Endocrine System and Pituitary Gland Practice Flashcards
Overview of the Endocrine System
The endocrine system is composed of several major glands produced in various parts of the body: * Pituitary Gland * Parathyroid Gland * Thyroid Gland * Pancreas * Adrenal Glands * Ovaries * Testes
Structure and Relationship of the Hypothalamus and Pituitary Gland
Hypothalamus: Acts as the primary regulator for the pituitary gland. It contains nuclei that produce hormones for storage and secretion as well as hormones that regulate the anterior pituitary.
Structure of the Pituitary Gland: * Adenohypophysis (Anterior Pituitary): * Composition: Consists of glandular epithelium. * Function: Both produces and secretes its own hormones. * Neurohypophysis (Posterior Pituitary): * Composition: Consists of neural tissue. * Function: Secretes only. It does not produce hormones; it stores and secretes hormones actually produced by the hypothalamus.
Posterior Pituitary (Neurohypophysis) Hormones
Hormone Production Sites in the Hypothalamus: * Supraoptic nucleus: Produces Antidiuretic Hormone (ADH). * Paraventricular nucleus: Produces Oxytocin (OT or OXT).
Antidiuretic Hormone (ADH) / Vasopressin: * Function: Primary role is the conservation of . * Mechanism of Action: * The hypothalamus contains osmoreceptors that detect an increase in osmotic pressure. * This stimulation triggers the secretion of ADH. * ADH stimulates the kidney tubules to reabsorb water into the interstitial fluid and then into the blood by osmosis. * Vasopressin Action (‘Vessel Pressure Substance’): * Causes contraction of the smooth muscle in arteries. * Leads to an increase in Blood Pressure (BP). * Stimulus for Release: Increased solute concentration of the blood. * Inhibitor of Release: Decreased solute concentration of the blood. * Target Tissue: Kidneys and Brain.
Oxytocin (OT): * Function: * Stimulates uterine contraction during childbirth. * Stimulates milk ejection (‘milk let-down reflex’). Note: Milk will not release without the presence of Oxytocin. * Mechanism: Operates on a positive feedback loop. * Stimulus for Release: Stretching of the uterus or an infant suckling at the nipple. * Inhibitor of Release: Lack of appropriate stimuli. * Target Tissue: Uterus and Mammary gland.
Anterior Pituitary (Adenohypophysis) Anatomy and Control
Hypothalamic-Hypophyseal Portal System: * The relationship between the hypothalamus and the anterior pituitary is vascular, not neural like the posterior pituitary. * Sequential Pathway: 1. Hypothalamic neurons secrete releasing and inhibiting hormones into the hypothalamic capillary bed. 2. Hormones travel through portal veins in the infundibulum. 3. Hypothalamic hormones exit the anterior pituitary capillary bed. 4. Hormones bind to receptors on anterior pituitary cells to stimulate or inhibit secretion. * Key Vascular Components: Superior hypophyseal artery, hypothalamic neurosecretory cells, portal vein, target cells in adenohypophysis, and anterior hypophyseal vein.
Anterior Pituitary Structure: * Consists of the Pars tuberalis, Pars anterior, and Pars intermedia. * Anatomically adjacent to the Optic Chiasm, Mammary body, and Infundibulum (Pituitary stalk). * Cells are classified by stain (basophil, acidophil, chromophobes) or by secretion.
Classification of Anterior Pituitary Cells and Hormones
Cell Types by Secretion: * Somatotrophs: Produce Growth Hormone (GH). * Corticotrophs: Produce Adrenocorticotropic Hormone (ACTH). * Thyrotrophs: Produce Thyroid Stimulating Hormone (TSH). * Lactotrophs: Produce Prolactin (PRL). * Gonadotrophs: Produce Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH).
Tropic Hormones: Defined as hormones that target other endocrine glands.
Growth Hormone (GH) / Somatotropin
Short-term Effects (Metabolic): * Inhibits glucose uptake by skeletal muscle. * Stimulates gluconeogenesis in the liver (generation of new glucose). * Stimulates lipolysis in fat (fat breakdown). * Result: Increased blood glucose concentration and increased blood fatty acid concentration (providing fuel/materials for growth).
Long-term Effects: * GH acts on the liver, muscle, bone, and other tissues to promote the release of Insulin-like Growth Factor (IGF). * IGF Functions: * Stimulates glucose uptake by cells (decreasing blood glucose, opposing the short-term GH effect). * Stimulates cell division and rapid protein synthesis. * Increases bone growth (longitudinal) and muscle development in children. * In adults, GH regulates body mass and muscle development.
