Trauma to the Endocrine Glands: Thyroid and Pancreas, Summaries of Nursing

Download Trauma to the Endocrine Glands: Thyroid and Pancreas and more Summaries Nursing in PDF only on Docsity! Endocrine Disorders Diagnosis and Management  Endocrine Disorders Pituitary Gland Hypothalamus Opuc Third chiasm ventricie —_ Pituitary gland Intundibulum Seva turcica of sphenoid bone Hypothalamic nerve cell Sosrericr ee Ss hs ituite rowth MS a Liou at § hormone (GH) Adrenecsorticotropic Adrenal hormone (ACTH) cortex Thyreida- mali AS hormone (FSH) Gonadotropic i. Hormones (FSH and Le) Ovary  Pituitary gland (hypophysis) - Master gland - Sella turcica of sphenoid bone - lobes: a. Anterior (adenohypophysis) b. Posterior (neurohypophysis) P R I Y T U I T A D I S O R D E R S NEUROHYPOPHYSIS ADENOHYPOPHYSIS  HYPERPITUITARISM  HYPOPITUITARISM  SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)  DIABETES INSIPIDUS (DI) Patho:  ↑ PRL – hyperprolactinemia  ↑ GH – rapid growth of all body tissues  Gigantism : before closure of epiphyses  Acromegaly: after epiphyseal closure; bone and soft tissue deformity and enlargement of viscera, w/o an ↑in ht • Condition in which Growth Hormone is oversecreted after epiphyses of long bones have sealed. • Results from hyperplasia or a tumor of anterior pituitary • Assessment Findings: • Huge lower jaw • Thick lips, thickened tongue • Bulging forehead • Large hands & feet • Headache • Partial blindness • Enlarged heart, liver & spleen • Muscle weakness • Hypertrophied joints become painful & stiff • Increased facial hair & deepened voices • Male: Erectile dysfunction • Female: amenorrhea Local:  visual field abnormality, headache, somnolence Acromegaly High blood -[Growth Hormone] Pituitary adenoma (CT scan or MRI) Visual field defects Hypertrophy of sweat & sebaceous glands Prominent supraorbital ridge Galactorrhoea (prolactin) Large nose and jaw Teeth are separated or lacking Cardiamegaly Hypertension Abnormal glucose tolerance test Sexual dysfunction Glucosuria/polyuria Spade-shaped hands and feet Arthrosis Peripheral neuropathy Fig, 30-7 KMc management Destroy/remove tumor 1. Surgical resection of tumor  Craniotomy  Transphenoidal hypophysectomy Ω w/ nasal packing, w/c is removed p-2-5 days Ω monitor for rhinorrhea, post nasal drainage: CSF leakage: test for glucose Ω caution against coughing, sneezing, bending over from waist dislodge graft Ω mouth breathing impaired gas exchange; instruct on deep breathing; adequate fld intake to prevent mucosal drying Medications:  Somatostatin analogues octreotide acetate (Sandostatin), lantreotide (Somatuline depot)  Can be given as a monthly depot injection (Sandostatin LAR)  s/e: cholelithiasis  GH receptor antagonist pegvisomant (Somavert)  blocks the effect of excess GH in the body  DOC for patients who partially or don’t respond to Sandostatin  Dopamine agonist a. Bromocriptine (Parlodel)  Decreased PRL level  a/e: nausea, headache, dizziness, nasal stuffiness, hypotension, depression Nursing management Assessment  client reaction to dx, expectations for the surgery,educational needs r/t dx and tx plan  support network after discharge  PE: v/s, wt., neurologic assessment (pupil size, handgrip, LOC, orientation, response to stimuli, visual acuity and visual field) pre-op eye exam for post-op comparison  Monitor for meningitis report temp elevation, severe headache, irritability, or nuchal rigidity Brudzinski’s sign : involuntary flexion of the arm, hip and knee when neck is passively flexed Kernig’s sign :loss of ability to straighten leg when it is fully flexed at the knee and hip  Provide oral hygiene avoid toothbrush p to 2 weeks post-op; oral care with gauze sponge; lubricate lips with petroleum jelly  Monitor for CSF drainage POST-OP Inform pt: • Lifetime hormone replacement therapy • ACTH: take cortisone with meals, food, milk, antacid • ADH for DI: vasopressin  Sexual disturbances from ↑ LH and FSH s/sx: sexual precocity in children amenorrhea and galactorrhea Administer bromocriptine a.d.  