Endocrine 3

  1. thyroid hormone primary action
    • -maintain energy homeostasis
    • -stimulate cell metabolism and activity
  2. Thyroid gland innervation
    • -adrenergic fibers coming off the cervical ganglion
    • -cholinergic fibers from the vagus nerve
    • -autonomic innervation controls blood flow
  3. How does adrenergic stimulation affect blood flow to the thyroid gland?  What about cholinergic stimulation?
    • Adrenergic increases blood flow
    • Cholinergic decreases blood flow
  4. thyroid functional anatomy
    made up of follicles (acini), surrounded by a layer of follicular cells, and filled with colloid

    colloid is made up of thyroglobulin (a large glycoprotein)
  5. Where are thyroid hormones stored?
    In the thyroglobulin molecule that is in the colloid (which is in the follicle of the thyroid gland)
  6. How much thyroid hormone can the thyroid gland store?
    Enough to supply the body its usual requirement for 2-3 months
  7. T or F, iodine and thyroglobulin (which contains about 70 tyrosine AA) combine to form the thyroid hormones?
  8. The other name for T4
  9. Of the thyroid hormones, how much is T4 and how much is T3?
    • T4 90%
    • T3 9%
  10. Normal total level of T4 (thyroxine)?
    Normal free level of T4?
    • total 5-12 mcg/dl
    • free 1-2 ng/dl
  11. Biologic half life of T4
    6-8 days
  12. Is the free portion of the thyroid hormones bound or unbound?
    unbound to proteins
  13. Normal T3 level?
    Half life?
    • T3 level 80-200 ng/dl
    • Half life 24 hours
  14. How much iodine do we need?  Why?
    • 1 mg iodine / week
    • -essential for the formation of thyroid hormones
  15. T3's other name
  16. Which is more potent- T3 or T4?
  17. Do T3 and T4 have the same qualitative effects?
  18. Explain how ingested iodine is involved in forming T3 and T4
    • -Iodine that we ingest gets absorbed in the GI tract
    • -Gets converted to an anion (iodide)
    • -Actively transported to the thyroid
    • -Converted back to iodine and hooked onto AA tyrosine to from T3 and T4
  19. What percent of T3 and T4 are bound to specifically to TBG (thyroid binding globulin)?  What percent are protein bound?
    What effect does this have?
    • 70% bound to TBG
    • 99% protein bound 

    acts as a reservoir and delays elimination of thyroid hormones
  20. Why do we need to check free T4 levels as opposed to total T4 levels?
    Only the free T4 is active (pt may have a high amount of T4 bound to TBG, but this doesn't mean the pt is hyperthyroid as the bound portion is not available)
  21. To properly evaluate thyroid function what 2 labs should we look at?
    free T4 and TSH
  22. Explain the hypothalamic-pituitary-thyroid axis
    • -Hypothalamus makes and releases (TRH) thyrotropin releasing hormone
    • -This stimulates TSH release from the anterior pituitary
    • -This stimulates the thyroid to increase synthesis and release of T3 and T4
    • -The free T3 and T4 inhibit TRH and TSH via negative feedback
  23. Aside from high levels of T3 and T4, what else can inhibit thyroid hormone production (by inhibiting TSH)?
    • -dopamine
    • -somatostatin
    • -glucocorticoids
  24. What effect do the thyroid hormones have on CHO metabolism?
    • -stimulates all aspects of CHO metabolism
    • -rapid glucose uptake (increase glycolysis, gluconeogenesis, absorption from the GI tract, and insulin secretion)
    • -likely due to increase in cellular metabolic enzymes
  25. What effect do the thyroid hormones have on fat metabolism?
    • -stimulate fat metabolism
    • -lipids are mobilized from adipose
    • -fat stores decrease
    • -FA concentration in the plasma increases FA oxidation by the cells
    • -decreased cholesterol, phospholipids, and triglycerides
  26. Why will hypothyroid pts have increased cholesterol levels?
    Increased TH decreases the concentration of cholesterol in the plasma, since they lack TH, their cholesterol is high
  27. How do the thyroid hormones affect vitamin requirements, BMR, and body weight?
    • Vit requirent and BMR are increased
    • Body weight is decreased
  28. What effect do the thyroid hormones have on CV system?
    • -increased blood flow
    • -increased CO
    • -increased HR
    • -increased strength of contraction
    • -increased end products of metabolism as well (increased CO2 causing VD)
  29. How do the thyroid hormones affect MAP?
    MAP is unchanged
  30. How do the thyroid hormones affect respirations, GI motility, and CNS?
    • -Increased respirations and  GI motility
    • -CNS excitation.
