Human Anatomy & Physiology the Endocrine System: Part A

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10/26/2014

PowerPoint® Lecture Slides Endocrine System: Overview prepared by Human Anatomy Barbara& Physiology Heard, Atlantic Cape Community • Acts with nervous system to coordinate College Ninth Edition and integrate activity of body cells • Influences metabolic activities via C H A P T E R 16 hormones transported in blood • Response slower but longer lasting than nervous system The Endocrine • Endocrinology System: Part A – Study of hormones and endocrine organs

Endocrine System: Overview Endocrine System: Overview

• Controls and integrates • Exocrine glands – Reproduction – Nonhormonal substances (sweat, saliva) – Growth and development – Have ducts to carry secretion to membrane – Maintenance of electrolyte, water, and surface nutrient balance of blood • Endocrine glands – Regulation of cellular metabolism and energy – Produce hormones balance – Lack ducts – Mobilization of body defenses

Endocrine System: Overview Figure 16.1 Location of selected endocrine organs of the body. Pineal gland Hypothalamus Pituitary gland • Endocrine glands: pituitary, thyroid, Thyroid gland parathyroid, adrenal, and pineal glands Parathyroid glands (on dorsal aspect • Hypothalamus is neuroendocrine organ of thyroid gland) Thymus • Some have exocrine and endocrine functions Adrenal glands – Pancreas, gonads, placenta Pancreas • Other tissues and organs that produce

hormones Gonads • Ovary (female) – Adipose cells, thymus, and cells in walls of • Testis (male) small intestine, stomach, kidneys, and heart

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Chemical Messengers Chemistry of Hormones

• Hormones: long-distance chemical • Two main classes signals; travel in blood or lymph – Amino acid-based hormones • Autocrines: chemicals that exert effects • Amino acid derivatives, peptides, and proteins on same cells that secrete them – Steroids • Paracrines: locally acting chemicals that • Synthesized from cholesterol affect cells other than those that secrete • Gonadal and adrenocortical hormones them • Autocrines and paracrines are local chemical messengers; not considered part of endocrine system

Mechanisms of Hormone Action Mechanisms of Hormone Action

• Hormones act at receptors in one of two 2. Lipid-soluble hormones (steroid and thyroid ways, depending on their chemical nature hormones) and receptor location • Act on intracellular receptors that directly activate genes 1. Water-soluble hormones (all amino acid– • Can enter cell based hormones except thyroid hormone) • Act on plasma membrane receptors • Act via G protein second messengers • Cannot enter cell

Figure 16.2 Cyclic AMP second-messenger mechanism of water-soluble hormones. Slide 1 Figure 16.3 Direct gene activation mechanism of lipid-soluble hormones. Slide 1

Steroid Extracellular Recall from Chapter 3 that hormone Plasma G protein signaling mechanisms fluid membrane are like a molecular relay race. 1 The steroid hormone Hormone Receptor G protein Enzyme 2nd diffuses through the plasma 1 Hormone (1st messenger) (1st messenger) messenger membrane and binds an binds receptor. Cytoplasm intracellular receptor. Receptor Adenylate cyclase Extracellular fluid Receptor- protein hormone complex 2 The receptor- G protein (Gs) hormone complex enters the nucleus.

Receptor cAMP 5 cAMP activates Nucleus GTP protein kinases. Binding region The receptor- hormone Receptor 3 GTP complex binds a specific DNA ATP region. Inactive Active GDP GTP protein protein DNA kinase kinase 4 Binding initiates Triggers responses of transcription of the gene to target cell (activates mRNA. enzymes, stimulates mRNA cellular secretion, opens ion channel, etc.)

Cytoplasm

2 Receptor 3 G protein 4 Adenylate 5 The mRNA directs protein activates G activates cyclase converts synthesis. protein (Gs). adenylate ATP to cAMP (2nd cyclase. messenger). New protein

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Target Cell Specificity Target Cell Activation

• Target cells must have specific receptors • Hormones influence number of their to which hormone binds, for example receptors – ACTH receptors found only on certain cells of – Up-regulation—target cells form more adrenal cortex receptors in response to low hormone levels – Thyroxin receptors are found on nearly all – Down-regulation—target cells lose receptors cells of body in response to high hormone levels

Figure 16.4a Three types of endocrine gland stimuli. Slide 1 Humoral Stimulus Neural Stimuli Hormone release caused by altered levels of certain critical ions or nutrients.

