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Ednocrine Disorders

Endocrine Disorders by Lucy

Definition of Diabetes A chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, and or both.
Diabetes can contribute to... Leading cause: End stage renal disease, adult blindness, non-traumatic lower limb amputations.Major contributing factor:Heart disease & Stroke.
Acute Complications of Diabetes Diabetic ketoacidosis (DKA), Hyperosmolar hyperglycemic syndrome (HHS), Hypoglycemia.
Diabetic Ketoacidosis (DKA) Caused by profound deficiency of insulin. Characterized by:Hyperglycemia, Ketosis, Acidosis, and dehydration. Most likely occurs in type 1.
Precipitating Factors (DKA) Illness, infection, inadequate insulin dosage, undiagnosed type 1 poor self-management, and neglect.
When Supply of Insulin is insufficient in DKA Glucose cannot be properly used for energy body breaks down fats stores. Ketones are by-products of fat metabolism.Alters pH balance, causing metabolic acidosis, ketone bodies excreted in urine, and electrolytes become depleted.
S & Sx DKA Abdominal pain, N/V, Kussmaul respirations, rapid deep breathing, attempt to reverse metabolic acidosis, and sweet fruity odor.
DKA (cont'd) Serious condition and must be treated promptly. Depending on S % Sx may or may not need hospitalization.
Laboratory Findings for DKA Blood glucose >300 mg/dl Arterial blood pH <7.30 Serum bicarbonate level <15 mEq/L Ketones in blood and urine
Airway Management for DKA Oxygen administration
Correct Fluid/Electrolyte Imbalance in DKA IV infusion of 0.45% or 0.9% naCl, restore urine output, raise blood pressure. When blood glucose levels approach 150 mg/dl-5% dextrose added to regimen, prevent hypoglycemia. Potassium replacement, Sodium bicarbonate if pH <7.
Insulin Therapy and DKA Withheld until fluid resuscitation has begun. Bolus followed by insulin drip.
Hyperosmolar hyperglycemic syndrome (HHS) Life-threatening syndrome, less common than DKA, Increased serum osmolality.often occurs in patients over 60 years of age with type 2.
HHS Patients has enough circulating insulin so ketoacidosis does not occur. Produces fewer symptoms in earlier stages, Neurologic manifestations occur due to
Usually History of HHS Inadequate fluid intake. Increasing mental depression. Polyuria.
Laboratory values for HHS Blood glucose >400 mg/dl Increase in serum osmolality Absent/minimal ketone bodies
HHS (cont'd) Medical emergency. High mortality rate. Therapy similar to DKA - except HHS required greater fluid replacement.
Nursing Management DKA/HHS Patient closely monitored. Administration:IV fluids,insulin therapy,& electrolytes. Assessment:renal status,cardiopulmonary status,& level of consciousness. Signs of potassium imbalance,cardiac monitoring,& vital signs.
Hypoglycemia Low blood glucose. Occurs when: too much insulin in proportion to glucose in the blood blood glucose level less than 70 mg/dl
Common Manifestations of Hypoglycemia Confusion, irritability, diaphoresis, tremors, hunger, weakness, visual disturbances, & can mimic alcohol intoxication. Untreated can progress to loss of consciousness, seizures, coma, & death.
Hypoglycemic unawareness Person does not experience warning signs/symptoms, increasing risk for decreased blood glucose levels. Related to autonomic neuropathy.
Causes of Hypoglycemia Mismatch in timing. Food intake and peak action of insulin or oral hypoglycemic agents.
First Sign of Hypoglycemia Check blood glucose: If <70 mg/dl begin treatment. If >70 mg/dl investigate further for cause of signs/symptoms. If monitoring equipment not available, treatment should be initiated.
Treatment for Hypoglycemia If alert enough to swallow:15-20 g of a simple carbohydrate (4-6 oz fruit juice, regular soft drink). Avoid foods with fat:decreases absorption of sugar.
Interventions after Initial Treatment for Hypoglycemia Do not overtreat. Recheck blood sugar 15 min. after treatment. Repeat until blood sugar >70mg/dl. Patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia. Check blood sugar again 45 min. after treatment.
