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  1. 1. Endocrine Disorders - 1 ENDOCRINE DISORDERS ENDOCRINE DISORDERS reviews normal function and requirements of the endocrine system; identifies antecedents for errors in function; discusses the signs, symptoms, and treatment of disorders related to pituitary and adrenal cortex secretion; reviews the normal function of the thyroid gland and regulation of thyroid secretion; describes antecedents, signs and symptoms, and treatment for hyperthyroidism and hypothyroidism; describes hypoglycemia, its antecedents and signs and symptoms; identifies the normal function of the Islets of Langerhans in the pancreas and the action of its hormones: insulin and glucagon; explains antecedents, signs and symptoms, complications, and treatment of the two major types of diabetes mellitus. I. Overview of endocrine system A. Normal function of the endocrine system: communication and control of other body functions by secretion of hormones necessary for: 1. Metabolism of organic nutrients 2. Fluid and electrolyte balance 3. Sexual reproduction and lactaction B. Requirements for normal function: 1. Gland cells able to secrete functional hormones - X 2. Good blood supply for hormonal transport - Y + 3. Functional receptors on target cells Z + 4. System of regulation for secretion of hormones: Negative feedback loops - an increase in the secretion of one hormone causes a decrease in the secretion of its regulating substances.
  2. 2. Endocrine Disorders - 2 C. Errors in function: 1. Hypersecretion (too much) 2. Insufficient secretion (too little) 3. Not enough receptors 4. Clearance problems: liver failure, kidney failure --> faulty clearance of hormone from plasma--> excessive amounts of hormone D. Endocrine Hormones 1. Regulation of metabolism and blood sugar levels: Insulin lowers blood sugar by moving glucose into cells and promoting nutrient storage. Hormones that oppose insulin work to increase the blood sugar and promote the metabolism of glucose and other nutrients by the cells. Oppose insulin Insulin | Glucagon | Glucocorticoids | Thyroid hormones (T3, T4) | Growth hormone (GH) | Epinephrine (Epi) 2. Regulation of fluid and electrolyte balance: Mineralocorticoids (aldosterone) Antidiuretic hormone (ADH) Parathyroid hormone (PTH) Thyroid calcitonin (TCT)
  3. 3. Endocrine Disorders - 3 3. For regulating the secretion of other hormones Hormones from the hypothalamus regulate pituitary hormone secretion. Anterior pituitary trophic hormones stimulate the secretion of hormones in designated target glands. Hypothalamic Related pituitary Gland/hormone releasing hormones trophic hormones stimulated TRH | TSH | Thyroid/T3, T4 CRH | ACTH | Adrenal cortex/cortisol LRH | FSH, LH | Ovaries & Testes PIF (prolactin inhibitory factor) GIF (somatostatin - growth hormone inhibitor) 4. For regulation of reproduction: Estrogen Primarily Progesterone in females Oxytocin Prolactin (PRL) Androgens - secreted by gonads (primarily in males) and adrenal cortex ON YOUR OWN: Make a chart of all the hormones mentioned here, using the following headings: Hormone - Secreting gland - Target - Action on target - Regulation
  4. 4. Endocrine Disorders - 4 II. Pituitary hormones 11878 A. Normal functions 1. Anterior pituitary Growth hormone promotes somatic growth - stimulates hyperplasia (cell division) and hypertrophy (larger cells) especially cartilage and bone increases blood glucose mobilizes lipids and glycogen spares protein increases protein synthesis Prolactin necessary for lactation (production and secretion of milk) inhibits LRH, LH (inhibits ovulation) effect on muscle, adipose similar to that of GH TSH, ACTH, LH, FSH trophic hormones stimulate endocrine glands to increase secretion Controlled by hypothalamic release/inhibition
  5. 5. Endocrine Disorders - 5 2. Posterior pituitary Oxytocin stimulates smooth muscle contraction in uterus, mammary ducts. regulated by "suckling" reflex. ADH (Vasopressin) increases water reabsorption by kidney increases blood pressure produces profound vasoconstriction reflex regulation via osmoreceptors in hypothalamus B. Error of "too little" secretion 1. Antecedents: 2835 Tumors that destroy secretory cells Ischemia Head trauma Inflammation due to infection or autoimmune response Alteration in regulating factors from hypothalamus 2. Signs and symptoms of pan-hypopituitarism in anterior pituitary Decreased growth hormone 3405 dwarfism (if prior to puberty) less opposition to insulin --> hypoglycemia 3310 decreased muscle mass (atrophy)
