Thyroid (Welch) Flashcards

1
Q

Thyroid hormones are derivates of what amino acid?

A

Tyrosine

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2
Q

How are thyroid hormones named?

A

Based off number of iodines tyrosine has attached
MIT=monoiodotyrosine
DIT=diiodotyrosine

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3
Q

What makes up Triiodotyrosine?

A

MIT + DIT = T3

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4
Q

What makes up T4?

A

DIT + DIT = T4

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5
Q

What are the active binders to the thyroid receptors?

A

T3 and T4

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6
Q

What is key for the creation of MIT and DIT?

A

Iodide from the diet

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7
Q

What is the stimulus for the uptake of iodide by the cells of the thyroid?

A

Thyroid stimulating hormone (TSH) from anterior pituitary

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8
Q

When TSH binds to the membrane of the thyroid cell what is required for the uptake of the iodide?

A

Energy via N/K ATPase pump

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9
Q

When TSH binds to the membrane of the thyroid cell, what is required for the uptake of the iodide?

A

Energy via N/K ATPase pupm

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10
Q

What is the character of MIT and DIT and what do they require?

A

Unstable. Require binding to thyroglobulin to stabilize in the thyroid

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11
Q

What happens if you don’t have enough thyroglobulin?

A

MIT and DIT will not stabilize and therefore will not get TC and T4

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12
Q

What are the reactions that Thyroidal Peroxidase catalyzes in the production of T3 and T4?

A
  1. Change taken up iodide into iodine
  2. Binding of MIT and DIT to thyroglobulin to stabilize
  3. Binding of MIT and DIT to create T3 and T4
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13
Q

Peroxidase is activated by what?

A

TSH

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14
Q

What things does TSh stimulate in the production of T3 and T4?

A
  1. Iodide uptake
  2. Peroxidase action
  3. Activate adenyllate cyclase
  4. Activate lysosome droplet to release T3 and T4
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15
Q

What is Thyroid Colloid?

A

Protein and fat storage area with no enzymes to store and protect T3 and T4

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16
Q

What does the increase in Adenylate Cyclase by TSH stimulation cause?

A

Increase in cAMP which causes lysosome to destroy colloid and release the stored T3 and T4

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17
Q

What causes the release of TSH from the anterior pituitary?

A

Thyrotropic releasing hormone by hypothalamus

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18
Q

What inhibits both TRH from Hypothalamus and TSH from the anterior pituitary?

A

T3 and T4

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19
Q

What is assumed to be the cause of any thyroid problem until proven otherwise?

A

TSH (anterior pituitary) is the cause

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20
Q

What does TRH from the hypothalamus cause the release of?

A

TSH, Prolactin, and GH

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21
Q

What is the diagnostic use of TRH (Protirelin)?

A

Administer and measure TSH and Thyroid hormones

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22
Q

What is the characteristic of a primary defect upon administration of TRH?

A

TSH increases but T4 level remains the same

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23
Q

What is the characteristic of a secondary defect upon administration of TRH?

A

TSH does not increase

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24
Q

What is the characteristic of a secondary defect upon administration of TRH?

A

Both TSh and T4 increase

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25
Q

What is the drug of choice for determining where breakdown lies in the excretion of thyroid hormones?

A

Protirelin

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26
Q

If protirelin (synthetic TRH) given and there is no change in TSH or T3 and T4k where is the problem?

A

PItuitary defect

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27
Q

If protirelin (synthetic TRH) is given to a hypothalamic patient and TSH increases, but T3 and T4 do not change, where is the problem?

A

At level of thyroid

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28
Q

If protirelin (synthetic TRH) is given to hypothalamic patient and TSH increases and T3 and T4 increase, where is the problem?

A

At the level of the hypothalamus

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29
Q

Of the thyroid problem levels, which is the most difficult to treat?

A

The hypothalamus-level problem because it is inside the blood-brain barrier

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30
Q

Which is the larger molecule: TRH or TSH?

A

TSH (large glycopeptides)

TRH (small tripeptide)

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31
Q

TSH deficiency leads to what physical change in thyroid?

A

Atrophy

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32
Q

TSH excess leads to what physical change in thyroid?

A

Goiter (hypervascular, hypertrophic, hyperplastic)

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33
Q

What is a synthetic TSH used diagnostically to distinguish between hypopituitarism and primary hypothyroidism?

A

Thytropar

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34
Q

What must be used in conjunction with Thytropar for diagnosis and what is the contraindication?

A

Used with radioactive iodine 131-I

Contraindicated in pregnant women

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35
Q

If there are small quantities in the thyroid of the radioactive iodine after it has been administered in conjunction with the Thytropar (diagnostic TSH) where does the problem lie?

A

Abnormal thyroid

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36
Q

What are 3 places a high iodine concentration will shut down a thyroid cell?

A
  1. Poison the N/K ATPase pump stopping iodine uptake
  2. Inhibit peroxidase action
  3. Inhibit adenylate cyclase
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37
Q

What ist he name of the high iodine solution used prior to surgery to shut down the thyroid in order to avoid a dump to T3 and T4?