Patient is still Hypoglycemic after treatment Administer 1 mg of Glucagon IM or subQ (side effect:rebound hypoglycemia). In acute care settings: 20 to 50 ml of 50% dextrose IV push.
Angiopathy: Macrovascular Diseases of large and medium sized blood vessels. Occur with greater frequency and with an earlier onset in diabetes. Development promoted by altered lipid metabolism common to diabetes. Tight glucose control may delay athersclerotic process.
Risk Factors for Angiopathy Obesity, smoking, hypertension, high-fat intake, sedentary lifestyle. Patients with diabetes should be screened for dyslipidemia at diagnosis.
Areas most Noticeably affected by Angiopathy Eyes (retinopathy), kidneys (nephropathy), & skin (dermopathy).
clinical Manifestations in Angiopathy Usually appear after 10 to 20 years of diabetes.
What is Diabetic Retinopathy Microvascular damage to retina. Result of chronic hyperglycemia. Most common cause of new cases of blindness in people 20-74 years of age. Nonproliferative versus proliferative.
Nonproliferative Diabetic Retinopathy Most common form. Partial occlusion of small blood vessels in retina causes development and microaneurysms. Capillary fluid leaks out. Retinal edema and eventually hard exudates are intraretinal hemorrhages occur.
Proliferative Diabetic Retinopathy Most severe form. Involves retina and vitreous. When retinal capillaries become occluded body forms new blood vessels. Vessels are extremely fragile and hemorrhage easily produce vitreous contraction. Retinal detachment can occur.
Photocoaglution Treatment for Diabetic Retinopathy Most common. Laser destroys ischemic areas of retina and prevents further visual loss.
Cryotherapy Treatment for Diabetic Retinopathy used to treat peripheral areas of retina. Probe creates frozen area until reaches specific point on retina.
Vitrectomy Treatment for Diabetic Retinopathy Aspiration of blood, membrane, fibers from inside through small incision. Used when: Vitreal hemorrhage does not clear in 6 mos. Threatened or actual retinal detachment.
Diabetic Nephropathy Associated with damage to small blood vessels that supply the glomeruli of the kidney. Leading cause of end-stage renal disease.
Critical Factors for Prevention/delay of Diabetic nephropathy Tight glucose control. Blood pressure management. Angiotensin-converting enzyme (ACE) inhibitors. Used even when not hypertensive. Angiotensin II receptor antagonists.
Yearly Screening for Diabetic Nephropathy Microalbuminuria in urine. Serum creatinine.
Diabetic Neuropathy 60%-70% of patients with diabetes have some degree of neuropathy. Nerve damage due to metabolic derangements of diabetes. Sensory versus autonomic neuropathy.
Sensory Neuropathy Distal symmetric,most common form,affects hands &/or feet bilat,characteristics:loss/abnormal sensations,pain,& paresthesias.Worse at night.Foot injury & ulcerations w/out having pain.Can cause atrophy of small muscles of hands/feet.
Treatment for Sensory Neuropathy Tight blood glucose control. Drug therapy: topical creams, tricyclic antidepressants, selective serotonin and norepinephrine reuptake inhibitors, and antiseizure medications.
Autonomic Diabetic Neuropathy Can affect nearly all body systems. Complications: gastroparesis (delayed gastric emptying), cardiovascular abnormalities, sexual function, and neurogenic bladder.
Food Complications with Diabetic Neuropathy Most common cause of hospitalization in diabetes. Result from combination of microvascular and macrovascular diseases.
Risk Factors for Feet and Lower extremities with Diabetic Neuropathy Sensory Neuropathy, peripheral arterial disease, smoking, clotting abnormalities, impaired immune function, autonomic neuropathy.
Acathosis Nigricans Dark, coarse, thickened skin.
Necrobiosis Lipidoidica Diabeticorum Associated with type 1. Red-yellow lesions. Skin becomes shiny, revealing tiny blood vessels.
Granuloma annulare Associated mainly with type 1. Forms partial rings of papules.
