- Pathophysiology: most common cause is tumor. A deficiency in GH that inhibits somatic growth. The primary site od dysfunction seems to be the hypothalmus. There is a family history, with change in growth pattern, definitive diagnosis based on Radioimmunoassay of plasma GH levels
- Clinical Manifestations: headaches, visual changes (dec. peripheral and acuity), anosmia (loss of sense of smell, and seizures. Menstrual irregularities, diminished libido, and changes in secondary sex characteristics. Truncal obesity, decreased muscle mass, decreased energy, and reduced exercise capability, flat affect or appear depressed.
- Therapeutic & Nursing Management: Biosynthetic Growth hormone injections and other hormone replacements as needed. Nurses need to evaluate effectiveness of therapy while providing patient and family with teaching, provide support and prepare child for daily injections. As well as monitor for Creutzfeldt Jakob Disease (rare neurodegenerative condition report in some patients after receiving GH from a cadaver donor)
- Pathophysiology: Graves - autoimmune disease of unknown etiology, there is excessive thyroid hormone secretion. Some precipitating factors include insufficient iodine supply, infection, or stressful life events.
Toxic Nodular Goiters - thyroid secreting nodules that function independent of TSH, they are toxic if associated with hyperthyroidism, they can be present but body compensates for their release of thyroid hormones.
- Clinical Manifestations: increased metabolism, tissue sensitivity to stimulation, and cardiac output, exophthalmos (protusion of eyeballs from orbits), A-fib, Bruit over thyroid gland, Heat Intolerance, elevated basal temperature, may lead to Thyrotoxic crisis
- Therapeutic & Nursing Management: Antithyroid meds, radioactive iodine therapy, subtotal thyroidectomy.
- Pathophysiology: Result from insufficient circulating thyroid hormones, which may be caused by a number of abnormalities, but rarely from insufficient diet in the US. May be primary or secondary: Primary: results from destruction of thyroid tissue or defective hormone synthesis, while Secondary: is related to pituitary disease which causes a decrease in TSH secretion or hypothalamic dysfunction. Can also be due to discontinuation of thyroid hormone therapy.
- Clinical Manifestations: Vary depending on severity, duration, and age of onset. Characterized by slowing of body processes, decreased cardiac out put, contractility, decreased GI motility, Cold Intolerance, myxedema (periorbital edema, puffiness, masklike effect, prominent tongue causing slurred speech)
- Therapeutic & Nursing Management: restoration of euthyroid state as safely and rapidly as possible, low calorie diet, drug therapy, patient/family teaching, screen high risk populations (family history, hx of neck radiation, women over 50, and postpartum)
- Pathophysiology: condition involving an increased secretion of PTH which helps regulate calcium and phosphate levels. The over secretion of PTH is divided into three categories: Primary: due to increased secretion of PTH leading to disorders of calcium, phosphate, and bone metabolism, most commonly due to benign tumor. Secondary: is a compensatory response to conditons causing hypocalcemia such as Vit. D deficiencies, malabsorption, chronic renal failure, etc. Tertiary: occurs when there is hyperplasia of the parathyroid glands and a loss of negative feedback from circulating calcium levels.
- Clinical Manifestations: may be asymptomatic, or overt symptoms. Clinical manifestation are those associated with hypercalcemia like constipation, lethargy, weakness, increased need for sleep, emotional disorders, and shortened attention span.
- Therapeutic & Nursing Management: Main goal is the treatment of underlying cause and symptoms while preventing complications. Surgical intervention is the most effective treatment and is done with endoscope for removal of parathyroids. Nonsurgical therapy includes annual screenings, avoidance of immobilization and dieatary measures, etc. The nurse should monitor for fluid and electrolyte disturbances and tetany after operations. I&O, frequent VS, and measures to relieve symptoms.
- Pathophysiology: May be Autoimmune hypoparathyroidism: which is caused by a deficient production of PTH or Pseudohypoparathyroidism: due to production of PTH being increased but end organs are unresponsive to it, this is thought to be inherited as an X-linked dominant trait with variable expressivity.
- Clinical Manifestations: Dry, scaly skin with eruptions, brittle hair, thin nails with transverse grooves, Tetany, paresthesias, tingling, laryngeal stridor, Headache, seizures, emotional lability, depression, positive Chvostek's and/or Trousseau signs.
- Therapeutic & Nursing Management: Primary goal is to treat acute complications (tetany), and maintain normal serum calcium levels. Emergency treatment of tetany requires IV Calcium watch for extravasation at IV site.
