Endocrine Disorders

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  • Endocrine Disorders

    1. 1. MAJOR DISORDERS OF THE ENDOCRINE SYSTEM Nio C. Noveno, RN, MAN
    2. 3. HORMONE REGULATION: NEGATIVE FEEDBACK MECHANISM <ul><li>If the client is healthy, </li></ul><ul><li>the concentration of hormones </li></ul><ul><li>is maintained at a constant level. </li></ul><ul><li>When the hormone concentration rises, </li></ul><ul><li>further production of that hormone is inhibited. </li></ul><ul><li>When the hormone concentration falls, </li></ul><ul><li>the rate of production of that hormone increases. </li></ul>
    3. 4. HORMONE REGULATION: NEGATIVE FEEDBACK MECHANISM
    4. 5. DISORDERS OF THE ENDOCRINE SYSTEM <ul><li>Primary </li></ul><ul><li>Problem in the target gland; autonomous </li></ul><ul><li>Secondary </li></ul><ul><li>Problem in the pituitary </li></ul><ul><li>Tertiary </li></ul><ul><li>Problem in the hypothalamus </li></ul>
    5. 6. ANTERIOR PITUITARY DISORDERS
    6. 9. HYPERPITUITARISM <ul><li>May be due to overactivity of gland </li></ul><ul><li>or the result of an adenoma </li></ul><ul><li>Characterized by: </li></ul><ul><li>Excessive serum concentration </li></ul><ul><li>of pituitary hormones (GH, ACTH, PRL) </li></ul><ul><li>Morphologic and functional changes </li></ul><ul><li>in the anterior pituitary </li></ul>
    7. 10. GROWTH HORMONE HYPERSECRETION <ul><li>Gigantism </li></ul><ul><li>Prior to closure </li></ul><ul><li>of the epiphyses; </li></ul><ul><li>proportional growth </li></ul><ul><li>Acromegaly </li></ul><ul><li>After closure </li></ul><ul><li>of the epiphyses; </li></ul><ul><li>disproportional </li></ul><ul><li>growth </li></ul>
    8. 11. HYPERPITUITARISM: CLINICAL MANIFESTATIONS <ul><li>A rthritis </li></ul>C hest: barrel-shaped R ough facial features O dd sensations: hands and feet M uscle weakness & fatigue E nlargement of organs G rowth of coarse hair A menorrhea; breast milk production L oss of vision; headaches I mpotence; increased perspiration S noring
    9. 12. HYPERPITUITARISM: CLINICAL MANIFESTATIONS
    10. 13. HYPERPITUITARISM: MANAGEMENT <ul><li>Medication </li></ul><ul><li>Bromocriptine- </li></ul><ul><li>Cabergoline </li></ul><ul><li>(dopamine agonists) </li></ul><ul><li>GH hypersecretion </li></ul><ul><li>and prolactinoma </li></ul><ul><li>Ocreotide </li></ul><ul><li>(somatostatin) </li></ul><ul><li>GH hypersecretion </li></ul><ul><li>Radiation </li></ul><ul><li>Indicated for larger </li></ul><ul><li>tumors </li></ul><ul><li>Surgery </li></ul><ul><li>Trans-sphenoidal </li></ul><ul><li>hypophysectomy </li></ul>
    11. 14. TRANS-SPHENOIDAL HYPOPHYSECTOMY <ul><li>Post-surgery nursing care </li></ul><ul><li>Semi- to high- Fowler’s position </li></ul><ul><li>Protect from infection and stressful situations </li></ul><ul><li>Hormone replacement </li></ul><ul><li>Constant neurologic checks </li></ul><ul><li>MIOW to check for DI </li></ul><ul><li>WOF CSF leak </li></ul><ul><li>Encourage deep-breathing, but not coughing </li></ul><ul><li>Institute measures to prevent constipation </li></ul><ul><ul><li>[straining increases ICP] </li></ul></ul>
    12. 15. HYPOPITUITARISM <ul><li>Deficiency of one or more </li></ul><ul><li>anterior pituitary hormones </li></ul><ul><li>Causes </li></ul><ul><li>Infections / Inflammatory disorders </li></ul><ul><li>Autoimmune diseases </li></ul><ul><li>Congenital absence </li></ul><ul><li>Tumor </li></ul><ul><li>Surgery / Radiation therapy </li></ul>
    13. 16. HYPOPITUITARISM <ul><li>Simmonds' disease </li></ul><ul><li>[Panhypopituitarism] </li></ul><ul><li>Complete absence </li></ul><ul><li>of pituitary hormones </li></ul><ul><li>Cachexia: </li></ul><ul><li>most prominent feature </li></ul><ul><li>Follows destruction </li></ul><ul><li>of the pituitary </li></ul><ul><li>by surgery, infection, </li></ul><ul><li>injury, or a tumor </li></ul>Sheehan’s syndrome [Post-partum pituitary necrosis] A complication of delivery Results from severe blood loss and hypovolemia  Pituitary ischemia
    14. 17. HYPOPITUITARISM: CLINICAL MANIFESTATIONS <ul><li>Hypo -thermia, -glycemia, -tension </li></ul>Loss of vision, strength, libido, & secondary sexual characteristics
    15. 18. HYPOPITUITARISM: MANAGEMENT <ul><li>Medication </li></ul><ul><li>Hormonal substitution </li></ul><ul><li>[maybe for life] </li></ul><ul><li>Corticosteroids </li></ul><ul><li>Levothyroxine </li></ul><ul><li>Androgen / Estrogen </li></ul><ul><li>Growth hormone </li></ul><ul><li>Radiation </li></ul><ul><li>Indicated for larger </li></ul><ul><li>tumors </li></ul><ul><li>Surgery </li></ul><ul><li>Trans-sphenoidal </li></ul><ul><li>hypophysectomy </li></ul>