Infection Related to Diabetic Neuropathy Diabetics more susceptible to infections.Defect in mobilization of inflammatory cells.Impairment of phagocytosis by neutrophils and monocytes. loss of sensation may delay detection.Treatment must be prompt and vigorous.
Cushing Syndrome Caused by excess of corticosteroids, particularly glucocorticoids.Most common cause-iatrogenic administration of exogenous corticosteroids.85%of enodgenous cases due to ACTH secreting pituitary tumor.
Glucocorticoids Regulate metabolism and increase blood glucose. critical to physiologic stress response.
Mineralocorticoids Regulate Sodium balance and potassium balance.
Androgen Contributes Growth and development in both genders. Sexual activity in adult women.
Clinical Manifestation of Cushing Syndrome Related to excess corticosteroids. Weight gain most common feature: trunk (centripetal obesity), face ("moon face"), cervical area, transient weight gain from sodium and water retention.
hyperglycemia in Cushing Syndrome Glucose intolerance associated with cortisol-induced insulin resistance. Increased gluconeogenesis by liver.
Protein Wasting in Cushing Syndrome Catabolic effects of cortisol. Leads to weakness, especially in extremities. Protein loss in bones leads to osteoporosis, bone and back pain.
Clinical Manifestations of Cushing Syndrome Loss of collagen, wound healing delayed, mood disturbances, insomnia, irrationality, psychosis, and purplish red striae on abdomen, breast, or buttocks.
Mineralocorticoid Excess May cause hypertension secondary to fluid retention.
Adrenal Androgen Excess May cause pronounced acne, virilization in women, and feminization in men.
Diagnostic Studies for Cushing Syndrome 24-hour urine for free cortisol-levels of 50-100 mcg/day in adults indicates Cushing Syndrome. High-dose dexamethasone suppression test used for borderline results of 24-hour urine cortisol.False positive can occur with depression, stress, or alcoholism.
Diagnostic Studies for Cushing Syndrome Cont'd. Plasma cortisol levels may be elevated with loss of diurnal variation.CT & MRI of pituitary & adrenal glands.Hypokalemia and alkalosis are seen in ectopic ACTH syndrome and adrenal carcinoma. Plasma ACTH may be low,normal,or elevated depending on problem.
Diagnostic Studies for Cushing Syndrome Cont'd. High or normal ACTH levels indicate ACTH-dependent Cushing's disease. Low or undetectable ACTH levels indicate an adrenal or exogenous etiology.
Collaborative Care for Cushing Syndrome Primary goal is to normalize hormone secretion. Treatment depends on cause.
Treatment for Pituitary Adenoma Surgical removal of tumor and/or radiation.
Treatment for Adrenal Tumors or Hyperplasia Adrenalectomy
Treatment for Ectopic ACTH-secreting Tumors Managed by treating primary neoplasm.
Drug Therapy for Cushing Syndrome Goal of drug therapy is inhibition of adrenal function.
Mitotane Suppresses cortisol production. Alters peripheral metabolism of cortisol. Decreased plasma and urine corticosteroid levels.
Metyrapone, Ketoconazole, and Aminoglutethimide Inhibit cortisol synthesis. Common side effects of drug therapy: anorexia, nausea and vomiting, GI bleeding.
Common Side Effects of Drug Therapy Depression, Vertigo, Skin rashes, and Diplopia (double vision).
Nursing Diagnoses for Cushing Syndrome Risk for infection, Imbalanced nutrition related to decreased appetite, Disturbed self-esteem related to altered body image, and Impaired skin integrity.
Patient Goals for Cushing Syndrome Experience relief of symptoms. Have no serious complications. Maintain positive self-image. Actively participate in therapeutic plan.
Acute Intervention for Cushing Syndrome S&Sx of hormone and drug toxicity. Complicating conditions:Cardiovascular disease,diabetes militus,infection.Monitor:VS, daily weight,glucose,infection,S&Sx of abnormal thromboembolic phenomena.
