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  1. What are the functions of Thyroxine (T4) & Triiodothyronine (T3)?
    To regulate protein synthesis & enzyme activity & to stimulate mitochondrial oxidation.
  2. What is the primary goal of the Thyroid gland?
    • ^ bodies metabolism
    • necessary for G&D in children
  3. What 3 hormones are secreted by the Thyroid gland?
    Triiodothyronine (T3), Thyroxine (T4), Calcitonin
  4. Explain how the Feedback mechanism works.
    Regulates T4 & T3 secretion from the thyroid gland via the hypothalamus releasing Thyrotropin releasing hormone (TRH), which stimulates the release of TSH (Thyroid stimulating hormone), which stimulates the release of T3 & T4.
  5. What is the etiology of Hypothyroidism?
    Insufficient circulating thyroid hormone
  6. What are the causes of Hypothyroidism?
    • Atrophy of gland w/aging
    • Irradiation, iodine deficiency or excess, Hashimoto's thyroiditis
  7. What are the s/s of Hypothyroidism?
    • Fatigue, lethargy
    • <mental acuity
    • Personality & mental changes
    • <cardiac output & contractility
    • <GI motility: constipation, achlorhyria
    • Cold intolerance
    • Myxedema ->facial puffiness, periorbital edema, masklike affect
    • Weight gain
    • Dry coarse skin
  8. What medications are used to Tx Hypothyroidism?
    Levothyroxine (synthroid, levothroid); ^levels of T3 & T4 hormones
  9. What is a critical nursing assessment with a client on Levothyroxine?
    Apical pulse & BP
  10. What are the s/e of Levothyroxine?
    • Wt loss
    • tremors
    • insomnia
    • nervousness
    • HTN
    • Tachycardia
  11. What is the etiology of Hyperthyroidism?
    An ^in circulating T3 & T4 levels, which results form an overactive thyroid gland or excessive output of thyroid hormones
  12. Hyperthyroidism has two classifications, what are they?
    • Grave's disease
    • Thyrotoxicosis
  13. What are the s/s of the hyperthyroid issue known as Grave's disease?
    • Tachycardia, palpitations
    • Nervousness, irritability, hyperactivity, emotional lablility, <attention span
    • ^appetite, wt loss
    • Exophthalmos (Bulging eyes)
    • insomnia
    • warm sweaty skin w/velvety smooth texture
    • Frequent stools-diarrhea
  14. What is the action of the drugs used to Tx hyperthyroidism? (Propylthiouracil {PTU}, Methimazole {Tapazole})
    • Inhibits thyroid hormone synthesis 
    • *blocker drugs
  15. When are these drugs used?
    • In Tx of Thyrotoxic crisis
    • Preparation for subtotal thyroidectomy
  16. What are the s/e of the hyperthyroidism drugs (PTU & Tapazole)?
    Blood disorders: <WBC & <platelets, HA, rash, hypothyroidism, GI upset, liver damage
  17. What are the nursing interventions for PTU & Tapazole (hyperthyroidism drugs)?
    • Monitor: VS, Wt
    • Admin before breakfast
    • Check OTC labels before using
    • Report s/e & s/s 
    • Medic alert bracelet
    • Warn of Iodine effects & presense of iodized salt, shellfish, OTC cough meds
    • Do NOT abruptly stop taking
    • s/s of hypothyroidism
    • s/s of hyperthyroidism
  18. What do the Parathyroid glands do?
    Secrete PTH (parathyroid hormone), which regulates calcium levels in the blood.
  19. A decrease in serum calcium stimulates the release of what?
    PTH, which ^calcium levels by mobilizing calcium from the bone, promoting calcium absorption from the intestine & promoting calcium reabsorption from the renal tubules.
  20. What 3 glands produce the hormone Calcitonin?
    • Mainly Thyroid gland
    • some by the Parathyroid & Thymus gland
  21. What is the action of the hormone Calcitonin?
    • Inhibits calcium reabsorption by bone & ^renal excretion of calcium
    • *counteracts the action of PTH
  22. The drug Calcitriol (Rocaltrol) is used to Tx which issues?
    • Hypoparathyroidism
    • Hypocalcemia in chronic renal failure patients
  23. What are the s/e of Calcitriol (Rocaltrol)?
    Anorexia, N/V/D, drowsiness, HA, dizziness, lethargy, photophobia, hypercalciuria, hematuria, hyperphosphatemia
  24. What is the critical nursing assessment when a client is taking Calcitriol (Rocaltrol)?
    Calcium levels
  25. What are the two parts to the Adrenal Glands?
    • Adrenal Cortex
    • Adrenal Medulla
  26. What does the Adrenal Cortex do?
    produces 2 types of hormones or corticosteroids: Glucocorticoids (cortisol) & Mineralocorticoids (Aldosterone)
  27. What causes the Adrenal glands secrete Cortisol?
    A <in serum cortisol levels ^CRF & ACTH secretions, which stimulate the adrenal glands to secrete & release cortisol.
  28. What is the action of Corticosteroids (hormones)?
    Promote sodium retention & potassium excretion.