    16. 19. POSTERIOR PITUITARY DISORDERS
    17. 22. DIABETES INSIPIDUS <ul><li>Characterized by massive polyuria </li></ul><ul><li>due to either lack of ADH or renal insensitivity </li></ul><ul><li>Central DI </li></ul><ul><li>Due to a deficiency in ADH production </li></ul><ul><li>Nephrogenic DI </li></ul><ul><li>Due to a defect in the kidney tubules </li></ul><ul><li>that interferes with water absorption </li></ul><ul><li>Polyuria is unresponsive to ADH, </li></ul><ul><li>which is secreted normally. </li></ul>
    18. 23. DIABETES INSIPIDUS: DIAGNOSTICS <ul><li>Fluid deprivation test </li></ul><ul><li>Administration of desmopressin </li></ul><ul><li>24-hour urine collection </li></ul><ul><ul><li>for volume, glucose, and creatinine </li></ul></ul><ul><li>Serum for glucose, urea nitrogen, calcium, uric acid, potassium, sodium </li></ul>
    19. 24. DIABETES INSIPIDUS: MANAGEMENT <ul><li>Central DI : </li></ul><ul><li>Desmopressin, Lypressin [intranasal] </li></ul><ul><li>Vasopressin tannate in oil [IM] </li></ul><ul><li>Nephrogenic DI : </li></ul><ul><li>Indomethacin- </li></ul><ul><li>-hydrochlorothiazide </li></ul><ul><li>-desmopressin </li></ul><ul><li>-amiloride </li></ul><ul><li>Clofibrate, chlorpropamide </li></ul>
    20. 25. SYNDROME OF INAPPROPRIATE ADH <ul><li>Disorder due to excessive ADH release </li></ul><ul><li>Clinical Manifestations </li></ul><ul><li>Persistent excretion of concentrated urine </li></ul><ul><li>Signs of fluid overload </li></ul><ul><li>Hyponatremia </li></ul><ul><li>LOC changes </li></ul><ul><li>No edema </li></ul>
    21. 26. SIADH: DIAGNOSTICS <ul><li>Low serum sodium [<135 mEq/L] </li></ul><ul><li>Low serum osmolality </li></ul><ul><li>High urine osmolality [>100 mOsmol/kg] </li></ul><ul><li>High urine sodium excretion [>20 mmol/L] </li></ul><ul><li>Normal renal function: low BUN [<10 mg/dL] </li></ul>
    22. 27. SIADH: MANAGEMENT <ul><li>Maintain fluid balance </li></ul><ul><li>MIOW </li></ul><ul><li>Fluid restriction </li></ul><ul><li>Loop diuretic </li></ul><ul><li>[If with evidence of fluid overload] </li></ul><ul><li>Lithium or demeclocycline </li></ul><ul><li>[Chronic treatment] </li></ul><ul><li>Maintain Na balance </li></ul><ul><li>Increased Na intake </li></ul><ul><li>Emergency treatment of 3% NaCl, followed by furosemide </li></ul><ul><li>[If serum Na <120, or if patient is seizing] </li></ul><ul><li>Excessively rapid correction of hyponatremia may cause central pontine myelinolysis! </li></ul>
    23. 28. THYROID DISORDERS
    24. 31. THYROID FUNCTION TESTS <ul><li>Serum TSH </li></ul><ul><li>Single best screening test [high sensitivity] </li></ul><ul><li>0.38 – 6.15 mcU/mL </li></ul><ul><li>If TSH is normal, fT 4 should be normal. </li></ul><ul><li>Screening required beginning 35 years, </li></ul><ul><li>then q 5 years thereafter </li></ul><ul><li>Also used for monitoring thyroid hormone </li></ul><ul><li>replacement therapy </li></ul>
    25. 32. THYROID FUNCTION TESTS <ul><li>Serum fT 4 </li></ul><ul><li>A direct measurement of free thyroxine, </li></ul><ul><li>the only metabolic fraction of T 4 </li></ul><ul><li>0.9 to 1.7 ng/L (11.5 to 21.8 pmol/L) </li></ul><ul><li>Used to confirm an abnormal TSH </li></ul>
    26. 33. THYROID FUNCTION TESTS <ul><li>Total serum T 3 and T 4 </li></ul><ul><li>T 3 70 to 220 ng/dL (1.15 to 3.10 nmol/L) </li></ul><ul><li>T 4 4.5 to 11.5 mcg/dL (58.5 to 150 nmol/L) </li></ul><ul><li>T 3 levels appear to be a more accurate </li></ul><ul><li>indicator of hyperthyroidism. </li></ul>
    27. 34. THYROID FUNCTION TESTS <ul><li>T 3 resin uptake test </li></ul><ul><li>Indirect measurement of unsaturated </li></ul><ul><li>thyroid-binding globulin (TBG) </li></ul><ul><li>25 – 35% uptake </li></ul><ul><li>Thyroid antibodies </li></ul><ul><li>5 – 10% of the population </li></ul><ul><li>Grave’s: 80% </li></ul><ul><li>Hashimoto’s: 100% </li></ul>
    28. 35. THYROID FUNCTION TESTS <ul><li>Thyroid scan / Radioscan / Scintiscan </li></ul><ul><li>Utilizes a gamma camera and radioisotopes </li></ul><ul><li>123 I, thallium, americium, </li></ul><ul><li>technetium-99m [ 99m Tc] pertechnetate </li></ul><ul><li>Results </li></ul><ul><li>Hot areas: increased activity </li></ul><ul><li>Cold areas: decreased activity </li></ul>
