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  1. 1. By Linda Self Assessment and Management of Patients with Endocrine Disorders
  2. 2. Glands of the Endocrine System  Hypothalamus  Posterior Pituitary  Anterior Pituitary  Thyroid  Parathyroids  Adrenals  Pancreatic islets  Ovaries and testes
  3. 3. Hypothalamus  Releasing and inhibiting hormones  Corticotropin-releasing hormone  Thyrotropin-releasing hormone  Growth hormone-releasing hormone  Gonadotropin-releasing hormone  Somatostatin-=-inhibits GH and TSH
  4. 4. Anterior Pituitary  Growth Hormone--  Adrenocorticotropic hormone  Thyroid stimulating hormone  Follicle stimulating hormone—ovary in female, sperm in males  Luteinizing hormone—corpus luteum in females, secretion of testosterone in males  Prolactin—prepares female breasts for lactation
  5. 5. Posterior Pituitary  Antidiuretic Hormone  Oxytocin—contraction of uterus, milk ejection from breasts
  6. 6. Adrenal Cortex  Mineralocorticoid—aldosterone. Affects sodium absorption, loss of potassium by kidney  Glucocorticoids—cortisol. Affects metabolism, regulates blood sugar levels, affects growth, anti- inflammatory action, decreases effects of stress  Adrenal androgens—dehydroepiandrosterone and androstenedione. Converted to testosterone in the periphery.
  7. 7. Adrenal Medulla  Epinephrine and norepinephrine serve as neurotransmitters for sympathetic system
  8. 8. Thyroid  Follicular cells—excretion of triiodothyronine (T3) and thyroxine (T4)—Increase BMR, increase bone and calcium turnover, increase response to catecholamines, need for fetal G&D  Thyroid C cells—calcitonin. Lowers blood calcium and phosphate levels
  9. 9. Parathyroid  Parathyroid hormone—regulates serum calcium
  10. 10. Pancreatic Islet cells  Insulin  Glucagon—stimulates glycogenolysis and glyconeogenesis  Somatostatin—decreases intestinal absorption of glucose
  11. 11. Kidney  1, 25 dihydroxyvitamin D—stimulates calcium absorption from the intestine  Renin—activates the RAAS  Erythropoietin—Increases red blood cell production
  12. 12. Ovaries  Estrogen  Progesterone—inportant in menstrual cycle,*maintains pregnancy,
  13. 13. Testes  Androgens, testosterone—secondary sexual characteristics, sperm production
  14. 14. Thymus  Releases thymosin and thymopoietin  Affects maturation of T lymphocetes
  15. 15. Pineal  Melatonin  Affects sleep, fertility and aging
  16. 16. Prostaglandins  Work locally  Released by plasma cells  Affect fertility, blood clotting, body temperature
  17. 17. Assessment  Health history—energy level, hand and foot size changes, headaches, urinary changes, heat and cold intolerance, changes in sexual characteristics, personality changes, others  Physical assessment—appearance including hair distribution, fat distribution, quality of skin, appearance of eyes, size of feet and hands, peripheral edema, facial puffiness, vital signs
  18. 18. Diagnostic Evaluation  Serum levels of hormones  Detection of antibodies against certain hormones  Urinary tests to measure by-products (norepinephrine, metanephrines, dopamine)  Stimulation tests—determine how an endocrine gland responds to stimulating hormone. If the hormone responds, then the problem lies w/hypothalmus or pituitary  Suppression tests—tests negative feedback systems that control secretion of hormones from the hypothalamus or pituitary.
  19. 19. Disorders of the Pituitary Pituitary Tumors  Eosinophilic tumors may result in gigantism or in acromegaly. May suffer from severe headaches, visual disturbances, decalcification of the bone, endocrine disturbances  Basophilic tumors may cause Cushing’s syndrome w/features of hyperadrenalism, truncal obesity, amenorrhea, osteoporosis  Chromophobic tumors—90% of pituitary tumors. Present with lowered BMR, obesity, somnolence, scant hair, low body temp, headaches, visual changes
  20. 20.  Growth hormone deficiency in childhood will result in primary dwarfism.
