Endocrinology 01a PDF

Homeostasis Nervous System Acts Rapidly (in milliseconds), but Short-lived Messenger = Electrical Signals → Neurotransmitters Very Specific receptor organs at the end of each neuron May Stim/Inh release of Hormones Primarily cause Musc. Ctx & secre...

Homeostasis Nervous System Acts Rapidly (in milliseconds), but Short-lived Messenger = Electrical Signals → Neurotransmitters Very Specific receptor organs at the end of each neuron May Stim/Inh release of Hormones Primarily cause Musc. Ctx & secretion of fluids from glands Endocrine System Acts Slowly (seconds to hours), but Long-lived Messenger = Hormones (Chemicals) Less Specific via Blood Stream to all Body cells Some hormones may Stim/Inh Nerve impulses Some hormones (Epi./NE) may be Neurotransmitters also and act in other target cells  Basic Concepts of Endocrine System Functions to keep the body in Homeostasis A state of equilibrium Keeps the body in a steady & balanced state so that the body systems can function optimally Involves: Body fluids Acid-base balance Temperature Metabolism Other factors  Endocrine Organs Hypothalamus Thymus Pineal Gland Pancreas Pituitary Gland Adrenal (Suprarenal) Glands Posterior Pituitary Adrenal Cortex Anterior Pituitary Adrenal Medulla Thyroid Gland Ovaries Parathyroid Glands Testes Hypothalamic-Pituitary-Target gland Axis Hypothalamus Produces Releasing and Inhibiting Hormones Stimulates Anterior Pituitary Gland Anterior Pituitary Gland Produces Stimulating Hormones Stimulates different “Target Organs” “Target Organs” Release their own Hormones  Intercellular Chemical Signals Hormones Released by endocrine glands Enter circulatory system Affect distant cells Ex.: Estrogen Autocrine Released by cells and have a local effect on same cell type from which chemical signals released Do NOT enter the blood Ex.: Prostaglandin Paracrine Released by cells and affect other neighborly cell types locally without being transported in blood Ex.: Somatostatin  Pheromones Secreted into environment and modify behavior and physiology Ex.: Sex pheromones Neurohormone Produced by neurons and function like hormones Mostly from Post. Pituitary Gland Ex.: Oxytocin & ADH Neurotransmitter or Neuromodulator Produced by neurons Secreted into extracellular spaces by presynaptic nerve terminals Travels short distances Influences postsynaptic cells Ex.: Acetylcholine. Locally-acting Chemicals – Do NOT enter the Blood Paracrine (“Para” = near) – Act upon cells next to secreting cells Autocrine (“Auto” = self) – Act upon the cell that secreted it In contrast… Other hormones may circulate for hrs & their effect being lost once inactivated or secreted  Hormonal Secretion 3 Patterns of Regulation of Hormone Secretion 1. Neural via Autonomic Nervous System (Ex.: Stress) 2. Non-Hormonal via concentration of a substance (Ex.: Glucose) 3. Hormonal via concentration of a hormone (Ex.: Thyroid hormones)  1. Nervous System Regulation Stimuli such as stress or exercise activate the sympathetic division of the autonomic nervous system Sympathetic neurons stimulate the release of epinephrine and smaller amounts of norepinephrine from the adrenal medulla. Epinephrine and norepinephrine prepare the body to respond to stressful conditions. Once the stressful stimuli are removed, less epinephrine is released as a result of decreased stimulation from the autonomic nervous system. 