  31. Why does thyroid hormone increase the rate of secretion of other hormones?
    It increases metabolism and therefore increases the requirement for other hormones
  32. How does thyroid hormone affect adipose tissue and muscle?
    Catabolic to both.  Leads to lipolysis and protein breakdown.  
  33. What is the most physiologically active form of thyroid hormone?
    • free T4
    • -represents only about 0.02% of the total T4 level
  34. What is the best measure of thyroid hormone at the cellular level?
  35. TSH normal values
    0.4-5 mU/L
  36. What is the incidence of hypothyroidism in adults?
  37. Primary hypothyroidism
    • -decreased production of thyroid hormone in the setting of increased or normal TSH
    • -95% of all cases
    • -usually from surgical removal or radiation
  38. Hashimoto's thyroiditis
    • -most common form of primary hypothyroidism
    • -Autoimmune process destroys thyroid tissue
    • -TSH can't exert it's effects on the thyroid (no thyroid hormone production)
  39. Secondary hypothyroidism
    • -due to hypothalamic or pituitary disease
    • -5% of cases
  40. Clinical manifestations of hypothyroidism
    • -cold intolerance
    • -somnulence
    • -slow and insidious onset
    • -mental and physical slowing, lethargy, apathy
    • -wt gain with decreased appetite (decreased BMR)
    • -large tongue, brittle hair, thick skin
  41. CV changes associated with hypothyroidism
    • -Decreased SV, HR, and CO
    • -impaired baroreflex
    • -ventricular arrhythmias
    • -increased peripheral vascular resistance, decreased blood volume
    • -increased cholesterol and triglycerides
  42. Why might someone with hypothyroidism be an aspiration risk?
    Due to decreased GI function
  43. Respiratory effects of hypothyroidism
    • -decreased VLC and diffusion capacity
    • -decreased ventilatory response to hypoxia and hypercarbia (careful with sedation)
  44. Diagnosis of hypothyroidism
    • *Increased TSH*
    • Decreased T3 and T4

    • Subclinical- increased TSH with normal T4 (few symptoms)
    • Overt- marked decrease in T4 and TSH 90 mU/L
  45. Hypothyroidism treatment
    • Levothyroxine
    • peaks in 10-12 days
    • half life 7.5 days (but varies if hypo or hyperthyroid due to changes in BMR)
  46. What does a total T4 level of < 1 mcg/ dl mean?
    Severe hypothyroidism, need to cancel elective surgery
  47. Pre-anesthesia evaluation for hypothyroidism
    • -airway!  pt may have tracheal deviation from enlarged thyroid or edema of VC and oral cavity
    • -? reflux due to delayed gastric emptying
  48. Is a pt with subclinical hypothyroidism ok to proceed with elective surgery?
  49. What Na+ abnormality may be seen with hypothyroidism
    -hyponatremia (dilutional due to impaired free water excretion)
