Pituitary Gland - Lesson 13 PDF

Pituitary gland = hypophysis - Small gland located in the sella turicac of sphenoid bone below the hypothalamus at the base of the brain - Median eminence = lowest portion of the hypothalamus that connects with pituitary stalk - Hypophysial stalk = pituitary stalk that connects the...

Pituitary gland = hypophysis - Small gland located in the sella turicac of sphenoid bone below the hypothalamus at the base of the brain - Median eminence = lowest portion of the hypothalamus that connects with pituitary stalk - Hypophysial stalk = pituitary stalk that connects the posterior pituitary to the hypothalamus - Anterior and posterior pituitary separated by paris intermedia which is relatively avascular Adenohypophysis = anterior pituitary Neurohypophysis = posterior pituitary Endocrine gland release hormones directly into the bloodstream, where they travel to cells throughout the body Exocrine gland secrete hormones into ducts Hormones - Peptide = short chains of amino acids - All hormones stimulated by the pituitary are peptides - Amine = tyrosine amino acid derivatives - Steroid = lipid-soluble and derived from cholesterol Adenohypophysis = anterior pituitary - Originates embryonically from Rathke's ouch - Comprised of epithelial cells - Highly vascular - Special neurons in the hypothalamus secrete hormones that control anterior pituitary secretion - Hypothalamic releasing hormone - Hypothalamic inhibiting hormone - Hormones from the hypothalamus are conducted to pituitary via the hypothalamic-hypophysial portal vessels - Prolactin-inhibiting hormone = dopamine rolactin-releasing hormone (PRH) as a specific, well-characterized hormone in humans does not exist. Instead, **prolactin secretion** is primarily regulated by **prolactin-inhibiting factors (PIFs)** and stimulatory mechanisms. Here\'s how it works: 1. **Stimulation of Prolactin Secretion**: - Prolactin release from the anterior pituitary is primarily stimulated by **thyrotropin-releasing hormone (TRH)** and, in some contexts, **oxytocin**. - Estrogen also plays a significant role in stimulating prolactin secretion, particularly during pregnancy. 2. **Inhibition of Prolactin Secretion**: - Dopamine, secreted by the hypothalamus, acts as the primary **prolactin-inhibiting factor (PIF)**. It binds to dopamine receptors on lactotroph cells in the anterior pituitary to suppress prolactin secretion. While the idea of a specific \"prolactin-releasing hormone\" has been hypothesized, research has yet to conclusively identify a distinct, independent hormone dedicated solely to this function in humans. Instead, TRH and other factors perform this role indirectly. - Releasing hormones from the hypothalamus play predominant role in all hormones except in prolactin which is mediated by positive feedback - Where do stimulating factors come from? Where do inhibiting factors come from? - Dopamine = positive feedback loop - Releasing and inhibiting factors are produced by the hypothalamus in response to negative feedback from target organs - "Releasing" in hormone name = hypothalamus origination - Anterior pituitary hormones - FSH - LH - Adrenocorticotropic hormone/corticotropin - Thyroid-stimulating hormone/thyrotropin = controls secretion of T4 and T3 - Prolactin = promotes mammary gland development and lactation - Endorphins - Growth hormone - Melanocyte-stimulating hormone - Anterior pituitary cell types for each hormone secreted by the anterior pituitary - Somatotropes produce human growth hormone - Corticotropes produce adrenocorticotropic hormone - Thryotropes produce TSH - Lactotropes produce prolactin - Gonadotropes produce FSH and LH - Neurohypophysis = posterior pituitary - Originates embryonically from outgrowth of the hypothalamus - Comprised of neural tissue primarily from glial-like cells called pituicytes - Magnocellular neurons located in supraoptic and paraventricular nuclei of hypothalamus - Secretes hormones synthesized by cell bodies in hypothalamus - ADH - Control rate of water excretion in urine - Primarily by supraoptic nuclei 5/6 and 1/6 from paraventricular nuclei - Oxytocin - Lactation and labor/delivery - Primarily by paraventricular nuclei 5/6 and 1/6 from supraoptic nuclei - No releasing hormones modulate release of posterior pituitary hormones - Exocytosis modulates release of posterior pituitary hormones - Posterior pituitary hormones (oxytocin and vasopressin/antidiuretic hormone, ADH) are not regulated by releasing hormones from the hypothalamus. Instead, they are synthesized in the hypothalamus (in the paraventricular and supraoptic nuclei) and transported along axons to the posterior pituitary, where they are stored and directly released into