  6. 6. Endocrine Disorders - 6 Decreased TSH, ACTH --> hypoglycemia Decreased MSH --> pale skin Decreased FSH, LH gonads not stimulated --> decreased estrogen, testosterone decreased secondary sexual characteristics amenorrhea due to lack of LH 3. Signs and symptoms of hypofunction of posterior pituitary Decreased ADH --> diabetes insipidus water not conserved can't concentrate urine --> polyuria (large volume of dilute urine) increased thirst --> polydipsia (increased fluid intake) low urine specific gravity, even if fluid-restricted dehydration large urinary bladder may also be caused by lack of renal responsiveness 4. Treatment for any hypopituitarism Replace missing hormones Avoid giving GH to increase height in normal children GH increases muscle mass but not strength or endurance (or anything else useful) in elderly
  7. 7. Endocrine Disorders - 7 C. Error of "too much" secretion 1. Antecedents Hthl Hyperfunctional tumors - Pit +/- Decrease in inhibitory input from hypothalamus Gld + Decrease in negative feedback from glands to their trophics 2. Signs and symptoms of hyperpituitarism (anterior pituitary) Increased GH if increased GH prior to puberty --> gigantism (increase in long bone growth) if increased GH in adults --> acromegaly (bones thicken) 3304, 3307, 3299 facial coarsening 3300-01 hands and feet large and wide spinal deformity (vertebrae thicken) osteoarthritis hyperglycemia may occur Increased prolactin --> 7146 galactorrhea (inappropriate secretion of milk in both men and women); amenorrhea (prolactin inhibits LH) Increased trophic hormones --> increased gland stimulation increased ACTH --> increased cortisol increased TSH --> increased T3, T4 (thyroid hormones)
  8. 8. Endocrine Disorders - 8 increased FSH and LH --> increased stimulation of sex steroids 11879 Visual complaints - partial blindness may occur due to pressure of pituitary against optic chiasm (May be one of the first symptoms of a pituitary tumor) 3. Signs and symptoms of hyperfunction of posterior pituitary Increased ADH --> syndrome of inappropriate ADH secretion (SIADH) concentrated urine water retention in plasma --> increased blood volume and blood dilution (decreased osmolarity) --> edema decreased serum Na + --> problems in excitable tissues (neurons and muscles) other causes ectopic ADH-secreting tumors 5-7 days post-operative status infectious pulmonary disease drugs, e.g., nicotine psychiatric disorder treatment for SIADH: fluid restriction hypertonic NACL in IV fluid stop antecedents
  9. 9. Endocrine Disorders - 9 4. Treatment for any hyperpituitarism Surgery to remove tumor/hyperplastic area Replace hormones in appropriate amounts III. Adrenal cortex hormones A. Normal function - two major classes of hormones 11872 1. Glucocorticoids (cortisol) Increases serum glucose mobilizes proteins and free fatty acids (ffa) from connective, adipose, and muscle tissue. increases gluconeogenesis in the liver (the mobilized ffa and proteins are converted to glucose) Redistributes fats from subcutaneous deposits on extremities to connective tissue on back of neck and abdomen Suppresses cell division in lymphocytes - prednisone used as antileukemic drug for lymphocytic leukemias Suppresses inflammatory response - cortisone used for severe arthritis and other inflammatory disorders Increases RBCs and neutrophils Increases HCl and pepsin secretion in stomach 2. Mineralocorticoids (aldosterone) Increases Na + reabsorption in kidney (saves Na +) Increases K + and H+ secretion in kidney
  10. 10. Endocrine Disorders - 10 B. Regulation of glucocorticoids and mineralocorticoids 1. Regulation of cortisol CRF - |+ stress + ACTH - |+ Cortisol 2. Regulation of Aldosterone - serum K + + aldosterone - BP + renin blood volume |+ | angiotensin I and II serum Na + |+ aldosterone C. Aldosteronism = too much aldosterone 1. Antecedents to aldosteronism Primary aldosteronism due to hypersecretory adrenal tumor or adrenal hyperplasia (Conn's syndrome). problem within adrenal cortex Secondary aldosteronism due to decreased renal flow or other increase in renin secretion. problem is outside of adrenal cortex 2. Signs and symptoms of aldosteronism Sodium and water retention --> increased blood volume --> edema