A

Lugall’s solution

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38
Q

Why is T3 more active than T4?

A

Less protein-bound, faster onset, 4 times more potent

Ten times greater receptor affinity

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39
Q

When would T3 be administered therapeutically?

A

In ER if euthyroidal

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40
Q

What is a stabilized euthyroidal patient given?

A

T4

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41
Q

Where is T4 converted to T3?

A

In liver by deiodinase enzymes

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42
Q

What percent of all T4 that is made is converted into T3 in the liver?

A

20%

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43
Q

What accounts for the pharmacokinetic difference between T3 and T4?

A

Amount of protein binding

44
Q

Which has the shorter half-life and faster onset: T3 or T4?

A

T3

45
Q

What are 3 general effects of thyroid hormones?

A
  1. Regulate growth and development
  2. Cariogenic effect
  3. Metabolic effect
46
Q

How do thyroid hormones regulate growth and development?

A

Stimulate protein synthesis in most organs

Control cell proliferation in brain (consider later for cretinism)

47
Q

How do Thyroid hormones exert a calorigenic effect?

A
  1. Increase basal metabolic rate particularly in heart, diaphragm, liver and kidney
  2. Increase number of adrenergic beta receptors in heart to sensitize to catecholamines
48
Q

What does thyroid have a major part in controlling with respect to the basal metabolic rate?

A

Temperature regulation

49
Q

What is the metabolic effect of Thyroid hormones?

A

Increase utilization of carbohydrates

50
Q

What is a risk of thyroid hormones increasing adrenergic beta receptors in the heart?

A

Increased tachycardia, arrhythmia risk

51
Q

Thyroid receptors are similar to what?

A

Steroid-like

52
Q

Thyroid receptors on cell work with insulin to do what?

A

Allow glucose and amino acids into the cell

53
Q

What is the intracellular action of T3 that is so important for the basal metabolic rate?

A

Acts on mitochondria to convert ADP to ATP which is critical for BMR.

54
Q

Growth and protein synthesis is the result of T3 binding where?

A

DNA

55
Q

What would be the signs of a patient that is hypothyroid and untreated?

A
  1. High Blood Pressure
  2. Low Energy
  3. Low proteins
56
Q

What is the primary cause of Hypothyroidism / Adult Myxedma?

A

Iodine deficiency

57
Q

What is the secondary cause of hypothyroidism / Adult Myxedema?

A

Defective TSH secretion

58
Q

What is the tertiary cause of hypothyroidism / Adult Myxedma?

A

Defective TRH secretion

59
Q

What would be the physiologic character of the thyroid in Hypothyroid / Adult Myxedema caused by iodine deficiency: Goiter or atrophy of the thyroid?

A

Goiter

60
Q

What would be the physiologic character of the thyroid in Hypothyroid / Adult Myxedmea caused by defective TSH or TRH secretion: goiter or atrophy of the thyroid?

A

Atrophy

61
Q

What are physical characteristics of a patient with Hypothyroidism / Adult Myxedema?

A
  1. Edem
  2. Thick, rough skin
  3. Hair loss
  4. Cold intolerance
  5. Lethargy
  6. Dullness
  7. Anorexia
  8. Constipation
  9. Anemia
  10. Amenorrhea
  11. Infertility
62
Q

What is Gull’s disease?

A

Rare severe hypothyroidism coupling iodine deficiency and defective TRH and TSH

63
Q

Why does hypothyroid contribute to infertility?

A

If you have a low T3 and T4, then there is no negative feedback to stop TRH which will cause prolactin release.
Prolactin decreases LH and FSH which stops ovulation in women and decreases spermatogenesis in men

64
Q

What is an immunologic disorder that has a humoral immunity response with antithyroid antibodies, causing inflammation?

A

Hashimoto’s thyroiditis

65
Q

What are the diagnostic findings for adult hypothyroidism?

A

Combination of low T4 and high serum TSH or the presence of antithyroid antibodies

66
Q

Endemic cretinism is due to what in infants?

A

Iodine deficiency

67
Q

Sporatic cretinism is due to what in infants?

A

Lack of thyroid development

68
Q

What are physical characteristics of juvenile myxedema / cretinism?

A
  1. Dwarfism
  2. Short extremities
  3. Mental retardation
  4. Hypoactive
  5. Hypothermia
  6. Slow heart rate
69
Q

What is the critical window in an infant with low thyroid?

A

2 months after birth, T3 and T4 are critical for myelination of neurons

70
Q

What is the only symptom of juvenile myxedema that is not reversible?

A

Mental retardation

71
Q

If chemotherapy is used to treat hypothyroidism, what is the drug of choice?

A

Levothyroxine (T4)

72
Q

What is the T3 drug for hypothyroidism?

A

Liothyronine IT3)

73
Q

A patient that needs a quick thyroid hormone uptake (e.g. in a coma) would be given what drug?

A

Liothyronine

74
Q

What was the theory of Liotrox, the T4:T3 4:1 ratio drug that is not used?