  21. 21. Pituitary Tumors—Assessment and Diagnostic Findings  H&P  Vision tests  CT, MRI  Serum levels of pituitary hormones, others
  22. 22. Diabetes Insipidus  Deficiency of ADH  Excessive thirst, large volumes of dilute urine  Can occur secondary to brain tumors, head trauma, infections of the CNS, and surgical ablation or radiation  Nephrogenic DI—relates to failure of the renal tubules to respond to ADH. Can be related to hypokalemia, hypercalcemia and to medications (lithium demeocycline)
  23. 23. Manifestations  Excessive thirst  Urinary sp. gr. of
  24. 24. Assessment and Diagnostic Findings  Fluid deprivation test—withhold fluids for 8-12 hours. Weigh patient frequently. Inability to slow down the urinary output and fail to concentrate urine are diagnostic. Stop test if patient is tachycardic or hypotensive  Trial of desmopressin and IV hypertonic saline  Monitor serum and urine osmolality and ADH levels
  25. 25. Pharmacologic Tx and Nursing Management  DDAVP—intranasal bid  Can be given IM if necessary. Every 24-96h. Can cause lipodystrophy.  Can also use Diabenese and thiazide diuretics in mild disease as they potentiate the action of ADH  If renal in origin—thiazide diuretics, NSAIDs (prostaglandin inhibition) and salt depletion may help  Educate patient about actions of medications, how to administer meds, wear medic alert bracelet
  26. 26. SIADH  Excessive ADH secretion  Retain fluids and develop a dilutional hyponatremia  Often non-endocrine in origin—such as bronchogenic carcinoma  Causes: Disorders of the CNS like head injury, brain surgery, tumors, infections or medications like vincristine, phenothiazines, TCAs or thiazide diuretics  Meds can either affect the pituitary or increase sensitivity to renal tubules to ADH  Management: eliminate cause, give diuretics (Lasix), fluid restriction, I&O, daily wt., lab chemistries
  27. 27. SIADH  Restoration of electrolytes must be gradual  May use 3% NaCl in conjunction with Lasix
  28. 28. Thyroid  T3 and T4  Need iodine for synthesis of hormones—excess will result in adaptive decline in utilization called the Wolf- Chaikoff mechanism  Thyroid is controlled by TSH  Cellular metabolism, brain development, normal growth, affect every organ in the body  T3 is five times as potent as T4  Calcitonin—secreted in response to high levels of serum calcium, increases deposition in the bone
  29. 29. Thyroid  Inspect gland  Observe for goiter  Check TSH, serum T3 and T4  T3 resin uptake test useful in evaluating thyroid hormone levels in patients who have received diagnostic or therapeutic dose of iodine. Estrogens, Dilantin, Tagamet, Heparin, amiodarone, PTU,steroids and Lithium can cloud the accuracy  T3 more accurate indicator of hyperthyroidism according to text
  30. 30. Thyroid  Antibodies seen in Hashimoto’s, Grave’s and other auto-immune problems.  Radioactive iodine uptake test measures rate of iodine uptake. Patients with hyperthyroidism exhibit a high uptake, hypothyroidism will have low uptake  Thyroid scan—helps determine the location, size, shape and size of gland. “Hot” areas (increased function) and “cold” areas (decreased function) can assist in diagnosis.