2. Action of Substance Other Than Hormone An increased blood glucose concentration stimulates increased insulin secretion from the pancreas Insulin increases glucose uptake by tissues, which decreases blood glucose levels. Autonomic nervous system also influences insulin secretion  3. Hormonal Regulation Negative and Positive Feedback At each level of the HPT Axis Prevents Over-secretion of any hormone Acts like a “Thermostat” of a house Stimulation (+) Inhibition (-) Homeostasis Values of variables fluctuate around a SET POINT This determines a normal range of values SET POINT Desired value What is the set point for Body Temperature? Negative Feedback Any deviation ( or ) from the set point is made SMALLER (ie.: Returning to normalcy) This occurs mostly in the body Positive Feedback Any deviation ( or ) from the set point is made GREATER (ie.: Going further away from normalcy) Not so common in the body  Transport & Distribution Hormones dissolve in blood 2 forms in bloodstream 1. Free Form 2. Bound to Binding Protein, reversibly Equilibrium of 2 forms Hormones distributed quickly thru body because they are in the blood Free Form Diffuse thru Capillary wall into Interstitial Fluid Follows concentration gradient Lipid-soluble Hormones Diffuse easily thru Capillary Cells Water-soluble Hormones Must pass thru Capillary Fenestrae Bound Form Reversibly bound as a “Reserve” on Binding Proteins (In Proteinuria, the Pt will lose these binding proteins in his urine and thus the hormone bound to them) Hormone/Target Cell Interaction Ligand Anything that binds to a receptor ie.: A Hormone is a Ligand Binding Site Where the Ligand binds to ie.: A Receptor Site is a Binding Site Ligand/Binding Site A proper connection will elicit a response by the Target Cell VERY SPECIFIC ie.: GH cannot bind to an Oxytocin Receptor site  Target Cells Highly specific receptors (proteins or glycoproteins) Geometry of receptors complement specific hormone Like a “Lock & Key” fit Up Regulation -  Sensitivity when Low Hormone level Down Regulation -  Sensitivity when High Hormone level  Receptors for Hormones Receptors for Catecholamines & Peptide Hormones are in the cell membranes of target cells Thyroid & Steroid Hormones cross the membrane and bind to receptors in the cytoplasm or nucleus  Classes of Receptors Membrane-bound Receptors Integral proteins with receptor site at cell surface These do NOT enter cell Interact with ligands that cannot pass through the plasma membrane Involves a 2nd Messenger within the cell a “Chain Reaction” occurs Ligands: – Water-soluble, Larger ligands, etc. Protein Hormones Polypeptide Hormones Catecholamines (Epi/NE) Intracellular Receptors In cytoplasm or in the nucleus These DO enter cell Interact with ligands that can pass through the plasma membrane Ligands: – Lipid-soluble, Smaller ligands, etc. Steroid Hormones Thyroid Hormones  Membrane-bound Receptors Ligand binds reversibly 1 of 2 Cascade of Events occurs: 1. Activation of G proteins  cAMP, Ca2+, Diacylglycerol (DAG) or Inositol Triphosphate (IP3) 2. Receptors Alter Activity of Intracellular Enzymes Directly  cGMP, Nitric oxide, or Ca2+  1. Activation of G Proteins Cascade of Events for  cAMP: 1. Hormone (1st Messenger) binds to “Surface Receptor” 2. This then binds to a G protein in the cell 3. The G protein is then activated as it binds GTP, displacing GDP 4. Adenylate Cyclase is activated 5. This produces cAMP (2nd Messenger) in cell 6. cAMP binds to Protein Kinase 7. Phosphorylation occurs on certain Proteins (requires ATP) 8. Activation of those Proteins occurs (ie.: the protein is made in response to what hormone “told” the cell) – 1 hormone molecule will activate a chain of cascades resulting in millions of