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Endo/Repro 2 Final > Thyroid and Anti-Thyroid Drugs > Flashcards

Thyroid and Anti-Thyroid Drugs Flashcards

1
Q

4 Thyroid Drugs

A
  1. Levothyroxine [T4]
  2. Liothyronine [T3]
  3. Liotrix [4:1 ratio of T4:T3]
  4. Thyroid desiccated
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2
Q

Anti-Thyroid Drugs

A
  1. Thioamides: Methimazole & PTU (propylthiouracil))
  2. Iodides: Potassium Iodide
  3. Radioactive Iodine (131I) sodium
  4. B-blockers: Metoprolol, propranolol, atenolol
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3
Q

Thioamides (Anti-thyroid agent)

A
  1. Methimazole
  2. Propylthiouracil (PTU)
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4
Q

Iodides (Anti-thyroid agent)

A
  • Potassium Iodide
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5
Q

B-Blockers (Anti-thyroid drugs)

A
  1. Metaprolol
  2. Propanolol
  3. Atenolol
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6
Q

How are thyroid hormones made? (steps)

A
  1. NIS (Na+/iodide symporter) moves [iodide] into the thyroid follicular cells from blood.
  2. Pendrin, a iodide transporter enzyme, transports iodide from [across the apical membrane of follicular cell => colloid].
  3. @ apical cell membrane:
    1. TPO (thyroid peroxidase): [iodide => iodine] via oxidation.
  4. In thyroglobulin molecule (gylcoprotein w a shit ton of tyrosine):
    1. Iodide organification: iodine undergoes iodination of tyrosine resides => DIT and MIT
    2. [DIT + DIT] => T4 (thyroxine); [MIT + DIT] => T3 (triiodothyronine)
  5. T3/T4, MIT and DIT go from colloid => apical membrane of the follicular cell via proteolysis and exocytosis,
  6. Released into blood in 5:1 T4:T3 ratio, bound to TBG (thyroxine-binding globulin) in plasma.
  7. T4 deiodinated to T3 (4x more portent than T4) or reverse T3 (metabollically inavtive)
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7
Q

How is T4 inactivated?

A
  1. Deamination
  2. Decarboxylation
  3. Conjugation
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8
Q
A
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9
Q

Bioavailability and 1/2-life of thyroid hormones (T3/4)

A
  • T4
    • Bioavailability = 80% (best in duodenum and ileum)
    • 1/2 life = 7 days
  • T3
    • Bioavailability = 95%
    • 1/2 life = 1 day
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10
Q

What thyroid drug is given for [thyroid replacement therapy] and why?

A

T4 (Levothyroxine)

  1. Longer 1/2 half = once a day administration
  2. More stable
  3. Cheap
  4. Lack of allergic foreign protein
  5. Easy to measure
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11
Q

Even though T3 is more potent (bioavailability of 95% vs 80%), why is it not recommended for replacement therapy?

A
  1. Shorter 1/2 life = 3/4x/day
  2. More expensive
  3. Difficult to monitor
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12
Q

Where is oral T4 best absorbed within the GI tract?

A

Duodenum and ileum

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13
Q

Absorption of T4 and T3 may be affected by what underlying condition?

A

Myxedema w/ ileus but NOT by mild hypothyroidism

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14
Q

1/2-life and clearance of T3/4 in a Hyperthyroid vs. Hypothyroid state

A
  • Hyperthyroid = T4/T3 clearance is ↑ and half-life ↓
  • Hypothyroid = T4/T3 clearance is ↓ and half-life ↑
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15
Q

Which 6 agents prevent peripheral conversion of T4 =>T3 by inhibiting 5’-deiodinase => [↑ reverse T3 levels and decrease in T3], and what is their purpose?

A

Agents that inhibit [T4 => T3 conversion] are given to patients with thyroid storm [thyrotoxic crisis] => reduce T3 levels.

  1. Radiocontrast agents: iopanoic acid and ipodate
  2. Amiodarone
  3. β-blockers
  4. Corticosteroids
  5. PTU
  6. Flavanoids
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16
Q

List 9 drugs/agents that ↓ T4 absorption

A
  1. Antacids (aluminum hydroxide, calcium carbonate)
  2. Ferrous sulfate
  3. Cholestyramine
  4. Colestipol
  5. Ciprofloxacin
  6. PPI’s
  7. Bran, Soy, and Coffee
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17
Q

7 drugs that (+) liver CYP450s and ↑ the metabolism of T4 and T3?