  31. 31. Nursing Implications  Be aware of meds patient is taking (see list in text) that can affect accuracy of testing  Also be aware if patient is taking multivitamins and food supplements
  32. 32. Hypothyroidism  Most common cause is Hashimoto’s thyroiditis  Common in those previously treated for hyperthyroidism  Atrophy of gland with aging  Medications like lithium, iodine compounds, antithyroid meds can cause  Radiation treatments to head and neck  Infiltrative diseases like amyloidosis, scleroderma  Iodine deficiency and excess  Hypothalamic or pituitary abnormality  More common in women, especially over age 50
  33. 33. Manifestations  From mild symptoms to myxedema  Myxedema –accumulation of mucopolysaccharides in sc and interstitial tissues. Is the extreme form of hypothyroidism. Can progress to shock.  S/S—fatigue, hair loss, dry skin, brittle nails, numbness and tingling of the fingers, amenorrhea, weight gain, decreased heart rate and temperature, lassitude, cognitive changes, elevated cholesterol levels, constipation, hypotension
  34. 34. Pharmacologic Management of hypothyroidism  Levothyroxine is preferred agent  Dosage is based on TSH  Desiccated thyroid used infrequently due to inconsistent dosing  Angina can occur when thyroid replacement is initiated as it enhances effects of cardiovascular catecholamines (in pt. w/pre-existent CAD). Start at low dose.  Hypnotics and sedatives may have profound effects on sensorium
  35. 35. Management in Myxedema  Cautious fluid replacement  Glucose to restore to normal glycemic levels  Avoid rapid overheating due to increased oxygen demands but keep warm  May give levothyroxine intravenously With recovery,  Modify activity  High fiber foods  Home health for follow-up
  36. 36. Hyperthyroidism  Extreme form is Grave’s disease  Caused by thyroiditis, excessive amount thyroid hormone, abnormal output by immunoglobulins  Is more common in women
  37. 37. Manifestations of hyperthyroidism  Thyrotoxicosis—nervousness, irritable, apprehensive, palpitations, heat intolerance, skin flushing, tremors, possibly exophthalmos  Have an increased sensitivity to catecholamines  Can occur after irradiation or presence of a tumor
  38. 38. Assessment and Diagnosis  Thyroid thrill and or bruit may be present  Thyroid may be enlarged  Decreased TSH, increased free T4 and an increased radioactive iodine uptake
  39. 39. Management  Reduce thyroid hyperactivity—usually use radioactive iodine, antithyroid meds or surgery)  Beta blockers  Can be relapse with antithyroid meds
  40. 40. Pharmacologic Therapy  Irradiation with administration of radioisotope iodine 131—initially may cause an acute release of thyroid hormones. Should monitor for thyroid storm  S/S of thyroid storm—high fever. Tachycardia, delirium, chest pain, dyspnea, palpitations, weight loss, diarrhea, abdominal pain  Management of thyroid storm—oxygen, IV fluids with dextrose, hypothermic measures, steroids to treat shock or adrenal deficiency, iodine to decrease output of T4, beta blockers, PTU or Tapazole impedes formation of thyroid hormone and blocks conversion of T4 to T3
  41. 41. Antithyroid Medications  PTU—propylthiouracil—blocks synthesis of hormones  Tapazole (methimazole)—blocks synthesis of hormones. More toxic than PTU.  Sodium Iodide-suppresses release of thyroid hormone  SSKI (saturated solution of potassium chloride)– suppresses release of hormones and decreases vascularity of thyroid. Can stain teeth  Dexamethazone—suppresses release of thyroid hormones
  42. 42. Surgical Management  Reserved for special circumstances, e.g. large goiters, those who cannot take antithyroid meds, or who need rapid normalization  Subtotal thyroidectomy  Before surgery, give PTU until s/s of hyperthyroidism have disappeared  Iodine may be used to decrease vascularity
  43. 43. Nursing Management  Reassurance r/t the emotional reactions experienced  May need eye care if has exophthalmos  Maintain normal body temperature  Adequate caloric intake  Managing potential complications such as dysrhythmias and tachycardias  Educate about potential s/s of hypothyroidism following any antithyroid tx.