activated proteins which, in turn, make billions of the substance the protein is suppose to release This is why it responds RAPIDLY !!!! Other 2nd Messengers: Ca2+ Diacylglycerol (DAG) Inositol Triphosphate (IP3) Understand cAMP’s mechanism (illustrated in the past few slides) Don’t worry about the mechanisms of other 2nd messengers You can view the next 3 Diagrams to see how other 2nd messenger mechanisms occur…… Notice the chain of events BEFORE the 2nd messenger begins are the same as with cAMP’s mechanism 2. Receptors that Directly Alter the Activity of Intracellular Enzymes (Simpler Cascade as G-Protein is NOT involved) Cascade of Events for  cGMP 1. Hormone (1st Messenger) binds to “Surface Receptor” 2. The inner portion of this receptor activates Guanylate cyclase 3. This converts GTP to cGMP (2nd Messenger) 4. cGMP acts on certain Proteins 5. Activation of those Proteins occurs Phosphodiesterase inactivates cGMP to GMP This Pathway also responds RAPIDLY !!!!  Intracellular Receptors Thyroid & Steroid Hormones > 90% are bound to proteins in blood These hormones diffuse into target cells Binds to DNA in Nucleus A specific mRNA is made and synthesizes a certain protein that the hormone “tells” the target cell to make There is no amplification (ie.: 1 structure does not tell 4 structures what to do at the same time) This is why it responds SLOWLY !!!  Hypothalamus (Neural Functions) Coordinates HR, BP & Resp. rate from: Pons Medulla oblongata Regulates: Temperature Hunger / Thirst Sleep Endocrine Functions……… Where the Nervous & Endocrine Systems interact Releasing & Inhibiting Hormones 7 Major Hormones (Ex. TRH, GnRH, PIH, etc.) Synthesized, Stored AND Secreted by Hypothalamus Target Organ is Anterior Pituitary Gland ADH & Oxytocin Synthesized by Hypothalamus Stored & Secreted by Posterior Pituitary Gland May still find their way into the bloodstream if the Posterior Pituitary Gland is compromised since they are still both synthesized  Pineal Gland (Body) Circadium Rhythm Biological Clock “Jet Lag” issue Releases Melatonin (NOT Melanin) Daylight (-) / Darkness (+) May control Onset of Puberty?? Melatonin ’s during puberty Pituitary Gland (Hypophysis) “The Master Gland” Sits in Sella Turcica Bony “cup” in the sphenoid bone Actually Two (2) Glands: 1. Anterior Pituitary Gland (Adenohypophysis) – Synthesizes, Stores & Secretes 7 Major Hormones from itself into bloodstream – 75% of Pituitary – Evolved from floor of mouth (Rathke’s Pouch) 2. Posterior Pituitary Gland (Neurohypophysis) – Stores and Secretes 2 hormones (*** These are actually synthesized in Hypothalamus) – Evolved from base of brain An “Extension” of the Hypothalamus via Infundibulum  Anterior Pituitary Gland (Histology) Acidophils (Pinkish) Cells that contain Polypeptide Hormones Somatotropes which produce GH Lactotropes which produce PRL Basophils (Bluish) Cells that contain Glycoprotein Hormones Thyrotropes which produce TSH Gonadotropes which produce LH or FSH Corticotropes which produce ACTH Chromophobes (Colorless) These are cells that have minimal or no hormonal content Anterior Pituitary Gland Hormones Thyroid Stimulating Hormone (TSH) Stimulates thyroid gland to secrete thyroid hormones (T 3 & T4) Growth Hormone (GH) Stimulates most tissues to grow Adrenocorticotropic Hormone (ACTH) Stimulates adrenal (cortex) gland to secrete its hormones (mostly Cortisol) Follicle Stimulating Hormone (FSH) Stimulates follicles (egg sacs) to grow in ovaries Stimulates sperm production in testicles Luteinizing Hormone (LH) Releases progesterone from ovaries