  11. 11. Endocrine Disorders - 11 hypertension headache retinopathy (severe hypertension --> fluid leaks out of vessels into retina) Decreased potassium --> weakness Decreased hydrogen --> metabolic alkalosis D. Cushing's syndrome (too much cortisol) 1. Antecedents Primary = hyperplasia, hyperfunctional tumor that secretes cortisol Secondary iatrogenic - due to drug therapy e.g., prolonged high dose steroids for inflammatory/autoimmune disorders. increase in ACTH e.g., due to a pituitary tumor or due to oat cell carcinoma of lung 2. Signs and symptoms of Cushing's syndrome 3342-43 Problems due to excessive protein breakdown: skin breakdown 3337 striae - purple/white stretch marks slow wound healing --> prone to development of infections 3338-39 muscle atrophy osteoporosis (matrix mobilized from bone)
  12. 12. Endocrine Disorders - 12 weak vessel walls --> bruising and petechiae (small reddish hemorrhagic spots) Problems due to increased gluconeogenesis: increased likelihood of hyperglycemia 3325 Problems due to fat redistribution: trunkal obesity and moon face arms and legs get thin thick abdomen buffalo hump at back of neck round face Problems due to lymphocyte suppression: impaired immunity Problems due to increased gastric acid secretion: peptic ulcers Emotional lability laughing, crying, instability of mood psychotic episodes may occur; may be linked to suppression of ACTH through negative feedback mechanism If Cushing's is due to primary hyperplasia, will also see s/sx of: aldosteronism (as in Conn’s) increased adrenal androgens 3344, 8303 hirsutism (increased hair growth on face, chest, abdomen) deepening of the voice
  13. 13. Endocrine Disorders - 13 3. Treatment for excess adrenocortical secretion Surgical removal of adrenal glands and hormone replacement Adrenal suppression by drugs E. Addison's disease (adrenal insufficiency) 1. Antecedents - 80% loss of both glands, due to: TB induced inflammatory response --> scarring of adrenal tissue Metastatic tumor Idiopathic Addison's disease due to autoimmune response 2. Signs and symptoms of Addison's disease Problems due to decreased cortisol: fasting hypoglycemia due to depleted glycogen stores plus decreased gluconeogenesis--> weakness, fatigue 3369, 3373-74 increased ACTH due to loss of negative feedback --> fragment of ACTH acts like MSH on skin --> bronzed appearance of skin - a classic sign of Addison's disease weight loss and fluid and electrolyte problems due to anorexia, nausea, vomiting and diarrhea Problems due to decreased aldosterone sodium and water depletion --> decreased blood volume --> postural (orthostatic) hypotension --> fainting increased heart rate vascular collapse (shock) may occur in response to additional stressors, such as trauma, infection, or diarrhea.
  14. 14. Endocrine Disorders - 14 decreased flow to kidney --> increased renin secretion - -> angiotensin II --> vasoconstriction but no way to increase blood volume increased serum potassium --> irritable muscles and heart arrhythmias Problems due to decreased androgens: loss of body hair 3. Treatment = replace needed hormones IV. Thyroid hormones T3 (triiodothyronine) and T4 (thyroxine). The number in T3, T4 refers to the number of iodine atoms contained in the hormone molecule. A. Normal function of thyroid hormones 1. Increase basal metabolic rate (BMR - the rate at which molecules are combusted with oxygen to make ATP) Increases the production and consumption of ATP. Heat is released as a byproduct 2. Promote liver clearance of cholesterol 3. Influences somatic growth: Low but normal levels promote protein synthesis High levels - burn protein 4. Increase myocardial contractility 5. Involved in central nervous system (CNS) development
  15. 15. Endocrine Disorders - 15 B. Regulation - TRH (from hypothalamus) + - TSH (from pituitary) + T3, T4 In addition to stimulating the production of T3 and T4, TSH also promotes increased cell division (hyperplasia) in the thyroid gland. C. Hyperthyroidism (thyrotoxicosis) = error of "too much" thyroid hormone E.g., Grave's disease 1. Antecedents to Grave's disease: Familial tendency Autoimmune disorder in which IgG antibodies (thyroid-stimulating immunoglobins - TSI) bind onto TSH receptors on thyroid cells and stimulate increased cell division and increased production of thyroid hormones. 2. Signs and symptoms of hyperthyroidism 3091-92 Goiter (enlargement of thyroid gland due to hyperplasia) 2358, 3080 Increased BMR 3125-26 excess heat production --> heat intolerance, vasodilation of cutaneous vessels --> sweating with warm skin. increased appetite, yet weight loss
