Endocrine Lecture 3 Thyroid

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cmatthews
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236533
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Endocrine Lecture 3 Thyroid
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2013-09-23 18:49:12
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BC CRNA PV3 Endocrine
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Endocrine Lecture 3 Thyroid
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  1. Primary physiologic effect of thyroid hormones is..........
    to stimulate cell metabolism and activity
  2. Describe the anatomy of the thyroid (where it is and the what are the parts)
    • Anterior to the trachea.
    • Two lobes connected by bridge of tissue (referred to as the isthmus) below the pyramidal lobe.
    • Isthmus itself will extend across the ventral surface of the trachea
  3. Thyroid weighs between ___ - ___g in the adult
    15-20
  4. Why can you sometimes hear a bruit over the thyroid gland?
    It has significant blood flow, can increase dramatically in goiter and cause a bruit
  5. What kind of nerve innervation does the thyroid have?
    • Autonomic innervation controls the blood flow.
    • Innervated by adrenergic fibers coming off the cervical ganglion (increased blood flow)
    • Cholinergic fibers from the vagus nerve (decreased blood flow)
  6. Describe the MICROSCOPIC anatomy of the thyroid
    Multiples follicles (acini) surrounded by a layer of follicular cells (FC) and filled with colloid (C).
  7. Colloid makes up __% of the thyroid gland (in terms of mass) and a major constituent of colloid is ____________, a large glycoprotein.
    30; thyroglobulin
  8. Each molecule of thyroglobulin contains about __ ___ ____ ___which then combine with iodine to form the thyroid hormones.
    70 tyrosine amino acids
  9. Thyroid hormones form within the thyroglobulin molecule and are stored in the .........
    colloid of the follicle
  10. What makes the thyroid gland unique among the endocrine glands?
    its ability to store large amounts of hormone such that the thyroid hormones stored in the follicles is enough to supply the body with its normal requirements for 2-3 months
  11. The thyroid gland stores enough thyroid hormones (in the follicles) to supply the body for how many months?
    will supply normal requirements for 2-3 Months!
  12. TRUE or FALSE. 90% of thyroid hormone secreted is T3
    FALSE! 90% is T4!
  13. T4 normal  total serum level = 5-12 mcg/dl and the free T4 = _____
    • T4 Normal total serum level = 5-12 mcg/dl
    • Free T4 = 1-2 mg/dl
  14. Biologic ½ life of T4
    6-8 days
  15. TRUE or FALSE. Thyroxine is T3
    FALSE. Thyroxine is T4 and Triiodothyronine is T3
  16. T3 is ___% of thyroid hormone secreted
    9%
  17. What is the normal T3 level?
    Normal = 80-200 ng/dl
  18. What is the 1/2 life of T3?
    24 hours
  19. Which has a longer 1/2 life, T3 or T4?
    T4 (6-8days) where T3 is only 24 hrs
  20. In really extreme cases of hyper secretion of the thyroid hormones, the BMR will increase __-___% above normal.
    60-100%
  21. Describe the role of iodine in forming hormones T3 and T4
    Iodine we ingest must get absorbed from GI tract and converted to charged Iodide (has minus charge) gets actively transported to thyroid where it converts back to iodine. And then hooked on to the AA tyrosine to form the hormones T3 and T4.
  22. How much iodine must we get to prevent a deficiency? Where do we get it?
    • 1 mg dietary Iodine/wk
    • Most of it is through iodized table salt 1part sodium iodide to every 100,000 parts of NaCl.
  23. Although they have similar qualitative effects, which is more potent, T3 or T4?
    T3
  24. 4 Step process of thyroid hormone synthesis
    • 1. Iodide is actively transported into the thyroid
    • 2. Iodide (I-) is oxidized to the active form iodine (I)
    • 3. Iodine is incorporated into tyrosine residues that are bound to thyroglobulin
    • 4. Iodinated tyrosine molecules are coupled forming T-3 & T-4
  25. Why does iodide need active transport?
    because it has a negative chargde
  26. About ___% of T3 and T4 are bound to a protein called ______________.
    70%; thyrobindinglobulin (TBG)
  27. Besides thyrobindinglobin (TBG) there are other proteins the thyroid hormones bind to. What % (total) of thyroid hormones is bound to protein?
    over 99%
  28. What will happen if the patient has high levels of TBG?
    • the amount of free hormone will decrease because more of it will be bound.