AND Triggers ovulation (release of egg from ovary) Releases testosterone from testicles Prolactin (PRL) Stimulates breasts to make milk Melanocyte Stimulating Hormone (MSH) Stimulates melanocytes to secrete melanin  Posterior Pituitary Gland (Histology) Neuroglia Pituicytes Nerve fibers (Axons) Fenestrated Capillaries “Little holes” to allow the hormones to enter blood Posterior Pituitary Gland Hormones Anti-Diuretic Hormone (ADH)  Urine →  Blood volume →  BP Oxytocin (OXY) Ejects milk from breasts Contracts uterus during labor  ANTERIOR Pituitary Gland Tropic Hormones (Tropins) All Anterior Pituitary Hormones are tropins Regulate hormone secretions of target endocrine tissues  ANTERIOR Pituitary Gland 1. Growth Hormone (GH) (a.k.a. Somatotropin) *** Stimulates Cell Growth in all body cells (Increases Height & Weight in Puberty) Excess – (Symptoms differ if Growth plates are fused or not) Gigantism – (In Children) – Symmetrical growth of long bones Growth plates are NOT fused yet Acromegaly – (In Adults) – Facial features become wider & enlarged Growth plates are already fused – Enlarged Hands, Face & Jaw – HTN – Death due to Heart Failure Pituitary Gland lies adjacent to Optic Chiasm Large Pituitary Tumor can press against Optic Chiasm Causes “Tunnel Vision” (Bitemporal Hemianopsia) (Inferior View)  Deficiency – Pituitary Dwarfism (In Children) Short stature, but with normal body proportions Growth plates are NOT fused yet NOTE: Not all causes of Dwarfism are due to GH deficiency.  Dwarfism ACHONDROPLASIA – (m.c. form of Dwarfism (70%)) Long bones stop growing in childhood Normal torso, short limbs Failure of cartilage growth in Epiphyseal Plate Spontaneous mutation produces mutant dominant allele PITUITARY DWARFISM Lack of Growth Hormone (GH) Normal proportions with short stature 2. Thyroid Stimulating Hormone (TSH) (a.k.a. Thyrotropin) Stimulates Thyroid gland to secrete Thyroid Hormones T3 T4 3. Adrenocorticotropic Hormone (ACTH) Stimulates Adrenal (Cortex) gland to secrete 3 Hormones: Aldosterone Cortisol Androgens (Sex Steroids (Testosterone & Estrogen)) Binds directly to Melanocytes and releases Melanin 4. Follicle Stimulating Hormone (FSH) In Females (acts on Ovaries) Develops Follicles Produces Mature Ova Secretes Estrogen In Males (acts on Testes) Stimulates Production of Sperm 5. Luteinizing Hormone (LH) In Females (acts on Ovaries) Triggers Ovulation Stimulates Corpus Luteum to secrete Progesterone (Corpus Luteum → ruptured site where egg was released) In Males (acts on Testes) Secretes Testosterone 6. Prolactin (PRL) Stimulates the Development of Milk Glands (During Puberty) Stimulates the Production of Milk (During Pregnancy) 7. Melanocyte Stimulating Hormone (MSH) Not truly a significant hormone NOT produced in adults In Pregnancy: Stimulates Melanocytes in skin to release Melanin (Produces Pigmentation in face & Abdomen) ACTH also stimulates Melanocytes  POSTERIOR Pituitary Gland 1. Antidiuretic Hormone (ADH, Vasopressin) Reabsorbs H2O from Kidneys  Urine Volume →  Blood volume →  BP  Vasoconstriction →  BV Diameter →  BP Excess Syndrome of Inappropriate ADH (SIADH) – Lung Cancer (m.c.c.) → Produces an ADH-like hormone    Urine →    Blood volume → HTN    Vasoconstriction →    BV Diameter → HTN Deficiency Diabetes Insipidus (DI)    Urine →    Blood volume → HYPOtension VERY Rare POLYDIPSIA = Increase in Thirst POLYURIA = Increase in Urine output 2. Oxytocin Stimulates Uterus to contract Begins labor Stimulates the Release of Milk (Lactation) When baby cries or sucks  Thyroid Gland 2 Lobes connected by the Isthmus Anterior to Trachea HIGHLY VASCULAR !!!!!!!  