  29. A deficiency of corticosteroids can result in serious illness or death because of their influence on what bodily functions?
    • electrolytes & carbohydrates, protein & fat metabolism.
    • regulates serum glucose
    • Suppresses inflammatory/immune response
    • Supports adaptation during stress
  30. What does the Adrenal glands Medulla secrete?
    Epinephrine & Norepinephrine
  31. A decrease in corticosteroid secretion is called what?
    • Adrenal hyposecretion
    • Adrenal insufficiency
    • Addison's Disease
  32. An increase in corticosteroid secretion is called what?
    • Adrenal hypersecretion
    • Cushing Syndrome
  33. A sudden and complete failure of the Adrenal Cortex is life threatening & called what?
    Adrenal Crisis
  34. What are the s/s of an Adrenal Crisis?
    • Confusion
    • Restlessness
    • Nausea
    • Vomiting
    • Hypotension
    • Circulatory collapse -> shock
  35. What are the medications used for replacement therapy in Addison's patients?
    • Glucocorticoids: hydrocortisone
    •                       methlyprednisolone
    •                       prednisone
    •                       triamcinolone
    •                       dexamethasone (Decadron)
    • Mineralcorticoid: Fludrocortisone acetate (Florinef)
  36. What should a client with Addison's be taught about potassium vs sodium?
    • ^Na+ intake during excess heat/humidity
    • <K+ d/t hyperkalemia
  37. In what forms can Corticosteroids (mineralocorticoids, glucocorticoids) be given?
    • Inhalations
    • Nasal sprays
    • Opthalmic
    • Otics
    • Topicals
    • IMs
  38. What is the action of the bodies natural Corticosteroids?
    promote sodium retention & potassium excretion.
  39. Name some Corticoid drugs.
    • Beclomethasone (Vanceril)
    • Fluticasone (Flonase)
    • Methylprednisolone (Solu-Medrol)
    • Hydrocortisone
    • Fludrocortsone (Florinef)
    • **Inhaled forms cause fewer systemic effects
  40. What are the s/e of the Glucocorticoid drugs?
    • Hyperglycemia (monitor w/DM clients)
    • ^risk for infection
    • Central obesity & Wt gain
    • HTN 
    • Cardivascular, fluid, electrolytes
    • Peptic ulcers
    • Skin fragility
    • Osteoporosis
    • CNS-euphoria, insomnia, behavioral
    • Growth failure
    • Inhaled: thrush
  41. What are the Corticosteroid drugs indicated for?
    • Respiratory disorders
    • Allergic reactions
    • Dermatologic disorders
    • GI disorders
    • Hemolytic disorders
    • Joint inflammation
    • Neoplastic diseases
    • Rheumatic disorders
    • Opthalmic disorders
    • Organ replacement
  42. What are the nursing implications for Glucocorticoids?
    • Give oral forms with milk, food or nonsystemic antacids (AL, Ca, or Mg salts) to minimize GI upset
    • Must avoid abrupt withdrawal
    • Avoid contact w/large crowds & those w/infections
    • Monitor for infections particularly fungal w/inhaled forms (oral or nasal)
    • Instruct patients to use topical forms exactly as ordered
    • Will need ^doses after stressful events such as surgery
  43. What is Cushing's Syndrome?
    • Overproduction of corticosteroids
    • Excessive administration of steroids
  44. What are the s/s of Cushing's Syndrome?
    • Wt gain-Truncal obesity
    • Acne
    • Muscle wasting
    • Osteoporosis, fractures
    • Thin, fragile skin (moon face, buffalo hump)
    • Hyperglycemia
    • HTN
    • Psychoses
  45. What is Diabetes Mellitus?
    • A chronic disease resulting from deficient glucose metabolism.
    • Caused by insufficient insulin secretion from the beta cells.
  46. Diabetes Mellitus is characterized by the "three P's".  What are they?
    • Polyuria: ^urine output
    • Polydipsia: ^thirst
    • Polyphagia: ^hunger
  47. What are the three types of Diabetes Mellitus?
    • Type 1; insulin-dependent DM
    • Type 2; non-insulin-dependent DM
    • Gestational
  48. Where is insulin released from?
    • Beta cells of the islets of Langerhans in pancrease.
    • Responds to ^in blood glucose
  49. What is the fxn of insulin?
    • Promotes uptake of glucose, amino acids & fatty acids
    • Converts to glycogen for future glucose needed in liver & muscles
  50. What are the s/s of Hyperglycemia?
    • Polyuria
    • Polyphagia
    • Polydipsia
    • Wt loss
    • Blurred vision
    • Fatigue
    • Fruity acetone odor of breath
  51. In Type 1 Diabetes (IDDM) the insulin makes little to no insulin.  Which age groups are prone to Type 1 Diabetes?
    Child, adolescent, young adult
  52. in Type 2 Diabetes (NIDDM), the pancreas produces insulin but what occurs with the receptors sites?
    The insulin receptor sites are either decreased or defective.