    • However because the free hormone level drop will stimulate the thyroid stimulating hormone, so that decrease in free hormone will only be temporary
  29. Why do we need to look at both free T4 and TSH instead of looking at total thyroid hromone?
    if a high level of TBG and only measuring total thyroid hormone, then  it will be high up but it doesn’t mean the pt is hyperthyroid.

    Need to look at free T4 and TSH to get better picture
  30. T3 and T4 act in negative way to inhibit both TRH and TSH in hypothalamus and ant pituitary. Is it total or free T3 and T4 that do this?
    FREE! that's the physiologically active kind!
  31. Besides T3 and T4, what else can inhibit the negative feedback pathway for axis?
    Dopamine, somatostatin and glucocorticoids.
  32. Thyroid hormones cause stimulation of CHO metabolism. Explain this
    • Rapid glucose uptake:
    • ↑ glycolysis
    • ↑ gluconeogenesis
    • ↑ absorption from GI tract
    • ↑ insulin secretion
  33. Thyroid hormones cause stimulation of fat metabolism. Explain this
    Lipids mobilized from adipose which decrease fat stores & increase fatty acids in plasma thereby increasing fatty acid oxidation by cells (↓ cholesterol, phospholipids, & triglycerides)
  34. Do thyroid hormones increase or decrease vitamin requirements?
    INCREASE (Vitamins act as coenzymes for metabolic processes)
  35. Do thyroid hormones increase or decrease BMR?
    INCREASE
  36. Do thyroid hormones increase or decrease body weight?
    DECREASE
  37. What are the effects of thyroid hormones on the CV system?
    • ↑ Blood flow ↑ C.O. (increase in end products of metabolism. CO2, increases, get vasodilation, increased blood flow and increase CO)
    • ↑ HR (tyrosine so cousins w/Epi & Norepi)
    • ↑ Strength of contraction
  38. If the BP increases d/t effects of thyroid hormones, why doesn't the MAP change?
    Systolic BP increases by 10-15mmHg but because of vasodilation, diastolic goes down so the mean is usually unchanged.
  39. What effect does the thyroid hormone have on respirations?
    • Increased respiration!
    • Increased O2 consumption and CO2 production, increased metabolic rate.
    • Expect increased depth and rate of respiration
  40. Does GI motility increase or decrease due to the effect of thyroid hormones?
    INCREASE GI motility
  41. What CNS effects are caused by the thyroid hormone?
    • CNS excitation (extreme cases could be nervousness and paranoia)
    • Altered sleep
  42. What muscle effects are caused by the thyroid hormones?
    Fine tremor
  43. Why is there an ↑ rate of secretion of other hormones from the effects of the thyroid hormones?
    2° ↑ requirements 2° ↑ metabolism (metabolic requirements are up, other hormones may need to increase levels to keep up w/that)
  44. A common test in the TFTs is free T4. How much does free T4 represent of the total T4?
    Only 0.02% of the total T-4 which measures both bound and unbound thyroxine
  45. Thyroxine (T4) is increased in ___% of patients with hyperthryoidism and decreased in ___% of patients with hypothyroidism.
    • ↑ in 90% of hyperthyroid patients
    • ↓ in 85% of hypothyroid patients
  46. What is the best measure of thyroid hormone function at the cellular level? What is the normal value?
    TSH = 0.4-5.0 mU/L
  47. Incidence of hypothyroidism
    0.5-0.8% of adults
  48. What is primary hypothyroidism?
    Decreased production of thyroid hormones in the setting of normal or elevated TSH
  49. 95% of all cases of hypothyroidism is primary or secondary?