  50. How are deep tendon reflexes affected with hypothyroidism?
    DTR are prolonged, pt may have increased NMB activity
  51. T or F, hypothyroidism causes MAC to be decreased?
    F, CO is decreased, so it only appears that MAC is decreased 
  52. Is neo or ephedrine preferred when treating hypotension in a hypothyroid pt?
    Ephedrine as neo will cause an increase in SVR and due to decreased CO the pt's heart might not be able to pump against the increased rx
  53. myxedema coma
    • -extreme hypothyroidism
    • -medical emergency, mortality > 50%
    • -most common in elderly women with long h/o hypothyroidism
    • -characterized by: delirium, unconsciousness, hypoventilation, hypothermia, bradycardia, hypotension, and severe dilution hyponatremia
  54. Myxedema coma treatment
    T3 and T4 (but remember they take a while to kick in)
  55. Hyperthyroidism causes
    • Grave's disease
    • toxic adenoma
    • toxic nodular goiter
  56. Clinical manifestations of hyperthyroidism
    • -hypermetabolic state
    • -anxiety, restlessness
    • -warm moist skin, flushed
    • -heat intolerance
    • -muscle weakness and wasting
    • -osteoporosis
    • -wt loss despite increased caloric intake
    • -tremor 
  57. What effect does thyroid hormone have on bones
    Promotes bone deposition and growth
  58. CV side effects of hyperthyroidism
    • -Tachycardia, palpitations, and arrhythmias
    • -Increased cardiac work
    • -hyperdynamic circulation (increased CO and myocardial contractility)
    • -cardiomegaly
  59. Subclinical hyperthyroidism
    • -Few s/sx 
    • -Increased HR
  60. Grave's disease
    • -autoimmune
    • -leading cause of hyperthyroidism
    • -0.4% of population
    • -F:M= 7:1
    • -usually ages 20-40 
  61. Grave's disease classic triad
    • -hyperthyroidism
    • -exopthalamus (abnormal connective tissue deposits in orbit and extraoccular muscles)
    • -dermopathy (edematous skin)
  62. Hyperthyroidism labs
    • -Increased T3 and T4
    • -Decreased TSH
  63. Medical hyperthyroidism treatment
    • -1st line treatment- anti-thyroid drugs- methimazole and PTU (propylthiouricil), inhibit synthesis of thyroid hormones
    • -Inorganic iodine- AKA Lugol's solution, (inhibits thyroid hormone release), immediate but short term effects
    • -radioiodine treatment (destroys thyroid gland)
    • -BB to relieve symptoms
  64. Surgical hyperthyroidism treatment
    • -subtotal or total thyroidectomy
    • -pts must be euthyroid first
    • -prompt control (stored hormones can't be released)
    • -corrects thyrotoxicosis in 95% of pts
  65. Complications of thyroidectomy
    • -hemorrhage with tracheal compression
    • -recurrent laryngeal nerve damage (hoarseness and dyspnea post-op)
    • -inadvertent removal of parathyroids
  66. Thyroid storm
    • AKA thyrotoxic crisis
    • -life threatening
    • -associated with major surgery or severe illness
    • -likely to occur 6-18-24 hours post-op
  67. CM of thyrotoxic crisis
    • -hyperthermia (105)
    • -severe tachycardia
    • -restlessness, agitation, tremor
    • -LOC, hypotension, HF
  68. Treatment of thyroid storm
    • -K iodine (Lugol's solution)
    • -PTU (not available IV)
    • -BB
    • -peripheral cooling, IVF
    • -glucocorticoids (hypermetabolic state may be linked to relative cortisol deficiency)
  69. Differentiation between MH and thyroid storm
    • -MH has muscle rigidity, increased CK levels, and acidosis
    • -thyroid storm does not
  70. Pre anesthesia evaluation of pts with hyperthyroidism
    • -elective surgery deferred until pt is euthyroid
    • -emergency cases require PTU, BB (esmolol), and cortisol
    • -AIRWAY!!
  71. What medications might you want to avoid with hyperthyroidism
    • -anticholinergics (increased HR)
    • -ex: scop patch

    -ketamine, pancuronium, epi, ephedrine
  72. Where are the parathyroids located?
    • Embedded within the thyroid
    • 2 in the superior thyroid
    • 2 in the inferior thyroid
    • -number and location may vary
  73. 2 types of parathyroid cells
    • -chief cells (majority)- produce and secrete parathyroid hormone
    • -oxyphil cells- unknown action
  74. What type of hormone is parathyroid hormone?
  75. parathyroid hormone target organ
    bones and kidneys
  76. Major effects of parathyroid hormone
    • -maintain Ca++ homeostasis according to plasma Ca++ levels
    • -increases plasma Ca++ level and decreases plasma phosphorus level
    • -bone resorption of Ca++ (moves Ca++ from the bone into the plasma)