Preoperative Care for Cushing Syndrome Control hypertension and hyperglycemia. High-protein diet helps correct protein depletion. Teaching depends on surgical approach.
Postoperative Care for Cushing Syndrome Risk of hemorrhage because of high vascularity of adrenal glands. Manipulation of glandular tissue may release hormones into circulation.BP,fluid balance,and electrolyte levels can be unstable because of hormone fluctuations.high doses of corticosteriods
Expected Outcomes For Cushing Syndrome Experience no S&Sx of infection. Attain weight appropriate for height. Increase acceptance of appearance. Maintain intact skin.
Addison's Disease Adrenocortical insufficiency.All 3 classes of adrenal corticosteriods are decreased:Glucocorticoids, mineralcoriticoids, androgens.Susceptibility genes have been identified. Other endocrine conditions often found.
Other Causes of Addison's Disease TB(rare in North America),infaction, fungal infection, infarction, AIDS, Metastatic cancer, Iatrogenic Addison's disease may be due to adrenal hemorrhage.
Addison's Disease Occurs in... Most often occurs in adults <60 years of age. Affects both genders equally. More common in white females if from autoimmune response.
Clinical Manifestations in Addison's Disease Does not become evident until 90% of adrenal cortex is destroyed. Disease usually advanced before diagnosis.
Primary Features of Addison's Disease Progressive weakness, Fatigue, Weight loss, Anorexia, and skin hyperpigmentation.
Hyperpigmentation in Addison's Disease In areas exposed to sun. At pressure points. Over joints, and In skin creases, especially palmar creases.
Clinical Manifestations of Addison's Disease Orthostatic hypotension, Hyponatremia, Hyperkalemia, nausea and vomiting and Diarrhea.
Addisonian Crisis caused by... Insufficient adrenocortical hormones. Sudden, sharp decrease in these hormones.
Addisonian Crisis Triggered by... Stress from infection, surgery, trauma, hemorrhage, psychological distress. Sudden withdrawal of corticosteroid replacement therapy.
Severe manifestations of Glucocorticosteroid and Mineralocorticoid Deficiencies Hypotension, Tachycardia, Dehydration, and Hyponatermia.
Manifestations of Addison's Disease hyperkalemia, hypoglycemia, fever, weakness, and confusion.
Complications of Addison's Disease Hypotension can lead to shock. Circulatory collapse is often unresponsive to usual treatment. GI manifestations include severe vomiting, diarrhea, and abdomen pain. Pain in lower back or legs.
Diagnostic Studies for Addison's Disease Abnormal laboratory findings: Hyperkalemia, Hypochloremia, Hyponatremia, hypoglycemia, Anemia, increased BUN, and Low urine cortisol levels.
Collaborative Care for Addison's Disease Hydrocortison: Most commonly used as replacement therapy. Treatment directed at: Shock management. high-dose hydrocortisone replacement. Large volumes of 0.9% and 5%dextrose administered to reverse hypotension and electrolyte imbalances until BP is normal
Nursing Implementation for Addison's Disease Frequent assessment. Assess VS and signs of fluid & Electroylyte imbalances every 30 min. to 4 hrs. for first 24 hrs. Take daily weights.
Acute Intervention for Addison's Disease Protect against infection. Assist with daily hygiene. Protect from extremes-light, noise, and temp. Discharge occurs before maintenance dose reached. Instruct on importance of follow-up appointments.
Ambulatory and Home Care for Addison's Disease Glucocorticoids usually given in divided doses. Mineralocorticoids given once in the morning (reflects normal circadian rhythm). Long-term care includes need for extra medication, stress management.
Interventions for Addison's Disease Teach S&Sx of corticosteroid deficiency and excess. Always wear medical alert bracelet. Provide handouts on drugs causing increase need for glucocorticoids. Instruct on how to take BP. Carry emergency kit with IM hydrocortisone.
Effects of Corticosteroid Therapy Long-term use of corticosteroids can lead to complications and side effects. Potential benefits must be weighed against risks. Should be taken in the morning w/food. Must not be stopped abruptly. Assess for corticosteroid-induced osteoporosis.