    primary; secondary is the remaining 5%
  50. What is the usual cause of primary hypothyroidism?
    Usually from surgical removal or radioactive iodine Rx
  51. What is idiopathic primary hypothyroidism?
    probably autoimmune with antibodies blocking TSH receptors in the thyroid
  52. What is Hashimoto’s thyroiditis ?
    autoimmune and causes destruction of the thyroid; characterized by goiter and hypothyroidism
  53. What is the most common cause of primary hypothyroidism?
    Hashimoto's thyroiditis
  54. What are the causes of secondary hypothyroidism?
    • Hypothalamic or pituitary disease
    • Lack of iodine
  55. TRUE or FALSE. You only get goiters in hyperthyroidism
    FALSE. You can get them in either hypo or hyper thyroidism
  56. Clinical Manifestations of hypothyroidism
    • Slow, insidious
    • Mental & physical slowing → apathy, listlessness
    • Fatigue → lethargy (somnolence) 
    • Weight gain with decreased appetite
    • Cold intolerance, decreased sweating
    • Periorbital & peripheral edema
    • Thickened skin, brittle hair, hoarse voice, large tongue
    • Goiter
    • Muscle aches
    • Amenorrhea
    • Psychosis
    • Constipation
  57. You can have ↓ stroke volume & ↓ HR → ↓ cardiac output with hypothyroidism. What other CV things are related to this.
    • ↓ myocardial contractility 2° systolic & diastolic dysfunction → cardiomegaly (severe cases)
    • Percardial effusions
    • Impaired baroreflex
  58. What type of EKG changes would you see in hypothyroidism?
    • EKG: flattened or inverted T’s, low amplitude P & QRS, SB
    • Ventricular arrhythmias
  59. Why do you see pale cool skin in hypothyroidism?
    ↑ peripheral vascular resistance & ↓ blood volume
  60. Why are people w/hypothyroidism at risk for CAD?
    ↑ cholesterol & triglycerides because thyroid hormones aren't working w/regard to fat metabolism
  61. What kind of Na+ level do you see in hypothyroidism?
    • Hyponatremia (dilutional) because of Impaired free water excretion
    • Mechanism not well understood. Might be an inability to maximally suppress ADH.
  62. What happens to the respirations during hypothyroidism?
    • ↓ Maximum breathing capacity, diffusion capacity, & ventilatory response to hypoxia & hypercarbia
    • Decreased response of hypoxia and hypercarbia be careful w/sedation
  63. What happens to the GI function w/hypothyroidism?
    • ↓ GI function (constipation)
    • **Aspiration risk!
  64. What happens to the deep tendon reflexes in hypothyroidism?
    • Prolonged relaxation phase in deep tendon reflexes
    • Monitoring for NMB
  65. What levels would you see in diagnosis of hypothyroidism?
    ↓ T 4, T 3, ↑ TSH
  66. what is Subclinical hypothyroidism?
    T 4 is normal with ↑ TSH (mean = 18 mU/L) = (few symptoms)
  67. What is Overt hypothyroidism?
    Marked ↓ T 4 & mean TSH of 90 mU/L
  68. What is the normal TSH level?
    Normal TSH is 0.4-5 mU/L
  69. L-thyroxine is the treatment for hypothyroidism. Describe the onset, peak and 1/2 life.
    • Gradual onset (6-12 hours)
    • Peak = 10-12 days
    • T ½ = 7.5 days (Average, varies on whether the pt is euthryoid. If hyperthyroid, ½ life is 3-4 days metabolizing quickly. If hypothyroid could take up to 10 days.)
  70. You get TFTs and the total T4 is  <1mcg/dl. What do you do?
    Well Free T4 and TSH are important but if the total T4 is that then it's severe hypothryoidism = cancel surgery
  71. What are our airway concerns in hypothyroidism?
    • Edema of oral cavity, vocal cords
    • Goiter (tracheal deviation)
  72. What labs would you get for a patient w/hypothyroidism?
    Na (dilutional hyponatremia), HCT, coags, glucose
  73. TRUE or FALSE. Patients with subclinical disease of hypothyroidism present no problems
    TRUE
  74. IV T3 has onset of ___ and peaks in ___
    Onset of 6 hours & peak BMR in 36-72hrs
  75. Why would we need steroid coverage for hypothyroidism?
    may have decreased adrenal cortical function, the question of steroid coverage may be raised.