    29. 36. THYROID FUNCTION TESTS <ul><li>Radioactive iodine uptake (RAIU) </li></ul><ul><li>Measures the proportion of administered tracer </li></ul><ul><li>dose of ¹²³I present in the thyroid gland </li></ul><ul><li>at a specific time after administration </li></ul><ul><li>Results </li></ul><ul><li>Hyper: high uptake </li></ul><ul><li>Hypo: low uptake </li></ul>
    30. 37. THYROID FUNCTION TESTS <ul><li>Fine-needle aspiration biopsy </li></ul><ul><li>Sampling of thyroid tissue to detect malignancy </li></ul><ul><li>Initial test for evaluation of thyroid masses </li></ul><ul><li>Results </li></ul><ul><li>Negative [benign] </li></ul><ul><li>Positive [malignant] </li></ul><ul><li>Indeterminate [suspicious] </li></ul><ul><li>Inadequate [non-diagnostic] </li></ul>
    31. 38. THYROID FUNCTION TESTS <ul><li>Nursing Implications </li></ul><ul><li>Determine whether the patient has taken medications or agents that contain iodine [antiseptics, multivitamins, cough syrup, amiodarone] because these may alter the test results. </li></ul><ul><li>Assess for allergy to iodine or shellfish. </li></ul><ul><li>For scans, tell patient that radiation is only minimal. </li></ul>
    32. 39. HYPERTHYROIDISM <ul><li>Increased basal metabolic rate (BMR) </li></ul><ul><li>Causes </li></ul><ul><li>Grave’s disease (autoimmune) </li></ul><ul><li>Initial manifestation of thyroiditis </li></ul><ul><li>TSH-screening pituitary tumor </li></ul><ul><li>Toxic adenoma </li></ul><ul><li>Factitious thyrotoxicosis </li></ul><ul><li>Amiodarone therapy </li></ul>
    33. 40. HYPERTHYROIDISM: CLINICAL MANIFESTATIONS <ul><li>G I hypermotility </li></ul>R apid weight loss A pprehension V olume deficit; voracious appetite E xophthalmos; erratic menses S ystolic BP elevated; sweating [tremors, tachycardia, palpitations]  in secondary disease  in primary disease TSH
    34. 41. HYPERTHYROIDISM: CLINICAL MANIFESTATIONS
    35. 42. THYROID STORM / THYROTOXIC CRISIS <ul><li>Marked delirium </li></ul><ul><li>Severe tachycardia </li></ul><ul><li>Vomiting </li></ul><ul><li>Diarrhea </li></ul><ul><li>Dehydration </li></ul><ul><li>High fever </li></ul>Occurs in patients with existing but unrecognized thyrotoxicosis, stressful illness, thyroid surgery, RAI Increased systemic adrenergic activity: Severe hypermetabolism
    36. 43. HYPERTHYROIDISM: MANAGEMENT <ul><li>Anti-thyroid drugs </li></ul><ul><li>Propylthiouracil (PTU); methimazole </li></ul><ul><li>Blocks thyroid hormone (TH) synthesis </li></ul><ul><li>Used for pregnant women and patients </li></ul><ul><li>who have refused surgery or RAI treatment </li></ul><ul><li>During pregnancy, PTU is DOC. </li></ul><ul><li>1% of infants born to mothers on anti- </li></ul><ul><li>thyroid therapy will be hypothyroid. </li></ul><ul><li>WOF agranulocytosis. </li></ul>
    37. 44. HYPERTHYROIDISM: MANAGEMENT <ul><li>RAI (¹³¹I), K or Na iodide, SSKI (Lugol’s) </li></ul><ul><li>Adjunct to other anti-thyroid drugs </li></ul><ul><li>in preparation for thyroidectomy </li></ul><ul><li>Treatment for thyrotoxic crisis </li></ul><ul><li>Inhibit release and synthesis of TH </li></ul><ul><li>Decrease vascularity of the thyroid gland </li></ul><ul><li>Decrease thyroidal uptake of RAI </li></ul>
    38. 45. HYPERTHYROIDISM: MANAGEMENT <ul><li>Medications to relieve the symptoms </li></ul><ul><li>related to the increased metabolic rate: </li></ul><ul><li>Digitalis, propranolol (Inderal), phenobarbital </li></ul><ul><li>Well-balanced, high-calorie diet </li></ul><ul><li>with vitamin and mineral supplements </li></ul><ul><li>Subtotal or total thyroidectomy </li></ul>
    39. 46. RAI THERAPY : NURSING IMPLICATIONS <ul><li>NPO post-midnight prior to administration </li></ul><ul><li>[Food may delay absorption] </li></ul><ul><li>After initial dose: </li></ul><ul><li>Urine and saliva slightly radioactive x 24H </li></ul><ul><li>Vomitus highly radioactive x 6-8H </li></ul><ul><li>Institute full radiation precautions. </li></ul><ul><li>Instruct the patient to use appropriate disposal methods when coughing and expectorating. </li></ul>
    40. 47. K OR NA IODIDE, SSKI (LUGOL’S) : NURSING IMPLICATIONS <ul><li>Dilute oral doses in water or fruit juice and give with meals to prevent gastric irritation, to hydrate the patient, and to mask the very salty taste. </li></ul><ul><li>Give iodides through a straw to avoid teeth discoloration. </li></ul><ul><li>Force fluids to prevent fluid volume deficit. </li></ul><ul><li>Warn patient that sudden withdrawal may precipitate a thyrotoxic crisis. </li></ul><ul><li>Store in a light-resistant container. </li></ul>