  44. 44. Parathyroid Glands  Parathormone maintains sufficient serum calcium levels  Excess calcium can bind with phosphate and precipitate in various organs, can cause pancreatitis  Hyperparathyroidism will cause bone decalcification and development of renal calculi  More common in women  Secondary hyperparathyroidism occurs in those with chronic renal failure and renal rickets secondary to excess phosphorus retention (and increased parathormone secretion)
  45. 45. Manifestations of Hyperparathyroidism  May be asymptomatic  Apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension and cardiac dysrhythmias  Excess calcium in the brain can lead to psychoses  Renal lithiasis can lead to renal damage and even failure  Demineralization of bones with back and joint pain, pain on weight bearing, pathologic fractures  Peptic ulcers and pancreatitis can also occur
  46. 46. Assessment and Diagnostic Findings  Persistent elevated calcium levels  Elevated serum parathormone level  Bone studies will reveal decreased density  Double antibody parathyroid hormone test is used to distinguish between primary hyperparathyroidism and malignancy  Ultrasound, MRI, thallium scan, fine needle biopsy also can be used to localize cysts, adenomas, or hyperplasia
  47. 47. Management  Recommended treatment for hyperparathyroidism is surgical removal  Hydration therapy necessary to prevent renal calculi  Avoid thiazide diuretics as they decrease renal excretion of calcium  Increase mobility to promote bone retention of calcium  Avoid restricted or excess calcium in the diet  Fluids, prune juice and stool softeners to prevent constipation  Watch for s/s of tetany postsurgically (numbness, tingling, carpopedal spasms) as well as cardiac dysrhythmias and hypotension
  48. 48. Hypercalcemic crisis  Seen with levels greater than 15mg/dL  Can result in life-threatening neurologic, cardiovascular and renal symptoms  Treatments include: hydration, loop diuretics to promote excretion of calcium, phosphate therapy to promote calcium deposition in bone and reducing GI absorption of calcium  Give calcitonin or mithramycin to decrease serum calcium levels quickly
  49. 49. Hypoparathyroidism  Seen most often following removal of thyroid gland, parathyroid glands or following radical neck surgery  Deficiency of parathormone results in increased bone phosphate and decreased blood calcium levels  In absence of parathormone, there is decreased intestinal absorption of dietary calcium and decreased resorption of calcium from bone and through kidney tubules
  50. 50. Clinical Manifestations of Hypoparathyroidism  Irritability of neuromuscular system  Tetany—hypertonic muscle contractions , numbnes, tingling, cramps in extremities, laryngeal spasm, bronchospasm, carpopedal spasm ( flexion of the elbows and wrists, dorsiflexion of the feet), seizures
  51. 51. Assessment and Diagnostic Findings  Trousseau’s sign—can check with a BP cuff  Chvostek’s sign—tapping over facial nerve causes spasm of the mouth, nose and eye  Lab studies may reveal calcium levels of 5-6 mg/dL or lower  Serum phosphate levels will be decreased
  52. 52. Management of Hypoparathyroidism  Restore calcium level to 9-10 mg/dL  May need to give IV calcium gluconate for immediate treatment  Use of parathormone IV reserved for extreme situations due to the probability of allergic reactions  Monitor calcium levels  May need bronchodilators and even ventilator assistance  Diet high in calcium and low in phosphorus; thus, avoid milk products, egg yolk and spinach.