Capillary (low Ca2+ • Nerve fibers stimulate hormone release in blood) – Sympathetic nervous system fibers stimulate Thyroid gland (posterior view) Parathyroid adrenal medulla to secrete catecholamines glands

Parathyroid glands PTH

Stimulus: Low concentration of Ca2+ in capillary blood. Response: Parathyroid glands secrete parathyroid hormone (PTH), which increases blood Ca2+. © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc.

Figure 16.4b Three types of endocrine gland stimuli. Slide 1 Neural Stimulus Hormonal Stimuli Hormone release caused by neural input. CNS (spinal cord) • Hormones stimulate other endocrine organs to release their hormones – Hypothalamic hormones stimulate release of most anterior pituitary hormones Preganglionic sympathetic fibers – Anterior pituitary hormones stimulate targets to secrete still more hormones Medulla of adrenal gland – Hypothalamic-pituitary-target endocrine organ feedback loop: hormones from final target Capillary organs inhibit release of anterior pituitary

Stimulus: Action potentials in preganglionic hormones sympathetic fibers to adrenal medulla. Response: Adrenal medulla cells secrete epinephrine and norepinephrine. © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc.

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Figure 16.4c Three types of endocrine gland stimuli. Slide 1 Hormonal Stimulus Nervous System Modulation Hormone release caused by another hormone (a tropic hormone). Hypothalamus • Nervous system modifies stimulation of endocrine glands and their negative feedback mechanisms Anterior pituitary gland – Example: under severe stress, hypothalamus and sympathetic nervous system activated Thyroid AdrenalGonad gland cortex (Testis) •  body glucose levels rise • Nervous system can override normal endocrine controls

Stimulus: Hormones from hypothalamus. Response: Anterior pituitary gland secretes hormones that stimulate other endocrine glands to secrete hormones. © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc.

Duration of Hormone Activity Interaction of Hormones at Target Cells

• Limited • Multiple hormones may act on same target – Ranges from 10 seconds to several hours at same time – Effects may disappear as blood levels drop – Permissiveness: one hormone cannot exert – Some persist at low blood levels its effects without another hormone being present – Synergism: more than one hormone produces same effects on target cell  amplification – Antagonism: one or more hormones oppose(s) action of another hormone

Figure 16.5a The hypothalamus controls release of hormones from the pituitary gland in two different ways (1 of 2). The Pituitary Gland and Hypothalamus Slide 1

Paraventricular nucleus • Pituitary gland (hypophysis) has two Hypothalamus 1 Hypothalamic neurons synthesize oxytocin or major lobes antidiuretic hormone (ADH). Posterior lobe of pituitary Optic – Posterior pituitary (lobe) chiasma Supraoptic nucleus • Neural tissue Infundibulum (connecting stalk) 2 Oxytocin and ADH are transported down the axons of Inferior the hypothalamic- hypophyseal – Anterior pituitary (lobe) Hypothalamic- hypophyseal tract to the posterior pituitary. hypophyseal artery (adenohypophysis) tract Axon terminals 3 Oxytocin and ADH are • Glandular tissue stored in axon terminals in Posterior lobe the posterior pituitary. of pituitary Oxytocin 4 When hypothalamic neurons fire, action potentials arriving at ADH the axon terminals cause oxytocin or ADH to be released into the blood.

