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Endorine > Thyroid Pharmacology (5/20) > Flashcards

Thyroid Pharmacology (5/20) Flashcards

1
Q

What is thyroglobulin?

A

Glycoprotein mc produced by thyroid containing iodinated tyrosine residues (MIT, DIT). These residues are coupled to form T3/T4

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2
Q

Describe the biosynthesis of thyroid hormones with enzymes

A
  1. Active iodide transport (NIS)
  2. Oxidation of iodine and iodination of tyrosine residues (TPO)
  3. Coupling of pairs of iodotyrosine mcs to form T3/T4 (TPO)
  4. Fusion with lysosome, proteolysis of TG, releasing T4/T3 and iodotyrosines (recycled)
  5. SiosinrION
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3
Q

How much more T4 is there to T3?

A

14x

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4
Q

What are the half lives of T4, T3?

A

T4: 7 days (long)
T3: 1 day

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5
Q

Where does peripheral conversion of T4 to T3 occur?

A

Brain, muscles, liver, kidneys and other organs via peripheral deiodinase

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6
Q

What hormones inc in hypothy?

A

TRH and TSH

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7
Q

What is primary hypothy?

A

Thyroid gland doesn’t work…very high levels of TSH

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8
Q

What is central/secondary hypothyroidism

A

Hypothyroidism due to insufficient stimulation by thyroid stimulating hormone (TSH) of an otherwise normal thyroid gland.

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9
Q

What hormones are dec in hyperthy?

A

TRH and TSH

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10
Q

What is levothyroxine?

A

Synthetic T4, drug of choice (LT4)

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11
Q

What is the goal of therapy?

A

Replacement, not cure since cure is not possible. Most pts req lifelong therapy

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12
Q

What is liothyronine?

A

Synthetic T3, only used in certain situations

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13
Q

Why do we treat with t4 and not T3?

A
  • Longer 1/2 life of T4 makes dosing easier (1x/d) and monitoring easier (T4 is more consistent)
  • T4 is converted to T3 in peripheral tissues anyway
  • Ppl can still have persistent symptoms maybe because their D2 doesn’t convert to T3 efficiently
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14
Q

When would we use T3 therapy?

A
  • Thyroid cancer pts before radioactive iodine therapy or scans
  • Pts suffering from myxedema coma
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15
Q

What are the side effects of LT4?

A
  • From inappropriate dosing (ppl are very sensitive to dose)
  • ->symp of hypo or hyper thy
  • Sensitivity to fillers
  • Can have coloring dye sensitivity

-Be careful in pregnancy! TSH is bad for the baby

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16
Q

How do we do dosing of LT4?

A
  • Dosing dep on age and deg of thyroid failure

- Older=lower doses because worry about T3 stim effects on heart

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17
Q

How do we monitor LT4?

A

Check TSH levels every 6 wks

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18
Q

What should TSH levels be

A

Target is normal range of 0.5-2.5

–>Can’t trust TSH levels in secondary (pit or central) hypothyroidism

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19
Q

Why would TSH on therapy be higher than expected?

A
  • Non compliance/missed dose
  • Some drugs dec LT4 absorption
  • Some conditions dec LT4 abs (small intestinal dis)
  • Some drugs inc hepatic LT4 metab (anti-seizure meds)
  • Things that inc TBG (like pregnancy, estrogens or acute hepatitis due to leakage from damaged cells)
  • Progression of endogenous thyroid dis (Hashimotos)
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20
Q

Why would TSH on therapy be lower than expected?

A
  • XS LT4 administered
  • Central hypothyroidism (dopamine, high dose glucocorticoids=transient dec in TSH)
  • Dec TBG (more FT4) due to androgen steroids, nephrotic syndrome, chronic liver dis, systemic illness
  • Reactivation of Graves’ or dev of autonomous nodules
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21
Q

What drugs cause primary hypothyroidism?

A
  • Lithium
  • Amiodarone
  • Iodine contrast dye
22
Q

What is Amiodarone

A

Drug that blocks T4–>T3 conversion and has iodine effect

23
Q

What drugs cause secondary hypothyroidism?

A

Bexarotene (retinoid)

24
Q

What are two situations in which the TSH level is very important?

A
  1. Pregnancy

2. Thyroid cancer (TSH goals are different)

25
Q

What is myxedema coma

A

Severe hypothyroidism

26
Q

How do we treat myxedema coma?

A
  • IV hydrocortisone first until assess for adrenal insufficiency (to avoid causing a crisis)
  • LT4 and LT3 IV
  • Supportive rx for any associative metabolic disturbances
  • Rx precipitating factors, esp infection
  • Be aware of dec metab of most meds, esp avoid sedatives
27
Q

What is a class of antithyroid drugs?

A

Thionamides (PTU and Tapazole are the brand names)

28
Q

How do thionamides work?

