Hormonal and Glucose Regulation PDF

Hormonal & Glucose Regulation Learning Objectives 1. Explain the hypothalamus-pituitary-hormone axis and feedback system 2. Recognize the hormones that originate in the anterior and posterior pituitary glands 3. Differentiate between diseases associated with hyperfunction versus hypofunctio...

Hormonal & Glucose Regulation Learning Objectives 1. Explain the hypothalamus-pituitary-hormone axis and feedback system 2. Recognize the hormones that originate in the anterior and posterior pituitary glands 3. Differentiate between diseases associated with hyperfunction versus hypofunction of the pituitary, thyroid, and adrenal glands 4. Identify the risk factors for type 1 diabetes, type 2 diabetes, and metabolic syndrome 5. Recognize the signs,symptoms, and clinical manifestations of type 1 diabetes and type 2 diabetes 6. Describe the pathological mechanism that cause type 1 and type 2 diabetes 7. Recognize the potential complications of uncontrolled diabetes and untreated metabolic syndrome Exemplars Diabetes 1 and 2 Hypo/hyperglycemia ○ Metabolic syndrome ○ Starvation Hypo/hyperthyroidism Cushings’ Syndrome Addison’s Disease Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Diabetes Insipidus (DI) Hormone Cell to Cell Communication Paracrine pathway > hormones are produced in a cell, secreted, and act directly on nearby receptive cells Autocrine pathway > the same as the paracrine pathway except that the receptor cells are also secretory cells so, in essence, the cell is able to produce the hormone and exert an effect on itself Endocrine pathway > hormones are produced in a cell, secreted, and travel through blood vessels to distant cells, attach to receptors, and act on that cell Synaptic pathway > hormones (neurotransmitters) are produced in the neuron, secreted, and travel along the axon to the synapse where they are released and taken up by a nearby neuron with the appropriate receptors to exert an effect Neuroendocrine pathway > hormones (neurohormones) are produced in a neuron, secreted, travel along the axon to the synapse, are released, are taken up into the vascular system, and travel to distant cells with the appropriate receptors to exert an effect Hypothalamus and Pituitary Interaction The hypothalamus produces several releasing and inhibiting hormones that act on the pituitary glands, stimulating the the release of pituitary hormones ○ The hormones produce in the hypothalamus are corticotrophin-releasing hormone, dopamine, growth hormone-releasing hormone, somatostatin, gonadotrophin-releasing hormone and thyrotrophin-releasing hormone  Two hormones are produced by the hypothalamus and then stored in the posterior pituitary gland before being secreted into bloodstream ○ Hormones known as posterior pituitary hormones are synthesized by hypothalamus, and include oxytocin and antidiuretic hormone (ADH or Vasopressin). The hormones are then stored in neurosecretory vesicles (Herring bodies) before being secreted by the posterior pituitary into the bloodstream The hypothalamus produces several releasing and inhibiting hormones that act on the pituitary gland, stimulating the release of pituitary hormones Of the pituitary hormones, several act on other glands located in various regions of the body, whereas other pituitary hormones directly affect their organs Disorders of Pituitary Function Hypothalamus (Grape size) produces antidiuretic hormone and oxytocin and then stores them in the posterior pituitary The hypothalamus and the anterior pituitary communicate via a portal system ○ Pituitary gland (pea size) is also called “Hypophysis” ○ Pituitary gland is the “master gland” Responsible for regulating other glands ○ Two portions; each with unique functions Anterior Posterior Anterior pituitary ○ TSH, ACTH, LH, FSH, GH, Prolactin Posterior Pituitary ○ Oxytocin, vasopressin Pituitary Hormones Anterior ○ ACTH > adrenocorticotropic hormone, or corticotropin, stimulates release of corticosteroids Adrenal cortex ○ GH > growth hormone-triggers growth Bone ○ TSH > thyroid stimulating hormone - stimulates thyroid gland ○ FSH > follicle stimulating hormone-stimulates graafian follicles and seminiferous tubules Testis, Ovary ○ LH > luteinizing hormone-stimulates production of androgens (testosterone) and rupture of follicle to release ovum Testis, ovary ○ Prolactin > stimulates milk production > mammary gland Posterior ○ ADH > antidiuretic hormone or vasopressin - decreases diuresis by controlling renal function Kidney tubules ○ Oxytocin > stimulates contraction of uterus and letdown in lactating females  Uterus smooth muscle, mammary gland Hypopituitarism: Growth Hormone Deficiency Inhibits somatic growth Primary site of dysfunction appears to be in the hypothalamus S/S > short stature, obesity, immature facial feature, delayed