Endocrine Glands PDF

ENDOCRINE SYSTEM FRANCIS JOE M. FUENTES, RN, USRN, CCRN, MANc EXOCRINE GLAND ENDOCRINE GLAND Adrenal Hypothalamus Ovaries Pancreas Parathyroid Pituitary...

ENDOCRINE SYSTEM FRANCIS JOE M. FUENTES, RN, USRN, CCRN, MANc EXOCRINE GLAND ENDOCRINE GLAND Adrenal Hypothalamus Ovaries Pancreas Parathyroid Pituitary Testes A Thyroid 1.Functions 1.Maintenance and regulation of vital functions 2.Response to stress and injury 3.Growth and development 4.Energy metabolism 5.Reproduction 6.Fluid and Electrolytes Balance HORMONES RISK FACTORS Age Poor diet Heredity Congenital factors Trauma Environmental factors Consequence of other health problems or surgery  Pituitary Gland The master gland; located at the base of the brain Influenced by the hypothalamus; directly affects the function of the other endocrine glands Promotes growth of body tissue, influences water absorption by the kidney, HORMONES A. ANTERIOR PITUITARY GLANDS Adrenocorticotropic hormone (ACTH) Follicle-stimulating hormone (FSH) Growth hormone (GH) Luteinizing hormone (LH) Melanocyte-stimulating hormone (MSH) Prolactin (PRL) Somatotropic growth-stimulating hormone Thyroid-stimulating hormone (TSH) B. POSTERIOR PITUITARY GLANDS These hormones are produced by the hypothalamus, stored in the posterior lobe, and secreted into the blood when needed: Oxytocin Vasopressin, antidiuretic hormone (ADH) C. THYROID GLANDS T3 T4 CALCITONIN D. PARATHYROID GLAND PARATHYROID HORMONE (PTH) Glucocorticoids: Cortisol, Cortisone, Corticosterone Responsible for glucose metabolism, protein metabolism, fluid and electrolyte balance, suppression of the inflammatory response to injury, protective immune response to invasion by infectious agents, and resistance to stress. Mineralocorticoids: Aldosterone Regulation of electrolyte balance by promoting sodium retention and potassium excretion F. ADRENAL MEDULLA EPINEPHRINE NOREPINEPPHRINE G.OVARY ESTROGEN & PROGESTERONE H. TESTES TESTOSTERONE I. PANCREAS INSULIN,GLUCAGON, SOMATOSTATI ENDOCRINE PROBLEMS OF ADULT PITUITARY GLANDS PROBLEM A. HYPOPITUITARISM B. HYPERPITUITARISM C. DIABETES INSIPIDUS D. SIADH CAUSES: -tumors -trauma -encephalitis autoimmunit y -stroke Hormones most often affected are: growth hormone (GH) gonadotropic hormones (luteinizing hormone, follicle-stimulating hormone), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), antidiuretic hormone (ADH) (GH, TSH) Reduced cardiac output (GH, ADH) Infertility, sexual dysfunction (gonadotropins, ACTH) Fatigue, low blood pressure (TSH, ADH, ACTH, GH) Tumors of the pituitary also may cause headaches and visual defects (the pituitary is located near the optic nerve).  Hypersecretion of growth HYPERPITUITARISM hormone by the anterior pituitary gland in an adult; (ACROMEGLY) caused primarily by pituitary tumors  sment ge hands and feet ckening and protrusion of the jaw hritic changes and joint pain ual disturbances phoresis , rough skin anomegaly pertension, atherosclerosis, cardiomegaly, rt failure ysphagia eepening of the voice ickening of the tongue, narrowing of the airway, sleep apnea yperglycemia lon polyps, increased colon cancer risk VASSOPRESIN INSUFFICIENCY  Diabetes Insipidus 1.Hyposecretion of ADH by the posterior pituitary gland caused by stroke, trauma, or surgery, or it may be idiopathic 2.Kidney tubules fail to reabsorb water. 3.In central diabetes insipidus there is decreased ADH production. 