  53. 53. Management of Hypoparathyroidism  Keep calcium gluconate at bedside  Ensure has IV access  Cardiac monitoring  Care of postoperative patients who have undergone thyroid surgery, parathyroidectomy or radical neck surgery. Be watchful for signs of tetany, seizures, and respiratory difficulties
  54. 54. Adrenals--Pheochromocytoma  Usually benign tumor  Originates from the chromaffin cells of the adrenal medulla  Any age but usu. Between 40-50 years old  Can be familial  10% are malignant  May be associated with thyroid carcinoma or parathyroid hyperplasia or tumor
  55. 55. Clinical Manifestations  Headache, diaphoresis, palpitations, hypertension  May have hyperglycemia related to excess epinephrine secretion  Tremors, flushing and anxiety as well  Blurring of vision  Feeling of impending doom  BPs exceeding 250/150 have occurred
  56. 56. Assessment and Diagnostic Findings  Associated with the 5 H’s—hypertension, headache, hyperhidrosis, hypermetabolism and hyperglycemia  Urinary catecholamines and metanephrine are direct and conclusive tests  Serum epinephrine and norepinephrine levels will be elevated  Urinary vanillymandelic acid also diagnostic  Must avoid coffee, tea, bananas, chocolate, vanilla and ASA, nicotine, amphetamines, decongestants before 24h urine testing  Clonidine suppression test—in normal individual, would block catecholamine release  Imaging studies
  57. 57. Management  Bedrest  Elevated HOB  ICU  Nipride  Calcium channel blockers and Beta blockers  Surgical management (manipulation of the tumor can cause excessive release of catecholamines)  Steroid therapy if adrenalectomy performed  Hypotension and hypoglycemia can occur post-op
  58. 58. Addison’s Disease  Adrenocortical insufficiency  Autoimmune or idiopathic atrophy  Can be caused by inadequate ACTH from pituitary  Therapeutic use of steroids
  59. 59. Manifestations  Muscle weakness  Anorexia  Dark pigmentation  Hypotension  Hypoglycemia  Low sodium levels  High potassium levels  Can result in Addisonian crisis
  60. 60. Addisonian crisis  Circulatory shock  Pallor, apprehension, weak&rapid pulse, rapid respirations and low blood pressure  Headache, nausea, abdominal pain and diarrhea  Can be brought on by overexertion, exposure to cold, acute infection, decrease in salt intake
  61. 61. Assessment and Diagnostic Findings  Early morning serum cortisol and plasma ACTH are performed. Will distinguish between primary and secondary adrenal insufficiency. In primary, will have elevated ACTH levels and below normal cortisol levels.  If the adrenal cortex is not stimulated by the pituitary, a normal response to doses of exogenous ACTH (see text)  Blood sugar levels and electrolyte values
  62. 62. Management  Restore circulatory status—fluids, steroids  May need antibiotics if infection precipitated crisis  May need lifelong steroid therapy and mineralocorticoid therapy  May need additional salt intake  Check orthostatics  Daily weights  Aware that stressors can precipitate crises  Medic alert bracelet or similar identification of history
  63. 63. Cushing’s Syndrome  Results from excessive adrenocortical activity  May be related to excessive use of corticosteroid medications or due to hyperplasia of the adrenal cortex  Oversecretion of corticosteroids can also be caused by pituitary tumor  Can be caused by bronchogenic carcinoma or other malignancy
  64. 64. Manifestations of Cushing’s syndrome  Cataracts, glaucoma  Hypertension, heart failure  Truncal obesity, moon face, buffalo hump, sodium retention, hypokalemia, hyperglycemia, negative nitrogen balance, altered calcium metabolism  Decreased inflammatory responses, impaired wound healing, increased susceptibility to infections  Osteoporosis, compression fractures  Peptic ulcers, pancreatitis  Thinning of skin, striae, acne  Mood alterations
  65. 65. Assessment and Diagnostic Findings  Overnight dexamethasone suppression test frequently used for diagnosis  Administered at 11pm and cortisol level checked at 8am  Suppression of cortisol to less than 5mg/dL indicates normal functioning  Measurement of plasma ACTH (radioimmunoassay) in conjunction with dexamethasone suppression test helps distinguish pituitary vs. ectopic sites of ACTH.  MRI, CT and CT also help detect tumors of adrenal or pituitary
  66. 66. Medical Management  If pituitary source, may warrant transphenoidal hypophysectomy  Radiation of pituitary also appropriate  Adrenalectomy may be needed in case of adrenal hypertrophy  Temporary replacement therapy with hydrocortisone or Florinef  Adrenal enzyme reducers may be indicated if source if ectopic and inoperable. Examples include: ketoconazole, mitotane and metyrapone.  If cause is r/t excessive steroid therapy, tapering slowly to a minimum dosage may be appropriate.