Hyperaldosteronism Excessive aldosterone secretion-sodium retention, potassium, & hydrogen ion excretion.
Hallmark of Hyperaldosteroinism Hypertension with hypokalemic alkalosis.
Primary hyperaldosteronism Usually caused by adrenocortical adenoma.
Secondary hyperaldosteronism due to renal artery stenosis, renin-secreting tumors, and chronic kidney disease.
Elevated Levels of Adosterone sodium retention and elimination of potassium.
Sodium Retention Leads to... Hypernatermia, Hypertension, and headache.
elimination Potassium leads to.... Hypokalemia, muscle weakness, fatigue, cardiac dysrhythmias, glucose intolerance, metabolic alkalosis, and may lead to tetany.
Diagnostic Studies for Hyperaldosteronism Primary aldosteronism: increased plasma aldosterone levels, increased sodium levels, decreased potassium levels, decreased renin activity. adenomas are localized by CT or MRI.
Treatment for Hyperalodosteronism Preferred treatment of primary hyperaldosteronism is surgical removal of the adenoma.
Before surgery Patients need... Low-sodium diet. Potassium-sparing diuretics. antihypertensive agents. Assess: BP and Fluid/electrolyte balances.
Pheocromocytoma Caused by tumor of the adrenal medulla. Produces excessive catecholamines. Mostly in young to middle-aged adults. Results in severe hypertension. If untreated:diabetes millitus, cardiomyopathy, and death.
Clinical Manifestations of Pheochromocytoma Severe episodic hypertension, severe pounding headache, Tachycardia with palpitations. Profuse sweating. Abdominal or chest pain.
Diagnostic Studies Best test is measurement of urinary fractionated metanephrines and catecholamines in 24-hour collection. Plasma catecholamines are elevated. CT and MRI used for tumor localization.
Treatment for Pheochromocytoma Surgical removal of tumor. Calcium channel blockers control BP. Sympathetic blocking agents may:decrease BP and Decrease symptoms of catecholamine excess. Beta blockers to decrease dysrhythmias. Monitor BP. Monitor glucose.
Hyperthyroidism Is hyperactivity of the thyroid gland with sustained increase in synthesis and release of thyroid hormones.
Thyrotoxicosis Refers to the physiologic effects or clinical syndrome of hypermetabolism that results from excess circulating levels of T4, T3, or both.
Grave's disease Is an autoimmune disease of unknown etiology marked by diffuse thyroid enlargement and excessive thyroid hormone secretion.
Clinical Manifestations of Grave's Disease Toxic Nodular Goiters-are thyroid hormone-secreting nodules that function independent of TSH stimulation. Exophthalmos-a protrusion of the eye-balls from the orbits.
Drug Therapy for Grave's Disease The first-line antithyroid drugs are propylthiouracil(PTU) and methimazole (Tapazole). These drugs inhibit the synthesis of thyroid hormones. PTU also blocks peripheral conversion of T4 to T3.
Diagnostic Studies for Hyperthyroidism The two primary laboratory findings used to confirm the diagnosis of hyperthyrooidism are decreased TSH levels and elevated free thyroxine (free T4) levels. The RAIU test is used to differentiate Graves' disease from other forms of thyroiditis.
Hypothyroidism Results from insufficient circulating thyroid hormone as a result of a variety of abnormalities. Can be r/t destruction of thyroid tissue or defective hormone synthesis or to pituitary disease with decreased TSH secretion of hypothalamic dysfunction.
Cretinism Hypothyroidism that develops in infancy and is caused by thyroid hormone deficiencies during fetal or early neonatal life.
Myxedema The accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues. The mucinous edema causes puffiness, periorbital edema, and masklike affect.
Diagnostic Studies for Hypothyroidism The most common and reliable laboratory tests are those that measure TSH and free T4. These values correlated with symptoms gathered from the history and physical examination, confirm the diagnosis.
Collaborative Care with Hypothyroidism Thyroid hormone replacement. Monitor thyroid hormone levels and adjust dosage. Nutritional therapy to promote weight loss.
Created by: tiniekittie12