Presentation 1 202 2023 Endocrine System PDF

202 SUMMARY PLATES FOR PRESENTATION 1 MATERIAL Endocrine Required Textbook Readings: (Nonsequential) Chapters 17  HORMONE: ‘TO EXCITE’ Copyright © 2010 Pearson Education, Inc.  hypothalamus...

202 SUMMARY PLATES FOR PRESENTATION 1 MATERIAL Endocrine Required Textbook Readings: (Nonsequential) Chapters 17  HORMONE: ‘TO EXCITE’ Copyright © 2010 Pearson Education, Inc.  hypothalamus * pineal gland * pituitary gland * ENDOCRINE GLANDS: (LISTED FROM SUPERIOR TO INFERIOR; AND IN ORDER OF STUDY) Traditional endocrine glands – pineal, hypothalamus, pituitary, thyroid, parathyroid, thymus, adrenal, pancreas, ovaries, & testes. The pancreas and gonads produce both hormones and exocrine products The ovaries & testes will be studied in detail with the Reproductive Systems Additional endocrine tissues – cutis, brain, osseous, adipose, heart, stomach & small intestine, liver, kidneys, and placenta. COMPARISON OF THE NERVOUS AND ENDOCRINE SYSTEMS Speed and persistence of response Nervous: reacts quickly (1 to 10 ms), stops quickly Endocrine: reacts slowly (hormones release in seconds or days), effect may continue for weeks – including permanent cellular changes Adaptation to long-term stimuli Nervous: response declines (adapts quickly) Endocrine: response persists (adapts slowly) Area of effect Nervous: usually, targeted and specific (one organ) Endocrine: usually general, widespread effects (many organs)  ENDOCRINE VS. NERVOUS: The Endocrine System is able to regulate long-term processes such as growth, development, or reproduction, which affects metabolic activities in virtually every cell in the human the body. The Nervous system is able to handle situations that require fraction of a second response (Crisis Response). 1° MECHANISM OF DYSFUNCTION 1° → Primary dysfunction is when a problem originates in a particular gland. 2° → Secondary dysfunction – when a problem occurs outside the gland and causes an effect (origination is elsewhere)  THE PINEAL GLAND Pineal gland—is a small pine cone-shaped gland attached to roof of third ventricle beneath the posterior end of corpus callosum After age 6 or 7, it undergoes involution (shrinkage) Down 75% by end of puberty Tiny mass of shrunken tissue in adults Secretory cells are called pinealocytes sets the rhythm for all cells PINEAL GLAND Outside of the BBB (Blood Brain Barrier) May contain radiopaque “brain-sand” (calcium salts) Possible causes: High Stress Accumulation of fluoride Standard American Diet (40%) Animal Fat & Animal Protein Possibly aging PINEAL GLAND Melatonin is involved with: Day/night cycles Peak levels occur from ten to midnight (drowsy) Begins at sunset Low levels occur at ten to noon (alert) Jet lag? RETINAL STIMULATION OF THE PINEAL ↑Melatonin receptors in Suprachiasmatic nucleus (SCN) of the Hypothalamus (reset switch*) on test Physiological processes that show rhythmic variations (body temperature, sleep, dreams, brain states, menstrual cycle, and appetite) Protects body from neurodegeneration and plays important role in navigation Many other chemicals are released but an adequate understanding of the Pineal gland remains elusive. PINEAL GLAND PP. 762-763 At night, the secretor y product of pinealocytes is Melatonin (a monoamine synthesized from serotonin) Melatonin inhibits the gonads and sexual maturation Hypo-states cause premature sexual maturation/ precocious puberty Children have ↑ Melatonin levels than Adults to inhibit puberty; A marked decrease stimulates puberty LONG WINTER NIGHTS ↑Melatonin Darkness Stimulates + Pineal Inhibits - gonads (and pigment cells in animals) LONG SUMMER DAYS ↓ Melatonin Light inhibits - Pineal Stimulates + gonads (and pigment cells in animals) SEASONAL AFFECTIVE DISORDER (SAD) AKA WINTER DEPRESSION Seasonal affective disorder (SAD) primarily occurs in winter or northern/ southern latitudes (~20%) ↓ light exposure (decreased light during daylight hours) ↑ Melatonin Hyper-melatonin state Increased in Daytime or Increased Overall Initial Symptoms: depression, lack of pleasure, decreased sex drive, lack of energy, sleepiness, PMS, difficulty concentrating, and weight gain. Treatment: Two to 3 hours of exposure to bright light each day reduces the melatonin levels and the symptoms (phototherapy/ lightbox (full exposure)) REVERSE SEASONAL AFFECTIVE DISORDER (RSAD) AKA SUMMER ONSET SEASONAL AFFECTIVE DISORDER Reverse Seasonal affective disorder (RSAD) primarily occurs in summer, or equatorial climates (~20%) ↑ light exposure Visual Brightness FYI 0.0001 lux – Moonless night ↓ Melatonin 0.1 lux – Deep Twilight 50 lux – Public areas (Indoor) Hypo-melatonin state 400 lux* - Offices (Sunrise /set) 20,000 lux – Full day (not direct) Decreased Overall to 100,000+ lux – Full Sun Initial Symptoms: anxiety, irritability, agitation, hyperactivity, increased sex drive, rapid speech, insomnia, decreased desire to sleep, hypomania, and weight loss. Treatment: Melatonin, location change, sunglasses, sun block, hat, increased time in dark/ cool rooms. THE HYPOTHALAMUS AND PITUITARY GLAND Hypothalamus (nervous tissue) Major control center of the endocrine and autonomic nervous system (ANS) Packed with nuclei Right and left paraventricular nuclei produce OT, TRH, CRH, GHIH (SS) Supraoptic nucleus produce ADH Preoptic nucleus produce GnRH Suprachiasmatic nucleus as biological clock Arcuate nucleus – Secretes GHRH, PRH, PIH, & regulates appetite THE HYPOTHALAMUS AND PITUITARY GLAND Infundibulum – hypothalamic stalk (neural) Pituitary Gland (two structures: neural and mucosal tissue) Neurohypophysis (posterior pituitary) Downgrowth from brains neurohypophyseal bud Adenohypophysis (anterior pituitary) * Arises from hypophyseal pouch (outgrowth of mucosal tissue – Rathke’s pouch) on test  PO P P PO SCN SCN SO A SO A P = Paraventricular PO = Preoptic SCN = Suprachiasmatic SO = Supraoptic A = Arcuate ADENOHYPOPHYSIS Has no neural connection Linked to hypothalamus only by hypophyseal portal system Primary capillaries in hypothalamus connected to secondary capillaries in adenohypophysis by hypophyseal portal venules Hypothalamic hormones regulate adenohypophysis  A B C NEUROHYPOPHYSIS Linked to hypothalamus by infundibulum axons Nerve tissue, not a true gland Nerve cell bodies in hypothalamus pass down the stalk as hypothalamo–hypophyseal tract and end in posterior lobe Hypothalamic neurons secrete hormones that are stored in neurohypophysis until released into blood The Posterior lobe of the pituitary is actually a part of the BRAIN  HYPOTHALAMIC HORMONES The hypothalamus sends chemical stimulus to the anterior pituitary via the Hypophyseal RH- from hypothalamus Portal System (All AA based) on test on test Releasing hormones (RH) ***CRH is both a regulator and a stimulate the pituitary to neurotransmitter; synthesis and release *May be the stress response integrator hormones of their own for the body. on test Inhibiting hormones (IH) shut off the synthesis and release of pituitary hormones Hypothalamic Hormones: TRH; CRH; GnRH; GHRH; PRH; PIH; GHIH HYPOTHALAMIC HORMONES (9) & NEGATIVE FEEDBACK LOOPS FOR RH’S TRH - Thyrotropin-releasing hormone CRH – Corticotropin-releasing hormone GnRH – Gonadotropin-releasing hormone GHRH – Growth hormone-releasing hormone PRH – Prolactin-releasing hormone (not in text) PIH – Prolactin-inhibiting hormone (Dopamine) GHIH – Growth hormone-inhibiting hormone (also known as Somatostatin) ANTERIOR AXIS OF CONTROL hypothalamic hormone  Hypothalamus Origin: Arcuate nucleus GHRH Anterior pituitary GH Fat, muscle, *also indirect cartilage, bone* pathways GH Stimulates Target cells Inhibits OT ADH HYPOTHALAMIC HORMONES – STORED AND RELEASED FROM NEUROHYPOPHYSIS OT - Oxytocin ADH – Antidiuretic Hormone ♥xyt♥cin OXYTOCIN (OT) - ♥XYT♥CIN Regulated by a positive feedback mechanism of oxytocin in the blood Promotes positive mood, nurturing, love, affection, trust behavior, and the feelings of sexual satisfaction and emotional bonding between partners Also known as the “cuddling hormone” in non lactating females and in males. Plays