Thyroid releases 3 Hormones: 1. Triiodothyronine (ACTIVE Hormone State) (T3) Increases the rate of Metabolism Dependent on Iodine from the Diet 2. Thyroxine (INACTIVE Hormone State) (T4) Converts to T3 by Liver 3. Calcitonin (Secreted when Calcium blood levels are high, NOT by TSH) Decreases Calcium in the blood Deposits Calcium into the bone (Opposite action of Parathyroid Hormone) EUTHYROIDISM = Thyroid is releasing hormones at a proper steady state.  Thyroid Gland (Histology) Follicle Cells (Thyroid Epithelial cells) Synthesizes Colloid Colloid Stores T3 and T4 Stored on Thyroglobulin and gradually released into blood Parafollicular Cells (C cells) Synthesizes Calcitonin  Synthesis of Thyroid Hormones 1. Thyroglobulin is synthesized and discharged into the lumen of follicle 2. Iodides (I–) are actively taken into the cell, oxidized to iodine (I2), and released into the lumen 3. Iodine attaches to Tyrosine, mediated by Peroxidase enzymes, forming T1 (Monoiodotyrosine, or MIT), and T2 (Diiodotyrosine, or DIT) 4. Iodinated Tyrosines link together to form T3 and T4 5. Colloid is then endocytosed and combined with a Lysosome, where T3 and T4 are cleaved and diffuse into the bloodstream Transport and Regulation of T4 & T3 1. T4 and T3 bind to Thyroxine-Binding Globulins (TBGs) produced by the liver 2. Both bind to target receptors, but T3 is ten times more active than T4 3. Peripheral tissues convert T4 to T3 4. Mechanisms of activity are similar to steroids 5. Regulation is by negative feedback Hypothalamic Thyrotropin-Releasing Hormone (TRH) can overcome the Negative Feedback  Know ALL the Functions of T3  Thyroid Enlargement Definitions: Thyromegaly Mild to Moderate enlargement Goiter Chronic & Progressive enlargement NOTE: May have Enlarged Thyroid and be Euthyroid. Etiology of Thyroid Enlargements 1. Simple Goiter (a.k.a. Nontoxic Goiter; Endemic Goiter) Lack of Iodine (in soil & diet) Thyroid enlarges to “grab” more iodine 2. Adenoma / Nodule (Adematous Goiter / Nodular Goiter) (Multinodular Goiter → Many nodules) Thyroid enlarges that part(s) only 3. Autoimmune Disease Graves’ Disease Causes Hyperthyroidism (w/ Goiter) Hashimoto’s Thyroiditis Causes Hypothyroidism (w/Goiter) Excess – Hyperthyroidism (a.k.a. Thyrotoxicosis) (2nd m.c. Endocrine Dz, next to Diabetes Mellitus) Females > Males Does NOT affect Calcitonin   T3/T4 →   Metabolism Signs/Symptoms: Thyromegaly / Goiter Hand Tremors Tachycardia / Palpitations / Restlessness / Diarrhea Weight Loss Irritability Heat Intolerance (Skin warm & Sweaty) – Graves’ Disease (m.c. form of Hyperthyroidism) (Autoimmune disease) Body produces antibodies that TURNS ON TSH receptors   T3/T4 Additional Sx specific to Graves’ Dz: – Diffuse Toxic Goiter Entire Thyroid is enlarged – Exophthalmos (Proptosis) B/L Bulging eyeballs – Pretibial Myxedema Skin of Anterior tibiae is edematous, dry & coarse Deficiency – Hypothyroidism (a.k.a. Myxedema) (m.c.c. is Treatment of Hyperthyroidism: Radioactive Iodine Subtotal Thyroidectomy) Does NOT affect Calcitonin  T3/T4 →  Metabolism Signs/Symptoms: Bradycardia / Constipation Weight Gain / Obesity Cold Intolerance Skin → Thickened; Edematous; Dry Hair → Dry; Brittle; Falls out Depression / Lethargy / Decreased Libido – Hashimoto’s Thyroiditis (m.c. form of Hypothyroidism) Chronic inflammation & progressive destruction of Thyroid (Autoimmune disease) Body produces antibodies AGAINST Thyroid Gland   T3/T4 → HYPOthyroidism Stages: 1. Inflamed Thyroid → Goiter 2. Thyroid tissue destroyed → Scar Tissue replaced (Small Thyroid) – Cretinism Congenital Hypothyroidism In Children NO Thyroid Hormone synthesis Irreversible if NOT treated early Sx.: *** Mental Retardation *** Dwarfism Protruding Tongue Lack of hair & teeth Pot-belly Rare in USA, as every child born is routinely tested for this disease prior to leaving hospital after birth Parathyroid Hormone (PTH) Secreted when Ca2+ blood levels are low Opposite action of Calcitonin Mechanisms of increasing Ca2+ into the blood 1.  