Given if without pituitary tumor  Inhibits PRL secretion  Panhypopituitarism (Simmond’s dse) Total lack of both anterior and posterior pituitary hormones  Dwarfism insufficient growth hormone during childhood  Invasion --- tumors  Infarction --- Sheehan’s syndrome, pituitary apoplexy  Infiltration --- sarcoidosis, hemochromatosis  Injury --- head trauma, child abuse  Immunologic --- lymphocytic hypophysitis  Iatrogenic --- surgery, radiation therapy  Infectious --- mycoses, TB, syphilis  Idiopathic --- familial  Isolated – deficiency of an anterior pituitary hormone short stature: stunted growth from deficiency or lack of GH  sexual and reproductive d/o (LH and FSH deficiency) ↓sex drive, sterility, ↓secondary sex characteristics Infertility, amenorrhea Diminished spermatogenesis, testicular atrophy  Secondary adrenocortical deficiency  Absence of lactation in post-partum women Management  Removal of causative factor  Replacement of hormones secreted by target glands Human growth hormone injections, corticosteroids, thyroid hormones, sex hormones Nursing management • Assessment: focus on target organ hyposecretion • Nursing interventions directed at problems resulting from hormone deficiency Diabetes Insipidus • Diagnostic test: • Fluid Deprivation Test: • Fluids are withheld for 8-12 hrs • Urine specific gravity & osmolarity are determined at the beginning & end of the test. • Failure to concentrate urine during the period of fluid deprivation. • Urinalysis • Colorless urine of low specific gravity. • 24-hour urine output – abnormally large MANAGEMENT 1. Replace ADH  desmopressin acetate (DDVAP or Stimate) ADH synthetic analog Nasal spray  Has no vascular effects of ADH  Vasopressin (Pitressin )  SC, intranasal  IM :q24-96hrs; given in evening; rotate sites Other meds:  Chlorpropamide (Diabinase)  Chlofibrate - For patients with residual ADH production (stimulates release of endogenous ADH) 2. Ensure adequate fluid replacement 3. Identify and correct underlying intracranial pathology DIABETES \NS1e1 DUS 1S TBF DV_ & MEAD oR PiyurtTary oR CRAIMIorTOMY + Histo RY oF —> Rex: VASOPRESSIN bDDAVP C S VPTS 2oL VRINE/DAY V SPECIEIC GRAVITY VY OSMoLARITY WYPa VoL EMMA A THIRST TACHYCARDIA vv Be ————————— <—_ RYRSING sage eerie re MON iToR Flops REPLACE FLUIDS YNELRO STATUS YVITAL SIGNS Mr veous MEMBRANES SS  Syndrome of Inappropriate Antidiuretic Hormone Secretion • Renal reabsorption of water rather than its normal excretion • Etiology: : often non-endocrine in origin • Lung tumors • CNS disorders • Brain tumors • CVA • Head trauma • Drugs (vasopressing, tricyclic antidepressants) • Oral hypoglycemics • Assessment Findings: • Water retention • Headache • Muscle cramps • Anorexia • As condition worsen: • N&V • Muscle twitching • Changes in level of consciousness • Decreased serum sodium levels & serum osmolarity • Increased urine sodium levels & osmolarity LABS: • Hyponatremia: S. Na+ < 135 mEq/L • Elevated serum ADH • Decreased serum osmolality S. Na+ decreased  cerebral edema, lethargy • 121-125 mEq/L: nausea, malaise • 115-120 mEq/L: HA, lethargy, obtundation • 110-114 mEq/L : SZ and coma • Management: • Check for signs of fluid overload: • Confusion • Dyspnea • Pulmonary congestion • Hypertension • Check for signs of hyponatremia • Weakness • Muscle cramps • Anorexia & diarrhea • Headache NURSING DIAGNOSES • Fluid volume excess r/t fluid retention • Risk for injury r/t altered neurologic function NURSING INTERVENTIONS  Explain the rationale for fluid restriction  Provide oral care  Identify patients at risk  Monitor:  Neurologic, fluid volume, and cardiac status  Daily weights, I&O, serum and urinary Na+ and osmolality Hyperthyroidism • Also called “Graves’ disease” • Pathophysiology & Etiology: • Autoimmune or inherited • Thyroid or pituitary tumors • Hypothalamic malignancies • Stress or infection Oversecretion of thyroid hormones Increase in metabolic rate Gamma probe measuring thyroid gland radioactivity | Nuclear Medicine Thy id San Radioactive iodine is ingested • Management: • Antithyroid drugs: • Propylthiouracil (PTU) • Methimazole (Tapazole) • Potassium iodide (lugol’s solution) • 131I –destroy hyperplastic thyroid tissue by radiation • Subtotal thyroidectomy (partial removal of the thyroid gland) • Monitor HR, BP & weights • Increase caloric intake • Total thyroidectomy (removal of the thyroid gland) Complications of thyroidectomy: • Accidental removal or alteration in the blood supply to the parathyroid glands – results to hypocalcemia • Hemorrhage • Thyrotoxicosis (Thyroid storm) • Damage to the recurrent laryngeal nerve – affects the vocal cords • Assessment Findings: • 41˚C temp. • Inc PR & cardiac dysrhythmias • Vomiting • Extreme restlessness • Chest pain & dyspnea • Marked elevation of thyroid hormone • Management: • Antithyroid drugs • IV corticosteroid • IV sodium iodide – prevents thyroid gland from releasing thyroid hormones • Propanolol • IV fluids • Antipyretic • Oxygen therapy Hypothyroidism • Insufficient or failure of thyroid gland to secrete hormones • Pathophysiology: Insufficient TSH Slowing of all metabolic processes • Myxedema – severe hypothyroidism • Myxedema coma – untreated myxedema • Hypothermia • Hypotension • Hypoventilation • Management: • Thyroid replacement therapy: • Levothyroxine sodium (Synthroid) • Liothyronine sodium (Cytomel) • VS & weight monitoring • High fiber foods Endemic & Multinodular Goiters Disorders of Parathyroid Glands Hyperparathyroidism • Etiology & Pathophysio: • Primary hyperparathyroidism • Adenoma of one of the parathyroid glands. • Increased urinary excretion of phosphorus & loss of calcium from bones • Renal stones may develop • Secondary hyperparathyroidism • Parathyroid glands secrete excessive parathormone in response to hypocalcemia • May result from Vit. D deficiency, chronic renal failure, large doses of thiazide diuretics & laxatives. Hypoparathyroidism • Etiology & Pathophysiology: • Trauma to the glands • Inadvertent removal of all or nearly all these structures during thyroidectomy • May be autoimmune • Congenital absence of parathyroids Decrease calcium absorption from the GI tract Hypocalcemia: neuromuscular hyperexcitability • Spastic muscle contractions • paresthesias • Assessment Findings: • Tetany • Numbness & tingling in fingers or toes or around the lips • Involuntary jerking spasm • Muscle cramping • Tonic flexion of an arm or a finger • Chvostek’s sign • Trousseau’s sign • Laryngeal spasm – dyspnea • Increased serum phosphorus level • Chronic hypoparathyroidism – increased bone density • Management: • IV calcium salt ( Calcium Gluconate) • Bronchodilators • Oral calcium & Vit. D Adrenal Insufficiency (Addison’s Disease) • Etiology & Pathophysiology: • Primary Adrenal Insufficiency: (Addison’s Disease) • Destruction of the adrenal cortex by diseases • Autoimmune • Unknown • Hypoglycemia • Decreased urea nitrogen excretion • Secondary Adrenal Insufficiency: • Surgical removal of both adrenal glands (Bilateral adrenalectomy) • Hemorrhagic infarction of the glands • Hypopituitarism • Corticosteroids – suppresses adrenal function • Assessment Findings: • Low serum sodium & fasting blood glucose • Increase serum potassium, calcium & blood urea • Hypoglycenia • Hunger, headaches sweating weakness, loss of consciousness, visual disturbances, disorientation • Synthetic ACTH (Cosyntropin (Cortrosyn)) • Screening test for adrenal function. • Absent or a low cortisol response: adrenal insufficiency • Management: • Daily corticosteroid replacement Fludrocortisone (Florinef) • Avoid exposure to infections & excessive fatigue • Weigh client daily • If with excessive perspiration – increase fluid & salt intake • Offer 6 meals a day rather than 3 meals. • Assessment Findings: • Anorexia • N&V • Diarrhea & abd. Pain • Profound weakness • Headache • Hypotension & vasomotor collapse - death • Restlessness • Fever • Shock may develop • Management: • IV Corticosteroids in normal saline & glucose • Antibiotics • VS monitoring Cushing’s Syndrome (Adrenocortical Hyperfunction) • Etiology & Pathophysiology: • Overproduction of adrenocortical hormones results from: • Benign or malignant tumors of the pituitary gland or adrenal cortex • Prolonged administration of high doses of corticosteroids. • Overproduction of ACTH by the pituitary gland Hyperplasia of the adrenal cortex Excessive production & secretion of glucocorticoids, mineralocorticoids & androgens Physical changes