important role in sexual arousal and orgasm when primed by sex hormones Stimulates uterine contractions and propulsion of semen ♥XYT♥CIN – BY PARAVENTRICULAR NUCLEI Promotes emotional bonding between lactating mother and infant; parental “attachment’ bonding Suckling reflex also promotes release of Oxytocin Also triggers milk ejection (“letdown” reflex) in women producing milk during lactation from PRL Stimulates labor contractions during childbirth - Stimulates by mobilizing Ca2+ Synthetic and natural oxytocic drugs are used to induce or hasten labor ANTIDIURETIC HORMONE (ADH) – BY SUPRAOPTIC NUCLEUS Antidiuresis is the water suppression or reduction of urinary volume by the kidneys. Prevents dehydration ADH also called Arginine Vasopressin (AVP); also a brain neurotransmitter ↑↑↑ ADH as seen in severe blood loss and trauma leading to “pressor effects” → Vasoconstriction of blood vessels and an ↑BP ANTIDIURETIC HORMONE Hypothalamic receptors respond to changes in the solute concentration of the blood If solute concentration is high (low water) ADH is synthesized and released, inhibiting urine formation (to increase blood volume) If solute concentration is low (high water) ADH is not released, allowing water loss ANTIDIURETIC HORMONE ADH targets kidney collecting ducts and aquaporins Pain, low blood pressure, nicotine, and morphine all stimulate ADH release. Alcohol and diuretic drugs (for heart failure and edema) inhibit ADH release and cause copious urine output (dehydration) Excessive water intake also inhibits ADH release HOMEOSTATIC IMBALANCES OF ADH ADH hyposecretion → Diabetes Insipidus (DI) ADH hypersecretion → Syndrome of inappropriate ADH secretion (SIADH) DIABETES INSIPIDUS (“OVERFLOW, TASTELESS”) Result of ADH hyposecretion (“not present” or “doesn’t work”) Frequently caused by blow to the head or surgical trauma that damages the hypothalamus. As long as patient is conscious and hydrated it is not life threatening. DI in children can interfere with appetite, weight gain, and growth. Polyuria - Huge output of urine (as Adults can stay healthy for much as 15 L/day) Polydipsia - Huge decades with adequate water thirst consumption SYNDROME OF INAPPROPRIATE ADH EXCESS (SIADH) Hyper- secretion of ADH Caused by meningitis, pneumonia, cancer, neurosurgery, drugs (anesthesia and depression SSRI’s (Selective Serotonin Re-uptake Inhibitors)) Symptoms include retained fluid, headaches, and disorientation due to brain edema and weight gain. Can lead to seizures and coma.  PITUITARY CONCEPTS “Trophic” – to turn on, to change, to regulate other endocrine glands. (FSH, LH, ACTH, TSH) GH & PRL exert major effects on non- endocrine targets Very little hormone storage in Anterior Lobe of Pituitary. (RH most important) ANTERIOR PITUITARY HORMONES (6) 1. Follicle-stimulating hormone (FSH) 2. Luteinizing hormone (LH) 3. Thyroid-stimulating hormone (TSH) or thyrotropin 4. Adrenocorticotropic hormone (ACTH) 5. Prolactin (PRL) 6. Growth hormone (GH) GONADOTROPIN: FOLLICLE- STIMULATING HORMONE (FSH) ABSENT FROM THE BLOOD IN PREPUBERTAL BOYS AND GIRLS Stimulates secretion of ovarian sex hormones, development of ovarian follicles, and sperm production FiSH production  Gonadotropin: Luteinizing hormone (LH) Absent from the blood in prepubertal boys and girls In females LH works alone to trigger ovulation on test LH stimulates ovulation, stimulates corpus luteum to secrete progesterone, stimulates testes to secrete testosterone, ovaries to release estrogens THYROID-STIMULATING HORMONE (TSH) OR THYROTROPIN Stimulates secretion of thyroid hormone and normal development of the thyroid ADRENOCORTICOTROPIC HORMONE (ACTH) OR CORTICOTROPIN Stimulates the adrenal cortex to secrete glucocorticoids (chiefly cortisol) PROLACTIN (PRL) After birth, stimulates mammary glands to synthesize milk; enhances secretion of testosterone by testes ANTERIOR AXIS OF CONTROL  GROWTH HORMONE (GH) OR SOMATOTROPIN Stimulates mitosis and cellular differentiation Targets bone, cartilage, fat, and muscle Exerts its effects