  16. 16. Endocrine Disorders - 16 Wasting of protein muscle weakness, atrophy soft, fine hair and skin; some hair loss osteoporosis Effects on excitable cells fatigue, anxiety, tremor, hyperreflexia, irritability increased heart rate (may lead to atrial fibrillation, which can throw a clot that occludes a cerebral vessel--> ischemic stroke) palpitations, increased stroke volume, increased cardiac output, slight increase in systolic BP increased smooth muscle motility --> diarrhea 3101, 3112, 3129 Exopthalmos (infiltrative ophthalmopathy): protrusion of the eyes related to infiltration of orbital tissues with lymphocytes and edema 3127 may also happen to skin on front of legs Menstrual irregularity Decreased serum cholesterol 3. Treatment for hyperthyroidism Surgical removal and replacement of thyroid hormones Thyroid blocking drugs Radioactive iodine - destroys the overactive thyroid tissue Screen for low TSH (high thyroid hormone levels) in late middle age (especially in women) as a marker for increased risk for atrial fibrillation and stroke
  17. 17. Endocrine Disorders - 17 D. Hypothyroidism = error of "too little" thyroid hormone 1. Antecedents Primary causes: autoimmune thyroiditis thyroidectomy iodine deficiency 3157 atrophy or malfunction due to trauma, destructive tumor, congenital problem Secondary causes: decreased TSH or TRH Uncle Toby 2. Signs and symptoms of adult onset hypothyroidism (myxedema) 3090 Goiter (in primary hypothyroidism) - TSH + Thyroid gland T3, T4 and increased cell division With a decrease in production of thyroid hormones, there is a loss of negative feedback to the pituitary. Thus, the pituitary continues to secrete TSH, which continues to stimulate cell division in the thyroid gland.
  18. 18. Endocrine Disorders - 18 Decreased BMR decreased heat production --> cold intolerance, decreased body temp., vasoconstriction --> pale (yellowish) cool dry skin, decreased sweating decreased appetite with weight gain Slow movements, speech and thinking Impaired sensation and delayed reflexes Decreased heart rate, stroke volume, cardiac output, and nl BP Muscle aching and stiffness; weakness and fatigue Headache Decreased smooth muscle motility --> constipation 3165 Brittle hair and nails 3164, 3167 Skin thickening and peripheral edema/effusions; puffy face, thick tongue and hoarseness due to deposits of protein- mucopolysaccaride complexes which pull fluid into the area. Excessive menstrual bleeding or amenorrhea Increased serum cholesterol 3. Signs and symptoms of congenital hypothyroidism = cretinism 3135 Blood tests (T3, T4, TSH) performed shortly after birth detect low thyroid hormone levels Decreased BMR cold, mottled skin, subnormal temperature decreased appetite, feeding problems
  19. 19. Endocrine Disorders - 19 Somnolence, lethargy Slow pulse Constipation Prolonged jaundice Sparse hair, dry skin 3133 Hoarse cry and protruding tongue and abdomen Slowed growth and development; short stature; flat, wide face; coarse features; slow bone and tooth development Prolonged jaundice Mental retardation 4. Treatment for hypothyroidism Replace T3, T4 (but be alert for decreased bone density) Replace iodine if deficient V. Islets of Langerhans in pancreas A. Normal function: insulin and glucagon oppose each other. 1. Insulin secreted by beta cells - decreases blood glucose Promotes increased entry/use of glucose in muscle and adipose cells Promotes increased lipogenesis (fat synthesis: glucose --> lipids as storage form) in adipose tissue Promotes increased glycogenesis (glycogen synthesis: glucose --> starch as a storage form) in muscle cells Promotes increased protein synthesis
  20. 20. Endocrine Disorders - 20 2. Glucagon secreted by alpha cells - increases blood glucose Increases glycogenolysis (breakdown of starch to glucose) in the liver. Increases gluconeogenesis (making of glucose from free fatty acids and amino acids) in the liver. Mobilizes glucose from liver Promotes cellular burning of fatty acids --> ketones B. Regulation of insulin and glucagon: 1. Short loop negative feedback blood glucose blood glucose - - insulin + glucagon + 2. Insulin is secreted in response to increased blood glucose. Then, as blood glucose drops, the stimulus for insulin secretion is lost and insulin secretion stops. 3. Glucagon is secreted in response to low blood glucose levels. Then, as blood glucose levels rise, the stimulus for glucagon secretion is lost and glucagon secretion stops. C. Hypoglycemia 1. Blood sugar < 50 mg% Typical, but not absolute cutoff