Ca2+ Removal from bone via Osteoclasts 2.  Ca2+ Reabsorption via Kidneys 3.  Ca2+ Absorption from Diet via Vitamin D Excess – Hyperparathyroidism   PTH →   Ca+2 in Blood Sx: Hypercalcemia Brittle Bones Duodenal Ulcers Kidney stones - (Kidneys are overwhelmed of Excess Ca+2 being excreted) Psychoses Deficiency – Hypoparathyroidism (Accidental removal of Parathyroid glands during Thyroidectomy)   PTH →   Ca+2 in Blood Sx: – Hypocalcemia – Hyperexcitability of Nerves & Muscle Twitching → Convulsions → DEATH!!! Muscle cramps TETANY (sustained muscle spasm)  Parathyroid Gland (Histology) Distinctly different from a Thyroid gland Chief Cells Synthesize PTH Arrange in rather dense cords or nests around abundant capillaries Oxyphil Cells Unknown Function (Large pale cells)  Thymus Gland Located posterior to Sternum In Children Large gland Receives Lymphoblasts that migrate from the red marrow Thymosins (Hormones) secreted Mature Lymphoblasts to become T-cell Lymphocytes In Adults Much smaller gland NOT functional in adulthood  Pancreas Located Posterior to the Stomach Head of Pancreas is tucked in Duodenum loop As an Endocrine Gland – Releases 3 major hormones: 1. Glucagon Stimulated when Blood Glucose is low Breaks down Glycogen (stored glucose in liver & muscle) to form Glucose into bloodstream 2. Insulin Stimulated when Blood Glucose is high Transports Glucose into cells 3. Somatostatin Same as GHIH from Hypothalamus INHIBITS Growth hormone, Glucagon & Insulin  Glucagon A 29-amino-acid polypeptide Hormone HYPERglycemic agent Its major target is the Liver (& Muscle) Functions: Glycogenolysis Breakdown of glycogen to glucose Gluconeogenesis Synthesis of glucose from lactic acid and noncarbohydrates Release of glucose to the blood from liver cells  Insulin A 51-amino-acid protein Hormone HYPOglycemic agent Synthesized as part of proinsulin and then excised by enzymes, releasing functional insulin Functions:  blood glucose levels  transport of glucose into body cells Counters metabolic activity that would enhance blood glucose levels  Pancreas (Histology) Acinar Cells Exocrine (Digestive) Portion of Pancreas 99% of Pancreas Islets of Langerhans Scattered circular endocrine portions of Pancreas Pancreas has several million of these islets *** Only making 1% of Pancreas Contain 4 different Cell Types Alpha, Beta, Delta, F cells Alpha Cells (20%) Synthesize Glucagon Beta Cells (70%) Synthesize Insulin Delta Cells (5%) Synthesize Somatostatin Also released from Hypothalamus as GHIH Inhibits Glucagon, Insulin and GH F Cells (5%) Synthesize Pancreatic Polypeptide Inhibits Somatostatin Deficiency – Diabetes Mellitus (DM) Statistics # 1 Endocrine Dz # 1 Risk factor for Coronary Artery Dz # 7 cause of Death in USA   Insulin →   Glucose in blood (Hyperglycemia) (Glucose cannot get into the cells!!!) Sx: Glycosuria = (Glucose in the urine) Polyuria = ( Urine) Polydipsia = ( Thirst) Polyphagia = ( Appetite)  3 Types of DM 1. Gestational DM Occurs during pregnancy (~10% of all pregnancies) (20% of these women develop DM later in life) 