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THYROID DISORDERS

PATHOPHYSIOLOGY. thyroid hormone secretion leads to hyperthyroidismWhat you see in this is called: thyrotoxicosis. . WHAT DO THYROID HORMONES AFFECT?. Metabolism in all body organsStimulate the heart heart rate stroke volume cardiac output blood flow. . . . . HYPERTHYROIDISM. I

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THYROID DISORDERS

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    1. THYROID DISORDERS HYPERTHYROIDISM HYPOTHYROIDISM

    2. PATHOPHYSIOLOGY thyroid hormone secretion leads to hyperthyroidism What you see in this is called: thyrotoxicosis

    3. WHAT DO THYROID HORMONES AFFECT? Metabolism in all body organs Stimulate the heart heart rate stroke volume cardiac output blood flow

    4. HYPERTHYROIDISM INCREASED THYROID HORMONES: Hypermetabolism sympathetic nervous system activity Effects protein, lipid and carbohydrate metabolism

    5. EFFECTS ON PROTEIN METABOLISM Protein synthesis and degradation More breakdown than buildup Leads to loss of protein Called negative nitrogen balance Degradation (breakdown)Degradation (breakdown)

    6. EFFECTS ON GLUCOSE Glucose tolerance decreased Leads to hyperglycemia

    7. EFFECTS ON FAT METABOLISM fat metabolism body fat appetite food intake; food intake does not meet energy demands weight nutritional deficiencies with prolonged disease

    8. CAUSES GRAVES DISEASE: Client has a goiter (enlarged thyroid gland (p1484) Autoimmune problem Antibodies attach to gland causing it to enlarge SYMPTOMS: exophthalmos (protrusion of the eyes) p1484) Pretibial myxedema (dry, waxy swelling of the frontal surfaces of the lower legs)

    9. ADDITIONAL CAUSES OF HYPERTHYROIDISM TOXIC MULTINODULAR GOITER: multiple thyroid nodules, milder disease EXOGENOUS HYPERTHYROIDISM: excessive use of thyroid replacement hormones THYROID STORM: untreated or poorly controlled hyperthyroidism; life threatening

    10. WHO GETS IT Most often women between 20-40 yrs

    11. ASSESSMENT Recent wgt loss Increased appetite Increase in # BM/day ****heat intolerance Diaphoresis even when temperatures comfortable for others Palpitations/chest pain Dyspnea with or without exertion

    12. ASSESSMENT VISUAL PROBLEMS MAY BE EARLIEST PROBLEM: Infiltrative Exophthalmopathy (abnormal eye appearance or function) Blurring/double vision/tiring of eyes Increased tears Photophobia Eyelid retraction(eyelid lag) (p1483) Globe lag (eyeball lag) (p1483) Infiltrative Exophthalmopathy (abnormal eye appearance or function): the wide-eyed or startle look is due to edema in the extraocular muscles and increased fatty tissue behind the eye which pushes the eyeball forward. Pressure on the optic nerve may impair vision Swelling and shortening of the muscles may cause problems with focusing Corneal ulcers or infection: if eyelid fails to close completely leaving eye unprotected Eyelid retraction(eyelid lag) (p1483): upper eyelid fails to descend when the client gazes slowly downward Globe lag (eyeball lag) (p1483: upper eyelid pulls back faster than the eyeball when the client gazes upward To assess: ask client to look down and then look up and document the response Infiltrative Exophthalmopathy (abnormal eye appearance or function): the wide-eyed or startle look is due to edema in the extraocular muscles and increased fatty tissue behind the eye which pushes the eyeball forward. Pressure on the optic nerve may impair vision Swelling and shortening of the muscles may cause problems with focusing Corneal ulcers or infection: if eyelid fails to close completely leaving eye unprotected Eyelid retraction(eyelid lag) (p1483): upper eyelid fails to descend when the client gazes slowly downward Globe lag (eyeball lag) (p1483: upper eyelid pulls back faster than the eyeball when the client gazes upward To assess: ask client to look down and then look up and document the response

    13. GOITER Thyroid gland may be 4 X normal Bruits (turbulence from increased blood flow) heard with stethoscope

    14. CARDIAC PROBLEMS systolic BP tachycardia dysrhythmia

    15. FURTHER SYMPTOMS Fine, soft, silky hair Smooth, moist skin Muscle weakness Hyperactive deep tendon reflexes Tremors of hands Restless, irritable, mood swings Decreased attention span Fatigued, inability to sleep

