Endocrine Conditions Student Notes PDF

Endocrine Conditions Objectives 1. Differentiate between the disorders caused by hypopituitary and hyperpituitary dysfunction. 2. Describe the manifestations of thyroid hypofunction and hyperfunction and the care of children with the disorders. 3. Distinguish between the manif...

Endocrine Conditions Objectives 1. Differentiate between the disorders caused by hypopituitary and hyperpituitary dysfunction. 2. Describe the manifestations of thyroid hypofunction and hyperfunction and the care of children with the disorders. 3. Distinguish between the manifestations of adrenal hypofunction and hyperfunction. 4. Differentiate among the various categories of diabetes mellitus. 5. Discuss care of the child with diabetes mellitus in the acute care setting. 6. Distinguish between a hypoglycemic and a hyperglycemic reaction. 7. Design a teaching plan for a child and family with diabetes mellitus. Fig. 51.1 Principal anterior and posterior pituitary hormones and their target organs.  May be due to organic defects or idiopathic Disorders etiology of Single hormonal or a combination Pituitary Clinical manifestations depend on the Function hormone(s) involved Symptoms may be related to overproduction or underproduction Panhypopituitarism 4 Hypopituitarism  Diminished or deficient secretion of pituitary hormones  Inhibits somatic growth and development of secondary sex characteristics  Consequences: Depend upon the degree of dysfunction  Gonadotropin deficiency  Growth hormone (GH) deficiency  Thyroid-stimulating hormone (TSH) deficiency  Corticotropin deficiency Hypopituitarism  Clinical manifestations  Slowed growth curve after first year  Appear overweight due to stunted height  Delayed sexual development  Diagnostic evaluation  Various diagnostic methods (skeletal surveys)  Growth patterns and previous health status Hypopituitarism 7  Treatmentis directed toward correction of the underlying disease process  Replacement with GH is successful in 80% of affected children.  Thedecision to stop GH therapy is made jointly by the child, family, and health care team. – Criteria: growth rate of less than 2.5 cm/year, decision that patient is tall enough, and a bone age of 14 for girls and 16 for boys  Pituitary Hyperfunction 8 Gigantism Acromegaly   Excess GH after epiphyseal Excess GH before closure of epiphyseal shafts results in closure overgrowth of long bones.  Typical facial features include  overgrowth of the following: Results in heights of 2.4 m or  Head more  Lips, tongue, jaw, nose  Vertical growth plus increased  Paranasal and mastoid sinuses muscles and viscera  Malocclusion of the teeth in the  Weight generally in proportion enlarged jaw to height  Increased facial hair, thickened, deeply creased skin Precocious Puberty Traditionally defined as sexual development before age 9 in boys or before age 8 in girls Occurs more frequently in girls Potential causes—see Box 51.4  Central precocious puberty  80% of children with this disorder  Peripheral precocious puberty  Premature development of breasts (thelarche), sexual hair (pubarche), and menses (menarche) Precocious Puberty  Therapeutic management  Treatment of specific cause, when known  May be treated with leuprolide acetate  Slows prepubertal growth to normal rates Treatment is discontinued at age for normal pubertal changes to resume  Nursing care  Psychological support for child and family  Diabetes Insipidus (DI)  Primary causes: familial (idiopathic)  Secondary causes: trauma, tumours, central nervous system (CNS) infection, granulomatous disease, vascular abnormalities  Therapeutic management  Daily hormone replacement of intranasal, oral or parenteral desmopressin (DDAVP)  Nursing care  Family education that treatment is lifelong (primary)  DI is different from diabetes mellitus (DM)  Older children assume responsibility for their own injections  Medical alert bracelet Syndrome of Inappropriate Antidiuretic Hormone (SIADH)  Fluid retention and hypotonicity  Anorexia, nausea and vomiting, stomach cramps, irritability, personality changes  Nursing care  Child is on fluid restriction so ensure accurate intake and output (I&O), measure daily weight  Observe for signs of fluid overload  Seizure precautions  Administer ADH-antagonizing medications  Child and family education Disorders of Thyroid Function  Thyroid secretes two types of hormones:  TH which is made up of Thyroxin (T4) Triiodothyronine (T3)  Calcitonin  May have hypothyroidism or hyperthyroidism  Mayhave disturbance in secretion of thyroid-stimulating hormone (TSH) or thyrotropin-releasing factor (TRF) Juvenile Hypothyroidism  Congenital or acquired  Can occur when dietary iodine is deficient  Presenting symptoms are decelerated growth  Other manifestations include: myxedematous skin changes (dry skin, puffiness around the eyes, sparse hair), constipation, sleepiness, and mental decline  Therapeutic management  Oral TH replacement  Nursing care  Importance of adherence to treatment  Periodic monitoring of response to therapy  Goitre  Hypertrophy of the thyroid gland  May occur with hypothyroid, hyperthyroid, or euthyroid TH secretion  Congenital or acquired  Therapeutic management  Thyroid enlargement at birth may compromise the newborn’s airway. Supplemental oxygen, tracheostomy set available Hyperextension of neck may facilitate breathing  Large goitres may be obvious; smaller nodules are evident only on palpation Lymphocytic Thyroiditis 16  Hashimoto disease, juvenile autoimmune thyroiditis  Most common thyroid dx in children  Mostly 6yrs or older  May be hypo/eu/hyperthyroid  Enlarged thyroid (goitre)  Hyperthyroidism (Graves’  Disease) The most common cause of hyperthyroidism in childhood is Graves’ disease.  