    41. 48. HYPOTHYROIDISM <ul><li>A state of low serum TH levels </li></ul><ul><li>or cellular resistance to TH </li></ul>A utoimmune D evelopmental D ietary I odine deficiency O ncologic D rugs I atrogenic N on-thyroidal E ndocrine
    42. 49. HYPOTHYROIDISM <ul><li>Causes </li></ul><ul><li>Chronic autoimmune [Hashimoto’s] thyroiditis </li></ul><ul><li>Hypothalamic failure to produce TRH </li></ul><ul><li>Pituitary failure to produce TSH </li></ul><ul><li>Inborn errors of TH synthesis </li></ul><ul><li>Thyroidectomy / Radiation therapy </li></ul><ul><li>Anti-thyroid therapy </li></ul><ul><li>Iodine deficiency </li></ul>
    43. 50. HYPOTHYROIDISM <ul><li>Classified according to the time of life in which it occurs </li></ul><ul><li>Cretinism </li></ul><ul><li>In infants and young children </li></ul><ul><li>Lymphocytic thyroiditis </li></ul><ul><li>Appears after 6 years of age </li></ul><ul><li>and peaks during adolescence; self-limiting </li></ul><ul><li>Hypothyroidism without myxedema </li></ul><ul><li>Mild thyroid failure in older children and adults </li></ul><ul><li>Hypothyroidism with myxedema </li></ul><ul><li>Severe thyroid failure in older individuals </li></ul>
    44. 51. HYPOTHYROIDISM: CLINICAL MANIFESTATIONS <ul><li>D ry, brittle hair; dry, coarse skin </li></ul>E dema (periorbital) R educed BMR [bradycardia, bradypnea] A pathy; anorexia; anemia I ncreased weight; intolerance to cold L ethargy; loss of libido E nlarged tongue D rooling  in secondary disease  in primary disease TSH
    45. 52. MYXEDEMA COMA <ul><li>Hypotension </li></ul><ul><li>Bradycardia </li></ul><ul><li>Hypothermia </li></ul><ul><li>Hyponatremia </li></ul><ul><li>Hypoglycemia </li></ul><ul><li>Respiratory failure </li></ul><ul><li>Coma </li></ul>Precipitating Factors Acute illness Rapid withdrawal of thyroid medication Anesthesia / Surgery Hypothermia Opioid use
    46. 53. HYPOTHYROIDISM: MANAGEMENT <ul><li>Prevention </li></ul><ul><li>Prophylactic iodine supplements to decrease </li></ul><ul><li>the incidence of iodine-deficient goiter </li></ul><ul><li>Symptomatic cases </li></ul><ul><li>Hormonal replacement </li></ul><ul><li>Levothyroxine (Synthroid) </li></ul><ul><li>Liothyronine (Cytomel) </li></ul><ul><li>Liotrix (Thyrolar) </li></ul><ul><li>Dosage increased q 2-3 weeks </li></ul><ul><li>especially in elderly patients </li></ul>
    47. 54. HYPOTHYROIDISM: MANAGEMENT <ul><li>Tell patient to WOF: </li></ul><ul><li>Chest pain, palpitations, sweating, </li></ul><ul><li>nervousness, and other S/S of overdosage </li></ul><ul><li>Instruct the patient to take TH at the same time </li></ul><ul><li>each day to maintain constant hormone levels. </li></ul><ul><li>Suggest a morning dosage to prevent insomnia. </li></ul><ul><li>Monitor apical pulse and BP. </li></ul><ul><li>If pulse >100 bpm, withhold drug. </li></ul>
    48. 55. HYPOTHYROIDISM: NURSING INTERVENTIONS <ul><li>Diet : high-bulk, low-calorie </li></ul><ul><li>Encourage activity </li></ul><ul><li>Maintain warm environment </li></ul><ul><li>Administer cathartics </li></ul><ul><li>and stool softeners </li></ul><ul><li>To prevent </li></ul><ul><li>myxedema coma , </li></ul><ul><li>tell patient to continue </li></ul><ul><li>course of thyroid </li></ul><ul><li>medication even if </li></ul><ul><li>symptoms subside. </li></ul>Maintain patent airway Administer medications: Synthroid, glucose, corticosteroids IV fluid replacement Wrap patient in blanket Treat infection or any underlying illness
    49. 56. PARATHYROID DISORDERS
    50. 59. HYPERPARATHYROIDISM <ul><li>Primary </li></ul><ul><li>Single adenoma </li></ul><ul><li>Genetic disorders </li></ul><ul><li>Multiple endocrine neoplasias </li></ul><ul><li>Secondary </li></ul><ul><li>Rickets </li></ul><ul><li>Vitamin D deficiency </li></ul><ul><li>Chronic renal failure </li></ul><ul><li>Phenytoin or laxative abuse </li></ul>
    51. 60. HYPERPARATHYROIDISM: CLINICAL MANIFESTATIONS <ul><li>C onstipation </li></ul>A pathy L ordosis C ardiac dysrhythmias U pset GIT L ow energylevels I ncreased BP  PO 4  PTH Calcium Alkaline phospatase