- Pathophysiology: is the result of a lack of ACTH, with Glucocorticoids, mineralocorticoids, and androgens all being decreased. The common cause in industrialized countries is autoimmune response to adrenal tissue. Genetic have been discovered. Other causes include: TB, infarction, fungal infections, AIDS, metastatic cancer, iatrogenic Addison's disease may be due to renal hemorrhage. MOst common in adults <60 years, most common in white females if autoimmune, if not it is equal in both genders
- Clinical Manifestations: not evident until 90% of adrenal cortex is destroyed. Progressive weakness, fatigue, weight loss, anorexia, skin hyperpigmentation (in arease exposed to sun, pressure points, over joints, skin creases), Ortho Hypo,
- Pathophysiology: excessive aldosterone secretion (which causes sodium retention and potassium excretion), which may be caused by adrenal tumor or androgenital syndromes. Primary: is caused by adrenocortical adenoma, Secondary: is due to renal artery stenosis, renin secreting tumors and chronic kidney disease.
- Clinical Manifestations: Hallmark is hypertension with hypokalemic alkalosis. Sodium retention and thus water retention, hypernatremia, hypertension, headache, hypokalemia, weakness, fatigue, Cardiac dysrhythmias, glucose intolerance, could lead to tetany.
- Pathophysiology: Theories link the cause to single and combinations of factors that include; Genetics, autoimmune, viral, and environmental.
- Type 1: is normally the end result of a long standing process, like the progressive destruction of pancreatic B cells by autoantibodies.
- Type 2: is the most prevalent form of diabetes. It has a genetic basis with greater rates in African Americans, Asian Americans, Hispanic Americans, and Native Americans. (Native americans and Alaskans have highest rates in world). It occurs when pancreas still produces some insulin, but amount is either insufficient or poorly utilized. Obesity, Genetic mutations can cause this
- Type 1: Polyuria, polydipsia, polyphagia, sudden recent weight loss, There is a long preclinical time and people usually present to the ER with Diabetic Ketoacidosis.
- Type 2: Gradual onset with nonspecific symptoms, fatigue, recurrent infections and vaginal yeast or monilia infections, prolonged wound healing, visual changes.
- Acute Complications: Diabetic Ketoacidosis (profound deficiency of insulin, most likely with type 1 - remember to keep airway patent), Hypoglycemia (low blood glucose), and Hyperosmolar hyperglycemic syndrome (life-threatening, less common, medical emergency)
- Chronic Complications: Angiopathy (Macro and Microvascular disease that effects large and medium blood vessels as well as capillaries and arterioles), Retinopathy (damage to retina due to chroinc hyperglycemia, common cause of blindness in 20-74 yr olds), Nephropathy (leading cause of end stage renal disease), Infections, integumentary problems.
- A. Monitoring: testing is done normally with finger sticks and glucometer by the patients. Normally this is done before meals but may also be told to check before and after exercise to determine how it effects metabolic control.
- B. Medications: include several types of insulin (rapid acting, Short acting (regular, onset in 1/2 - 1 hour, peak 2-3 hours, duration 3-6 hours), Intermediate acting (NPH, onset 2-4 hours, Peak 4-10 hours, duration 10-16 hours), long acting (glargine, Onset 1-2 hours, no pronounced peak, duration 24+ hours). There are also oral agents that are used to help control diabetes.
- C. Diet: The goals of nutritional management of diabetes is to live as near a normal life as possible by preventing or reducing the risk of complications.
- D. Exercise: This can help the body naturally adjust and maintain a normal level of glucose. This will help increase insulin receptors and insulin production.
- This is the most challenging part of diabetes treatment for many patients. It must take into consideration the background of the patient, including ethnicity, cultures, religious beliefs, etc. The main goals of nutritional therapy are as follows:
· Maintain blood glucose levels to as near normal as safely possible to prevent or reduce the risk for complications of diabetes.
· Achieve lipid profiles and blood pressure levels that reduce the risk for cardiovascular disease
· Modify lifestyle as appropriate for the prevention and treatment of obesity, dyslipidemia, cardiovascular disease, and nephropathy.
· Improve health through healthy food choices and physical activity.
· Address individual nutritional needs while taking into account personal and cultural preferences and respecting the individual's willingness to change.
- Type 1: should be based on indifvidual's food intake and balaced with insuli and exercise patterns.
- Type 2: has an emphasis for nutrition therapy that achieve glucose, lipid, and blood pressure goals.
- Food Composition: should include 45-65% of total energy intake to come from carbohydrates and monounsaturated fats. Fats should compose no more than 25-30%, protein 10%, and alcohol should be avoided for providing no nutritional value but many claories