puberty, hypoglycemia, seizures, obesity, insulin resistance The pituitary secretes hormones that are essential to growth and reproduction Evaluation of GH Deficiency and GH replacement Family history Growth patterns and health history Definitive diagnosis bases of radioimmunoassay of plasma GH levels Hand x-rays to evaluate growth potential vs ossification Endocrine studies to detect deficiencies Prognosis GH replacement successful in 80% of patients Growth rate of 3.5-4 cm/yr before treatment and increase to 8-9 cm/yr after treatment Response varies based on age, length of treatment, frequency of doses, dosage, weight, and GH receptor amount Family support needs Child’s body image Preparing child for daily injections Treatment very expensive ( $20,000 - $ 30,000 a year) Pituitary Hyperfunction of GH: Clinical Manifestations Excess GH before closure of epiphyseal shafts results in overgrowth of long bones Reach heights of 8 feet or more Vertical growth and increased muscle Weight generally in proportion to height Excess GH after epiphyseal closure is called acromegaly ○ Gigantism if before Typical facial features Acromegaly > symptoms = pituitary adenoma, hypertrophy of sweat/sebaceous glands, galactorrhoea ( prolactin), cardiomegaly hypertension, sexual dysfunction, peripheral neuropathy, visual field defects, prominent supraorbital ridge, large nose and jaw (teeth are separated or lacking), abnormal glucose tolerance test (glucosuria/polyuria), spade shaped hands and feet, arthrosis Diagnostic Evaluations and Management Caused by non-cancerous tumor in anterior pituitary gland called adenoma Radiologic studies, endocrine studies Surgical treatment to remove tumor Radiation and radioactive implants Hormone replacement therapy after surgery in some cases Early identification of patients with excessive growths rates Early treatment for improved outcomes  ○ Emotional support, body image concerns, unusual in US early intervention prevents Diabetes Insipidus (DI) The principle disorder of the posterior pituitary Results from hyposecretion of ADH Produces uncontrolled diuresis Primary causes > familial or idiopathic Secondary causes > trauma, tumors, CNS, infection, aneurysm History of head injury, pituitary tumor, or craniotomy Clinical Manifestations of DI and TX Cardinal signs > polyuria and polydipsia First sign is often enuresis (involuntary urination) The urine is highly dilute with a low specific gravity. Loss of fluids leads to serum hyperosmolality and severe dehydration. Shock and death can occur if untreated Infants > irritability relieved with feedings of water but not milk, dehydration often occurs Instruct parents in difference between diabetes insipidus and diabetes mellitus Daily hormone replacement of vasopressin ○ Drug of choice = DDAVP ○ Nasal spray or IV administration ○ Requires treatment for life S/S > up to 20 L urine per day, lower specific gravity, hypovolemia, increased thirst, tachycardia, low BP, lower osmolarity Syndrome of Inappropriate Antidiuretic Hormone: SIADH Produced by hypersecretion of the posterior pituitary (increased ADH) S/S > fluid retention and hypotonicity (low sodium), anorexia, nausea/vomiting, irritability, personality changes Symptoms disappear when ADH is decreased Diagnosis > hyponatremia (serum sodium less than 135 mEq/L), hypotonicity (plasma osmolality less than 280 mOsm/kg), decreased urine volume, highly concentrated urine with a high sodium content Treatment ○ Accurate I and O ○ Observe for signs of fluid overload ○ Water restriction ○ Seizure precautions ○ Hypertonic saline in severe cases ○ Administer ADH-antagonizing meds Diabetes Insipidus vs SIADH Diabetes Insipidus SIADH High urinary output Low urinary output Low levels of ADH High levels of ADH  Hypernatremia Hyponatremia Dehydrated Over hydrated Lose too much fluid Retain too much fluid Both will present with excessive thirst Thyroid Function Thyroid hormone regulates Basal metabolic rate Thyroid secretes two types of hormones ○ Thyroid hormone, which is made up of Thyroxine (T4) Triiodothyronine (T3) May have hypothyroidism or hyperthyroidism May have disturbance in secretion of TSH Hypothyroidism Deficient thyroid hormones Acquired or congenital Congenital hypothyroidism occurs during fetal development and results in thyroid gland underdevelopment, insufficient synthesis of thyroid hormone, or problems with TSH secretion. In utero, maternal T4 crosses the placenta; therefore, the newborn appears unaffected at birth. If the child is untreated after birth, the lack of thyroid hormone production and secretion results in intellectual disability and impaired growth Acquired hypothyroidism can result from 1.) deficient thyroid hormone synthesis; 2.) destruction of the thyroid gland; or 3.) impaired TSH or TRH secretion Common causes of acquired