    52. 61. HYPERPARATHYROIDISM: MANAGEMENT <ul><li>Surgery to remove adenoma </li></ul><ul><li>Force fluids; limit dietary calcium intake </li></ul><ul><li>For life-threatening hypercalcemia: </li></ul><ul><li>Furosemide </li></ul><ul><li>Bisphosphonates </li></ul><ul><li>[Etidroanate (Didrodinel), pamidronate] </li></ul><ul><li>Calcitonin (Cibacalcin, Miacalcin) </li></ul><ul><li>Plicamycin (Mithracin) + glucocorticoid </li></ul><ul><li>Mithramycin </li></ul>
    53. 62. HYPOPARATHYROIDISM <ul><li>Causes </li></ul><ul><li>Congenital absence </li></ul><ul><li>or malfunction of the parathyroids </li></ul><ul><li>Autoimmune destruction </li></ul><ul><li>Removal or injury to one or more </li></ul><ul><li>parathyroids during neck surgery </li></ul><ul><li>Massive thyroid radiation therapy </li></ul><ul><li>Ischemic parathyroid infarction during surgery </li></ul>
    54. 63. HYPOPARATHYROIDISM: CLINICAL MANIFESTATIONS <ul><li>D yspnea; dysrhythmias </li></ul>E xtremities: tingling F otophobia I ncreased bone density C hvostek sign; cramps I rritability T rousseau sign; tetany  PO 4  PTH Calcium Alkaline phospatase
    55. 64. HYPERTHYROIDISM: MANAGEMENT <ul><li>IV Ca chloride or gluconate [emergency treatment] </li></ul><ul><li>DOC post-thyroidectomy </li></ul><ul><li>Oral Ca salts (Ca carbonate or gluconate) </li></ul><ul><li>Vitamin D supplementation </li></ul><ul><li>Increase intestinal Ca absorption </li></ul><ul><li>Dihydrotachysterol, ergocalciferol </li></ul>
    56. 65. T rousseau’s & Chvostek’s E levated serum PO 4 ; low Ca 2+ T ingling A lkalosis; Arrhythmias N arrowing of airway I rritability C ramps
    57. 66. HYPOPARATHYROIDISM <ul><li>Parathormone injections [in acute attacks] </li></ul><ul><li>WOF allergies </li></ul><ul><li>Diet: High-calcium [spinach], low-phosphate [milk, cheese, egg yolks] </li></ul><ul><li>Al(OH) 2 , Gelusil, Amphogel p.c. </li></ul><ul><li>Pentobarbital (Nembutal) </li></ul><ul><li>[calm environment] </li></ul>
    58. 67. T C AKE ARE ETANY RACHEOSTOMY ALCIUM GLUCONATE ALCIUM 8.6 – 10.6 mg / dL
    59. 68. PHEOCHROMOCYTOMA
    60. 69. ADRENAL GLANDS
    61. 70. ADRENAL MEDULLA <ul><li>Release cathecholamines </li></ul><ul><ul><li>Epinephrine </li></ul></ul><ul><ul><li>Norephinephrine </li></ul></ul><ul><li>Released during “fight or flight” situations (sympathetic effect) </li></ul>
    62. 71. PHEOCHROMOCYTOMA <ul><li>Adrenal tumor </li></ul><ul><li>Increased Epi and NEpi </li></ul><ul><li>Heredity </li></ul>
    63. 72. PHEOCHROMOCYTOMA <ul><li>H eadache </li></ul><ul><li>A nxiety </li></ul><ul><li>N ausea </li></ul><ul><li>E ye disturbances </li></ul><ul><li>S evere hypertension </li></ul>
    64. 73. PHEOCHROMOCYTOMA BP HR Diaphoresis BMR VMA Glucose
    65. 74. PHEOCHROMOCYTOMA <ul><li>Adrenalectomy </li></ul><ul><li>Steroid treatment </li></ul><ul><li>Antihypertensive and antidysrhythmic </li></ul><ul><li>nitroprusside (Nipride) </li></ul><ul><li>propranolol (Inderal) </li></ul><ul><li>phentolamine (Regitine) </li></ul>
    66. 75. PHEOCHROMOCYTOMA <ul><li>MBP / MIO </li></ul><ul><li>Fluid replacements </li></ul><ul><li>Decrease environmental stimulation </li></ul><ul><li>Maintenance doses of steroids </li></ul><ul><li>Follow-up check up </li></ul><ul><li>24-hour urine specimens </li></ul><ul><li>[VMA and catecholamine studies] </li></ul><ul><li>Avoid : coffee, chocolate, beer, wine, citrus fruit, bananas, and vanilla 24h before test </li></ul>
    67. 76. ADDISON'S DISEASE
    68. 77. ADRENAL CORTEX HORMONES <ul><li>Glucocorticoids </li></ul><ul><ul><li>Cortisol, corticosterone </li></ul></ul><ul><ul><li>Increase blood glucose levels by increasing rate of gluconeogenesis </li></ul></ul><ul><ul><li>Increase protein catabolism </li></ul></ul><ul><ul><li>Increase mobilization of fatty acids </li></ul></ul><ul><ul><li>Promote sodium and water retention </li></ul></ul><ul><ul><li>Anti-inflammatory effect </li></ul></ul><ul><ul><li>Aid the body in coping with stress </li></ul></ul>
    69. 78. ADRENAL CORTEX HORMONES <ul><li>Mineralocorticoids </li></ul><ul><ul><li>Aldosterone, Corticosterone, Deoxycorticosterone </li></ul></ul><ul><ul><li>Regulate fluid and electrolyte balance </li></ul></ul><ul><ul><li>Stimulate reabsorption of sodium, chloride and water </li></ul></ul><ul><ul><li>Stimulate potassium excretion </li></ul></ul><ul><li>Under the control of Renin-Angiotensin-Aldosterone system (RAAS) </li></ul>
    70. 80. ADRENAL CORTEX HORMONES <ul><li>Sex hormones </li></ul><ul><ul><li>Androgens, Estrogens </li></ul></ul><ul><ul><li>Influences the development of sexual characteristics </li></ul></ul>