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Figure 16.5b The hypothalamus controls release of hormones from the pituitary gland in two different ways (2 of 2). Slide 1 Posterior Pituitary and Hypothalamic Hormones

Hypothalamus Hypothalamic • Oxytocin and ADH neurons synthesize GHRH, GHIH, TRH, – Each composed of nine amino acids Anterior lobe CRH, GnRH, PIH. of pituitary Superior hypophyseal – Almost identical – differ in two amino acids artery 1 When appropriately stimulated, 2 Hypothalamic hormones hypothalamic neurons secrete travel through portal veins to releasing or inhibiting hormones the anterior pituitary where into the primary capillary plexus. they stimulate or inhibit release of hormones made in Hypophyseal the anterior pituitary. portal system • Primary capillary 3 In response to releasing plexus A portal hormones, the anterior • Hypophyseal system is two pituitary secretes hormones portal veins into the secondary capillary capillary plexus. This in turn empties • Secondary plexuses into the general circulation. capillary plexus (beds) connected GH, TSH, ACTH, by veins. FSH, LH, PRL

Anterior lobe of pituitary

ADH Anterior Pituitary Hormones

• Diabetes insipidus • Growth hormone (GH) – ADH deficiency due to hypothalamus or • Thyroid-stimulating hormone (TSH) or posterior pituitary damage thyrotropin – Must keep well-hydrated • Adrenocorticotropic hormone (ACTH) • Syndrome of inappropriate ADH • Follicle-stimulating hormone (FSH) secretion (SIADH) • Luteinizing hormone (LH) – Retention of fluid, headache, disorientation – Fluid restriction; blood sodium level • Prolactin (PRL) monitoring

Growth Hormone (GH, or Somatotropin) Homeostatic Imbalances of Growth Hormone • Produced by somatotropic cells • Hypersecretion • Direct actions on metabolism – In children results in gigantism – Increases blood levels of fatty acids; – In adults results in acromegaly encourages use of fatty acids for fuel; protein • Hyposecretion synthesis – In children results in pituitary dwarfism – Decreases rate of glucose uptake and metabolism – conserving glucose –  Glycogen breakdown and glucose release to blood (anti-insulin effect)

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Figure 16.6 Growth-promoting and metabolic actions of growth hormone (GH). Figure 16.7 Disorders of pituitary growth hormone. Hypothalamus secretes growth Inhibits GHRH release Feedback hormone–releasing Stimulates GHIH release Anterior hormone (GHRH), and pituitary GHIH (somatostatin) Inhibits GH synthesis and release

Growth hormone (GH)

Indirect actions Direct actions (growth- (metabolic, promoting) anti-insulin)

Liver and other tissues

Produce

Insulin-like growth factors (IGFs)

Effects Effects

Fat Carbohydrate Skeletal Extraskeletal metabolism metabolism

Increases, stimulates Reduces, inhibits Increased protein Initial stimulus Increased cartilage Increased Increased blood synthesis, and formation and fat breakdown glucose and other cell growth and Physiological response skeletal growth and release anti-insulin effects proliferation Result © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc.

Thyroid-stimulating Hormone (Thyrotropin) Figure 16.8 Regulation of thyroid hormone secretion. Hypothalamus

• Produced by thyrotropic cells of anterior TRH pituitary • Stimulates normal development and Anterior pituitary secretory activity of thyroid • Release triggered by thyrotropin-releasing TSH hormone from hypothalamus • Inhibited by rising blood levels of thyroid Thyroid gland hormones that act on pituitary and Thyroid hypothalamus hormones Stimulates Target cells Inhibits

Adrenocorticotropic Hormone Gonadotropins (Corticotropin) • Regulation of ACTH release • Follicle-stimulating hormone (FSH) and – Triggered by hypothalamic corticotropin- luteinizing hormone (LH) releasing hormone (CRH) in daily rhythm • Secreted by gonadotropic cells of anterior – Internal and external factors such as fever, pituitary hypoglycemia, and stressors can alter release • FSH stimulates gamete (egg or sperm) of CRH production • LH promotes production of gonadal hormones • Absent from the blood in prepubertal boys and girls

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Thyroid Gland Thyroid Hormone (TH)

• Two lateral lobes connected by median • Actually two related compounds

mass called isthmus – T4 (thyroxine); has 2 tyrosine molecules + 4 • Composed of follicles that produce bound iodine atoms glycoprotein thyroglobulin – T3 (triiodothyronine); has 2 tyrosines + 3 bound iodine atoms • Colloid (fluid with thyroglobulin + iodine) fills lumen of follicles and is precursor of • Affects virtually every cell in body thyroid hormone • Parafollicular cells produce the hormone calcitonin