A
  1. Rifampin
  2. Rifabutin
  3. Phenobarbital
  4. Phenytoin
  5. Protease inhibitors
  6. Carbamazepine
  7. Imatinib
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18
Q

5 drugs that cause AI thyroid disease w/ hypo- or hyperthyroidism.

A
    • Interferon-α / Interferon-β
    • IL-2
    • Lithium
    • Amiodarone
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19
Q

How do drugs/conditions that change the clearance in patients with a NL thyroid react?

A

Thyroid starts to hyperfunction = maintain NL hormone concentration

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20
Q

MOA of Thyroid Hormone

A
  1. T3/T4 enter cell via active transport
  2. T4 => converted to T3 via 5’-deiodinase
  3. T3 enters nucleus => binds to TR (thyroid receptor)
  4. Corepressor is released and coactivator binds
  5. TR homodimer separtaes
  6. TR binds to RXR (retanoid X receptor)
    • transciption
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21
Q

In the absence of hormone, what is the structure of the TR (thyroid receptor)?

A
  1. TR (homodimer) bound to corepressor protein, which is bound to DNA on the TRE (thyroid hormone response element)
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22
Q

How long after administering thyroid hormone does it take to see the effects and why?

A

Lag time of hours or days due effects at the level of gene transcription

23
Q

What are T3 preparations best used for clinically?

A

Short-term suppression of TSH

24
Q

How can we ↓ thyroid activity and hormones?

A
  1. Block synthesis of TH
  2. Modify the tissues response to TH
  3. Destroy thyroid w/ radiation or surgery
25
Q

Thiomides

  • Drugs
  • MOA (general)
A
  • Methimazole and PTU (propylthiouracil)
  • Block synthesis of thyroid hormone
26
Q

PTU

Bioavailability, absorption,, metabolism, half-life, and dosing

A
  • BA of 50-80% that is rapidly absorbed, peaking in our serum at 1 hour => vitually all metabolites are excreted in 24 hours
    • BA is low d/t incomplete absorption and large 1st-pass effect.
  • 1/2 life = 1.5 hour
  • Dose = 3- 4x/ day
27
Q

Methimazole

Bioavailability, absorption, metabolism, half-life, and dosing

A
  • BA is 100% (completely absorbed) and excreted slower (65% in 48 hours)
  • 1/2 life = 6 hours
  • Dosing = 1x day
28
Q

Thiomides in pregnancy and when breastfeeding

A
  • Pregnancy: cross placental barrier and concentrates in thyroid = n_ot recommended_
    • If must give = give PTU in 1st trimester and methimazole in 2nd/3rd trimerst
  • Breastfeeding: safe (secreted in milk at low concentrations)
29
Q

If you must give thiomides during pregnancy, what is recommended?

A
  • 1st trimester = PTU
  • 2nd/3rd = Methimazole
30
Q

MOA of Thioamides (Methimazole and PTU)

A

Block synthesis of TH => thus, takes 3-4 weeks before stores are depleted

  1. Inhibit thyroidal peroxidase (TPO) catalyzed rxns
  2. Blocks iodide organification
  3. Inhibits coupling of MIT and DIT to form T3 and T4
  4. *****PTU ALSO BLOCKS PERIPHERAL CONVERSION OF T4=> T3, DROPPING T3 LEVELS EVN MORE
  5. Does NOT block thyroid gland uptake of iodide
31
Q

How does the fall in T3 concentration with PTU + iodine differ from that of Methimazole + iodine?

A

FALL EVEN MORE bc PTU blocks peripheral conversion of T4 –> T3;

32
Q

What effect to PTU and Methimazole have on thyroid gland iodide uptake?

A
  • Do NOT block thyroid gland iodide uptake
  • Inhibit hormone synthesis, rather than release
33
Q

AE’s PTU or Methimazole?

Which is most severe? ***

A
  1. Maculopapular pruritic rash, at times accompanied by: Fever + nausea + GI distress
  2. Agranulocytosis (granulocyte count < 500 cells/mm3) ****
    1. Reverse by DQing drug or CSF
34
Q

Risk of agranulocytosis in ppl taking Thiomides is higher for who?

A
  • Risk ↑ in older pt’s and those receiving high-dose methimazole
35
Q

Potassium Iodide (Anti-thyroid) MOA

A

Prevents the release of TH.

  • Inhibits organification and hormone release
  • ↓ size and vascularity of hyperplastic thyroid gland
36
Q

3 clinical uses of Potassium Iodide?

