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Adv Pharm 1 > Endo (pt 4/7) Thyroid > Flashcards

Endo (pt 4/7) Thyroid Flashcards

1
Q

Where is TSH produced?

A

Anterior Pituitary Gland

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2
Q

What regulates the secretion of TSH?

A

Hypothalamus hormone Thyrotropin-releasing hormone (TRH)

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3
Q

Increased levels of Thyroid Hormone _____ the secretion of TSH from the pituitary.

A

Inhibit

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4
Q

There is a negative feedback between the thyroid hormones and the ______, and weakly on the ______.

A

Pituitary; hypothalamus

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5
Q

What conditions increase/decrease TRH?

A

Increase: cold, acute psychosis, and circadian & pulsatile rhythms
Decrease: Severe stress, heat

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6
Q

What hormones offer negative inhibition of TSH (that are not thyroid hormones)?

A

-Corticoids
-Somatostatin
-Dopamine

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7
Q

What is the primary determinant of TSH secretion and TRH secretion?

A

Thyroid hormone

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8
Q

T/F: Thyroid hormone levels can override TRH influence from the hypothalamus

A

True; TH is the primary determinant of TSH secretion

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9
Q

T/F: Iodide uptake and TH synthesis is dependent on TSH

A

False; these processes are independent of TSH.

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10
Q

Large doses of iodine cause what?

A

Inhibition of iodide organification (Wolff-Chaikoff block), reducing TH levels

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11
Q

High Na diets of iodized salts can inhibit what?

A

Iodine organification

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12
Q

-Chronic lymphocyte thyroiditis
-Most common cause of hypothyroidism in US
-Autoimmune dz, antibodies directed against thyroid gland

A

Hashimoto’s Thyroiditis

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13
Q

Lack of Wolff-Chaikoff block means what?

A

Loss of the inhibitor mechanism.

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14
Q

Loss of the Wolff-Chaikoff block in patients with a multinodular goiter causes what?

A

Hyperthyroidism

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15
Q

90% of the hormone secreted by the thyroid is _____, and 10% is _____.

A

T4; T3

However, a great portion of T4 is converted to T3 peripherally.

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16
Q

Which thyroid hormone is more potent?

A

T3 is about 4x more potent than T4, but there is much smaller quantities and it lasts for a much shorter time. (shorter 1/2 life)

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17
Q

Which thyroid hormone is the biologically active form?

A

T3

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18
Q

The Hypocalcemic hormone produced in the walls of the thyroid follicles where T3 and T4 are stored.

A

Calcitonin

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19
Q

What are the 4 phases by which thyroid hormones are synthesized?

A

Trapping, Binding, Coupling, and Release

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20
Q

The cells of the thyroid gland are remarkable in that they can concentrate iodide above plasma levels. Then, the trapped iodide is oxidized to iodine so that it readily binds to tyrosine (an Amino Acid).

A

Trapping

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21
Q

After iodide is oxidized to iodine by TPO, tyrosine constituents in thyroglobulin (the large glycoprotein synthesized and secreted by thyroid cells) are iodinated to form monoiodotyrosine (MIT) and diiodotyrosine (DIT).

A

Binding

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22
Q

These precursors of the thyroid hormone are then stored in the thyroid gland (in the colloid) until the coupling of 1 diiodotyrosine and 1 monoiodotyrosine forms triiodothyronine T3 and 2 molecules of diiodothyrosine form thyroxine (T4). T3 and T4 remain stored in the colloid.

A

Coupling

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23
Q

Stimulated by TSH from anterior pituitary.

A

Release

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24
Q

Synthesis of thyroid hormones starts with ?

A

The thyroid cells synthesizing and secreting a large glycoprotein, thyroglobulin. Each molecule contains 140 tyrosine amino acids

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25
Q

How does iodide (ionic form of Iodine = I-) get into the thyroid gland?

A

By the cell protein NIS (Sodium/Iodide Symporter)

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26
Q

Iodide is oxidized by what to iodine ?

A

Thyroid peroxidase (TPO)

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27
Q

Iodine rapidly combines with what within the thyroglobulin molecule to form MIT (monoiodotyrosine) and DIT (diiodotyrosine)?

A

Tyrosine residues

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28
Q

2 DITs combine to form?

A

L-Thyroxine (T4)

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29
Q

1 DIT + 1 MIT =

A

T3

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30
Q

How are Thyroxine, T3, MIT, and DIT released from thyroglobulin?