Figure 16.10 Synthesis of thyroid hormone. Slide 1 Thyroid Hormone Thyroid follicular cells

Colloid

1 Thyroglobulin is synthesized and • Major metabolic hormone discharged into the follicle lumen. Tyrosines (part of thyroglobulin molecule) Capillary 4 Iodine is attached to tyrosine • Increases metabolic rate and heat in colloid, forming DIT and MIT. Golgi production (calorigenic effect) apparatus Rough Thyro- ER Iodine globulin 3 Iodide DIT MIT colloid • Regulation of tissue growth and is oxidized to iodine. development Iodide (I−) 2 Iodide (I–) is trapped (actively transported in). T4 5 Iodinated tyrosines are T linked together to form T3 Lysosome 3 – Development of skeletal and nervous systems and T4.

T4 – Reproductive capabilities 6 Thyroglobulin colloid is endocytosed and combined T3 7 Lysosomal enzymes with a lysosome. Colloid in T4 cleave T and T from • Maintenance of blood pressure 4 3 lumen of T thyroglobulin and hormones 3 diffuse into bloodstream. follicle

To peripheral tissues

Transport and Regulation of TH Figure 16.8 Regulation of thyroid hormone secretion. Hypothalamus

• T4 and T3 transported by thyroxine-binding TRH globulins (TBGs) Anterior pituitary • Both bind to target receptors, but T3 is ten times more active than T4 TSH • Peripheral tissues convert T4 to T3 Thyroid gland

Thyroid hormones Stimulates Target cells Inhibits

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Homeostatic Imbalances of TH Figure 16.11 Thyroid disorders.

• Hyposecretion in adults—myxedema; goiter if due to lack of iodine • Hyposecretion in infants—cretinism • Hypersecretion—most common type is Graves' disease

Calcitonin Parathyroid Glands

• Produced by parafollicular (C) cells • Four to eight tiny glands embedded in • No known physiological role in humans posterior aspect of thyroid • Antagonist to parathyroid hormone (PTH) • Contain oxyphil cells (function unknown) • At higher than normal doses and parathyroid cells that secrete parathyroid hormone (PTH) or – Inhibits osteoclast activity and release of Ca2+ from bone matrix parathormone 2+ – Stimulates Ca2+ uptake and incorporation into • PTH—most important hormone in Ca bone matrix homeostasis

Figure 16.12 The parathyroid glands. Figure 16.13 Effects of parathyroid hormone on bone, the kidneys, and the intestine.

Hypocalcemia (low blood Ca2+)

PTH release from parathyroid gland

Pharynx (posterior aspect) Osteoclast activity Ca2+ reabsorption Activation of in bone causes Ca2+ in kidney tubule vitamin D by kidney Capillary 3- and PO4 release into blood

Thyroid Parathyroid gland cells Parathyroid (secrete glands parathyroid Ca2+ absorption Esophagus hormone) from food in small intestine Trachea Oxyphil cells

Ca2+ in blood

Initial stimulus Physiological response

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Homeostatic Imbalances of PTH Adrenal (Suprarenal) Glands

• Hyperparathyroidism due to tumor • Paired, pyramid-shaped organs atop – Bones soften and deform kidneys – Elevated Ca2+ depresses nervous system and • Structurally and functionally are two contributes to formation of kidney stones glands in one • Hypoparathyroidism following gland – Adrenal medulla—nervous tissue; part of trauma or removal or dietary magnesium sympathetic nervous system deficiency – Adrenal cortex—three layers of glandular – Results in tetany, respiratory paralysis, and tissue that synthesize and secrete death corticosteroids

Figure 16.14 Microscopic structure of the adrenal gland. Homeostatic Imbalances of Aldosterone

Hormones Capsule secreted Zona glomerulosa Aldosterone • Aldosteronism—hypersecretion due to adrenal tumors Zona fasciculata + Adrenal gland – Hypertension and edema due to excessive Na • Medulla • Cortex Cortex + Cortisol – Excretion of K leading to abnormal function of and androgens Kidney neurons and muscle