    16. LABORATORY ASSESSMENT IN HYPERTHYROIDISM: T3 T4 TSH in Graves disease Radioactive Thyroid Scan Ultrasonography: used to determine goiter or nodules EKG: note tachycardia

    17. DRUG THERAPY ***antithyroid drugs: thioamides propylthiouracil (PTU) methimazole (Tapazole) carbimazole (Neo-Mercazole) ACTION: blocks thyroid hormone production; takes time Need to control cardiac manifestations (tachycardia, palpitations, diaphoresis, anxiety) until hormone production reduced: use beta-adrenergic blocking drugs: propranolol (Inderal, Detensol)

    18. DRUG THERAPY Iodine preparations: Lugols Solution SSKI (saturated solution of potassium iodide) Potassium iodide tablets, solution, and syrup ACTION: decreases blood flow through the thyroid gland This reduces the production and release of thyroid hormone Takes about 2 wks for improvement Leads to hypothyroidism

    19. DRUG THERAPY Lithium Carbonate ACTION: inhibits thyroid hormone release NOT USED OFTEN BECAUSE OF SIDE EFFECTS: depressions, diabetes insipidus, tremors, N&V

    20. DRUG THERAPY RADIOACTIVE IODINE THERAPY: Receives RAI in form of oral iodine Takes 6-8 Weeks for symptomatic relief Additional drug therapy used during this type of treatment Not used on pregnant women

    21. SURGICAL MANAGEMENT Why use surgery? Used to remove large goiter causing tracheal or esophageal compression Used for pts who do not have good response to antithyroid drugs TWO TYPES OF SURGERIES: Total thyroidectomy (must take lifelong thyroid hormone replacement) Subtotal thyroidectomy

    22. PREOPERATIVE CARE Low weight: Hi protein, hi CHO diet for days/weeks before surgery

    23. PRE-OPERATIVE CARE Antithyroid drugs to suppress function of the thyroid Iodine prep (Lugols or K iodide solution) to decrease size and vascularity of gland to minimize risk of hemorrhage, reduces risk of thyroid storm during surgery Tachycardia, BP, dysrhythmias must be controlled preop

    24. PREOPERATIVE TEACHING Teach C&DB Teach support neck when C&DB Support neck when moving reduces strain on suture line Expect hoarseness for few days (endotracheal tube)

    25. POST-OP THYROIDECTOMY NURSING CARE VS, I&O, IV Semifowlers Support head Avoid tension on sutures 5. Pain meds, analgesic lozengers

    26. POSTOP THYROIDECTOMY NURSING CARE Humidified oxygen, suction First fluids: cold/ice, tolerated best, then soft diet Limited talking , hoarseness common Assess for voice changes: injury to the recurrent laryngeal nerve

    27. POSTOP THYROIDECTOMY NURSING CARE CHECK FOR HEMORRHAGE 1st 24 hrs: Look behind neck and sides of neck Check for c/o pressure or fullness at incision site Check drain REPORT TO MD CHECK FOR RESPIRATORY DISTRESS Laryngeal stridor (harsh hi pitched resp sounds) Result of edema of glottis, hematoma,or tetany Trach set/airway/ O2, suction CALL MD for extreme hoarseness Check every 30-60 min for extreme hoarseness (S&S) of respiratory distressCheck every 30-60 min for extreme hoarseness (S&S) of respiratory distress

    28. TETANY accidental removal of the parathyroid gland during surgery can happen This disturbs the Ca metabolism low blood calcium: see hyper-irritability of the nerves, spasms of the hands and feet, muscle twitchings occur, tingling, around mouth/toes/fingers RISK: laryngospasm, airway obstruction TREAT: IV calcium gluconate or calcium chloride

    29. POSTOP NURSING CARE CHECK FOR THYROID STORM: 25% mortality rate result of release of TH during surgery Observe for fever, tachycardia, systolic hypertension, agitation leading to seizures, delirium and coma, heart failure and shock TREAT: Patent airway, cardiac monitor Antithyroid drugs IV: PTU, propyl-Thyracil, Tapazole, sodium iodide solution Inderal, Detensol for cardiac symptoms Glucocorticoids (hydrocortisone IV) Antipyretics and cooling blanket for fever