  76. What do you want to avoid pre-op for the patient w/hypothyroidism?
    Sedation! (not normal response to hypercarbia and hypoxia)
  77. What do we think about regarding induction for a patient w/hypothyroidism?
    • ?RSI, ?awake intubation (Esp if huge goiter and tracheal deviation
    • Ketamine (unless psychosis)
    • Succinylcholine or intermediate acting NDMR (if reflux not significant)
  78. what type of monitoring do we do if the patient has hypothyroidism?
    • As indicated by patient assessment, surgical procedure
    • Monitor temp and keep pt warm (peripherally vasoconstricted)
    • Monitor TOF (muscle skeletal weakness
  79. Do we have decreased MAC in hypothyroidism?
    NO, just a decrease in CO
  80. Why should we be careful w/volatiles in the patient w/hypothyroidism?
    They have decreased CO so careful volatiles & other myocardial depressants
  81. What are our concerns regarding emergence of the patient w/hypothyroidism?
    • May be delayed (lower metabolic rate)
    • Careful reversal of neuromuscular blocker
    • If giving NDMR, give lower end dose, go carefully
  82. Your patient w/hypothyroidism has a low BP, which is a better choice, phenylephrine or ephedrine?
    • Ephedrine!
    • Phenylephrine you get vasoconstriction, increased SVR. So you add resistance and already decreased CO and heart may not pump well against the resistance.
  83. Myxedema coma is a medical emergency with mortality > ___%
    50%
  84. Which patient population is myxedema coma common in?
    Most common in elderly women with long Hx of hypothyroidism
  85. What is the s/s of myxedema coma?
    • Delirium
    • Unconsciousness
    • Hypoventilation
    • Hypothermia
    • Bradycardia
    • Hypotension
    • Dilutional hyponatremia (severe)
  86. What is the treatment of myxedema coma?
    T 4 & T 3; but it doesn't kick in as quickly as you would like.
  87. What is myxedema coma?
    EXTREME hypothyroidism
  88. What is the etiology of hyperthyroidism?
    • Grave’s disease (99%)
    • Toxic nodular goiter (nodes function independently of negative feedback)
    • Toxic adenoma
    • Also iatrogenic cause: excessive administration of thyroxine.
  89. Clinical manifestations of hyperthyroidism (think hypermetabolic state)
    • Anxious, restless, hyperkinetic
    • Skin is warm & moist & face flushed
    • Heat intolerance, diaphoresis
    • Muscle weakness, wasting (proximal limbs)
    • Fatigue but unable to sleep
    • Osteoporosis
    • Weight loss despite ↑ caloric intake
    • Hyperactive reflexes, tremor
  90. What are the cardiac clinical manifestations of hyperthyroidism?
    • ↑ HR & palpitations/arrhythmias → ↑ cardiac work
    • Hyperdynamic circulation↑ myocardial contractility & c.o.
    • Cardiomegaly
    • Thyrotoxic cardiomyopathy
  91. If someone has subclinical hyperthyroidism, what would you see?
    few s/s but INCREASED HR
  92. What % of the US population has Grave's disease?
    0.4% of US population
  93. Who is most likely to get Graves disease  a 30yr old female or a 50yr old man?
    • 30yr old female
    • Female to male ratio is 7:1 and usually appears between age 20-40yr
  94. What causes Grave's disease?
    Appears to be autoimmune (antibodies bind to TSH receptors → hypersecretion of T 3 & T 4)
  95. What is the classic triad of hyperthyroidism?
    • Hyperthyroidism
    • Exopthalamos (d/t abnormal connective tissues deposits in the orbit and extraocular muscles)
    • Dermopathy (edematous skin, pretibial myxedema, occurs over dorsum of feet and legs &  in 10-15% of cases)
  96. What TFTs do you expect in hyperthyroidism?
    ↑ T 3 & T 4 & ↓ TSH
  97. What is the first line of treatment in hyperthyroidism? What do they do?
    • Antithyroid drugs: Propylthiouracil (PTU) & Methimazole (Tapazole)
    • Inhibit oxidation of inorganic iodide & coupling of iodothyronine preventing synthesis of thyroid hormones
    • Suppressing conversion of T4 to T3
    • **Don't destroy existing hormones
  98. How long do the antithyroid drugs take to work?
    • 6-8 weeks (on Sue's slide)
    • Sue said it takes 3-12weeks to create a euthryoid state.