    71. 82. ADDISON'S DISEASE <ul><li>Hyposecretion of adrenocortical hormones </li></ul><ul><li>Destruction of the cortex </li></ul><ul><li>Idiopathic atrophy </li></ul>
    72. 83. ADDISON'S DISEASE <ul><li>W eakness </li></ul><ul><li>E xcess stress </li></ul><ul><li>A / N / V / D </li></ul><ul><li>K & ACTH elevation; Low Na, BP, cortisol, glucose </li></ul>
    73. 85. ADDISON'S DISEASE <ul><li>Replacement of hormones </li></ul><ul><li>Hydrocortisone; Fludrocortisone </li></ul><ul><li>PNSS (0.9 NaCl) </li></ul><ul><li>Dextrose </li></ul><ul><li>Diet : </li></ul><ul><li>High-CHO & CHON </li></ul><ul><li>Low potassium, high sodium </li></ul>
    74. 86. ADDISON'S DISEASE <ul><li>VS, weight, and serum glucose level </li></ul><ul><li>24-hour urine specimens </li></ul><ul><li>[LOW 17- hydroxycorticosteroids & 17-ketosteroids] </li></ul><ul><li>Electrolyte levels:  K;  Na </li></ul><ul><li>Bronze-skin </li></ul><ul><li>Changes in energy or activity </li></ul>
    75. 87. ADDISON’S DISEASE
    76. 88. ADDISON'S DISEASE <ul><li>MVS [4x / day] </li></ul><ul><li>Infection, Addisonian crisis, dehydration </li></ul><ul><li>MIOW / MBP / MBG </li></ul><ul><li>Give steroids with milk or an antacid </li></ul><ul><li>Avoid : Contacts & Stress </li></ul>
    77. 89. CUSHING'S SYNDROME
    78. 90. CUSHING'S DISEASE <ul><li>A drenal hyperplasia / tumor </li></ul><ul><li>C ushing’s disease </li></ul><ul><li>T umor-secreting ACTH </li></ul><ul><li>H ypothalamic </li></ul>
    79. 91. <ul><li>B uffalo hump </li></ul><ul><li>U nusual behavior (depression, personality changes, fatigability) </li></ul><ul><li>F acial features (moonface, hirsutism in women) </li></ul><ul><li>F at (truncal obesity) </li></ul><ul><li>A CTH and cortisol in blood elevated; </li></ul><ul><li>L oss of muscle mass </li></ul><ul><li>O verextended skin (abdominal striae with easy bruisability) </li></ul>
    80. 92. <ul><li>H ypertension, hyperglycemia, hypernatremia </li></ul><ul><li>U rinary cortisol elevated </li></ul><ul><li>M enstrual irregularities </li></ul><ul><li>P orosity of bones (osteoporosis) </li></ul>
    81. 93. CUSHING’S SYNDROME
    82. 94. CUSHING'S SYNDROME <ul><li>Remove exogenous steroids </li></ul><ul><li>Hypophysectomy or irradiation </li></ul><ul><li>Adrenalectomy </li></ul>
    83. 95. CUSHING'S SYNDROME <ul><li>Cyproheptadine (Periactin) </li></ul><ul><li>Metyrapone </li></ul><ul><li>Mitotane (Lysodren) </li></ul><ul><li>Aminoglutethamide (Cytadren) </li></ul><ul><li>Potassium supplements </li></ul><ul><li>High-CHON; Low Na </li></ul>
    84. 96. CUSHING'S SYNDROME <ul><li>MVS, MIOW, MBP, MBG </li></ul><ul><li>Electrolyte levels: Na & K </li></ul><ul><li>Urine specimens </li></ul><ul><li>[LOW 17- hydroxycorticosteroids & 17-ketosteroids] </li></ul><ul><li>Physical appearance </li></ul><ul><li>Changes in coping & sexuality </li></ul><ul><li>[verbalization] </li></ul><ul><li>Stress reduction </li></ul>
    85. 97. DIABETES MELLITUS
    86. 98. DIABETES MELLITUS <ul><li>Insulin resistance [GDM, age] </li></ul><ul><li>Failure in production </li></ul><ul><li>Blockage of insulin supply </li></ul><ul><li>Autoimmune response </li></ul><ul><li>Excess body fat </li></ul><ul><li>Heredity </li></ul>
    87. 99. DIABETES MELLITUS <ul><li>Type I [juvenile ]/IDDM </li></ul><ul><li>Type II [adult- onset type]/ NIDDM </li></ul><ul><ul><li>gradual onset </li></ul></ul><ul><li>diet and exercise obesity </li></ul><ul><li>Pancreatectomy, Cushing's syndrome, drugs </li></ul>
    88. 100. DIABETES MELLITUS <ul><li>Low insulin leads to : </li></ul><ul><li>Hyperglycemia </li></ul><ul><li>Glucosuria </li></ul><ul><li>Polyuria </li></ul><ul><li>Gluconeogenesis </li></ul>
    89. 101. DIABETES MELLITUS <ul><li>Complications </li></ul><ul><li>Microvascular </li></ul><ul><li>Retinopathy & Renal failure </li></ul><ul><li>Macrovascular </li></ul><ul><li>CV and PVD </li></ul><ul><li>Peripheral neuropathy </li></ul>
    90. 102. P olyuria olydipsia olyphagia ruritus aresthesia oor healing oor eyesight
    91. 103. Normal Impaired DM FBS <110mg/dl 110-125mg/dl ≥ 126mg/dl 2H OGTT <140mg/dl ≥ 140; <200mg/dl ≥ 200 mg/dl
    92. 104. DIABETES MELLITUS <ul><li>Diet </li></ul><ul><li>complex CHO [50% to 60%] </li></ul><ul><li>water-soluble fiber </li></ul><ul><li>oat, bran, peas, beans, pectin-rich FV </li></ul><ul><li>CHON [12% to 20%] </li></ul><ul><li>60 and 85 g </li></ul><ul><li>CHOO [<30%] </li></ul><ul><li>70 to 90 g/day / MUFA </li></ul>