    30. HYPOTHYROIDISM Decreased levels of Thyroid Hormone

    31. CAUSES Cells damaged; no longer function Cells might be normal, person doesnt ingest enough iodide & tyrosine needed to make thyroid hormones

    32. SYMPTOMS Blood levels of thyroid hormones are low Decreased metabolic rate Hypothalamus and anterior pituitary gland make stimulatory hormones (TSH) as compensation Thyroid gland enlarges forming goiter

    33. MYXEDEMA DEVELOPS With low metabolism metabolites build up inside the cells which increases mucous and water leading to cellular edema Edema changes clients appearance Nonpitting edema appears everywhere especially around the eyes, hands, feet, between shoulder blades Tongue thickens, edema forms in larynx, voice husky

    34. INCIDENCE OF HYPOTHYROIDISM 30-60 yrs of age Mostly women

    35. ASSESSMENT Increased sleeping (14-16 hours daily) Generalized weakness Anorexia Muscle aches Paresthesias Constipation Cold intolerance Decreased libido, woman:difficulty becoming pregnant, changes in menses;men/impotence

    36. ASSESSMENT Coarse features Edema around eyes and face Blank expression Thick tongue Overall muscle movement is slow Lethargic, apathetic, drowsy, poor attention span, poor memory

    37. LABORATORY ASSESSMENT T3 T4 TSH

    38. DRUGS THAT IMPAIR THYROID FUNCTION lithium carbonate (Lithane) Aminoglutethimide Sodium or potassium perchlorate Thiocyanates cobalt

    39. NURSING DIAGNOSES Decreased cardiac output RT altered heart rate and rhythm as a result of decreased myocardial metabolism Ineffective Breathing pattern RT to decreased energy, obesity and fatigue Disturbed thought processes RT to impaired brain metabolism and edema Imbalanced nutrition More than body requirements RT to excessive intake in relation to metabolic needs Hypothermia RT to decreased metabolic rate Constipation RT to decreased motility of the GI tract Disturbed body image RT to illness Deficient knowledge of condition, diagnosis and TX RT to cognitive limitationDecreased cardiac output RT altered heart rate and rhythm as a result of decreased myocardial metabolism Ineffective Breathing pattern RT to decreased energy, obesity and fatigue Disturbed thought processes RT to impaired brain metabolism and edema Imbalanced nutrition More than body requirements RT to excessive intake in relation to metabolic needs Hypothermia RT to decreased metabolic rate Constipation RT to decreased motility of the GI tract Disturbed body image RT to illness Deficient knowledge of condition, diagnosis and TX RT to cognitive limitation

    40. NURSING INTERVENTIONS EXPECTED OUTCOMES: Maintains HR greater than 60/min Maintains BP within normal limits No dysrhythmia, peripheral edema, neck vein distension

    41. TREATMENT LIFELONG THYROID HORMONE REPLACEMENT levothyroxine sodium (Synthroid, T4, Eltroxin) IMPORTANT: start at low does, to avoid hypertension, heart failure and MI Teach about S&S of hyperthyroidism with replacement therapy

    42. MYEXEDEMA COMA Rare serious complication of untreated hypothyroidism Decreased metabolism causes the heart muscle to become flabby Leads to decreased cardiac output Leads to decreased perfusion to brain and other vital organs Leads to tissue and organ failure LIFE THREATENING EMERGENCY WITH HIGH MORTALITY RATE

    43. PROBLEMS SEEN WITH MYXEDEMA COMA Coma Respiratory failure Hypotension Hyponatremia Hypothermia hypoglycemia

    44. TREATMENT OF MYEXEDEMA COMA Patent airway Replace fluids with IV NSSS Give levothyroxine sodium IV Give glucose IV Give corticosteroids Check temp, BP hourly Monitor changes LOC hourly Aspiration precautions, keep warm

    45. PARATHYROID DISORDERS HYPERPARATHYROIDISM HYPOPARATHYROIDISM

    46. RESPONSIBILITY OF GLANDS Maintain calcium and phosphate balance

    47. INCREASED PTH EFFECTS ON KIDNEY acts directly on the kidney causing increased kidney reabsorption of calcium and increased phosphate excretion Leads to hypercalcemia and hypophosphatemia

    48. INCREASED PTH EFFECTS ON BONE Increase bone resorption (bone loss of calcium) by decreasing osteoblastic (bone production) activity and increasing osteoclastic (bone destruction activity) This process releases Ca and phosphate into the blood and reduces bone density