hypothyroidism include autoimmunity, iodine deficiency, surgical removal or or radiation therapy to the thyroid gland, medications that destroy the thyroid gland, and genetic defects that affect the thyroid hormones. Hashimotos is an autoimmune cause more common in females Clinical Manifestations of Hypothyroidism Low metabolic rate Fatigue, cold intolerance, weakness, weight gain, constipation, impaired reproduction, impaired memory Myxedematous skin changes (swelling of the skin and underlying tissue) ○ Dry skin ○ Sparse hair ○ Periorbital edema S/S > hair loss, apathy, lethargy, dry skin, muscle aches/weakness, constipation, receding hairline, facial/eyelid edema, dull blank expression, extreme fatigue, thick tongue/slow speech, anorexia, brittle nails/hair ○ Late clinical manifestations > subnormal temperature, bradycardia, weight gain lowered level of consciousness, thickened skin, cardiac complications Hypothyroidism TX  Lifelong thyroid hormone replacement therapy is initiated and increased gradually until optimal hormone levels and clinical improvement are achieved. The most common drug used to treat hypothyroidism is levothyroxine (synthroid, levoxyl) Levothyroxine is a synthetic form of T4 Hyperthyroidism (Graves Disease) Common cause of hyperthyroidism is Graves disease ○ Enlarged thyroid gland and exophthalmos ○ Peak incidence 12-14 years age, but may be present at birth ○ Familial association Manifestations develop gradually, often over 6-12 months Diagnosis based on increased levels of T4 and T3 with suppressed TSH Hyperthyroidism Clinical Manifestations Excessive metabolic rate Weight loss, agitation, restlessness, sweating, heat intolerance, diarrhea, tachycardia, heart palpitations, tremors, fine hair, oily skin, irregular menstruation, weakness Goiter > enlargement of thyroid gland Exophthalmos (protrusion of the eyeballs) is also characteristic of Graves disease. This protrusion is usually bilateral and results from the interaction of TSH-sensitized antibodies interacting with fibroblast antigens found in extraocular muscles and tissues. The interaction results in lymphocyte infiltration, edema, and fibroblast accumulation, which displaces the eyeballs forward. Exophthalmos often persists despite treatment of hyperthyroidism T3, T4, TSH Triiodothyronine (T3), thyroxine (T4), thyroid stimulating hormone (TSH) PTU > given to those with graves disease to decrease thyroid hormone levels Synthroid > if TSH is high want to make sure T4 increases, also give if lacking T4 Pituitary issue > everything low T3 and T 4 high and TSH low > hyperthyroid give PTU Hypothyroid if T3 and T4 down, TSH elevated Types of Hormone Normal Ranges TSH 0.5 - 4.5 mIU/L Total T4 (TT4) 5.4 -11.5 mcg/dl Total T3 (TT3) 80 - 220 ng/dl Thyroid Crisis or Storm May occur from sudden release of hormone ○ Unusual in children but can be life threatening in adults May be precipitated by infection, surgery, or discontinuation of anti-thyroid therapy Treatment of thyroid storm ○ Antithyroid drugs ○ Propranolol Nursing Considerations Identify clients with hyper and hypothyroidism Be alert for signs and symptoms Client needs quiet environment, rest periods Help family cope with emotional lability associated with disorder Dietary requirements to meet client’s increased metabolic rate Medications > side effects Disorders of Adrenal Function Adrenal cortex secretes three groups of steroids ○ Glucocorticoids (cortisol, corticosterone) Regulates metabolism, inflammatory/immune response, and the stress response Increase in cortisol = increase blood sugar ○ Mineralocorticoids (aldosterone) Regulates sodium and potassium levels, regulates water balance and blood pressure ○ Sex steroids (androgens, estrogens, and progestins) Contribute to pubic and axillary hair growth; minimally affect sexual function Adrenal medulla secretes catecholamines: epinephrine and norepinephrine Altered levels of these produces significant dysfunction Catecholamine-secreting tumors are the primary of adrenal medullary hyperfunction (pheochromocytoma) Pheochromocytoma Adrenal tumor that secretes catecholamines Clients often have bilateral, multiple, benign tumors Increased production of catecholamines > may mimic other disorders Surgical removal of tumor (s) May require bilateral adrenalectomy and lifelong glucocorticoid and mineralocorticoid therapy Cushing Syndrome  A characteristic group of manifestations caused by excessive circulating free cortisol May be caused by excessive or prolonged steroid therapy Condition is reversible once steroids are discontinued Abrupt withdrawal of steroids may precipitate acute adrenal insufficiency Etiologies of Cushing Syndrome Long-term administration of corticosteroid medications (such as prednisone) Tumors of the pituitary gland that stimulate excess ACTH production Tumors of the