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Transcript
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 selfmanagement Hormones Responsible for regulating: – Reproduction – Growth & Development – Energy production & use – Maintenance of internal environment Catecholamines Amino Acid derivatives – Epinephrine – Norepinephrine – Thyroxin Easily replaced Many can be oral 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 Steroids Formed from cholesterol Easily produced for replacement Most can be oral Include Adrenal and Sex Glands: – Aldosterone – Cortisol – Estrogen – Testosterone Pharmacologic Uses Diagnostic – ACTH to stimulate the Adrenals – Thyroglobin to check thyroid response Replacement – Insulin – Estrogen – Thyroid Pharmacologic Effects – Steroids to decrease inflammation 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. Feedback Loops Hypothalamus __ Releasing Factor Pituitary Hormone A Target Organ Hormone B Biologic Effect __ Negative Feedback Loop Physiologic Changes with Aging Reduction in hormone production Changes in hormone clearance Decreased cellular responsiveness Changes in; – Physical activity level – Nutritional status – Body composition Causes of Disease Over or Under Production Transport abnormalities Inability of target tissues to respond Problems with the feedback mechanism Primary Secondary 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 Hypothalamus Neuro Secretory Cells Releasing Factor Producing Cells Portal Vessel Anterior Posterior Hormone Producing Cells 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) Anterior Pituitary Growth 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. 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 Anterior Pituitary Gonadotropic Hormone Gonadotropin-releasing hormone (GnRH) – Produced and released from the hypothalamus. Stimulates the secretion of follicle stimulating hormone (FSH) and lutenizing hormone (LH), from the anterior pituitary. Anterior Pituitary Adrenocorticotropic Hormone (ACTH) Stimulates the adrenal cortex to synthesize and release cortisols in response to stress. Anterior Pituitary Thyroid 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 Posterior Pituitary Oxytocin – Uterine contraction – Milk let down ADH (Vasopressin) – Renal conservation of water – Vasoconstriction – Increase GI motility – Released in response to plasma osmolarity 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 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 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 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 Addison's Adrenocorticol insufficiency Autoimmune Sxs - weight loss, anorexia, weakness, low BP, low sodium, high potassium, nausea & vomiting, diarrhea Tx - Glucocorticoids – Mineralcorticoids Adrenal Crisis Adrenal Medulla Pheochromocytoma – Neoplasm increasing catecholamines – Surgical removal Sxs - episodic HTN, increased metabolism, hyperglycemia Lab - urine metanephrines Monitor wide BP fluctuations 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 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 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. 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 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 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 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 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 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 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 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) 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. Diabetes Causes Inability to use CHO Insulin action ineffective at tissue site or not enough Insulin available 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 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 Type I Beta cell destruction Rapid onset Must be given Insulin Ketoacidosis prone 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 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 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 Baby Effects Increase amounts of amniotic fluid Large fetus Hypoglycemic reactions after birth Respiratory Distress Syndrome Tests Blood Sugar Glycosylated Hemoglobin (HbA1c) – The higher the number the poorer the control. GTT - Glucose Tolerance Test Capillary Blood Glucose (CBG) Treatment Diet – ADA Exchange list – Individually prescribed Exercise – Type I - IDDM Increases Insulin sensitivity of cells Reduce Insulin dose or snack before exercise – Type II - NIDDM Increases Insulin binding at receptors May initially elevate blood sugars Insulin Treatment Goal: Match Normal Secretion Patterns of the Body Multiple types of Insulin Administration techniques Site Rotations Pumps New Technology Somogyi Effect Wide difference in CBG’s – Low in early AM – High after breakfast Counter regulatory to hypoglycemia during the night Treatment - lower Insulin dose in the evening or increase food intake before bed Dawn Phenomenon High CBG’s and possibly Ketones in the morning Dawn release of Growth Hormone or Cortisol Treatment - Change Insulin times and/or increase Insulin dose Look at client’s entire management program Sulfonylureas Must be producing some Insulin Action: – Stimulate Beta cell release of Insulin – Increase Insulin receptor sensitivity – May decrease liver glucose production Do Not Take Extra if Overeats! Hypoglycemia may be prolonged Hypoglycemics Alpha-Glycosidase Inhibitors – Delay digestion and absorption of CHO Biguanides – Decrease glucose absorption, decrease glucose production in liver, and improves insulin sensitivity in tissues Meglitinides – Stimulates Beta cells and improves insulin response to glucose Thiazolidinediones – Lowers insulin resistance by re-sensitizing the body to its own insulin Hypoglycemia Too much Insulin or not enough food Symptoms due to rapid drop in Blood Sugar Adrenergic (Fight or Flight) Symptoms Glyconeurogenic (Brain) Symptoms Beta Blockers mask the symptoms Elderly often present with Brain symptoms FIRST DKA - Diabetic Ketoacidosis No Insulin leads to: – Use of glucose – Breakdown of fats to fatty acids to Ketones – Acidosis causes K+ to leave cells and water loss – Severe dehydration with high serum K+ levels Jamie HHNK Hyperglycemic Hyperosmolar NonKetosis Enough Insulin to Avoid DKA High Blood Glucose Levels lead to Osmotic Diuresis Hypovolemia Treatment = Insulin and Rapid IV Fluid Replacement Prevent by Pushing Fluids When Serum Osmolarity Nears 320 2(Na+K) + BS + BUN 18 2.8 Chronic Complications 80% of Medical Spending Increasing as Population Ages Microvascular Macrovascular PATIENT EDUCATION Arthur Pattern Management Rule Target Glucose Goals Regular CBG’s Record CBG’s & events Study a 3 day pattern Determine Insulin responsible for problems s Insulin by 1 or 2 Units One change at a time Treat low CBG’s FIRST 3 days before another change Client #1 A.M. NOON P.M. H.S. 2/1 84 191 114 97 2/2 78 222 104 135 2/3 90 201 117 103 2/4 86 186 129 132 Client #2 A.M. NOON P.M. H.S. 2/1 64 191 114 67 2/1 68 262 204 135 2/3 50 201 47 103 2/4 86 66 129 132 Client #3 A.M. NOON P.M. H.S. 2/1 254 271 314 397 2/2 278 282 304 335 2/3 264 261 387 403 2/4 286 286 329 332 Home Causes Oral Medication Errors – Dose, Timing, Double Medication – Bring ALL Meds from home Insulin Errors – Technique Problems – Observe technique ASAP – Check dose and timing at home Diet Misinformation / Changes