the bloodstream when needed. - In contrast, anterior pituitary hormones are regulated by hypothalamic releasing and inhibiting hormones via the hypothalamic-pituitary portal system. - Posterior pituitary cell types - Magnocellular neurons - Secretion of hormones from posterior pituitary - Cell bodies in the hypothalamus synthesize ADH and oxytocin - Hormones travel from hypothalamus down pituitary stalk to posterior pituitary - Posterior pituitary secretes ADH and oxytocin - Posterior pituitary secretion is controlled by nerve signals from hypothalamus - Anatomic neighbors to the pituitary gland - Optic nerve and optic chiasm - Cavernous sinus key structures = internal carotid, oculomotor nerve, trochlear nerve, ophthalmic division of trigeminal nerve, maxillary division of trigeminal nerve, abducens nerve - Anterior pituitary hormones mnemonic = FLAT-PEG - Tropic hormones = FLAT = act on other endocrine glands = FSH, LH, Adrenocorticotropic hormone, thyroid stimulating hormone - Direct hormones = exert effects on organs = prolactin, endorphin, growth hormone - Posterior pituitary = direct hormones = ADH and oxytocin - Know hormone function, where they come from, what stimulates production, what inhibits it - Negative feedback loop for all hormones except prolactin - FSH - Stimulated by GnRH - inhibited by estrogen - function = stimulates ovulation and spermatogenesis - LH - Stimulated by GnRH - inhibited by testosterone, progesterone, inhibin - function= stimulates development of corpus luteum and release of estrogen, progesterone, and testosterone - HPA = hypothalamic-pituitary-adrenal axis - Adrenocorticotropic Hormone (ACTH) - Stimulated by CRH and anything that increases hypothalamic synthesis of CRH (e.g. stress, catecholamines, dopamine, serotonin, Ach, histamine) - Inhibited by cortisol - Function = target adrenal gland to secrete cortisol - Affected by circadian rhythm - TSH - Stimulated by TRH - Inhibited by thyrotropin, high levels of T3 and T4 - Function = stimulates thyroid to release T3 and T4 and calcitonin - Prolactin - Stimulated by PRH - Inhibited by PIH/dopamine - Function = development of breasts and lactation - Positive feedback loop = infant breastfeeds so more prolactin produced so more milk produced - Endorphins - Stimulated by pain, stress, exercise, sex - Inhibited by GABA - Function alleviate pain, lower stress, improve mood, enhance sense of well-being - Growth hormone - Stimulated by GHRH - Secreted in a pulsatile pattern - Affected by nutrition, stress, dopamine, serotonin - Inhibited by GHIH/somatostatin - Function = stimulate growth of all cells in body - ADH/vasopressin - Secretion of ADH is regulated by extracellular fluid osmolality and circulating blood volume - Formed primarily in the supraoptic nuclei - Osmoreceptors in supraoptic nuclei detect changes in osmolarity - Increased osmolarity increases secretion of ADH - Decreased osmolarity decreases secretion of ADH - Stretch receptors in atria, carotid arteries, aorta, pulmonary \_\_\_ detect blood volume - Increased circulating blood volume stimulates stretch receptors and causes decreased ADH secretion - Decreased circulating blood volume (by 15-25%) causes increased ADH secretion - ADH decreases excretion of water by kidneys - Increased ADH levels result in SIADH - Decreased ADH levels result in DI - Oxytocin - Stimulates contraction of the pregnant uterus and plays an important role in the letdown of milk - The love hormone -- affects both males and females - Released during stress [Pituitary tumors and disease ] - Pituitary adenomas are common and most are benign - Anterior pituitary adenomas can lead to excess production of hormones - Most common pituitary adenomas are prolactinomas - MEN1 = multiple endocrine neoplasia tumors = MEN1 is characterized by a combination of tumors of the anterior pituitary, parathyroid, gastrointestinal tract, and pancreas - Tumors are classified by size and cell of origin - Functional adenoma secretes hormones while a non-functioning adenoma does not - Symptoms of functional adenomas depend on cell type and hormone excess - Non-functioning adenomas are usually macroadenomas - Mass effect - Mass effect symptoms are due to compression of surrounding structures from large, usually non-functioning adenomas - Symptoms - Headache common - Visual field deficits = bitemporal hemianopsia - Cranial nerve palsy - Diabetes insipidus - Panhypopituitarism - hypothyroidism, hypoadrenalism, hypogonadism - Stalk effect - **Pituitary apoplexy** = rupture of the pituitary usually as the result of bleeding - **Sheehan's syndrome** occurs when anterior pituitary is damaged due to significant blood loss e.g. OB hemorrhage - Emergency! - Treatment = surgical decompression, steroid therapy, hormone replacement - Signs of meningeal irritation - Brudzinski sign = Involuntary bending of the knees and hips occurs when the neck is flexed - Kernig sign = Pain or resistance occurs when the leg is straightened at the knee while the hip is flexed at 90° - Positive of either sign indicates meningeal irritation - GH excess - Gigantism and acromegaly occur due to excess GH - Preadolescent = **gigantism** due to stimulation of GH on all tissues - Bony growth plates are not sealed yet - Bones can continue to grow longer - Post-adolescence = **acromegaly** due to stimulation of GH on all tissues except bone - Bony growth plates are sealed - Bones grow thicker instead of longer - Usually diagnosed in adults - Treatment - Anesthetic management of acromegaly - Proliferation of connective tissue and bone = everything is bigger and barrel-chested - Anticipate difficult airway in every aspect of airway management (mask, laryngoscopy, and intubation) - Will have subglottic stenosis so have smaller ETT available - Avoid nasal intubation due to enlarged turbinates - Multi-organ dysfunction due to acromegaly = DM, HTN, cardiomyopathy, heart failure, ventricular hypertrophy, CAD, OSA - Stress-level glucocorticoids may be indicated if impairment of adrenal axis - Decreased GH - Congenital = dwarfism = insufficient bone maturation and short stature - Acquired/child = panhypopituitarism = do not pass through puberty and do not develop adult sexual functions - If only GH is abnormal, these pts will develop normally but are short in stature - Acquired/adult - Causes = tumor compressing pituitary, thrombosis of pituitary blood vessels - Effects = hypothyroidism, hypogonadism, lethargy, weight gain, loss of sex functions - **Cushing's disease** = pituitary tumor produces **excessive amounts of ACTH** - Excess ACTH leads to increased cortisol release from adrenal glands - Excess cortisol leads to symptoms of glucocorticoid excess - Cushing's syndrome = glucocorticoid excess - Causes = excess ACTH, adrenal cancers, excess iatrogenic administration - Tumor types outside of the pituitary that can secrete ACTH and cause Cushing's = small cell tumors of lung, islet cell tumors of pancreas, medullary thyroid tumors - Signs and symptoms of Cushing's disease - Hyperglycemia - HTN - Weight gain, central obesity - Hypokalemia - Increased infection and poor wound healing - Alkalosis - Hirsutism, acne, loss of libido, menstrual disturbances - Osteopenia and osteoporosis - Skeletal muscle weakness - Cataracts - Skin striae, spontaneous ecchymosis, facial plethora - Depression, cognitive dysfunction, emotional lability - Anesthetic management considerations in Cushing's - Preop assessment = BP, glucose, intravascular fluid volume, electrolytes - Buffalo hump and OSA may complicate airway management - Use caution with positioning dur to osteopenia, fragile skin - Increased infection and DVT/PE risk - AVOID etomidate in these patients - Muscle relaxants have exaggerated effects in hypokalemia and myopathy - **Pituitary prolactinoma** = excess prolactin - Most common pituitary hypersecretion syndrome in men and women! - Symptoms - In women will cause breast milk production/galactorrhea, infertility problems, amenorrhea, anovulation, osteoporosis - In men will cause decreased sex drive, gynecomastia, galactorrhea - Treatment - Microadenoma = dopamine agonists, monitoring - Macroadenoma = surgical resection - Thyrotropin secreting adenoma = excess TSH - Rare! - Treatment = surgical resection - Gonadotroph adenomas = excess FSH and LH - Rare! - More likely to be seen from mass effects syndromes - Diabetes insipidus = too little ADH - Central DI = related to the brain - Nephrogenic DI = related to the kidney's inability to respond to ADH - Caused by reduced secretion of ADH - Symptoms - Increased and dilute urine output with low specific gravity - High serum osmolality and hypernatremia i.e. intravascularly depleted - Treatment - Maintain intravascular volume - DDAVP/desmopressin - Anesthetic considerations - Preop assessment = electrolyte imbalances (especially Na+), hydration status, renal function, plasma osmolarity - Fluid management = calculate water deficit, isotonic fluid administration, frequent labs - If urine output is \>300mL/hour for \>2 hours = DDAVP - Calculating total body water deficit -- won't be tested on this - SIADH = too much ADH - Caused by increased secretion of ADH - Symptoms - Water intoxication, dilutional hyponatremia - Hypertonic urine with high specific gravity - Low serum osmolality and hyponatremia - Treatment - Correct underlying cause - Fluid restriction - Consider hypertonic caline if symptomatic or Na+\