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GOOD MORNING

GOOD MORNING. Endocrine System. Regulates body systems Hormones secreted into the blood stream Each hormone has 1 or more target organs (receptor sites) Rhythmic pattern of release Problems arise from either production or receptor sites Most problems are chronic requiring self-management.

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GOOD MORNING

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  1. GOOD MORNING

  2. Endocrine System • Regulates body systems • Hormones secreted into the blood stream • Each hormone has 1 or more target organs (receptor sites) • Rhythmic pattern of release • Problems arise from either production or receptor sites • Most problems are chronic requiring self-management

  3. Hormones • Responsible for regulating: • Reproduction • Growth & Development • Energy production & use • Maintenance of internal environment

  4. Catecholamines • Amino Acid derivatives • Epinephrine • Norepinephrine • Thyroxin • Easily replaced • Many can be oral

  5. Proteins & Peptides • Chains of Amino Acids • Difficult to isolate & engineer • None survive the GI system • Proteins: • Larger molecules • Insulin, Calcitonin, Growth Hormone, FSH • Peptides: • Releasing Factors in Hypothalamus & Posterior Pituitary (Neurohypophysis) • Oxytocin, Vasopressin

  6. Steroids • Formed from cholesterol • Easily produced for replacement • Most can be oral • Include Adrenal and Sex Glands: • Aldosterone • Cortisol • Estrogen • Testosterone

  7. Pharmacologic Uses • Diagnostic • ACTH to stimulate the Adrenals • Thyroglobin to check thyroid response • Replacement • Insulin • Estrogen • Thyroid • Pharmacologic Effects • Steroids to decrease inflammation

  8. Feedback • Secreted when the body identifies a need • Changes in the blood level or other hormones may cause an increase or decrease in secretion • Negative Feedback: • Hormone produces an effect, when it is strong enough, further hormone secretion is inhibited, decreasing physiologic effect.

  9. Feedback Loops __ Hypothalamus Negative Feedback Loop Releasing Factor __ Pituitary Hormone A Target Organ Hormone B Biologic Effect

  10. Physiologic Changes with Aging • Reduction in hormone production • Changes in hormone clearance • Decreased cellular responsiveness • Changes in; • Physical activity level • Nutritional status • Body composition

  11. Causes of Disease • Over or Under Production • Transport abnormalities • Inability of target tissues to respond • Problems with the feedback mechanism • Primary • Secondary

  12. Pituitary • Anterior Pituitary • Hypothalamic releasing factors stimulate the release or inhibit the release of hormones • Posterior Pituitary • Hormones produced in the hypothalamus are stored in the posterior lobe until stimulated by the hypothalamus via nerve impulses

  13. Hypothalamus Neuro - Secretory Cells Releasing Factor Producing Cells Portal Vessel Anterior Posterior Hormone Producing Cells

  14. Anterior Pituitary • Growth Hormone (GH) • Gonadotropic • Lutenizing Hormone (LH) • Follicle Stimulating Hormone (FSH) • Adrenocorticotropic Hormone (ACTH) • Thyroid Stimulating Hormone (TSH) • Prolactin (PRL) • Melanocyte-stimulating Hormone (MSH)

  15. Anterior PituitaryGrowth Hormone (Somatotropin) • Growth Hormone increases bone growth and tissue cell size by changing metabolism, antagonizing the action of insulin, and increasing fat mobilization for energy use. • Deficiency - Dwarfism = delay in all body parts with no mental impairment. • Excess - Gigantism in childhood, acromeglia in adults.

  16. Acromegaly • Acromegaly is the Greek word for "extremities" and "enlargement” • Signs and symptoms vary, dependent upon how long the patient has had the disease, but may include… • Swelling of the hands and feet • Facial features become coarse as bones grow • Body hair becomes coarse as the skin thickens and/or darkens • Increased perspiration accompanied with body odor • Protruding jaw • Voice deepening

  17. Anterior PituitaryGonadotropic Hormone • Gonadotropin-releasing hormone (Gn-RH) • Produced and released from the hypothalamus. Stimulates the secretion of follicle stimulating hormone (FSH) and lutenizing hormone (LH), from the anterior pituitary.

  18. Anterior PituitaryAdrenocorticotropic Hormone (ACTH) Stimulates the adrenal cortex to synthesize and release cortisols in response to stress.

  19. Anterior PituitaryThyroid Stimulating Hormone (TSH) Hypothalamus releases TRH Stimulates the anterior pituitary to produce TSH Regulates the amount of thyroid hormone produced and released into the bloodstream by the thyroid gland

  20. Posterior Pituitary • Oxytocin • Uterine contraction • Milk let down • ADH (Vasopressin) • Renal conservation of water • Vasoconstriction • Increase GI motility • Released in response to plasma osmolarity

  21. SIADH - Syndrome of Inappropriate ADH • ADH release • Water Reabsorption into circulation -Renal Tubules • Extravascular Fluid • Plasma Osmolality • Glomerular Filtration Rate • Serum Sodium Levels CEREBRAL EDEMA

  22. Diabetes Insipidus • ADH Deficiency • Water excretion and blood concentration • ADH is a peptide and can not be taken orally • Treatment: • Vasopressin (Pitressin) - short acting injection • Lypressin and Desmopressin - nasal spray

  23. Adrenal Cortex • Glucocorticoids (Cortisol) • Release is under ACTH control • Mineral-corticoids (Aldosterone) • Renin-Angiotensin system and K+ levels • Stimulated by NaCl depletion • Androgens • Growth of hair follicles • Stress increases cortisol and aldosterone to maintain CV tone. • Impairment of release leads to adrenal crisis