    49. CHRONIC CALCIUM EXCESS Calcium is deposited in soft tissues

    50. CAUSES OF HYPERPARATHYROIDISM Tumors Trauma Radiation Vit D deficiency Chronic renal failure with hypocalcemia

    51. ASSESSMENT High levels of PTH: Cause renal calculi Pathologic fractures Osteoporosis High levels of Calcium: Anorexia, N/V, constipation, wgt loss, peptic ulcers Fatigue/lethargy Mental confusion, psychosis, coma, death if serum Ca greater than 12 mg/dL

    52. LABORATORY ASSESSMENT Serum calcium elevated: normal range: 9-10.5mg/dL Serum phosphate decreased: Normal 3.0-4.5mg/dL Serum parathyroid hormone increased: Normal 50-330 pg/ml

    53. NONSURGICAL MANAGEMENT GOAL: reduce serum calcium levels Hydration: IV saline in large volumes promotes renal excretion of calcium Diuretics: furosemide (Lasix, Uritol) - increases kidney excretion of calcium

    54. INTERVENTIONS Assess cardiac function and I&O q2-4 hrs during hydration therapy Continuous cardiac monitoring Close monitoring of serum calcium levels reporting precipitous drops to MD Sudden drops may lead to tingling/numbness in muscles

    55. DRUG THERAPY PHOSPHATES: oral phosphates inhibit bone resorption and interfere with calcium absorption IV only used when serum calcium levels need rapid lowering

    56. DRUG THERAPY CALCITONIN: Decreases the release of calcium and increases the kidney excretion of calcium Best effect when combined with glucocorticoids

    57. DRUG THERAPY CALCIUM CHELATORS: Lower calcium levels by binding (chelating) calcium which reduces the levels of free calcium FIRST EXAMPLE: mithramycin (cytotoxic agent), one IV dose can lower serum calcium in 48 hrs DANGER: THROMBOCYTOPENIA, increased tendency to bleed, kidney and liver toxicity SECOND CALCIUM CHELATOR: penicillamine (Cuprimine, Pendramine)

    58. SURGICAL REMOVAL OF PARATHYROID GLAND Used to manage hyperparathyroidism Surgery similar to that of removal of thyroid gland

    59. HYPOPARATHYROIDISM

    60. PATHO Rare disorder Parathyroid function decreased Either lack of PTH secretion or lack of effectiveness of PTH secretion End Result: hypocalcemia Caused by: removal of glands during thyroidectomy, or hypomagnesemia (seen in alcoholics or chronic renal disease, or malnutrition); causes impairment of PTH secretion

    61. ASSESSMENT Mild tingling and numbness due to tetany Tingling and numbness around the mouth or in the hands and feet reflect mild to moderate hypocalcemia Severe muscle cramps, carpopedal spasms, and seizures (with no loss of consciousness or incontinence), mental changes from irritability to psychosis reflect a more severe hypocalcemia)

    62. ASSESSMENT Positive signs indicating potential tetany CHVOSTEKS SIGN: sharp tapping over facial nerve causes twitching of mouth, nose and eye TROUSSEAUS SIGN: carpopedal spasm induced by application of BP cuff

    63. LABORATORY ASSESSMENT EEG CT scan (shows brain cacifications from chronic hypocalcemia) Serum calcium: Serum phosphate: Serum magnesium: Serum vitamin D:

    64. INTERVENTIONS CORRECT HYPOCALCEMIA: IV calcium with 10% solution of calcium chloride or calcium gluconate over 10-15 minutes; then long term oral therapy Calcium 0.5-2G daily Oral calcium: OSCAL Calcium gluconate Calcium lactate Calcium carbonate

    65. INTERVENTIONS CORRECT VITAMIN D DEFICIENCY: large doses of vit D to increase absorption of Calcium; acute treated with calcitriol (Rocaltrol) CORRECT HYPOMAGNESEMIA: acute is treated with 50% magnesium sulfate either IM or IV Then long term is treated with 50,000 to 400,000 Units of ergocalciferol daily

    66. INTERVENTIONS DIET: high in calcium, low in phosphorus Avoid milk, yogurt and processed cheeses because of high phosphorus content aluminun hydroxide (Amphogel) with or before meals to decrease phosphate levels THERAPY FOR HYPOCALCEMIA IS LIFELONG WEAR MEDIC ALERT

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