  67. 67. Primary Aldosteronism or Conn’s Syndrome  Excessive aldosterone secondary to adrenal tumor  retain sodium and excrete potassium  Results in alkalosis  Hypertension—universal sign of hyperaldosteronism  Inability of kidneys to concentrate the urine  Serum becomes concentrated  Excessive thirst  Hypokalemia interferes with insulin secretion thus will have glucose intolerance as well
  68. 68. Assessment and Diagnostic Findings  High sodium  Low potassium level  High serum aldosterone level  Low renin level  Aldosterone excretion rate after salt loading is diagnostic for primary aldosteronism  Renin-aldosterone stimulation test
  69. 69. Management  Surgical removal of tumor  Correct hypokalemia  Usual postoperative care with abdominal surgery  Administer steroids  Fluids  Monitoring of blood sugar  Control of hypertension with spironolactone
  70. 70. Corticosteroid Therapy  Hydrocortisone--Cortisol  Cortisone--Cortate  Prednisone--Deltasone  Prednisolone-Prelone  Triamcinolone--Kenalog  Betamethasone--Celestone  Fludrocortisone (contains both mineralocorticoid and glucocorticoid) Florinef
  71. 71. Indications  RA  Asthma  MS  COPD exacerbations  Lupus  Other autoimmune disorders  Dermatologic disorders
  72. 72. Dosing  Lowest dose  Limited duration  Best time to give dose is in early morning between 7-8 am  Need to taper off med to allow normal return of renal function
  73. 73. Side Effects of Steroids  Hypertension, thrombophlebitis, accelerated atherosclerosis  Increased risk of infection  Glaucoma and corneal lesions  Muscle wasting, poor wound healing, osteoporosis, pathologic fractures  Hyperglycemia, steroid withdrawal syndrome  Moon face, weight gain, acne
  74. 74. Case Study 1  35 year old male presents with BP of 188/112 at a yearly physical exam. Previous exams noted blood pressures of 160/94 and 158/92. On questioning, patient admits to twice a month episodes of apprehension, severe headache, perspiration, rapid heartbeat, and facial pallor. These episodes had an abrupt onset and lasted 10-15 minutes.  Routine hematology and chemistry studies are wnl and chest xray and ECG are normal.  What is your impression?  What labs would you draw?
  75. 75. Case Study 2  50 year old woman presents with enlargement of left anterior neck. She has noted increased appetite over the past month with no weight gain, and more frequent bowel movements over the same period. Patient feels jittery at times, experiences palpitations and feels “hot” a lot recently.  She is 5’8” tall and weighs 150#. Heart rate is 110 and blood pressure is 110/76.  What might be this patient’s problem?  What lab tests might you draw?
  76. 76. Case study 3  48 year old woman with a past history of mental illness presents with a new onset of bizarre psychotic behavior. She had been well over the past two years.  She is 5’5” tall and weighs 138#. Her heart rate is 65, irreg and BP is 130/75. Exam is normal except that she is confused to place, time and year. Patient c/o joints aching and of feeling fatigued.  Lab tests reveal serum calcium level of 13.8mg/dL (reference range is 8.4-10.1)  Phosphorus is 2.4 (reference range is 2.5-4.5)  What is your diagnosis?
  77. 77. Case Study 4  40 year old deeply tanned woman presents with a 6 month history of increasing fatigue. For the past three months she has suffered from recurrent URIs, poor appetite, abdominal cramps, fatigue and diarrhea. She has lost 25#. She has noted joint pains, muscle weakness, and has not menstruated for the past 3 months.  Labs reveal blood glucose of 59, Na+ 130, K+ 6.0.  What disorder do you expect?
  78. 78. Case Study #5  27 year old woman presents with depression, insomnia, increased facial fullness and recent increase in acne. She had an episode of depression and acute psychosis following uncomplicated delivery of normal baby boy 9 months previously. Her menses have been irregular since their resumption after the birth (she is not breast feeding). Patient relates has had several vaginal yeast infections recently.  Heart rate is 90bpm, BP is 146/100. Her face is puffy and has acne vulgaris. Thin extremities and with truncal obesity.  What are your suspicions?  What labs will you draw?