both directly and indirectly by inducing the Liver* to produce insulin-like growth factors (IGF) and others Hormone half-life—the time required for 50% of the hormone to be cleared from the blood GH half-life: about 10 minutes* IGF half-life: about 20 hours  PROTEIN SYNTHESIS Promotes Amino Acid Uptake from blood and protein synthesis at the ribosomal level for cell growth. Requires amino acids (AA) for building material LIPID METABOLISM Mobilizes fatty acids from adipocytes into the blood and encourages the use of fats for fuel. “The Protein-sparing effect” Provides Energy for other growing tissues CARBOHYDRATE METABOLISM Mobilizing fatty acids from adipocytes reduces dependence on glucose. Liver also synthesizes glucose. “The Glucose-sparing effect” Spares Glucose for the brain “Diabetogenic effect” – anti-insulin* Chronic oversecretion Insulin resistance Glucose intolerance Frank Diabetes ELECTROLYTE BALANCE Electrolyte balance: promotes Na+, K+, and Cl− retention by kidneys, enhances Ca2+ absorption in intestine A FURTHER LOOK AT GROWTH HORMONE Has a 24 hour cycle (Elevated in evening sleep) Secretion highest during first 2 hours of sleep (usually SWS* bursts) Can peak in response to vigorous exercise Declines with age (Muscle Atrophy) GH Supplementation may spur muscle growth, reduce body fat, and help physique. Increased GH related to Cancer and DM* HOMEOSTATIC IMBALANCES OF GROWTH HORMONE Hypersecretion In children results in gigantism (symmetrical) In adults results in acromegaly Hyposecretion In children results in pituitary dwarfism (symmetrical) Robert Wadlow compared to his father, Harold Franklin Wadlow (±1.82 m (5 ft 11 1⁄2 in))  HOMEOSTATIC IMBALANCES OF GROWTH HORMONE Hypersecretion In children results in gigantism (before plate closure) In adults results in acromegaly Usually results in Bitemporal Hemianopsia (tunnel vision (David & Goliath) HOMEOSTATIC IMBALANCES OF GROWTH HORMONE Hyposecretion In children results in pituitary symmetrical dwarfism If also decrease in TSH and Gonadotropins the child will be malproportioned In Adults results in fatigue, weight change, and emotional instability. Achondroplasia* Note: GHRH or hGH* replacement therapy and abuse/ parental administration. HOMEOSTATIC IMBALANCE: ACROMEGALY Hypersecretion after plate closure Gradual increased size of hands, feet, ears, lips, and tongue. (First noticed by non fitting rings, gloves, and shoes) GH counteracts insulin so increases Blood Glucose. Non-reversible. Treatment: GHIH(SS); Tumor Removal Side note: AA uptake stimulates GH secretion  ACROMEGALY* Growth of many somatic tissues Skin, muscle, heart, liver, and gastrointestinal tract Without treatment results in significant morbidity Joint deformity, hypertension, pulmonary insufficiency, and heart failure André René Roussimoff Fezzik, the giant in the film The Princess Bride THYROID GLAND The largest endocrine gland is located in the anterior neck and connected by a median tissue mass called the isthmus Composed of follicles that produce the glycoprotein thyroglobulin Colloid (thyroglobulin + iodine (I2)) fills the lumen of the follicles and is the precursor of thyroid hormone Other endocrine cells, the parafollicular cells, produce the hormone calcitonin *Oxidation of two iodide ions = iodine (I2) THYROID HORMONES Consists of two related iodine-containing compounds. on test 2% as ACTIVE T3 – triiodothyronine; has two tyrosines with three bound iodine atoms (MIT and a DIT) 98% as T4 – thyroxine; has two tyrosine molecules plus four bound iodine atoms (Two DIT’s) Iodine deficiency is more common in inland areas. Why? Identify I on the inner vs. outer benzyl ring (MIT vs. DIT) - T3, T4, rT3 Nature = top  TRANSPORT AND REGULATION OF TH T3 and T4 bind to thyroxine-binding globulins (TBGs) produced by the liver Both bind to target receptors, but T3 is ten times more active than T4 Peripheral tissues convert T4 to T3 (Deiodinate) Mechanisms of activity are similar to steroids Regulation is by negative feedback to Hypothalamus EFFECTS OF