A

By exocytosis and proteolysis

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31
Q

MIT & DIT stay within the ____, are _____ and the iodine is reused.

A

gland; deiodinated

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32
Q

The ratio of T4:T3 within thyroglobulin is ?

A

5:1

33
Q

Most of the thyroid hormone released is?

A

T4 (thyroxine)

34
Q

80% of circulating T3 in the blood is derived from?

A

Peripheral metabolism of Thyroxine

35
Q

20% of circulating T3 is from?

A

Direct thyroid secretion

36
Q

What is the primary pathway for the peripheral metabolism of Thyroxine?

A

Deiodination by three 5’deiodinase enzymes (D1, D2, and D3)

37
Q

What drugs block the three 5’deiodinase enzymes?

A

Amiodarone
Contrast Dye
Beta Blockers
Corticosteroids

Severe illness and starvation also

38
Q

What is the effect of sedatives/analgesics in hypothyroidism? Hyperthyroidism?

A

Hypo: increased sedation and respiratory depressant effects from sedatives and opioids in hypothyroidism

Hyperthyroid: Opposite

39
Q

Note that thyroid function is impacted by multiple drugs.

A

Noted

40
Q

Thyroxine is best absorbed where?

A

In Duodenum & Ileum

41
Q

What is the drug of choice for tx of hypothyroidism?

A

Levothyroxine (T4)

42
Q

What are some pros of Levothyroxine?

A

-Stable, uniform, inexpensive
-Lacks allergens
-Easily measured
-1/2 life 7 days
-Daily to weekly dosing (!)
-Converts to T3 = giving both hormones (!!!)

43
Q

What is the best drug to give for short-term TSH suppression?

A

Liothyronine (T3)

44
Q

Describe Liothyronine (T3)

A

-3-4 xs more potent than T4
-More biologically active, doesn’t have to be converted (95% absorbed)
-Not recommended for routine therapy due to higher cost and difficulty monitoring
-Multiple daily doses
-Avoid in cardiac patients due to increased risk of toxicity.

45
Q

What are the two pathways anti-thyroid drugs work?

A

1) Interfere with the production of thyroid hormones
2) Modify the tissue response to thyroid hormones

46
Q

What are the 3 types of antithyroid drugs?

A

1) Thioamides
2) Iodides (no longer used for sole therapy)
3) Radioactive iodine

47
Q

What are the thioamides?

A

-Propylthiouracil (PTU)
-Methimazole

48
Q

Describe the mechanism of action of the thioamides (PTU and methimazole)?

A

Are transported to the thyroid gland and inhibit further release of thyroid hormones by inhibiting thyroid peroxidase, the enzyme that catalyzes the incorporation of iodide into thyroglobin.

PTU also blocks peripheral conversion.

49
Q

Can be used in the 1st trimester of pregnancy as it does not cross the placenta as easily due to higher protein binding.

A

Propylthiouracil (PTU)

But still not rly used (pregnancy category D - evidence of human fetal risk) due to potential for fetal hypothyroidism

50
Q

Does PTU have a BBW?

A

Yes, BBW for severe hepatitis

51
Q

What is the DOC in adults and children for antithyroid agents?

A

Methimazole

10xs more potent than PTU

52
Q

Which anti-thyroid drug is associated with congenital malformations, and therefore not used in pregnancy?

A

Methimazole

53
Q

The ______ group is essential for antithyroid activity.

A

Thiocarbamide

54
Q

Describe the absorption, excretion, etc of PTU.

A

-50-80% bioavailable
-Due to incomplete absorption or large 1st pass effect in Liver
-Renal excretion
-T1/2 of 1.5 hrs
-Administer q 6-8 hrs
-100 mg dose inhibits organification by 60% for 7 hrs

55
Q

Describe the absorption, excretion, etc of Methimazole.

A

-Completely absorbed
-Renal excretion (slower than PTU)
-T1/2 of 6 hrs
-30 mg dose exerts anti-thyroid effects for >24 hrs

56
Q

How do the thioamides prevent thyroid hormone synthesis?

A

By inhibiting thyroid peroxidase catalyzed reactions.
-Slow onset of action
-3-4 weeks before T4 stores are depleted

Blocks iodine organification and also blocks the coupling of iodotyrosines

57
Q

PTU also inhibits what?

A

The deiodination of T4 and T3 (!!!)

58
Q

What are the adverse effects associated with the Thioamides (PTU and Methimazole)?