    93. 105. DIABETES MELLITUS <ul><li>Insulin dose adjustments depend on : </li></ul><ul><ul><li>physical and emotional stresses </li></ul></ul><ul><ul><li>specific type of insulin </li></ul></ul><ul><ul><li>condition and needs of the client </li></ul></ul>
    94. 106. Insulin Onset Peak Duration Ultra rapid acting insulin analog (humalog) 10-15 min 1 H 3 H SAI (humulin regular) ½ - 1 H 2-4 H 4-6 (8) H IAI (humulin lente, Humulin NPH) 3-4 H 4-12 H 16-20 H LAI (Protamine zinc, humulin ultralente) 6-8 H 12-16 H 20-30 H Premixed insulin (NPH-regular [80-20, 70-30, 50-50]) ½-1 H 2-12 H 18-24 hrs Insulin glargine (Lantus ) Slower than NPH No Peak 24 H
    95. 107. DIABETES MELLITUS <ul><li>Somogyi effect </li></ul><ul><li>Epinephrine & Glucagon </li></ul><ul><li>Glycogenolysis </li></ul><ul><li>[iatrogenically-induced hyperglycemia] </li></ul><ul><li>Lowering insulin dosage at night </li></ul><ul><li>MBG </li></ul>
    96. 108. DIABETES MELLITUS <ul><li>Insulin pump </li></ul><ul><li>Basal doses of regular insulin delivered every few minutes bolus doses delivered pc </li></ul><ul><li>Appropriate amount of insulin for 24 hours plus priming is drawn into syringe </li></ul><ul><li>The administration set is primed and needle inserted aseptically, usually into abdomen </li></ul>
    97. 109. DIABETES MELLITUS <ul><li>Client teaching points: </li></ul><ul><li>Proper insulin preparation using aseptic technique </li></ul><ul><li>When to remove the pump (e.g., before showering or sexual relations) </li></ul><ul><li>MBG at home </li></ul>
    98. 110. INSULIN ADMINISTRATION <ul><li>Increases the hypoglycemic effects of insulin </li></ul><ul><li>Aspirin, alcohol, oral anticoagulants, oral hypoglycemics, beta blockers, tricyclic antidepressants, tetracycline, MAOIs </li></ul>Increases blood glucose levels Glucocorticoids, thiazide diuretics, thyroid agents, oral contraceptives Increase the need for increased insulin dose Illness, infection, and stress
    99. 111. ORAL HYPOGLYCEMIC AGENTS <ul><li>Sulfonylureas </li></ul><ul><li>Promotes increase insulin secretion from pancreatic beta cells through direct stimulation </li></ul><ul><li>First Generation Agents : </li></ul><ul><li>Acetohexamide </li></ul><ul><li>Tolbutamide (Orinase) </li></ul><ul><li>Tolzamide (Tolinase) </li></ul><ul><li>Chlorpropamide (Diabenese) </li></ul><ul><li>Second Generation Agents : </li></ul><ul><li>Glipizide (Minidiab, Glucotrol) </li></ul><ul><li>Glyburide (DiaBeta, Glynase, Micronase) </li></ul><ul><li>Glimepiride (Amaryl) </li></ul>
    100. 112. ORAL HYPOGLYCEMICS <ul><li>Biguanides </li></ul><ul><li>Reduces hepatic production of glucose by inhibiting glycogenolysis </li></ul><ul><ul><li>Decrease the intestinal absorption of glucose and improving lipid profile </li></ul></ul><ul><li>Agents : </li></ul><ul><li>Phenformin </li></ul><ul><li>Metformin (Glucophage, Glucophage XR) </li></ul><ul><li>Buformin </li></ul>
    101. 113. ORAL HYPOGLYCEMICS <ul><li>Alpha-glucosidase inhibitors </li></ul><ul><ul><li>Inhibits alpha-glucosidase enzymes in the small intestine and alpha amylase in the pancreas </li></ul></ul><ul><ul><li>Decreases rate of complex carbohydrate metabolism resulting to a reduced rate postprandially </li></ul></ul><ul><ul><li>Agents : </li></ul></ul><ul><li>Acarbose (Precose, Gluconase, Glucobay) </li></ul><ul><li>Miglitol (Glyset) </li></ul>
    102. 114. ORAL HYPOGLYCEMICS <ul><li>Thiazolidinediones </li></ul><ul><li>Enhances insulin action at the cell and post-receptor site and decreasing insulin resistance </li></ul><ul><li>Agents : </li></ul><ul><li>Pioglitazone (Actos) </li></ul><ul><li>Rosiglitazone (Avandia) </li></ul><ul><li>Rosiglitazone + Metformin (Avandamet) </li></ul>
    103. 115. DIABETES MELLITUS <ul><li>Other therapies include: </li></ul><ul><li>pancreas islet cell grafts </li></ul><ul><li>pancreas transplants </li></ul><ul><li>implantable insulin pumps </li></ul><ul><li>cyclosporin [Sandimmune, Neoral] </li></ul>
    104. 116. DIABETES MELLITUS <ul><li>MBG [done pc and hs ] + HbA1C </li></ul><ul><li>MBP + weight </li></ul><ul><ul><li>Renal function + MIO </li></ul></ul><ul><ul><li>Eye examination </li></ul></ul>
    105. 117. GLYCOSYLATED HEMOGLOBIN (HBA 1C ) <ul><li>Reflects effectiveness of treatment </li></ul><ul><ul><li>< 7.5% (good control) </li></ul></ul><ul><ul><li>7.6% - 8.9% (fair control) </li></ul></ul><ul><ul><li>> 9% (poor control) </li></ul></ul>