Zona reticularis

Adrenal medulla Epinephrine

Medulla and norepinephrine

Drawing of the histology of the Photomicrograph (115x) adrenal cortex and a portion of the adrenal medulla

Glucocorticoids Homeostatic Imbalances of Glucocorticoids

• Keep blood glucose levels relatively • Hypersecretion—Cushing's constant syndrome/disease • Maintain blood pressure by increasing – Depresses cartilage and bone formation – Inhibits inflammation action of vasoconstrictors – Depresses immune system • Cortisol (hydrocortisone) – Disrupts cardiovascular, neural, and – Only one in significant amounts in humans gastrointestinal function • Cortisone • Hyposecretion—Addison's disease • Corticosterone – Also involves deficits in mineralocorticoids • Decrease in glucose and Na+ levels • Weight loss, severe dehydration, and hypotension

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Figure 16.16 The effects of excess glucocorticoid. Gonadocorticoids (Sex Hormones)

• Most weak androgens (male sex hormones) converted to testosterone in tissue cells, some to estrogens • May contribute to – Onset of puberty – Appearance of secondary sex characteristics – Sex drive in women – Estrogens in postmenopausal women

Patient before onset. Same patient with Cushing's syndrome. The white arrow shows the characteristic "buffalo hump" of © 2013 Pearson Education, Inc. fat on the upper back. © 2013 Pearson Education, Inc.

Gonadocorticoids Adrenal Medulla

• Hypersecretion • Medullary chromaffin cells synthesize – Adrenogenital syndrome (masculinization) epinephrine (80%) and norepinephrine – Not noticeable in adult males (20%) – Females and prepubertal males • Effects • Boys – reproductive organs mature; secondary sex – Vasoconstriction characteristics emerge early – Increased heart rate • Females – beard, masculine pattern of body hair; clitoris resembles small penis – Increased blood glucose levels – Blood diverted to brain, heart, and skeletal muscle

Figure 16.17 Stress and the adrenal gland.

Adrenal Medulla Short-term stress Prolonged stress

Stress

Nerve impulses Hypothalamus • Hypersecretion CRH (corticotropin- – Hyperglycemia, increased metabolic rate, releasing hormone) rapid heartbeat and palpitations, Spinal cord

hypertension, intense nervousness, sweating Corticotropic cells of anterior pituitary Preganglionic To target in blood sympathetic fibers • Hyposecretion Adrenal cortex Adrenal medulla (secretes steroid (secretes amino acid– hormones) – Not problematic based hormones) ACTH

Catecholamines – Adrenal catecholamines not essential to life Mineralocorticoids Glucocorticoids (epinephrine and norepinephrine) Short-term stress response Long-term stress response • Heart rate increases • Kidneys retain • Proteins and fats converted • Blood pressure increases sodium and water to glucose or broken down • Bronchioles dilate • Blood volume and for energy • Liver converts glycogen to glucose and releases blood pressure • Blood glucose increases glucose to blood rise • Immune system • Blood flow changes, reducing digestive system activity supressed and urine output • Metabolic rate increases

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Pineal Gland Pancreas

• Small gland hanging from roof of third ventricle • Triangular gland partially behind stomach • Pinealocytes secrete melatonin, derived from • Has both exocrine and endocrine cells serotonin – Acinar cells (exocrine) produce enzyme-rich • Melatonin may affect juice for digestion – Timing of sexual maturation and puberty – Pancreatic islets (islets of Langerhans) – Day/night cycles contain endocrine cells – Physiological processes that show rhythmic variations • Alpha () cells produce glucagon (hyperglycemic (body temperature, sleep, appetite) hormone) – Production of antioxidant and detoxification molecules • Beta () cells produce insulin (hypoglycemic in cells hormone)

Figure 16.18 Photomicrograph of differentially stained pancreatic tissue. Glucagon