4.In nephrogenic diabetes insipidus, ADH production is adequate, but the kidneys do not respond appropriately to the ADH. Assessment 1.Excretion of large amounts of dilute urine 2.Polydipsia 3.Dehydration (decreased skin turgor and dry mucous membranes) 4.Inability to concentrate urine 5.Low urinary specific gravity 6.Fatigue 7.Muscle pain and weakness 8.Headache 9.Postural hypotension that may progress to vascular collapse without rehydration SYNDROME OF INAPPRORIATE ANTIDIURETIC HORMONE Condition of hyperfunctioning of the posterior pituitary gland in which excess ADH is released, but not in response to the body’s need for it. Causes: trauma, stroke, malignancies (often in the lungs or pancreas), medications, and stress. Treatment is directed at Assessment 1.Signs of fluid volume overload 2.Changes in level of consciousness and in status 3.Weight gain without edema 4.Hypertension 5.Tachycardia 6.Anorexia, nausea, and vomiting  ENDOCRINE PROBLEMS OF ADULT ADRENAL GLANDS PROBLEM Adrenal Cortex Addison’s disease Primary hyperaldosteronism (Conn’s syndrome) Cushing’s disease Cushing’s syndrome Adrenal Medulla Pheochromocytoma Adrenal cortex insufficiency (Addison’s Disease) 1.Primary Adrenal insufficiency 1.Also known as Addison’s disease, refers to hyposecretion of adrenal cortex hormones -glucocorticoids -mineralocorticoids -androgen CAUSE: autoimmune destruction 2.Secondary adrenal insufficiency is caused 3. Loss of glucocorticoids in Addison’s disease leads to decreased vascular tone, decreased vascular response to the catecholamines epinephrine and norepinephrine, and decreased gluconeogenesis. 4. In Addison’s disease, loss of the mineralocorticoid aldosterone leads to dehydration, hypotension, ASSESSMENT:  HEALTH TEACHING!!! Clients taking exogenous corticosteroids must establish a plan with their PHCPs or endocrinologist for increasing their corticosteroids during times of stress.  Cushing’s syndrome and Cushing’s disease (hypercortisolism) 1. Cushing’s syndrome 1.A metabolic disorder resulting from the 2.chronic and excessive production of cortisol by the adrenal cortex or from the administration of glucocorticoids in large doses for several weeks or longer (exogenous or iatrogenic) 3.ACTH-secreting tumors (most often of the 4. Cushing’s disease is a metabolic disorder characterized by abnormally increased secretion (endogenous) of cortisol, caused by increased amounts of ACTH secreted by the pituitary gland. D. Primary Hyperaldosteronism (Conn’s syndrome) Hypersecretion of mineralocorticoids (aldosterone) from the adrenal cortex of the adrenal gland CAUSE: ADENOMA 1.Excess secretion of aldosterone causes sodium Assessment 1.Symptoms related to hypokalemia, hypernatremia, and hypertension 2.Headache, fatigue, muscle weakness 3.Cardiac dysrhythmias 4.Paresthesias, tetany 5.Visual changes 6.Glucose intolerance 7.Elevated serum aldosterone Excessive amounts of epinephrine and  Catecholamine-producing tumor usually found in the adrenal medulla, but extra- adrenal locations include the chest, bladder, abdomen, and brain Assessment 1.Paroxysmal or sustained hypertension 2.Severe headaches 3.Palpitations 4.Flushing and profuse diaphoresis 5.Pain in the chest or abdomen with nausea and vomiting 6.Heat intolerance 7.Weight loss ENDOCRINE PROBLEMS OF ADULT THYROID GLANDS PROBLEM HYPOTHYROIDISM a. Hypothyroid state resulting from hyposecretion of thyroid hormones and characterized by a decreased rate of body metabolism b. The T3 &T4 is low and the TSH is elevated. c. In primary hypothyroidism, the source of dysfunction is the thyroid gland, and the thyroid cannot produce the necessary amount of hormones. Assessment 1.Hypotension 2.Bradycardia 3.Hypothermia 4.Hyponatremia 5.Hypoglycemia 6. Generalized edema 7. Respiratory failure 8. Coma  Myxedema Coma MYXEDEMA COMA A rare but serious disorder that results from persistently low thyroid production Coma can be precipitated by acute illness, rapid withdrawal of thyroid medication, anesthesia and surgery, hypothermia, or the use of sedatives and opioid analgesics. ENDOCRINE PROBLEMS OF ADULT THYROID GLANDS PROBLEM HYPERTHYROIDISM a. Hyperthyroid state resulting from hyper secretion of thyroid hormones (T3 and T4) b. Characterized by an increased rate of body metabolism c. A common cause is Graves’ disease, also known as toxic diffuse goiter. d. Clinical manifestations are referred to as thyrotoxicosis. e. The T3 and T4 are usually elevated and the TSH level is low. with uncontrollable hyperthyroidism. It can be caused by manipulation of the thyroid gland during surgery and the release of thyroid hormone into the bloodstream; it also can occur from severe infection and stress. Antithyroid medications, beta blockers, glucocorticoids, and iodides may be administered to the client before thy- roid surgery to prevent its occurrence.  