  99. Why are Betablockers used in treatment of hyperthyroidism?
    • relief of signs & sx
    • helpful for increased HR
  100. What does inorganic iodine do in the treatment of hyperthyroidism?
    • In high concentrations inhibits release of hormones
    • Immediate but short term effects so reserved for preparing patients for surgery (and to tx thyrotoxic crisis)
  101. Describe Radioiodine therapy in treatment of hyperthyroidism. (when do you use it, sucess rate, and disadvantages)
    • If hyperthyroidism recurs after antithyroid Rx
    • Remission rate = 80-98%
    • Disadvantage is incidence of subsequent hypothyroidism within 10 years (40-70%)
  102. What % of patients will have hypothyroidism within 10 years after radioiodine therapy?
    40-70%
  103. What is the remission rate of hyperthyroidism after radioiodine therapy?
    80-98%
  104. What must the patient be before surgical thyroidectomy (for both subtotal or total)?
    Euthyroid
  105. Which has a lower incidence of hypothyroidism after treatment for hyperthyroidism, radioiodine therapy or surgery?
    • Surgery 10-30%
    • Radioiodine therapy is 40-70%
  106. Surgery corrects thyrotoxicosis in ___% of patients
    95%
  107. What are the disadvantages/complications of surgery for hyperthyroidism?
    • Hemorrhage with tracheal compression
    • Recurrent laryngeal nerve damage
    • Inadvertent removal of parathyroids
  108. Does surgery provide prompt control of hyperthyroidism?
    yes, taking storage of hormones away
  109. Does the surgeon usually want the patient muscle relaxed for surgery on the thyroid?
    No! want to avoid causing recurrent laryngeal nerve damage so doesn't want the patient muscle relaxed
  110. The life threatening Thyrotoxic Crisis is associated with what?
    • major surgery or severe intercurrent illness 
    • 6-18-24 hrs post op is when it’s more likely to occur.
  111. What are the clinical manifestations of thyrotoxic crisis?
    • Profound hyperthermia (105 ° F)
    • Severe tachycardia
    • Restlessness, agitation, tremor
    • Loss of consciousness, hypotension, heart failure
  112. How can we differentiate between MH and thyrotoxic crisis?
    TC doesn't have associated w/muscle rigidity, or increased CK level, or a marked acidosis.
  113. What is the treatment for thyrotoxic crisis?
    • Potassium iodide
    • Propylthiouracil
    • Beta blocker (Esmolol)
    • Peripheral cooling, IV fluids
    • Glucocorticoids (cortisol 100-200mg if the patient is hypotensive because the hypermetabolic state would lead to a relative cortisol deficiency)
  114. TRUE or FALSE. In hyperthyroidism, elective surgery should be deferred until patient is euthyroid
    TRUE
  115. What do you do if there is an emergency case on a patient w/hyperthyroidism?
    Emergency cases require beta blockade (esmolol), PTU, cortisol (or decadron)
  116. What do we want to avoid with a patient who is hyperthyroid during pre-op?
    • Avoid anticholinergic
    • If doing awake fiber optic or RSI, sometimes want to dry up secretions but in this case wouldn't want to. If needed, give a betablocker first then give glyco
  117. What are the guidelines for Esmolol in a patient who is hyperthryoid?
    100-300mcg/kg/min IV until HR is less than 100.
  118. What are our concerns for induction and maintenance for a patient who is hyperthyroid?
    • Prepare for thyroid storm
    • Avoid ketamine, pancuronium
    • Thiopental has antithyroid activities 
    • No increase in MAC
    • Increase in drug metabolism can cause organ toxicity
    • Hyperthyroid patients may have co-existing muscle disease--Decrease dose of neuromuscular blocker and monitor TOF
    • Use glycopyrrolate with reversal instead of atropine
    • Avoid epinephrine, ephedrine
  119. What are our concerns during emergence of a patient w/hyperthyroidism?
    • AIRWAY!
    • In pt that may have airway compromise especially.
    • Want to ensure pt is well reversed, no airway edema, no RCL nerve damage before we extubate the patient

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