Regulation (Multi-tiered Feedback): * First-Tier: Hypothalamus releases GHRH (stimulatory) or Somatostatin (inhibitory). * Second-Tier: Anterior pituitary releases GH. * Third-Tier/Effects: GH affects liver, muscle, bone, and fat. IGF provides negative feedback to both the hypothalamus and anterior pituitary.
Stimuli for Release: GHRH, stress, exercise, ingestion of protein, and fasting.
Inhibitors of Release: Somatostatin.
Other Anterior Pituitary Hormones
Prolactin (PRL): * Target: Mammary glands (which are exocrine glands). * Function: Lactogenic hormone. Promotes breast development and stimulates milk production. Assists milk secretion after birth. * Regulation: Stimulated by hypothalamic Prolactin-releasing hormone (PRH) and inhibited by Prolactin-inhibiting factor (dopamine).
Thyroid Stimulating Hormone (TSH): * Target: Thyroid gland. * Regulation: Stimulated by hypothalamic Thyrotropin-releasing hormone (TRH); inhibited by increased thyroid hormone levels and somatostatin. * Function: Growth and development of the thyroid; production and secretion of and .
Adrenocorticotropic Hormone (ACTH): * Target: Adrenal cortex. * Regulation: Stimulated by hypothalamic Corticotropin-releasing hormone (CRH) and stress; inhibited by increased cortisol and aldosterone. * Function: Growth and development of adrenal cortex; stimulates secretion of adrenal steroids (glucocorticoids) and catecholamines.
Follicle Stimulating Hormone (FSH): * Target: Ovaries and Testes. * Female Action: Stimulates primary follicles to mature; releases estrogen from ovaries. * Male Action: Stimulates spermatogenesis. * Regulation: Stimulated by GnRH.
Luteinizing Hormone (LH): * Target: Ovaries (Female) and Interstitial cells of testes (Male). * Female Action: Stimulates ovulation; stimulates production/action of corpus luteum; stimulates corpus luteum to secrete Progesterone and Estrogen. * Male Action: Stimulates secretion of Testosterone. * Regulation: Stimulated by GnRH.
Pineal Gland
Function: Connects the nervous and endocrine systems.
Hormone: Melatonin.
Biological Clock: Regulated by the Suprachiasmatic nucleus, which receives input via the optic chiasm.
Thyroid Gland: Anatomy and Hormone Synthesis
Anatomy: Located in the neck. Contains thyroid follicles filled with colloid.
Follicular Cells: Produce thyroid hormone.
Parafollicular Cells (C Cells): Produce Calcitonin, which increases bone formation and inhibits bone breakdown to decrease blood calcium levels.
Thyroid Hormone Synthesis Checklist: 1. Follicle cells secretes Thyroglobulin (a large precursor protein) into the colloid. 2. Iodide ions () are absorbed from the blood via a symporter and transported across the cell by Pendrin into the colloid. 3. Iodide is converted to iodine atoms () via oxidation. 4. Iodination: Iodine atoms attach to tyrosyl residues on thyroglobulin. * 1 Iodine + Tyrosine = Monoiodothyronine (MIT). * 2 Iodines + Tyrosine = Diiodothyronine (DIT). 5. Conjugation: * (Triiodothyronine). * (Thyroxine). 6. Iodinated thyroglobulin enters the follicle cell by endocytosis. 7. Lysosomal enzymes cleave and from the protein. 8. and are released into the blood via MCT transporters.
Note on Active Forms: Most target tissues convert to the more active . has a longer half-life in the blood and acts as a reservoir.
Thyroid Hormone Functions and Disorders
Functions: * Metabolic Rate/Thermoregulation: Sets Basal Metabolic Rate (BMR). Increases ATP consumption; heat from reactions maintains core temperature. * Growth/Development: Required for normal bone, muscle, and nervous system development. * Synergism with SNS: Up-regulates receptors for sympathetic neurotransmitters, affecting heart rate and blood pressure.
Negative Feedback Loop: * Stimulus: Decreased levels or cold exposure. * Receptor: Hypothalamus. * Control 1: Hypothalamus secretes TRH. * Control 2: Anterior pituitary secretes TSH. * Effector: Thyroid secretes and grows.