ENDOCRINE PROBLEMS OF ADULT PARATHYROID GLANDS PROBLEM A. HYPOPARATHYROIDISM B. HYPOPARATHYROIDISM ASSESSMENT HYPOPARATHYROIDISM HYPERPARATHYROIDISM 1.Hypocalcemiaand 1.Hypercalcemia and hyperphosphatemia hypophosphatemia 2.Fatigue and muscle 2.Numbness and tingling n theface weakness 3.Muscle cramps and cramps in the 3.Skeletal pain and tenderness abdomen 4.Bone deformities that result in pathological or in the extremities 5.fractures 4. Positive Trousseau’s sign or 6.Anorexia, nausea, vomiting, Chvostek’s sign epigastric pain 7.Weight loss 5. Signs of over tetany, such as 8.Constipation bronchospasm, laryngospasm, 9.. Hypertension carpopedal spasm, dysphagia, 10. Cardiac dysrhythmias Can occur following thyroidectomy because of removal of parathyroid tissue PANCREAS PROBLEM metabolism of: carbohydrate protein and lipid caused by : deficiency of insulin or insulin resistance An absolute or relative deficiency of insulin results in hyperglycemia. TYPE 1 TYPE 2 Type 1 diabetes Type 2 diabetes mellitus is a nearly mellitus is a relative absolute deficiency lack of insulin or of insulin (primary resistance to the beta cell action of insulin; destruction); if usually, insulin is insulin is not given, sufficient to stabilize fats are fat and protein metabolized for metabolism but not energy, resulting in carbohydrate ketonemia metabolism. 1.Metabolic syndrome is also known as syndrome X, and the individual has coexisting risk factors for developing type 2 diabetes mellitus. Risk Factors: Abdominal obesity Hyperglycemia Hypertension, 1.Diabetes mellitus can lead to chronic health problems and early death as a result of complications that occur in the large and small blood vessels in tissues and organs. A. Macrovascular complications include coronary artery disease, cardiomyopathy, hypertension, cerebrovascular disease, and peripheral vascular disease. B. Microvascular complications include Assessment 1.Polyuria, polydipsia, polyphagia (more common in type 1 DM) 2.Hyperglycemia 2.Weight loss (common in type 1 diabetes mellitus, rare in type diabetes mellitus) 3.Blurred vision 4. Slow wound healing 5.Vaginal infections 6.Weakness and paresthesias 7.Signs of inadequate circulation to the feet 8.Signs of accelerated atherosclerosis (renal, cerebral, cardiac, peripheral) Diet a. The diabetic client’s diet should take into ac- count weight, medication, activity level, and other health problems. b. Day-to-day consistency in timing and amount of food intake helps control the blood glucose level. c. As prescribed by the PHCP or d. Carbohydrate counting may be a simpler approach for some clients; it focuses on the total grams of carbohydrates eaten per meal. The client may be more compliant with carbohydrate counting, resulting in better glycemic control; it is usually necessary for clients undergoing intense insulin therapy. e. Incorporate the diet into individual client needs, lifestyle, and cultural and Exercise a. Exercise lowers the blood glucose level, encourages weight loss, reduces cardiovascular risks, improves circulation and muscle tone, decreases total cholesterol and triglyceride levels, and decreases insulin resistance and glucose intolerance. b. Instruct the client in dietary adjustments when exercising; exercise to prevent hypoglycemia, it need not be deducted from the regular meal plan. If the blood glucose level is higher than 250 mg/dL (13.9 mmol/L) and urinary ketones (type 1 diabetes mellitus) are present, the client is instructed not to exercise until the blood glucose level is closer to normal and urinary ketones are absent. The client