adrenal gland that stimulate excess cortisol production Ectopic production ACTH or CRH from a tumor at a distant site, such as small cell carcinoma of the lung Diagnostic Evaluation Confirm excess cortisol levels X-rays: evaluate for osteoporosis and skull films to look for enlargement of sella turcica (bony depression in sphenoid bone) Laboratory tests ○ Fasting blood glucose ○ Serum electrolytes ○ 24 hr urine Cushing Syndrome Symptoms Excessive hair growth, red cheeks, weight gain and pendulous abdomen with red striae, poor wound healing, ecchymosis, moon face or buffalo hump Therapeutic management ○ Surgery or radiation ○ Replacement of growth hormone, ADH, TH, gonadotropins Acute Adrenocortical Insufficiency Adrenal crisis Diagnosis generally based on clinical symptoms Most serious endocrine disorder > hypotension, shock, death Autoimmune destruction of the layers of the adrenal cortex is the most common cause of the disease. Others result from adrenal gland granuloma, tumors, or drugs that block the synthesis of corticosteroids These conditions lead to the inability of the adrenal glands to produce any glucocorticoids, mineralocorticoids, or androgens. As a result, ACTH levels are elevated to increase the secretion of these three major steroid hormones from the adrenal glands. (excess melanin) Don't have the ability to fight or flight mode Chronic Adrenocortical Insufficiency: Addison Disease When it occurs, usually result of neoplasms or lesion of adrenal glands or idiopathic cause Symptoms appear gradually after 90% of adrenal tissue is nonfunctional Treatment: IV infusion of hydrocortisone then oral replacement of steroids following Deficient Hormones Clinical Manifestations Glucocorticoids Hypoglycemia, weakness, poor stress response, fatigue, anorexia, nausea, vomiting, weight loss, personality changes Mineralocorticoids Dehydration, hyponatremia, hyperkalemia, hypotension, weakness, fatigue, shock Androgens Sparse axillary and pubic hair Pancreatic Hormone Function Function of islets of langerhans  ○ Alpha cells produce glucagon ○ Beta cells produce insulin ○ Delta cells produce somatostatin (believed to regulate insulin and glucagon) ○ Insulin is needed for glucose uptake Decrease insulin secretion > lower blood glucose, increase alpha, high insulin Starvation Glucose is a major energy source for body tissues. In starvation, dietary glucose is unavailable for glucose-dependent tissues,such as the brain and muscle tissue. The body attempts to manufacture glucose in a process called gluconeogenesis by breaking down muscle proteins. The muscle then releases acidic byproducts, promoting metabolic acidosis Insulin is a hormone that promotes glucose production and uptake by cells and inhibits the use of fat stores for energy. If the body is to adapt to starvation effectively, insulin production must be suppressed to inhibit glucose uptake and gluconeogenesis, and another energy source must be used at a greater level than glucose This is accomplished through a compensatory increase in glucagon, cortisone, epinephrine, and growth hormone. These hormones all have anti-insulin effects and also stimulate enzymes on the adipocytes to release fatty acids for energy. The fatty acids travel to the liver and are converted to ketones. Ketones are the replacement energy source that allows sparing of muscle catabolism. The brain and other glucose-dependent tissues prefer glucose but will use ketones for energy as an adaptive response Diabetes Mellitus Type 1 Characterized by a total or partial deficiency of the hormone insulin Destruction of beta cells, usually leading to absolute insulin deficiency Typically, onset in childhood and adolescence, but can occur at any age Most DM of childhood is Type 1 Type 1 Type 2 The body does not make enough insulin The body cannot use insulin properly Insulin Dependent Insulin Resistant Usually ages 0-40 (mostly young children or Usually ages 40+ (mostly adults but occurring teens) in children and teens who are overweight and obese) Increased thirst/urination, weight loss, fatigue, Increased thirst/urination, weight loss, fatigue, fruity smelling breath, irritability, blurred blurred vision, slow healing sores or frequent vision, slow healing sores or frequent infections infections There is no way to prevent Type 1 Diabetes Most cases of Type 2 diabetes can be prevented Insulin injections, blood sugar checks, health Healthy eating/meal planning, increased  eating and meal planning, increased physical physical activity, oral medication, blood sugar activity checks, sometimes insulin injections Diabetes Mellitus Type 1 With a deficiency of insulin, glucose is unable to enter the cell, and remains in blood causing hyperglycemia When serum glucose exceeds renal threshold glucose spills into urine (glycosuria) Cells break down