross anatomy of the thyroid gland, anterior viewPhotomicrograph of thyroid gland follicles

Thyroid Hormone (TH)

Thyroid hormone is the body's major metabolic hormone, existing in two forms: T4 (thyroxine) and T3 (triiodothyronine). T4 is the predominant form in circulation, but T3 is more active and is produced from T4 in peripheral tissues. TH enters target cells, binds to nuclear receptors, and regulates gene transcription, affecting nearly every cell in the body.

  • Functions: Increases basal metabolic rate (BMR), heat production (calorigenic effect), regulates tissue growth and development, and maintains blood pressure.

  • BMR Calculation:

Regulation of Thyroid Hormone Release

TH release is regulated by a negative feedback loop involving the hypothalamus, anterior pituitary, and thyroid gland. Low TH levels stimulate the release of thyrotropin-releasing hormone (TRH) from the hypothalamus, which triggers thyroid-stimulating hormone (TSH) release from the anterior pituitary, stimulating the thyroid gland to produce TH.

Hypothalamic-pituitary-thyroid axis

Major Effects of Thyroid Hormone

System

Normal Effects

Hyposecretion

Hypersecretion

BMR/Temperature

Increases BMR, heat production

↓ BMR, cold intolerance, weight gain

↑ BMR, heat intolerance, weight loss

Metabolism

Stimulates glucose, fat, protein metabolism

↓ Metabolism, high cholesterol

↑ Catabolism, muscle wasting

Nervous System

Normal development/function

Mental sluggishness, developmental delay

Restlessness, insomnia

Cardiovascular

Increases heart rate, BP

↓ HR, ↓ BP

↑ HR, ↑ BP

Muscular/Skeletal

Normal growth/function

Weakness, stunted growth

Muscle atrophy, osteoporosis

GI/Reproductive/Integumentary

Normal motility, fertility, skin/hair health

Constipation, infertility, dry skin/hair

Diarrhea, menstrual irregularity, thin skin/hair

Major effects of thyroid hormone in the body

Thyroid Disorders

Hyposecretion: Myxedema and Goiter

Myxedema is severe hypothyroidism in adults, characterized by low metabolic rate, thick/dry skin, puffy eyes, and lethargy. If caused by iodine deficiency, the thyroid enlarges, forming a goiter. Treatment involves hormone replacement.

Clinical appearance of myxedemaClinical appearance of myxedema (side view)Enlarged thyroid (goiter) due to iodine deficiency

Congenital Hypothyroidism (Cretinism)

Usually due to poor thyroid development, pituitary problems, or maternal factors. Symptoms include weak cry, poor feeding, constipation, and prolonged jaundice. Lifelong TH replacement is necessary.

Clinical appearance of congenital hypothyroidismClinical appearance of congenital hypothyroidism (side view)

Hypersecretion: Graves' Disease

Graves' disease is an autoimmune disorder where antibodies mimic TSH, causing excessive TH release. Symptoms include high metabolic rate, sweating, rapid heartbeat, nervousness, weight loss, and exophthalmos (bulging eyes). Treatment includes thyroid removal or radioactive iodine.

Bulging eyes (exophthalmos) of Graves' disease

Calcitonin

Calcitonin is produced by parafollicular (C) cells in response to high blood calcium levels. It inhibits osteoclast activity, reducing calcium release from bone, and stimulates calcium uptake into bone. Its physiological role in humans is minor, but pharmacologically, it is used to treat osteoporosis.

Photomicrograph of thyroid gland follicles showing parafollicular cells

Parathyroid Glands

Anatomy and Function

The parathyroid glands are small glands located on the posterior aspect of the thyroid. They secrete parathyroid hormone (PTH), the most important hormone in calcium homeostasis. PTH is released in response to low blood calcium and acts on the skeleton, kidneys, and intestine to increase blood calcium levels.

Anatomy and histology of the parathyroid glands

Regulation of Calcium Homeostasis

PTH stimulates osteoclasts to release calcium from bone, enhances calcium reabsorption in the kidneys, and promotes activation of vitamin D, increasing intestinal absorption of calcium. Calcitonin acts as an antagonist to PTH.

Calcitonin and PTH regulation of calcium homeostasisPTH regulation of calcium homeostasis

Adrenal Glands

Structure and Hormones

The adrenal glands are paired organs atop the kidneys, consisting of an outer cortex and inner medulla. The cortex produces corticosteroids: mineralocorticoids (aldosterone), glucocorticoids (cortisol), and gonadocorticoids (androgens). The medulla produces catecholamines (epinephrine and norepinephrine).

Histology of the adrenal gland

Mineralocorticoids: Aldosterone

Aldosterone regulates sodium and potassium balance, affecting blood volume and pressure. Its secretion is controlled by the renin-angiotensin-aldosterone mechanism, plasma potassium, ACTH, and atrial natriuretic peptide (ANP).

Major mechanisms controlling aldosterone release

Disorders: Aldosteronism

Hypersecretion of aldosterone (aldosteronism) causes hypertension, edema, and hypokalemia, leading to muscle and neural dysfunction.

Glucocorticoids: Cortisol

Cortisol helps the body resist stress by increasing blood glucose, fatty acids, and amino acids. It is released in response to ACTH and regulated by negative feedback. Chronic excess leads to Cushing's syndrome, while deficiency causes Addison's disease.

Cushing's syndrome: buffalo humpAddison's disease: characteristic bronzing of skin

Gonadocorticoids

These weak androgens are converted to testosterone or estrogens in tissues. They contribute to puberty, secondary sex characteristics, and female libido. Hypersecretion can cause masculinization in females and precocious puberty in boys.

Masculinization in females due to adrenogenital syndrome

Adrenal Medulla: Catecholamines

The adrenal medulla secretes epinephrine and norepinephrine, which mediate the fight-or-flight response: increasing heart rate, blood pressure, and blood glucose, and diverting blood to essential organs. Effects are short-lived compared to cortical hormones.

Short-term stress response via adrenal medullaLong-term stress response via adrenal cortex

Summary Table: Adrenal Gland Hormones

Hormone

Regulation of Release

Target Organ and Effects

Effects of Hyper/Hyposecretion

Mineralocorticoids (aldosterone)

Renin-angiotensin, K+, ACTH, ANP

Kidneys: Na+ reabsorption, K+ excretion

↑: Aldosteronism; ↓: Addison's disease

Glucocorticoids (cortisol)

ACTH

Body cells: metabolism, stress resistance

↑: Cushing's; ↓: Addison's

Gonadocorticoids

ACTH

Sex characteristics, libido

↑: Masculinization; ↓: No effect

Catecholamines

Sympathetic nervous system

Fight-or-flight response

↑: Prolonged response; ↓: Unimportant

Summary table of adrenal gland hormones

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