THYROID HORMONE Increasing metabolic rate Resultant Increases in oxygen consumption Increasing Heat production (Calorigenic effect) –Thermogenesis* (Mitochondria* - ↑ ATP inefficient = ↑ Heat) Accelerates breakdown of carbohydrates, fats, and protein for fuel (releasing energy) To meet increased demand it also raises the respiratory rate, heart rate, and strength of heartbeat. Regulates tissue growth Develops fetal nervous system  HOMEOSTATIC IMBALANCES: Hyperthyroid pathology → Graves’ Disease Hypothyroid pathology in infants → Congenital hypothyroidism (Cretinism) Hypothyroid pathology in adults → Myxedema  ENDOCRINOLOGIC BASIS OF GRAVE’S DISEASE: Most common hyperthyroid pathology Autoimmune disease where antibodies mimic TSH and continuously stimulate TH release. Symptoms include an ↑ metabolic rate, sweating, nervousness, irritability, rapid/ irregular heartbeat, weight loss, exophthalmos (protrusion of the eyeballs), and toxic goiter of Graves’ disease. TRX: Surgical removal of thyroid gland or ingestion of radioactive iodine (destroys most active cells).  Toxic Goiter Early Diffuse Toxic Goiter ENDOCRINOLOGIC BASIS OF CRETINISM: Severe hypothyroidism in infants May reflect genetic deficiency of the fetal thyroid gland or deficiency of dietary iodine. S/S: Mentally retarded, short and disproportionate sized body, thick tongue, and neck. Preventable if diagnosed early (Not reversible once S/S appear) ENDOCRINOLOGIC BASIS OF MYXEDEMA: Hypothyroid syndrome of adults S/S: ↓ metabolic rate, constipation, feel chilled, edema, lethargy, and mental sluggishness (endemic goiter if the result of a lack of iodine). TRX: Depending on cause can be reversed by iodine supplements or HRT (hormone replacement therapy). Endemic Goiter  Hypothyroidism affects 1-2% of all adults at some time in their life. Note: In the World most common is Iron Deficiency In US the most common is Hashimoto thyroiditis Abnormal immune response, antithyroid antibodies against the follicular cells In this case the antibodies are not stimulatory Immune process that blocks and destroys thyroid function Develops slowly (Diverse Hypo Symptoms) Detected early by high TSH with normal T3 T4 It is believed that the SAD diet and Environmental triggers may cause (Infection, Stress, & Radiation). THYROID HORMONES: CALCITONIN [201 REVIEW] A hormone produced by the parafollicular, or C, cells Lowers blood calcium levels (especially in children) Antagonist to parathyroid hormone (PTH); also ↑ blood [Ca++] negative feedback on PTH CALCITONIN Calcitonin targets the skeleton, where it: Inhibits osteoclast activity (and thus bone resorption) and release of calcium from the bone matrix Stimulates calcium uptake and incorporation into the bone matrix Regulated by a humoral (calcium ion concentration in the blood) negative feedback mechanism PARATHYROID GLANDS Tiny glands embedded in the posterior aspect of the thyroid Cells are arranged in cords containing oxyphil and chief cells Chief (principal) cells secrete PTH PTH (parathormone) regulates calcium balance in the blood EFFECTS OF PARATHYROID HORMONE PTH release increases Ca2+ in the blood as it: Stimulates osteoclasts to digest bone matrix Enhances the reabsorption of Ca2+ and the secretion of phosphate by the kidneys Increases absorption of Ca2+ by intestinal mucosal  HOMEOSTATIC IMBALANCES: Hyperparathyroid pathology → Hyperparathroidism Excess PTH secretion, usually caused by a tumor, which can cause bones to become soft, deformed, & fragile Raises blood calcium levels Hypoparathyroid pathology → Hypoparathyroidism Deficient PTH secretion, usually due to surgery which can cause fatal tetany within 3 or 4 days blood calcium levels  TEST 1 INCLUDES: Presentation 1 Material Presentation 2 Material (next powerpoint) Make sure you are comfortable will all the anatomical terms, and all the lecture material. Read all the Test rules in the Syllabus. Posted slides may get additions or substitutions prior to in-class lectures This test is a 50-minute test. Afterword's we will review.