  53. Who are at risk for Type 2 Diabetes Mellitus (NIDDM)?
    Overweight, family Hx, Inactivity, certain ethnic groups, gestational diabetes, childhood obesity
  54. What are the Tx options for Type 2 Diabetes Mellitus (NIDDM)?
    • Weight loss
    • diet & excercise
    • oral hypoglycemics
  55. What are the s/s of Type 2 DM?
    • Polyuria
    • Slow healing cuts or sores
    • Numbness/tingling in hands or feet
    • Blurred vision &/or dizziness
    • itchy or dry skin
    • Fatigue
    • ^thirst
    • Frequent infections
  56. What are the complications to watch for with a client who has Diabetes Mellitus?
    • Kineys: Nephropathy
    • Nerve: Neuropathy
    • Circulatory system: peripheral vascular disease
    • Eyes: Retinopathy
    • Heart: Atherosclerotic Heart disease
    • Accelerated Atherosclerosis can lead to acute MI & Stroke
  57. What are the medications used to Tx Type 2 DM (NIIDM)?
    • Oral Anti-diabetic meds:
    • -sulfonylureas
    • -meglintinides
    • -biguanides
    • -thiazolidinediones (TZDs)
    • -alpha-glucosidase inhibitors
    • Insulins
  58. Where do the Anti-diabetic drugs Sulfonylureas work in the body?
    • Stimulate beta cells to ^insulin secretion
    • Alters sensitivity of peripheral insulin receptors

    in pancrease
  59. How often are Sulfonylureas taken in a NIDDM patient?
    Once a day
  60. Name the three Sulronylureas used for NIDDM patients.
    • Glyburide
    • Glimepiride
    • Glipizide
  61. Why are the three Sulfonylureas (glyburide, glimepiride, glipizide) able to work in patients with NIDDM (type 2)?
    Because in type 2 NIDDM the pancreas is still able to make some insulin
  62. What are the s/e of the three Sulfonylurea drugs? (glyburide, glimepiride, glipizide)
    • Hypoglycemia
    • Blood disorders
    • Wt gain
    • Seizures
    • coma
  63. What types of patients are Sulfonylureas cautioned in?
    • Liver or kidney dysfunction
    • elderly
    • malnourished
    • adrenal or pituitary insufficiency
  64. What is the action of the Meglintinide drugs (Starlix, Prandin) used for Type 2 NIDDM?
    Stimulate beta cells to ^insulin secretion from the pancrease
  65. What are the Meglintinide drugs used for Type 2 NIDDM?
    • Nateglinide (Starlix)
    • Repaglinide (Prandin)
  66. What is the main purpose of using the Meglintinide drugs in Type 2 NIDDM patients?
    • For <BS at mealtimes
    • they have a <chance of hypoglyceia
  67. What are the s/e of the Meglitinides (Starlix & Prandin)?
    • URI symptoms
    • HA
    • Hypoglycemia
    • Wt gain
  68. The Biguanides are used mainly for Type 2 NIDDM, what is their action? (Metformin/glucophage)
    • <glucose production by the liver
    • <intestinal absorption of glucose
    • ^use of glucose by muscles & fat cells
  69. What are the nursing implications with the Biguanide (Metformin/glucophage) drugs?
    • Take w/meals
    • Discontinue before giving contrast dye & restart after eval renal fxn
    • s/e: dizziness, fatigue, HA, agitation, metallic taste, GI distress, lactic acidosis, hepatotoxicity
  70. What is the action of the TZD drugs (Actos, Avandia) used to Tx Type 2 NIDDM?
    <insulin resistance by stimulating receptors on muscle cells to ^uptake of insulin
  71. What are the nursing implications with the TZD drugs Actos & Avandia?
    • Monitor Wt
    • s/e: URI's, hepatotoxicity, HA, edema, anemia, fluid retention, ^plasma volume
  72. Alpha-Glucosidase Inhibitor drugs work in the GI tract & are used for Type 2 NIDDM, what is their action? (Precose, Glyset)
    Inhibits enzyme that breaks down carbs, thus slows digestion.
  73. What are the two Alph-Glucosidase Inhibitor drugs used to Tx Type 2 NIDDM?
    • Acarbose (Precose)
    • Miglitol (Glyset)
    • *can be combined w/sulfonyurea
  74. What are the nursing implications for the Alpha-Glucosidase Inhibitors (Precose & Glyset)?
    • *give w/1st bite of each meal
    • s/e: GI ->flatulence, diarrhea, abdominal pain, cramping
  75. What are the contradictions with ALL oral anti-diabetic meds?
    • Known drug allergy
    • Severe Kidney disease
    • Sever Liver disease
    • Pregnancy
  76. What are the nursing implications with ORAL anti-diabetic meds?
    • *Liver & Kidney fxn tests
    • know what your administering: d/t combo drugs
    • ensure client can tolerate food & eat b4 admin
    • ensure there are orders for when pt is NPO
    • Teach: s/s hypo/hyperglycemia, avoid alcohol, medic alert bracelet
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2013-10-29 13:45:18

chap 51&52 PP page 3-
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