Pathology: * Hyperthyroidism: Characterized by over-production of hormone. Causes include Graves' disease. Symptoms: Diffuse goiter, Exophthalmos (bulging eyes), heat intolerance, and anxiety. * Hypothyroidism: Characterized by dry/sparse hair, thinning of lateral eyebrows, periorbital edema, and a puffy, dull face with dry skin. * Goiter: Enlargement of the thyroid gland. * Cancer: Thyroid cancer manifests as abnormal growth/masses.
Adrenal Gland Structure and Cortex Hormones
Location: Superior aspect of each kidney (pyramid-shaped).
Regions: * Adrenal Cortex: Outer region, typical endocrine gland. * Adrenal Medulla: Inner region, neuroendocrine organ (secretes neurohormones).
Zonations of the Adrenal Cortex: * Zona Glomerulosa (Outer): Densely packed cells. Produces Mineralocorticoids (Aldosterone). * Zona Fasciculata (Middle): Cells stacked in columns. Secretes Glucocorticoids (Cortisol) and Androgenic steroids. * Zona Reticularis (Inner): Thin layer, loosely arranged. Secretes Glucocorticoids and Androgenic steroids (Gonadocorticoids).
Aldosterone (Mineralocorticoid): * Regulated by the Renin-Angiotensin-Aldosterone System (RAAS). * Maintains Blood Pressure (increases smooth muscle tone in arteries). * Increases and water reabsorption. * Increases excretion of and in urine. * Hyperaldosteronism Symptoms: Hypokalemia (low ), hypernatremia (high ), and hypertension.
Cortisol (Glucocorticoid): * Stimulated by ACTH via the HPA (Hypothalamus-Pituitary-Adrenal) axis. * Involves the precursor molecule POMC, which is cleaved into ACTH, eta-lipotropin, eta-MSH, etc. * Actions: 1. Increases protein breakdown in muscle. 2. Liver gluconeogenesis from amino acids. 3. Increases lipolysis in adipose tissue. 4. Anti-inflammatory effects (inhibits white blood cells). * Excess Cortisol Note: Can lead to hyperglycemia and loss of protein.
Adrenal Pathology
Cushing’s Syndrome (Cortisol Excess): * Causes: Adrenal hyperplasia or tumor. * Symptoms: Thinning of scalp hair, emotional instability, acne, moon face, buffalo hump, osteoporosis, truncal obesity, striae of skin, easy bruising, muscle wasting (weakness/thin extremities), diabetes mellitus, and cardiac hypertrophy/hypertension.
Addison’s Disease (Adrenal Insufficiency): * Causes: Autoimmune adrenal atrophy, infection, or tumor metastasis. * Symptoms: Personality changes, anorexia, nausea, hyperpigmentation (specifically in palms of hands), cardiac insufficiency, hypotension, diarrhea, abdominal pain, and muscle weakness.
Androgen Disorders: Can result in Ambiguous Genitalia (e.g., clitoromegaly, posterior labial fusion).
Adrenal Medulla and Catecholamines
Hormones: Epinephrine (EPI) and Norepinephrine (NE).
Secretion Mechanism: * Stimulated by sympathetic preganglionic fibers releasing Acetylcholine (ACh). * Adrenal medullary secretory cells release hormones into the bloodstream. * Hormones reach target cells via Adrenergic receptors.
Effects: Increases heart rate/force, dilates bronchioles, constricts blood vessels to skin and digestive/urinary organs, increases metabolic rate, and dilates pupils.
Questions & Discussion
Clinical Reasoning (GH Excess): * Question 1: What happens if a patient has a tumor in the adenohypophysis that increases GH release? * Question 2: What happens if the patient is 10 years old? * Context: At age 10, epiphyseal plates are open. Excess GH results in Gigantism (excessive longitudinal growth). * Question 3: What happens if the patient is 56 years old? * Context: At age 56, epiphyseal plates are closed. Excess GH results in Acromegaly (growth of bone width and soft tissue, notably in hands, feet, and face).
Stress Response Identification: * Question: Which of the following is a major stress hormone that is released by way of ANS stimulation? * A. Aldosterone * B. Glucagon * C. Cortisol * D. Insulin * E. Epinephrine (Correct Answer) * Follow-up Discussion: Although both Epinephrine (E) and Cortisol are released during stress, the mechanisms of release are different. Epinephrine is stimulated via a neural pathway (direct ANS stimulation of the adrenal medulla), whereas Cortisol is stimulated via a hormonal pathway (the HPA axis involving CRH and ACTH).