    106. 118. DIABETES MELLITUS <ul><li>diet & weight </li></ul><ul><li>ketonuria </li></ul><ul><li>note infection </li></ul><ul><li>legs / feet / toenails check </li></ul><ul><li>[keep in between toes dry] </li></ul><ul><li>acceptance & understanding </li></ul>
    107. 119. DIABETES MELLITUS <ul><li>Administer insulin </li></ul><ul><li>sterile technique </li></ul><ul><li>rotating injection sites </li></ul><ul><li>dosage / types / strengths / peak </li></ul><ul><li>CHO source </li></ul><ul><ul><li>Avoid : tight shoes; smoking; heat </li></ul></ul>
    108. 120. DIABETES MELLITUS <ul><li>hypoglycemia </li></ul><ul><li>Headache </li></ul><ul><li>Nervousness </li></ul><ul><li>Diaphoresis </li></ul><ul><li>Rapid, thready pulse </li></ul><ul><li>Slurred speech </li></ul>
    109. 121. THE CLIENT IS TIRED! <ul><li>T </li></ul><ul><li>I rritability </li></ul><ul><li>R estlessness </li></ul><ul><li>E </li></ul><ul><li>D iaphoresis </li></ul><ul><li>Hypoglycemia: <50 mg/dL </li></ul><ul><li>Causes: </li></ul><ul><li>Overtreated hyperglycemia </li></ul><ul><li>Increased exercise </li></ul><ul><li>β -blockers </li></ul><ul><li>Gastric paresis </li></ul><ul><li>Alcohol intake </li></ul><ul><li>Erratic insulin absorption </li></ul>achycardia xcessive hunger xcitability remors
    110. 122. <ul><li>Mild : </li></ul><ul><li>S hakiness </li></ul><ul><li>T remors </li></ul><ul><li>E xcessive hunger </li></ul><ul><li>P aresthesias </li></ul><ul><li>P allor </li></ul><ul><li>D iaphoresis </li></ul><ul><li>Rx : </li></ul><ul><li>10-15 gm carbohydrate </li></ul><ul><ul><li>2 oz. (1 small tube of) cake icing </li></ul></ul><ul><ul><li>4 oz. orange juice </li></ul></ul><ul><ul><li>6 oz. regular soda </li></ul></ul><ul><ul><li>6-8 oz 2% skim milk </li></ul></ul><ul><ul><li>(4 to) 10 pieces of hard candy </li></ul></ul>
    111. 123. <ul><li>Moderate : </li></ul><ul><li>D rowsiness </li></ul><ul><li>I mpaired judgment </li></ul><ul><li>D ouble or blurred vision </li></ul><ul><li>H eadache </li></ul><ul><li>I nability to concentrate </li></ul><ul><li>M ood swings </li></ul><ul><li>I rritability </li></ul><ul><li>S lurred speech </li></ul><ul><li>Rx : </li></ul><ul><li>20-30 gm carbohydrate </li></ul><ul><li>Glucagon 1 mg SQ/IM </li></ul>
    112. 124. <ul><li>Severe : </li></ul><ul><li>S eizures </li></ul><ul><li>U nconsciousness </li></ul><ul><li>D isorientation </li></ul><ul><li>Rx : </li></ul><ul><li>25 gm D 50 dextrose IV </li></ul><ul><li>Glucagon 1 mg IM/IV </li></ul>
    113. 125. DIABETES MELLITUS <ul><li>diabetic coma </li></ul><ul><li>Restlessness </li></ul><ul><li>Hot, dry, flushed skin </li></ul><ul><li>Thirst </li></ul><ul><li>Rapid pulse </li></ul><ul><li>Nausea </li></ul><ul><li>Fruity odor to breath </li></ul>
    114. 126. <ul><li>K etoacidosis </li></ul><ul><li>U rinary changes </li></ul><ul><li>S unken eyeballs </li></ul><ul><li>S kin is warm & flushed </li></ul><ul><li>M embranes are dry </li></ul><ul><li>A rrhythmias </li></ul><ul><li>U pset GI system </li></ul><ul><li>L ow BP </li></ul><ul><li>S aline solution </li></ul><ul><li>Rx : </li></ul><ul><li>Regular insulin drip </li></ul><ul><ul><li>0.9% or 0.45% NSS </li></ul></ul><ul><ul><li>1:1 [100U:100cc] </li></ul></ul><ul><li>Nursing care: </li></ul><ul><li>Check glucose </li></ul><ul><ul><li>250-300 mg/dL [q30-60mins] </li></ul></ul><ul><ul><li>250 mg/dL </li></ul></ul><ul><ul><ul><li>DC the drip </li></ul></ul></ul>
    115. 127. <ul><li>NON </li></ul><ul><li>K etosis is absent </li></ul><ul><li>E lectrolyte imbalance [K + decrease] </li></ul><ul><li>T hirst </li></ul><ul><li>O btundation </li></ul><ul><li>T reat with regular insulin drip </li></ul><ul><li>I nitiate diet </li></ul><ul><li>C orrect hyperglycemia </li></ul>
    116. 128. <ul><li>N ormal creatinine? </li></ul><ul><li>E rythrocyte sedimentation rate [ESR: 0-20 mm/hr] </li></ul><ul><li>P oor glycemic control </li></ul><ul><li>H emodialysis </li></ul><ul><li>R estrict: Na + , CHON, K + , weight </li></ul><ul><li>O utput & input (MIO) </li></ul><ul><li>N o symptoms </li></ul>
    117. 129. <ul><li>R educed O 2 in the eye </li></ul><ul><li>E levated sugar & BP </li></ul><ul><li>T ension is high in the retina </li></ul><ul><li>I ncreased lens opacity </li></ul><ul><li>N O eyesight </li></ul><ul><li>A nnual eye exam [every 6-12 months] </li></ul>
    118. 130. MAJOR DISORDERS OF THE ENDOCRINE SYSTEM THANK YOU! Nio C. Noveno, RN, MAN

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