Diagnostic evaluation  Therapeutic management  Goal of therapy: to slow rate of hormone secretion  Antithyroid medications, surgery, ablation (radioactive iodine) -> often results in secondary hypothyroidism  Thyrotoxicosis (thyroid crisis or thyroid storm)  Nursing care Hypoparathyroidism  May be caused by a specific defect in the synthesis of PTH  May also occur secondary to other causes  Infection, autoimmune syndromes  Postoperatively after thyroidectomy  Present in the newborn due to  Maternal diabetes mellitus (DM)  Formula with high phosphate-to-calcium ratio  Clinical manifestations  Therapeutic management  Nursing care  Monitor renal function, blood pressure, serum vitamin D levels  Maintain seizure and safety precautions  Monitor for laryngospasm Hyperparathyroidism  Primary: adenoma of the gland  Secondary: chronic renal disease, renal osteodystrophy, congenital anomalies of urinary tract  Common factor is hypercalcemia  Clinical signs  Diagnostic evaluation  Therapeutic management  Depends on cause  Nursing care Disorders of Adrenal Function  Theadrenal cortex secretes three groups of “steroids”:  Glucocorticoids (cortisol, corticosterone)  Mineralocorticoids (aldosterone)  Sex steroids (androgens, estrogens, and progestins)  Altered levels of these produce significant dysfunction. Acute Adrenocortical Insufficiency  Adrenal crisis  Diagnosis is generally based on clinical symptoms.  Early clinical symptoms  Increased irritability, headache, weakness  Abdominal pain, nausea, vomiting, diarrhea  Box 51.9  Diagnostic evaluation  Treatment with cortisol confirms the diagnosis  Therapeutic management  Nursing care Chronic Adrenocortical Insufficiency (Addison's Disease)  Usuallyresult of infections, destructive lesions of the adrenal gland or neoplasms, autoimmune processes, or idiopathic.  Box 51.10  Therapeutic management  Oralsupplements of glucocorticoids (cortisol) and mineralocorticoids (aldosterone)  Nursing care  Parental guidance and education Cushing Syndrome A characteristic group of manifestations caused by excessive circulating free cortisol  Clinical manifestations  Diagnostic evaluation  Therapeutic management  Surgery  Replacement of GH, ADH, thyroid extract, gonadotropins, and steroids  Nursing care Congenital Adrenal Hyperplasia (CAH)  Disorders caused by decreased enzyme activity required for cortisol production in the adrenal cortex which results in overproduction of adrenal androgens  Results in virilization of the female fetus  Varying degrees of ambiguous genitalia  Salt-wasting crisis frequently occurs  Diagnosis based on congenital abnormalities  Newborn screening in many provinces Congenital Adrenal Hyperplasia (CAH)  Therapeutic management  Administration of glucocorticoids  Gender assignment is complex and controversial – requires support from interdisciplinary team  Reconstructive surgery may be required.  Not all children are diagnosed at birth.  Nursing care  Education and support for family  Disorders of Pancreatic Hormone Secretion  Diabetes mellitus (DM)  Characterizedby a total or partial deficiency of the hormone insulin  Diabetes type 1 – body does not produce insulin  Diabetes type 2 – body does not produce enough insulin or cannot process it  Endocrine Case Study 27 You are caring for an 8 year-old girl with newly diagnosed type 1 diabetes. She is the youngest child in her family with two older brothers, aged 12 and 14 years. She is in grade 3 and active in school and extracurricular sports. Her parents work full-time. She has felt unwell for the last 2-3 weeks and her outpatient bloodwork meets criteria for diagnosis of diabetes. 1. What signs and symptoms are common preceding diagnosis of type 2 diabetes? 2. What are the lab tests and thresholds to diagnose diabetes mellitus? What are considerations for testing and diagnosis in children? 3. What topics can you anticipate will be important for family health teaching? How will you prioritize these topics? 4. What considerations should be included in nutritional planning and teaching? 5. What is ketoacidosis? What factors may precipitate DKA? What is the most critical complication? 6. Identify and explain two ways to monitor the effectiveness of insulin therapy? 7. What are the long-term complications associated with diabetes mellitus?  Diabetes 28 Ketoacidosis Kussmaul's Respirations  Body breaks down alternate  Hyperventilation characteristic of sources of energy metabolic acidosis, respiratory system  eliminating excess CO2 by increased Ketones are released, and excess ketones are eliminated in urine depth and rate (ketonuria) or by the lungs (acetone breath) Diabetic Ketoacidosis (DKA)  Ketones in the blood are strong  progressive deterioration with acids that lower serum pH and dehydration, electrolyte imbalance, produce ketoacidosis acidosis, coma, may cause death  Therapeutic Management 29  Insulin therapy Long-Term Complications  Insulin preparations  Microvascular complications,  Dosage and methods of especially nephropathy, administration neuropathy, and retinopathy  Monitoring  Macrovascular disease  Glucose monitoring; goal near-  With poor control, vascular normal range of 4.4 to 6.6 mmol/L changes as early as 2.5 to 3  Measurement of hemoglobulin A1c years after diagnosis levels  With excellent control, can be  Urine delayed 20 years  Other: nutrition, exercise, hypoglycemia, hyperglycemia Diabetes Mellitus Type 2  Arises due to insulin resistance  Risk factors include: obesity, ethnicity, genetics  Screening and diagnostic evaluation  Therapeutic management  Risk reduction for type 2 diabetes