should try to exercise at the same time each day and should exercise when glucose from the meal is peaking, not when insulin or glucose-lowering medications are peaking. Insulin should not be injected into an area of the body that will be Instruct the client with diabetes mellitus to monitor the blood glucose level before, Oral hypoglycemic medications: (OHA) Oral medications are prescribed for clients with diabetes mellitus type 2 when diet and weight control therapy have failed to maintain Insulin Insulin is used to treat type 1 diabetes mellitus and may be used to treat type 2 diabetes mellitus when diet, weight control therapy, and oral hypoglycemic agents have failed to maintain satisfactory blood glucose levels. Illness, infection, and stress increase the blood glucose level and the need for insulin; insulin should not be withheld during times of illness, infection, or stress because hyperglycemia and diabetic ketoacidosis can The peak action time of insulin is important to explain to the client because of the possibility of hypoglycemic reactions occurring Regular insulin (U-100 strength) can be administered via IV injection (IV push). Regular insulin (U-100) and the short-duration insulins (lispro, aspart, and glulisine) can be administered (under close medical supervision) via IV infusion. A skin sensor device can be used that monitors the client’s blood glucose continuously; the information is transmitted to the pump, which determines the need for insulin, and then the insulin is injected. The pump holds up to a 3-day supply of insulin and can be disconnected easily if necessary for certain Continuous subcutaneous activities such as bathing. insulin infusion is administered by an externally worn device that contains a syringe and pump; different types of pumps are available and the one selected is based on the client’s Acute Complications of Diabetes Mellitus 1.Hypoglycemia occurs when the blood glucose level falls below 70 mg/dL (3.9 mmol/L) or when the blood glucose level drops rapidly from an elevated level. 2.Hypoglycemia is caused by too much insulin or too large an amount of an oral hypoglycemic agent, too little food, or excessive activity. 1.The client needs to be instructed always to keep some form of fast- acting simple carbohydrate available 2. If the client has a hypoglycemic reaction and does not have any of the recommended emergency foods available, any avail- able food should be eaten; high-fat foods slow the absorption of glucose, and the 3. Clients who experience frequent episodes of hypoglycemia, older clients, and clients taking β-adrenergic blocking agents may not experience the warning signs of hypoglycemia until the blood glucose level is dangerously low; this phenomenon is termed hypoglycemia unawareness. Assessment 1. Mild hypoglycemia: The client remains fully awake but displays adrenergic symptoms; the blood glucose level is lower than 70 mg/dL (3.9 mmol/L). 2. Moderate hypoglycemia: The client displays symptoms of worsening hypoglycemia; the blood glucose level is usually lower than 40 mg/dL (2.2 mmol/L). 3. Severe hypoglycemia: The client displays se-vere neuroglycopenic symptoms; Do not attempt to administer oral food or fluids to the client experiencing a severe hypoglycemic reaction who is semiconscious or unconscious and is unable to swallow. This client is at risk for aspiration. For this client, an injection of glucagon is administered subcutaneously, intra- muscularly, or intravenously. In the hospital or emergency department, the client may be treated with an IV injection of 25 to 50 mL (12.5 to 25 g) of 1.Extreme hyperglycemia occurs without ketosis or acidosis. 2.The syndrome occurs most often in individuals with type 2 diabetes mellitus. 3.The major difference between HHS and DKA is that ketosis and acidosis do not occur with HHS; enough insulin is present with HHS to prevent the breakdown of fats for energy, thus preventing ketosis. Mellitus