A

Treats:

  • 1) Thyroid storm and sx’s improve within 2-7 days (rapidly)
  • 2) Pre-op reduction of hyperplastic thyroid
  • 3) Block uptake of radioactive isotopes of iodine in a radiation emergency or other exposure to radioactive iodine
37
Q

AE’s Potassium Iodide?

A

AE = uncommon

    • Acneiform rash
    • Swollen salivary glands
    • Mucous membrane ulcerations
    • Conjunctivitis
    • Metallic taste
38
Q

Potassium Iodide in Pregnancy

A

Avoid: crosses placental barrier and cause goiter in BB

39
Q

Radioactive Iodione

  • TX
  • MOA
  • Administartion
  • CI
A
  • TX: thyrotoxicosis
  • Destroys thyroid parenchyma (epithlium swells and necrosis, follicle disrupts, edema and leukocyte infiltartaion)
  • Orally; rapidly absortbed => concentrated in thyroid and foollicles
  • DO NOT GIVE TO PG W or BREASTFEEDING
40
Q

Radioactive Iodine in PG and Breastfeeding

A

CI IN W WHO ARE PG OR BREASTFEEDING

41
Q

Advanages of Radioactive Iodine

A
  1. Easy to adminiter (oral)
  2. Effective
  3. Cheap
  4. No pain
42
Q

Which β-blockers are effective adjunctive agents in the management of thyrotoxicosis and which is most commonly used?

A

Those w/o sympathomimetic activity (i.e., metoprolol, propranolol, and atenolol)

  • Propranolol is most commonly use
43
Q

What effect do β-blockers have on thyroid levels?

A

- Improve hyperthyroid sx’s, but typically do not alter levels

  • High doses of propranolol have been shown to reduce T3 through blockade of peripheral conversion of T4 –> T3
44
Q

Treatment of Hypothyroidism

A
  • Levothyroxine (T4) on empty stomach; effects seen in 6-8 weeks
45
Q

What is a myxedema coma?

A

End state of untreated hypothyroidism = progressive weakness, stupor, hypothermia, hypoventillation, hypoglycemia, shock and death.

46
Q

Management of hypothyroidism in someone with myxedema coma

A

- Large loading dose of IV T4 (bc poor absorption) followed by smaller IV dosing

47
Q

Management of hypothyroidism in someone with myxedema + CAD

A

Correction of myxedema with T4 must be done cautiously to avoid provoking arrhythmia, angina, or acute MI (sx’s of elevated T4)

48
Q

Why is tx of hypothyroidism in pt’s _trying to get pregnan_t and those currently pregnant so important?

A
  • Trying to get pregnant & hypothyroidism = infertile
  • Pregnant = decelopment of brain depends on moms T4
49
Q

When is anti-thyroid drug therapy most useful for Grave’s disease and what are the preferred agents?

A
  • Most useful in young pt’s w/ small glands and mild disease
  • Methimazole or PTU administered until remission (12-18 mo. of tx)
  • Methimazole is preferable to PTU (EXCEPT in pregnancy) due to once-daily dosing
50
Q

When is a thyroidectomy the preferred tx for Grave’s disease and what % of these pt’s will require thyroid supplementation?

A
  • pt’s w/ very large glands or multinodular goiter

- 80-90% will require thyroid supplementation

51
Q

When is radioactive iodine the preferred tx for Grave’s disease; what about in pt’s w/ underlying heart disease, severe toxicosis, and the elderly?

A
    • Preferred tx for most pt’s >21 years of age
    • In pt’s w/ underlying heart disease, severe thyrotoxicosis, or elderly tx w/ anti-thyroids until pt is euthyroid is preferable
    • 80% will develop hypothyroidism and require replacement therapy
52
Q

What are the adjunct drugs which can be added to anti-thyroid therapy in pt with Graves?

A
  • β-blockers w/o intrinsic sympathomimetic activity may be helpful in controlling tachycardia, HTN, and a-fib
  • If β-blocker is CI can give the CCB, diltiazem, for management of tachycardia
53
Q

Thyroid storm (Thyrotoxic crisis) treatment

A
    1. B-blockers => control arrhythmia
    1. K+ iodide => prevent release of thyroid
    1. PTU/methimazole => prevent production of TH
    1. IV hydrocortisone => prevent shock and block conversion of T4=> 3 in peripheral tissue
    1. Supportive therapy

Endo/Repro 2 Final (11 decks)

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