A

Interfere with two steps of thyroid hormone synth by affecting TPO

  1. Intrathyroidal iodine utilization (ie to make MIT/DIT and to couple them to make T3/T4)
  2. Iodotyrosine coupling
29
Q

When do we use antithyroid drugs?

A
  • Graves’ Disease (most freq)
  • To bring down T3/T4 levels prior to surgery with radioactive iodine (“cool pt down”)
  • People not candidates for surgery/RAI
  • Children and adolescents
  • Adults in remission (use for 1-2 years)
30
Q

What is the half life for PTU vs methimazone?

A

1 hr vs 4-6 hrs

31
Q

What is the dif in protein binding betw PTU vs methimazone?

A

P: 80% bound
M: none bound

32
Q

What is a bonus of PTU that methimazone doesnt do?

A

PTU also dec T4–>T3 conversion

33
Q

What is the dif between PTU and methimazone in dose?

A

M: daily (longer half life of 4-6 hrs)
P: 3x/day (half life 1 hr)

34
Q

What is the dif between PTU and methimazone in freq of side effects

A

M: dose related, but less freq
P: no dose relationship (agranulocytosis, severe hepatitis, skin rxns)

35
Q

When do we use methimazole vs PTU?

A

Use methimazole in all Graves’ pts except

  1. 1st trimester preg
  2. Thyroid storm (use bonus T4–>T3 block)
  3. Adverse rxns to meth
36
Q

What can kill someone on antithyroid drugs?*** and what is the risk?

A

Agranulocytosis! Risk is 0.1-0.5%

-Can occur at any time or dose

37
Q

What other drugs besides antithyroids should you use in hyperthyroidism

A
  • Beta blockers (reduce HR and dec symptoms of hyperthyroidism)
  • NSAIDs for symptom relief
  • Iodine or glucocorticoids in addition to antithyroid drugs in severe thyrotoxicosis
38
Q

What drugs inhibit T4–>T3 conversion?

A
  • PTU
  • Glucocorticoids
  • Propanolol
39
Q

What do we use to treat thyroid storm?

A

PTU or methimazole
Propranolol
Hydrocortisone
K+ iodine drops (SSKI): also blocks conversion

40
Q

RLS in TH production?

A

Iodide transport via NIS Na+/I- active symporter which allows the thyroid gland to maintain iodide concentration 30-40x higher than plasma

41
Q

What regulates NIS?

A

TSH

42
Q

How does NIS adapt?

A

Low iodide inc NIS, high will decrease NIS and the thyroid can override dietary levels

43
Q

Where is NIS expressed?

A

Highly in thyroid (allows for radioactive iodine scanning and therapy of thyroid in selective manner)

Low levels in salivary glands, breast, gastric tissue

44
Q

What is optimal iodide intake?

A

150mcg/d, 220 if preg

-prolonged dec can cause endemic goiter and cretinism (in utero)

45
Q

What is the Wolff-Chaikoff Effect?

A
  • Normal autoreg of iodide prevents hyperthyroidism after iodine load
  • When iodide levels are high, NIS, iodide organification and thyroid hormone release is inhibited
  • In normal thyroid, the gland can escape this inhibitory effect when it needs to
  • In Hashimoto’s or Graves’, the suppressive effect may persist. So you can use iodide to treat hyperthyroidism in this case
46
Q

What is SSKI?

A
  • Saturated solution potassium iodide used for treatment of uncontrolled hyperthyroidism
  • Use 2 hours after PTU in thyroid storm
  • Blocks release of TH from thyroid
47
Q

What is Amiodarone?

A
  • Used to treat arrhythmias
  • Blocks T4–>T3 so can cause hypothyroidism plus iodine effect (ie can’t escape wolff)
  • Can also cause hyperthyroidism in toxic nodular dis or graves’ via inc TH production due to iodine effect (type 1) OR in pts with normal thyroids can lead to destructive thyroiditis–>inc thyroid hormone release due to direct toxic effect of the drug (type 2)–>ie it leaks TH because it destroyed thyroid cells
48
Q

What is the Jod-Basedow Phenomenon?

A

Iodine exposure produces thyrotoxicosis (excess TH production) in people with euthyroid goiters likely due to areas of autonomous fxn

49
Q

Radioiodine as a treatment

A
  • Emits gamma rays and beta particles
  • Used in low doses for diagnostic purposes, higher doses for therapy
  • Effects dose dependent
  • Do not give to breast feeding, preg women, or children
  • Stop antithyroid drugs 5 days prior
  • Low iodine diet to starve body for iodine so more gets uptaken
  • Need 24hr uptake 1st to det dose
  • Goal in graves is hyppthyroidism
50
Q

Describe the process of radioiodine treatment

A

-Necrosis of follicular cells followed by disappearance of colloid and fibrosis of glands over months

51
Q

Recombinant TSH

A

Used in thyroid cancer pts to look for sites of metast. by stimulating thyroid tissue for detection of thyroglobulin and radioidine scanning.

Avoids symptomatic hypothyroidism

Endorine (24 decks)

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