  21. 21. Endocrine Disorders - 21 2. Antecedents to hypoglycemia Too much insulin, due to: insulin overdose (can cause insulin shock) hypersecreting tumor (insulinoma) ingestion of alcohol + simple carbohydrates. Alcohol potentiates the ability of increased blood glucose to stimulate insulin secretion --> hypoglycemia 3 beers + chips --> hypoglycemia in 2-3 hours Decrease in hormones that oppose insulin decreased glucagon (disease of alpha cells of the pancreas) decreased cortisol (eg. Addison's disease) decreased epinephrine decreased GH (hypopituitarism) decreased thyroid hormones (myxedema) Liver disease --> decreased gluconeogenesis, decreased glycogen stores alcohol when fasting will have the same effect Malabsorption Errors of metabolism Starvation
  22. 22. Endocrine Disorders - 22 3. Signs and symptoms of hypoglycemia Signs and symptoms due to autonomic sympathetic stimulation (--> increased epinephrine release) sweating anxiety palpitations pallor weakness and tremor Signs and symptoms due to brain glucose deprivation initially (below 40 mg %): hunger headache confusion, amnesia, decreased attention blurred vision, paresthesias behavior/mood changes: drunken gait, aggressiveness, irritability severe hypoglycemia: hypothermia seizures coma
  23. 23. Endocrine Disorders - 23 D. Diabetes mellitus 1. Hormonal alterations Too little insulin Too much glucagon Insulin receptor failure 2. Antecedents to insulin dependent diabetes dellitus (IDDM) = type I. Beta cell failure (impaired insulin secretion) due to: autoimmune mechanism - antibodies and T-cells initially targeted against enzyme (GAD) made by beta cells and later to insulin genetic predisposition - polygenic, recessive viral disease, such as rubella, coxsackie, mumps - all have external proteins similar to the enzyme (GAD) look-alike 1841 destructive tumor pancreatitis Usually a rapid onset. Often occurs prior to age 25 (juvenile onset).
  24. 24. Endocrine Disorders - 24 3. Antecedents to non-insulin dependent diabetes mellitus (NIDDM) = type II Insulin resistance may be receptor deficiency - slow to regenerate receptors obesity - present in 80% of cases. Probable mechanism = frequent overeating --> excessive insulin secretion --> use up receptors multiparity - hormonal changes and weight gain--> insulin resistance --> maternal blood sugar can go more to the fetus than to her own cells may be problem in muscle-cell membrane (e.g., in its fatty acid makeup) rather in receptor may be glucose metabolism problem in cells, not just glucose transport (insulin) problem Genetic - autosomal dominant pattern Usually slow onset. Generally occurs in adults (aged 25-40) 4. Signs and symptoms of diabetes mellitus (DM) related to inability to store glucose --> glucose stays in the blood. Hyperglycemia (blood glucose > 140 mg%) Blood glucose measurement is normally obtained following an 8-12 hour fast. Glucose intolerance (blood glucose > 200 mg% when measured 2 hrs after glucose meal). Often glucose intolerance occurs prior to the development of fasting hyperglycemia.
  25. 25. Endocrine Disorders - 25 Glycosuria (starts when blood glucose is > 160-180 mg%) occurs in IDDM and severe NIDDM only osmotic diuresis - The glucose particles in the tubular filtrate pull extra water out into the filtrate, where it is lost in the urine -- > fluid & electrolyte loss polyuria polydipsia decreased blood volume --> decreased BP --> decreased blood flow to brain --> coma blood glucose is typically in the thousands mg% when this happens HHNK = hypergylcemic hyperosmolar non- ketotic syndrome also, dehydration, shock s/sx, fever wasting of ingested calories weight loss polyphagia - increased food intake fatigue, somnolence 5. Signs and symptoms of diabetes mellitus (DM) related to oxidation of free fatty acids to ketones (IDDM only) --> ketonemia (ketones in blood) Ketones are filtered into tubular filtrate and excreted in the urine (ketonuria).