  24. Cushing Syndrome • Excess of corticosteroids secreted by the adrenal cortex • Iatrogenic - prolonged use • Lab - 240 urine for cortisol • Tx - Surgery, Radiation, Suppress synthesis using drug therapy • Prolonged steroid use - TAPER doses • Post-op care

  25. Addison's • Adrenocorticol insufficiency • Autoimmune • Sxs - weight loss, anorexia, weakness, low BP, low sodium, high potassium, nausea & vomiting, diarrhea • Tx - Glucocorticoids • Mineralcorticoids • Adrenal Crisis

  26. Adrenal Medulla • Pheochromocytoma • Neoplasm increasing catecholamines • Surgical removal • Sxs - episodic HTN, increased metabolism, hyperglycemia • Lab - urine metanephrines • Monitor wide BP fluctuations

  27. The Thyroid Gland • Normal thyroid levels are essential to regulate cellular metabolism, and for normal growth and development. • Production of thyroid hormone is caused by release of TSH (stimulated by TRH) • Thyroxin - T4 • Triiodothyronine - T3

  28. Thyroid • Essential to regulate metabolism • Caused by release of TSH: • Thyroxin - T4 • Triiodothyronine - T3 • Stimulated by increased Ca++ in blood • Calcitonin - lowers blood levels by inhibiting bone re-absorption • Low calcium levels suppress the release of calcitonin • Elevated levels increase it’s secretion

  29. Prevalence of Thyroid Disorders • In the United States, approximately 7.5 percent of the population (about 1 in every 13 individuals) have been diagnosed with thyroid disorders, and nearly another 1 percent are estimated to have undiagnosed thyroid maladies.

  30. Hyperthyroid • Graves Disease • Multinodular Goiter • Symptoms: • Increased metabolism • Increase stimulation of sympathetic nervous system • Exopthalmos • Thyroid Storm – Thyrotoxicosis----Severe and life threatening • Treatment - Propylthiouracil, Inderol, Iodine, Radiation, Surgery

  31. Hypothyroid • Infants - long gestation, failure to thrive • Childhood - Autoimmune • Adult - Atrophy or Decreased TSH • Myxedema - interstitial edema, fatigue, lethargy, impaired memory leading to coma high mortality rate. • Long term - Sxs related to increased protein turnover • Cardiovascular, GI, and reproductive • Replacement Therapy

  32. Parathyroid • Maintains extracellular Ca++ levels • Parathormone - Calcitonin antagonist • Release stimulated by low blood levels of Ca++ or high levels of phosphates • Increases Ca++ blood levels • Reabsorption of Ca++ and Phos. from bones • Increase GI absorption • Increase reabsorption in kidneys

  33. Hyperparathyroid • Primary - Parathyroid tumor or hyperplasia • Secondary - Response to Low Ca++ levels • ESRD - Response to phosphate excretion problems • Nursing - increase fluids, low calcium diet, avoid immobility • Mithramycin - antihypercalcemic agent • Post-op removal - observe for tetany, fluid and electrolyte problems

  34. Hypoparathyroid • Accidental removal or vascular damage during surgery • Sxs - Tetany, Chvostek’s sign • Lab- low calcium, low PTH, and high Phos. • Tx - Vitamin D, Calcium supplements, and Phosphate binders

  35. Pancreas • Insulin • Beta cells of Langerhans • Stored in Beta Cells as Proinsulin • Catalyst to cellular metabolism • Promotes storage of CHO in liver, muscle cells, and fat deposits • Glucagon • Opposes the action of Insulin • Alpha cells produce • Acts to mobilize liver glycogen and convert to glucose

  36. Diabetes Mellitus • Chronic hyperglycemia---main feature in all types of diabetes mellitus. Resulting from: • Insulin secretion • Insulin action • Or both • Disease classified • Age of onset • Problem causing the lack of insulin • Severity of the deficiency

  37. Cost of Diabetes in the United States, 2002 • Total (direct and indirect): $132 billion • Direct medical costs: $92 billion • Indirect costs: $40 billion (disability, work loss, premature mortality)

  38. Blood Glucose Values • Normal – Fasting blood glucose levels of <110 mg/dL • Significant abnormal results – Levels>126mg/dL obtained on at least two occasions are diagnostic of diabetes, even in older adults.

  39. Diabetes Causes • Inability to use CHO • Insulin action ineffective at tissue site or not enough Insulin available

  40. Diabetes Causes • Glycogen fails to store in liver • Conversion of glycogen to glucose NOT affected • Increased metabolism of proteins and fats • Leads to Ketone production

  41. Insulin • Glucose transport across cell membrane • Storage of glucose as glycogen • Increased fat deposits • Decreased protein breakdown • Increased transport of amino acids into the cell for protein synthesis • Absence = Increased osmotic pressure • 3 Poly’s

  42. Type I • Beta cell destruction • Rapid onset • Must be given Insulin • Ketoacidosis prone

  43. Type II • Enough Insulin to prevent DKA • May have increased or decreased Insulin production • Decreased tissue response to Insulin • Abnormal liver glucose regulation • Oral Agent: • Increase Insulin production • Improve cell receptor binding • Regulate liver glucose production

  44. Impaired Glucose Tolerance • “Borderline Diabetes” • Blood Glucose levels above normal, but below levels to Dx Diabetes • May progress to Diabetes • Need close monitoring • Diet and Exercise

  45. Gestational • Intolerance of glucose during pregnancy • Insulin resistance to increase glucose available to the baby • Paced with placental hormones • GTT returns to normal in 3-5 weeks after delivery • Approximately 30% develop Diabetes within the next 5-10 years • Glucose Tolerance Test

  46. Baby Effects • Increase amounts of amniotic fluid • Large fetus • Hypoglycemic reactions after birth • Respiratory Distress Syndrome

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