A

-Maculopapular pruritic rash (most common)
-Severe/fatal hepatitis (BBW on PTU)
-Agranulocytosis (most dangerous complication)

59
Q

A granulocyte count <500 cells/mm3
-Immune suppression
-Infrequent but potentially fatal
-Inc risk in older patients and those taking >40 mg/day of methimazole
-Usually reversed when med discontinued

A

Agranulocytosis

60
Q

T/F: your patient has a rxn to PTU, so you should switch them to methimazole.

A

False: Cross sensitivity between PTU and methimazole is 50%. Do not switch drugs in patients with severe reactions.

61
Q

What is the only isotope of Iodine used in the treatment of thyrotoxicosis?

A

I 131

62
Q

Given to destroy the thyroid parenchyma via emission of Beta rays.
-Concentrated by the thyroid and incorporated by storage follicles
-Not painful
-Any part not taken up by the thyroid is excreted renally

A

Radioactive Iodine (I 131)

63
Q

What is the most widely used BB in thyrotoxicosis?

A

Propanolol

64
Q

Why do you use Beta Blockers with thyrotoxicosis?

A

-Inhibit SNS effects on heart and vessels
-Blocks the peripheral conversion of T4 to T3 (!!!) - propanolol

65
Q

What is important to monitor in a patient with a goiter?

A

Tracheal deviation/compression of trachea
(AIRWAY)

66
Q

What are dose adjustments to Levothyroxine made based on?

A

Serum TSH and free thyroxin levels
-takes 6-8 weeks for steady state
-Absorption is impaired with certain foods

67
Q

What is important to know regarding myxedema and CAD?

A

The low levels of circulating thyroid hormone in older persons (myxedema) is cardio-protective against increased demands that could lead to angina pectoris or MI.
-Correct with caution to avoid arrhythmias, angina, or acute MI.

68
Q

A medical emergency; the end state of untreated hypothyroidism.
-S/Sx: Severely depressed mental state, bradycardia, progressive weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia, water intoxication, shock, & death
-Tx: Loading Dose of Levothyroxine (300-400 mcg IV) followed by 50-100 mcg daily
-IV T3 can also be added

A

Myxedema Coma

69
Q

What are symptoms of Thyroxine toxicity in children?

A

-Restlessness, insomnia, accelerated bone maturation and growth

70
Q

What are symptoms of Thyroxine toxicity in adults?

A

-Inc nervousness
-Heat intolerance
-Episodes of palpitations and tachycardia
-Unexplained weight loss

71
Q

What are causes of hyperthyroidism?

A

-Grave’s Dz
-Toxic multinodular goiter
-Thyroiditis (antibodies to thyroid gland)
-TSH secreting pituitary tumors (adenomas, carcinomas)
-OD of thyroid replacement hormones

72
Q

The most common cause of hyperthyroidism.
-Antibodies directed at TSH receptors cause an increase in TH production

A

Grave’s Disease

73
Q

What are symptoms of hyperthyroidism?

A

Smooth, moist skin
Exophthalmus: collection of fluid, fat and inflammatory tissue (70% of pts)
Goiter
Tachycardia
Hyperactive tendon reflexes
Elevated skin temperature

74
Q

Treatment of Grave’s Disease?

A

-Thyroidectomy (Tx of choice)
-Anti thyroid drugs (Methimazole or PTU) or radioactive iodine (preferred medical mgmt for those >21 years old)

75
Q

The treatment of choice for patients with large glands or multinodular goiters.

A

Near-total Thyroidectomy

Need antithyroid drugs for 6 weeks prior to surgery
80-90% will require thyroid supplementation

76
Q

T/F: Thioamide therapy alone can be used for young patients with small glands and mild disease.

A

True; but a long tx period (up to 18 months) with a 50-60% incidence of relapse.

77
Q

How does radioactive iodine (I 131) work?

A

Excessive inorganic iodine will have a paradoxical effect on the thyroid gland (Wolff-Chaikoff effect), resulting in decreased ability of the thyroid to produce and release hormones.
-MUST be given after one of the thioamides.

78
Q

What are adjuncts used for the treatment of Grave’s Disease? (tachycardia, HTN, or AFib)

A

Propanolol or Metoprolol to inhibit SNS effects and block peripheral conversion of T4 to T3

Diltiazem can be used when beta adrenergic antagonists are contraindicated (Asthma)

Adv Pharm 1 (28 decks)

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