    • -increases kidneys reabsorption of Ca++ in the distal tubules
  77. What factors increase PTH release?
    • Hypocalcemia
    • Catecholamines
    • Hyperphosphatemia
  78. What factors supress PTH release?
    • Hypercalcemia
    • Vitamin D
    • Severe hypomagnesemia
  79. Where is calcitonin released from?
    Parafollicular cells of the thyroid
  80. What does calcitonin do?
    Decreases plasma Ca++ levels
  81. Which is more important in terms of regulating plasma Ca++ levels- calcitonin or PTH?
  82. How much Ca++ is in the body and where is the majority stored?
    • 1100 g
    • 99% in bones and teeth
  83. Various forms of Ca++ in the body and percentages
    • Ionized 50%
    • Protein bound 41%
    • Complexed to anions 9%
  84. What form of Ca++ is physiologically active?
  85. What form of Ca++ is able to diffuse thru a lipid membrane?
    • The Ca++ complexed to anions
    • -protein bound can't (too big)
    • -ionized can't (due to its charge, but it can go thru Ca++ channels)
  86. Total Ca++ normal value
    9-10 mg /dl
  87. Ionized Ca++ normal value
    4.5-5 meq/l
  88. What effect do PTH and calcitonin have on phosphorus levels?
    Decreases phos reabsorption (phos is excreted in the urine)
  89. Role of vitamin D on calcium levels
    • -enhances absorption of dietary Ca++ from the GI tract
    • -helps to reabsorb Ca++ from the renal tubules
    • -both help to increase plasma Ca++ levels
  90. Hypoparathyroidism
    • -impaired production of PTH
    • -may be associated with other endocrine disorders
    • -usual cause is surgical removal of the parathyroids
  91. Pseudohypoparathyroidism
    • -congenital disorder where the kidneys don't respond to PTH
    • -pts have MR, calcifications of basal ganglia, obesity, and structural abnormalities
  92. Hypoparathyroidism CM
    • -hypocalcemia
    • -chovstek and trousseaus sign
    • -paresthesias
    • -convulsions
    • -decreased myocardial contractility
    • -1st degree AVB
    • -laryngospasm
    • -CHF and hypotension
  93. Hypoparathyroidism treatment
    • -high Ca++ diet with vitamin D
    • -decrease renal Ca++ clearance with thiazide diuretics
    • -acute hypocalcemia treated with 10 ml of 10% calcium gluconate
  94. Hypoparathyroidism- anesthesia implications
    • -prevent further decreases in Ca++ levels
    • -(avoid hyperventilation as alkalosis will further decrease Ca++ levels)
    • -ACD PRBC preservative can bind to Ca++ 
    • -avoid albumin as it will bind to Ca+
    • -treat adverse effects of hypocalcemia
  95. Hyperparathyroidism
    • -excess secretion of PTH
    • -primary, secondary, or ectopic
    • -hallmark is serum total Ca++ of >5.5 meq/L or ionized > 2.5 meq/L
  96. Primary hyperparathyroidism
    • -90% due to benign parathyroid adenoma (also with hyperplasia, it's the most common presenting symptom of MEN type 1)
    • -also due to carcinoma
    • -excess PTH secretion
  97. Secondary hyperparathyroidism
    • -response of parathyroid to secrete excess PTH to counteract hypocalcemia from some other disease process (ex: renal disease)
    • -hypercalcemia does not usually occur as hypersecretion is 2/2 hypocalcema
    • -treatment is to control underlying disease
  98. Ectopic hyperparathyroidism
    • -AKA pseudohyperparathyroidism
    • -secretion of PTH by tissues other than the parathyroid
    • -occurs in CA of lung, breast, or kidney
  99. CM of hyperparathyroidism
    • -high Ca++ and low Phos levels
    • -s/sx r/t high ionized calcium
    • -decreased neuromuscular excitability
    • -muscle weakness, decreased muscle tone
    • -confusion, coma
    • -polyuria and polydipsia
  100. Hyperparathyroidism treatment
    • Temporizing: hydration with IV saline, loop diuretics to inhibit calcium reabsorption in L of H
    • Definitive: surgical, removal of abnormal or diseased gland, Ca++ levels normalize within 3-4 days
  101. Anesthesia implications of hyperparathyroidism
    • -maintain adequate hydration and UO
    • -careful with sedation and avoid ketamine 2/2 mental status changes and somnolence
    • -consider possibility of co-existing renal disease with drug selection
    • -assess if primary, secondary, or ectopic
Card Set
Endocrine 3
Thyroid and parathyroid