  26. 26. Endocrine Disorders - 26 ketone particles pull excess water into the filtrate (osmotic diuresis) --> fluid and electrolyte loss polyuria polydipsia decreased blood volume dehydration; decreased flow to the brain --> coma blood glucose is typically in the hundreds mg% when this happens Plasma ketones contribute to increased H+ in blood = diabetic ketoacidosis (DKA), a type of metabolic acidosis low serum pH respiratory centers stimulated; attempt to get rid of H+ by blowing off CO2 --> Kussmaul respirations (rapid, deep respirations) CNS is very sensitive to pH, so low pH --> coma blood glucose is typically in the hundreds mg% when this happens 6. Signs and symptoms of diabetes mellitus (DM) related to breaking down of amino acids for fuel (IDDM only). Increased nitrogenous wastes in the blood and urine (creatinine, urea, uric acid, etc.) Negative nitrogen balance - more nitrogen lost than gained --> impaired wound healing muscle wasting
  27. 27. Endocrine Disorders - 27 7. Signs and symptoms related to long-term complications of increased serum glucose and free fatty acids in both IDDM and NIDDM Vascular damage in both large and small vessels due to collagen cross-linking by glucose and by LDL binding to walls. in large vessels - atheroma development 80% of persons with IDDM or NIDDM have co-existing hypertension hypertension <---> atheroma development atherosclerotic plaques --> vascular occlusion --> ischemia of tissues downstream infarction (stroke, MI) foot ulcers (due to tissue hypoxia from peripheral vascular disease) 10251-53, 10245-46, 3248-49 necrosis --> gangrene of feet or lower legs --> amputation in small vessels - basement membrane problem --> thickening of walls, leakiness 3212 retinal damage related to increased retinal capillary permeability and obstruction, small aneurysms and ischemic damage to retina. DM is a major cause of blindness. glomerulosclerosis/nephrosclerosis --> hypertension, edema, uremia. DM is a major cause of renal failure.
  28. 28. Endocrine Disorders - 28 Neural damage due to autoimmune attack on peripheral neurons and due to accumulation of glucose metabolites (fructose and sorbitol) in cells --> osmotic swelling of cells. 3217 cells in lens of eye attract H2O --> cataracts (opaque lenses) Schwann cell disruption and axon degeneration --> loss of myelin sheath in peripheral neurons --> disruption of autonomic control of organs (bowel, bladder), and skeletal motor function (movement). inability to sense touch, pressure, pain in extremities (“stocking and glove” neuropathy), especially feet, causes increased risk of injuries going undetected --> further tissue damage, infection. 3246 (burn) problems in these tissues compounded by ischemia... Infection 1381 bacteria and molds thrive on extra glucose in fluids 399, 3261 4260-61 ischemic necrosis of tissues is good medium for infection 8. Increased risk of birth defects if mother requires insulin to control NIDDM, IDDM, or gestational diabetes 9. Treatment for diabetes mellitus If deficient, give insulin nasal spray (new) pump injection Transplant of pancreas or of islet cells
  29. 29. Endocrine Disorders - 29 Regulate diet coordinate food intake with insulin administration so that intake can be stored in cells. allow regeneration of receptors keep hyperglycemia to a minimum decrease intake of simple carbohydrates Monitor serum glucose (transdermal blood glucometers as well as finger stick variety); modify prescribed insulin dosage based on: exercise - with increased exercise, uptake and burning of glucose is enhanced. Need less insulin to get glucose into cells. If don't reduce insulin dose --> hypoglycemia infection, trauma, stress, pregnancy --> increased blood levels of epinephrine, cortisol, human placental lactogen, and GH which all oppose the action of insulin --> increased blood sugar - need more insulin !! Tight control of blood sugar levels significantly decreases incidence of complications !!!!! Prevent continued autoimmune destruction of beta cells immunosuppress with cyclosporin megadose of insulin early on to create tolerance Patient teaching essential to effective control of diabetes, including: diet, blood glucose monitoring, foot care, insulin administration, symptom identification, and dosage adjustments END OF ENDOCRINE DISORDERS