• Major target—liver Pancreatic islet • Causes increased blood glucose levels •  (Glucagon- producing) • Effects cells – Glycogenolysis—breakdown of glycogen to •  (Insulin- glucose producing) cells – Gluconeogenesis—synthesis of glucose from lactic acid and noncarbohydrates – Release of glucose to blood Pancreatic acinar cells (exocrine)

Figure 16.19 Insulin and glucagon from the pancreas regulate blood glucose levels. Insulin Stimulates glucose uptake by cells

Insulin Tissue cells • Effects of insulin Stimulates glycogen formationw Pancreas Glucose Glycogen – Lowers blood glucose levels Blood Liver glucose falls to – Enhances membrane transport of glucose into normal range. fat and muscle cells Stimulus Blood – Inhibits glycogenolysis and gluconeogenesis glucose level

– Participates in neuronal development and Stimulus Blood glucose level learning and memory Blood glucose rises to normal • Not needed for glucose uptake in liver, range. kidney or brain Pancreas

Glucose Glycogen

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Factors That Influence Insulin Release Homeostatic Imbalances of Insulin

• Elevated blood glucose levels – primary stimulus • Diabetes mellitus (DM) • Rising blood levels of amino acids and fatty – Due to hyposecretion (type 1) or hypoactivity (type 2) acids of insulin – Blood glucose levels remain high  nausea  higher • Release of acetylcholine by parasympathetic blood glucose levels (fight or flight response) nerve fibers – Glycosuria – glucose spilled into urine • Hormones glucagon, epinephrine, growth – Fats used for cellular fuel  lipidemia; if severe  hormone, thyroxine, glucocorticoids ketones (ketone bodies) from fatty acid metabolism • Somatostatin; sympathetic nervous system  ketonuria and ketoacidosis – Untreated ketoacidosis  hyperpnea; disrupted heart

activity and O2 transport; depression of nervous system  coma and death possible

Diabetes Mellitus: Signs Homeostatic Imbalances of Insulin

• Three cardinal signs of DM • Hyperinsulinism: – Polyuria—huge urine output – Excessive insulin secretion • Glucose acts as osmotic diuretic – Polydipsia—excessive thirst – Causes hypoglycemia • From water loss due to polyuria • Low blood glucose levels – Polyphagia—excessive hunger and food • Anxiety, nervousness, disorientation, consumption unconsciousness, even death • Cells cannot take up glucose; are "starving" – Treated by sugar ingestion

Table 16.4 Symptoms of Insulin Deficit (Diabetes Mellitus) Ovaries and Placenta

• Gonads produce steroid sex hormones – Same as those of adrenal cortex • Ovaries produce estrogens and progesterone – Estrogen • Maturation of reproductive organs • Appearance of secondary sexual characteristics • With progesterone, causes breast development and cyclic changes in uterine mucosa • Placenta secretes estrogens, progesterone, and human chorionic gonadotropin (hCG)

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Testes Other Hormone-producing Structures

• Testes produce testosterone • Heart – Initiates maturation of male reproductive – Atrial natriuretic peptide (ANP) decreases organs blood Na+ concentration, therefore blood – Causes appearance of male secondary pressure and blood volume sexual characteristics and sex drive • Kidneys – Necessary for normal sperm production – Erythropoietin signals production of red – Maintains reproductive organs in functional blood cells state – Renin initiates the renin-angiotensin- aldosterone mechanism

Developmental Aspects Developmental Aspects

• Hormone-producing glands arise from all three • Ovaries undergo significant changes with germ layers age and become unresponsive to • Most endocrine organs operate well until old age gonadotropins; problems associated with • Exposure to pesticides, industrial chemicals, arsenic, dioxin, and soil and water pollutants estrogen deficiency occur disrupts hormone function • Testosterone also diminishes with age, but • Sex hormones, thyroid hormone, and effect is not usually seen until very old age glucocorticoids are vulnerable to the effects of pollutants • Interference with glucocorticoids may help explain high cancer rates in certain areas

Developmental Aspects

• GH levels decline with age - accounts for muscle atrophy with age • TH declines with age, contributing to lower basal metabolic rates • PTH levels remain fairly constant with age, but lack of estrogen in older women makes them more vulnerable to bone- demineralizing effects of PTH