2. Type 1 DM (Autoimmune Dz) Body produces antibodies against pancreas portion that synthesizes insulin (Beta Cells) Absolutely NO INSULIN synthesized 3. Type 2 DM (Insulin Resistance) 90% of all DM cases Risks correlated to: Age / Obesity / Family History 80% of people with DM are Obese  Adrenal Glands Located on the superior poles of each kidney a.k.a. Suprarenal Glands Actually Two (2) Glands: 1. Cortex (outer layer) Releases 3 Hormones 2. Medulla (inner core) Releases 2 Hormones  Adrenal Cortex (Overview) *** Synthesizes and releases Steroid Hormones called Corticosteroids Zona Glomerulosa Synthesizes Mineralocorticoids Aldosterone Zona Fasciculata Synthesizes Glucocorticoids Cortisol Zona Reticularis Synthesizes Gonadocorticoids Androgens  Adrenal CORTEX 1. Aldosterone (Regulates Electrolyte balance) Factors that stimulate Aldosterone to be secreted:  K+ in blood  Na+ in blood  BP Functions: Reabsorbs Na+ → (H2O Follows Na+) →  BP Excretes K+ Aldosterone released by 3 mechanisms: 1. Renin-Angiotensin mechanism  BP → Kidneys release Renin → Angiotensin II → Aldosterone release 2. K+ / Na+ Concentrations in blood 3. ACTH Causes small increases of Aldosterone during stress ✓ Atrial Natriuretic Hormone (ANH) – (a.k.a. Atrial Natriuretic Peptide) (ANP) Secreted from HEART in response to high BP INHIBITS Aldosterone Excess – Hyperaldosteronism (a.k.a. Conn’s Disease)  Aldosterone →  BP (HTN) HTN Hypernatremia Hypokalemia → Muscle Weakness Deficiency – Hypoaldosteronism  Aldosterone →  BP (HYPOtension) Hypotension Hyperkalemia Hyponatremia 2. Cortisol – (Maintains body’s ability to counteract stress) – Breaks down Glycogen from Stress stimulation (NOT stimulated by low glucose levels as Glucagon does) – Functions: 1.  Gluconeogenesis →  Glucose 2.  Lipolysis (converts Triglycerides) →  Fatty Acids 3.  Protein Catabolism →  Amino Acids 4.  Vasoconstriction of BV →  BP 5.  Anti-inflammatory effects a.  Allergic Rxn’s b.  Immune System c. Wound Repair Excess – Cushing’s Syndrome Etiology Lung Cancer (m.c.c.) → Produces an ACTH-like hormone Other causes: → - Pituitary Tumor - Corticosteroids (chronic use) Sx: Hyperglycemia HTN  Weight Gain → Central Fat Distribution  Protein Synthesis → Wasting of muscles (“Egg on 2 sticks”)  Deficiency – Addison’s Disease Etiology 1. Autoimmune Disease (m.c.c.) Body produces antibodies against Adrenal Cortex 2. Hyposecretion of ACTH Usually affects ENTIRE Adrenal Cortex (mostly Cortisol though): Decrease Cortisol /Aldosterone /Androgens Sx: Hypoglycemia Weight loss / Muscle weakness Decrease ability to tolerate stress, disease or surgery HYPOtension Hyponatremia Hyperkalemia (Bronzed color to the skin) 3. Androgens Male hormones: (Precursors of TESTOSTERONE) Adolescent Male Onset of male puberty The appearance of secondary sex characteristics Stimulate body hair growth Adult Male (Very small insignificant amounts) Adult Female Sex Drive (Libido) Androgens are converted into ESTROGENS after Menopause This conversion occurs in Adipose Tissue  Adrenal MEDULLA Stimulated by Sympathetic Nervous System “Fight or Flight” Directly innervated by short Pre-ganglionic Fibers (ie.: Adrenal Medulla responds VERY QUICKLY!!!) Catecholamines 1. Epinephrine (Epi) (a.k.a. Adrenalin) (80%) 2. Norepinephrine (NE) (a.k.a. Noradrenalin) (20%) Excess – Pheochromocytoma (Pheo.) (Adenoma of Adrenal Medulla) Benign Tumor Increase Epi & NE → Severe HTN → STROKE Severe Headaches  Adrenal Gland (Histology) Capsule Connective Tissue covering Adrenal Cortex (3 Layers) 1. Zona Glomerulosa → Aldosterone 2. Zona