protein for conversion to glucose by the liver (glucogenesis) Type 1 DM believed to be autoimmune disease arising when a person with a genetic predisposition is exposed to a precipitating event such as viral infection Heredity is prominent factor in etiology High A1C > high blood sugar for long time DM Type 1: Ketoacidosis When glucose is unavailable for cellular metabolism, the body breaks down alternate sources of energy Ketones are released, and excess ketones are eliminated in urine (ketonuria) or by the lungs (acetone breath) Ketones in the blood are strong acids that lower serum pH and produce ketoacidosis Severe insulin deficiency, common complication of type 1 DM Characterized by hyperglycemia, metabolic acidosis, glucosuria, ketonuria, ketonemia Diabetic Ketoacidosis DKA Emergency situation Results from progressive deterioration with dehydration, electrolyte imbalance, acidosis, coma, and may cause death Treatment of DKA focuses on stabilizing blood glucose levels, correcting acidosis, replacing fluids and electrolytes, and improving tissue perfusion. These goals are accomplished through intravenous administration of insulin, fluid, and electrolyte solutions TX Type 1 DM Insulin therapy Glucose monitoring > goal range 80-120 mg/dl Urine testing for ketones ○ q3h during illness and whenever glucose is > 240 mg/dl when illness not present Nutrition, exercise Teach patient and family how to manage hypoglycemic episodes Illness management, management of DKA Kussmaul Respirations > Have with DKA Hyperventilation characteristics of metabolic acidosis, resulting from respiratory system’s attempt to eliminate excess CO2 by increased depth and rate Breath also has a sweet, fruity odor caused by the release of acetone, a volatile form of ketones Hypoglycemia A state of significantly low blood glucose that results in clinical manifestations, such as weakness, pallor, or cool/clammy skin  Most commonly found in individuals with type 1 diabetes who are undergoing insulin replacement therapy. Insulin replacement therapy requires the careful intake of adequate nutrients to match the injected insulin. Simple carbohydrates, such as that found in sugary foods like syrup, fruit juice, or honey, enter the blood and rapidly raise the blood sugar. This stimulates the rapid release of insulin. The insulin pulls this excess glucose into cells of the body and actually deprives the brain of glucose. Type 2 Diabetes Arises because of insulin resistance Onset usually after age 40 Native American, Hispanics, and African-American are at increased risk of type 2 DM Affected persons may or may not require insulin injections Symptoms are insidious and nonspecific. Potentially polydipsia, polyphagia, and polyuria may occur Usually related to long-term complications such as visual changes, changes in kidney function, coronary artery disease, peripheral vascular disease, recurrent infections, or neuropathy Metabolic Syndrome Metabolic syndrome is a condition that includes insulin resistance and a constellation of other metabolic problems, including obesity, high triglyceride levels, low high-density lipoprotein (HDL) levels, hypertension, and coronary heart disease Individuals diagnosed with type 2 diabetes must also be evaluated for metabolic syndrome to determine the full range of metabolic alterations Long-Term Complications of DM Microvascular complications, especially nephropathy and retinopathy Macrovascular disease, neuropathy Patient Education DM and Insulin Therapy Nature of disease Meal planning Insulin therapy > types of insulin, duration, onset and peak action, mixing and administration of types of insulin, rotation of injection sites Insulin pump therapy Glucose monitoring Recognition and treatment of hypoglycemia and hyperglycemia Management of minor illnesses Record keeping Hygiene, family support, acute care Khan Academy Videos Hormones = chemical messengers > communicate through body > wireless go into bloodstream and work on body without directly connecting ○ Endocrine >far distance ○ Paracrine > regionally ○ Autocrine > small distance in one cell or next Pituitary gland > master gland ○ Has an effect on thyroid > metabolism (T3 and T4) ○ TSH > acts on thyroid gland > stimulates gland to make thyroid hormone > regulate metabolism ○ Hyperthyroidism > fast metabolism ○ Hypothyroidism > slow metabolism ○ ACTH > acts on adrenal cortex, sit above kidney, make cortisol which regulates glucose metabolism, maintain BP, aldosterone ○ LH, FSH > act on gonads (ovaries,testes) sperm/egg production, testosterone ○ GH > optimal growth of long bones ○ Prolactin > lactation, breast feed Hypothalamus/ posterior pituitary > ADH and Oxytocin Adrenal gland ○ Cortex > steroids are made > cortisol and aldosterone ○ Medulla > catecholamine (epi,Nepi) Pancreas > blood sugar (insulin, glucagon)