A

Mimics the body’s T4:T3 ratio, but faster onset due to T3 being negated by the faster metabolism of T3

75
Q

What is given to protect T3 and T4 from degradation due to overly rapid endocytotic effects?

A

Thyroglobulin (Proloid)

76
Q

What is the benefit of using synthetic thyroid compounds?

A
  1. Pure
  2. Reproducable
  3. Few allergic reactions
77
Q

A simple goiter would be treated with what?

A

Levothyroxine (would remit)

78
Q

Myxedema and mild hypothyroidism would require what?

A

Replacement therapy for life

79
Q

What is the outcome if an infant is treated within three months of birth for low thyroid?

A

No physical or mental retardation

80
Q

What are potential side effects of hypothyroid therapy?

A
  1. Tachycardia
  2. Headache
  3. Insomina
  4. Heat intolerance
  5. Nausea
81
Q

What would be a symptom of a female on T4 therapy (Levothyroxine) that is discontinuing oral contraceptives?

A

Tachycardia due to decreased thyroid binding globulin and decreased T4 requirement

82
Q

What is a drug interaction on a patient on T4 treatment (Levothyroxine) should be warned about?

A

OTC with sympathomimetics (e.g. sedated) will be synergistic with thyroid hormones

83
Q

Should a patient that misses a dose of their thyroid hormone therapy catch up on that dose?

A

No

84
Q

What is one of the major drugs that decrease binding of thyroxine to thyroid binding globulin?

A

Salicylates (patient takes a lot of aspirin)

85
Q

If thyroid binding is decreased for any reason, what should be done to the dose?

A

Decrease the dose

86
Q

What is the most common form of hyperthyroidism?

A

Grave’s disease

87
Q

What is lacking in hyperthyroidism?

A

Negative feedback due to antibodies stimulating TSH receptors

88
Q

Thyrotoxicosis can lead to what in a hyperthyroid patient?

A
  1. Right heart failure

2. Atrial fibrilation

89
Q

Is thyrotoxicosis the same as hyperthyroidism?

A

No it’s a symptom

90
Q

What is a hyperthyroidism that results also from negative feedback lacking and a long-standing non-toxic goiter?

A

Plummer’s disease

91
Q

What is a difference in the long-term outcome between Grave’s disease and Plummer’s disease?

A

Grave’s disease spontaneously remits in 50% of cases

Plummer’s has no spontaneous remission

92
Q

Which hyperthyroid condition has a nodular goiter?

A

Plummer’s

93
Q

What are symptoms common to both hyperthyroid conditions (Grave’s and Plummer’s)?

A
  1. Tachycardia
  2. Excitable
  3. Tremors
  4. Weight loss
  5. Heat intolerance
94
Q

What are 2 treatments for hyperthyroidism?

A
  1. 131-I to emit beta radiation and kill nearby cells

2. Antithyroid drugs

95
Q

What antithyroid drugs can be given until patient spontaneously remits (if Grave’s) or in conjunction with 131-I to hasten recovery, and can be used to stabilize the patient until surgery?

A
  1. Propylthiouracil

2. Methimazole

96
Q

What is the drug of choice for hyperthyroid?

A

Propylthiouracil (fewer side effects, quicker onset, longer duration)

97
Q

How do propylthiouracil and methimazole act?

A

Inhibit thyroid peroxidase which blocks organification of iodide and blocks coupling of iodotyrosines

98
Q

Do propylthiouracil and methimazole affect iodide uptake or hormone release?

A

No

99
Q

Propylthiouracil inhibits peripheral conversion of T4 to T3 where and by what?

A

In the liver by iodothyronine 5’-diodinase-1

100
Q

What is given to a patient suffering a thyroid storm (massive let down of T3 and T4 causing Tachycardia, common during surgery)?

A
  1. Propylthiouracil
  2. Methimazole
  3. Propranolol (beta blocker)
101
Q

What is used to reduce the vascularity of thyroid in preparation for thyroidectomy?

A
  1. Lugol’s Iodine (5% I2)

2. Ipodate (iodinated contrast media 61% I2)

102
Q

Will propylthiouracil decrease the size or vascularity of the thyroid?

A

No

103
Q

What is the treatment for Grave’s disease hyperthyroidism?

A

131-I or antithyroids (Propylthiouracil or Methimazole) because expect spontaneous remission. Contraindicated in pregnancy.
Subtotal thyroidectomy in children.

104
Q

What is the treatment for Plummer’s disease hyperthyroidism?

A

131-I or surgery because no remission

105
Q

Antithyroid drugs (propylthiouracil or methimazole) are used how for Plummer’s disease hyperthyroidism?

A

Only for stabilization

106
Q

Where is the site of inhibition for the action of Propylthiouracil?

A

Deiodination of T4 to T3

107
Q

High dose iodide exert inhibition where?

A
  1. Inhibit T3 / T4 release
  2. Inhibit organization of iodine
  3. Inhibit coupling of iodotyrosine