Fasciculata → Cortisol 3. Zona Reticularis → Androgens Adrenal Medulla Chromaffin Cells (Clusters of Blue Columnar cells arranged around Medullary Veins) Sympathetic Nerve Ganglions (MANY)  Ovaries 1. Estradiol – (Most abundant Estrogen in a non-pregnant state) (Stimulated by FSH) From Follicle (and Corpus Luteum & Placenta) Corpus Luteum → ruptured site where egg was released Female Puberty Maintains female characteristics Follicle (egg sac) growth Endometrial proliferation (Prepares the uterus for pregnancy) 2. Progesterone (Stimulated by LH) From Placenta (and Corpus Luteum) Maintains pregnancy Suppresses ovulation (Required in Birth Control Pills) 3. Inhibin Inhibits FSH Release 4. Relaxin Increases flexibility of Symphysis Pubis during Childbirth  Testes (Testicles) 1. Testosterone (Stimulated by LH) Male Puberty Maintains male characteristics 2. Inhibin Inhibits FSH Release Other Hormone-Producing Organs Heart Atrial Natriuretic Hormone (ANH) – (a.k.a. Atrial Natriuretic Peptide) (ANP) – Inhibits Aldosterone Release  BP  Blood Volume  Na+ in blood Gastrointestinal tract Many digestive hormones Placenta Beta -Human Chorionic Gonadotropin (β-hCG) Maintains pregnancy during 1st Trimester Progesterone & Estrogen also Kidneys Erythropoietin Synthesizes RBC’s Renin Converts Angiotensin I to Angiotensin II →  BP Skin Calcitriol (Active form of Vitamin D) →  Ca2+ Adipose tissue Leptin  Hunger  Energy expenditure In Summary………  Lastly……… Further discussion of Thymus will be explored in Hematology & Immunology Further Anatomy discussions of Ovaries & Testes will be explored in Reproduction No further discussion of the Pineal Gland  Study Tips There are so many players and sites in the Endocrine system. Study Tips: Organize yourself (flash cards)…… This can make it easy. Draw diagrams as to who secretes what when released What do the hormones do Know why a hormone is stimulated/inhibited Where do the hormones live before secreted and where do they go when they enter the bloodstream Know what happens with “Hyper-” / “Hypo-” for each hormone What should you know from A&P? Know what each hormone’s Abbreviation means & any Synonyms. ADH stands for Anti-Diuretic Hormone Vasopressin is another name for ADH Know what Regulates (Stimulates & Inhibits) each hormone.  BP stimulates ADH to be secreted Know each hormone Origin (where it is Made, Stored and Secreted). ADH is made in the Hypothalamus ADH is stored & secreted from the Posterior Pituitary Gland Know where each hormone Targets (where are its Receptors located). ADH targets the Kidney & Blood vessels Know each hormone’s Function(s)…… There are usually a few!!! ADH reabsorbs Water →  Blood Volume →  BP ADH causes vasoconstriction →  BP  After comprehending each homone with the chart, you should then be able to discuss what happens when there is Too much (Hyper-) OR Too little (Hypo-) of the hormone. For instance……..  Now we can understand Diseases What happens when there is EXCESS of the hormone secreted?  ADH →  BP → HYPERtension What causes this hormone to be released too much? An Adenoma of the Posterior Pituitary will secrete a lot of ADH What is the name of this condition of secreting too much of this hormone? Syndrome of Inappropriate ADH (SIADH) What happens when there is DEFICIENCY of the hormone secreted?  ADH →  BP → HYPOtension What causes this hormone to be released too little? A Stroke to the Posterior Pituitary can secrete less ADH What is the name of this condition of secreting too little of this hormone? Diabetes Insipidus (D.I.)…… (NOT Diabetes Mellitus)