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Pharmacology II > Thyroid & Anti-thyroid Drugs > Flashcards

Thyroid & Anti-thyroid Drugs Flashcards

1
Q

what are the thyroid hormones?

what hormones trigger their release?

A

T3 and T4

hypothalmic-pituitary-thyroid axis:

  • TRH (hypothalamus) –> TSH (anterior pituitary) –> T3, T4 (follicular cells)
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2
Q

discuss the regulators of the hypothalamic-pituitary-thyroid axis?

A

inhibition:

TRH & TSH both by T3,T4 (feedback)

TRH: by chronic stress

TSH: by

  • somatostatin (also inhibits somatotrophes)
  • dopamine (also inhibits lactotrophes)
  • glucocorticoids
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3
Q

whta inhibits release of TRH from hypothalamus?

A
  • T3/T4 (negative feedback)
  • chronic stress
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4
Q

what are low, normal and high TSH levels

A
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5
Q

define hyperthyroidism / thyrotoxicosis

what are the major causes of hyperthryoidism?

A

= hypermetabolic state due to excess circulating T3, T4

major causes

  • primary
    • Grave’s (thyroid hyperplasia)
    • thyroiditis - inflammation/fibrosis damages thyroid & leads to excess TH release
      • granulomatous, subacute lympocytic
    • thyroid nodules / multdinodular goiter
  • excess consumption of: 1. iodine or 2. TH supplements
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6
Q

Graves is most common in what population?

A

women 20-40 yrs

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7
Q

what are the major manifestations of hyperthyroidism / thyrotoxicity?

A

= hypermetabolic state

  • too hot (heat intolerant)
  • weight loss (increased metabolic rate)
  • inc GI activity –> diarrhea
  • rapid DTRs
  • tachycardia / tachyarrythmias –>. HF
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8
Q

hyperthyoidism is managed generally by what drug classes?

(list the drugs in each class)

A
  1. antithyroid drugs:
    • thioamides: methimazol, propylthiouracil (PTU)
    • iodies (KI)
  2. radioactive iodine (131I)
  3. thyroidectomy
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9
Q

thioamides

  • incudes what drugs?
  • have what MOA?
  • have what clinical uses?
  • what general AEs?
A

methimazole, propylthiouracil (PTU)

  • MOA: both inhibit TH synthesis by inhibition of thyroperoxidase (no thyroglobulin iodination) PTU also inhibits T4–>T3
  • clinical use: hyperthyroidism
  • AEs: 1. hepatotoxicity, 2. dangerous in pregnancy
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10
Q

methimazole

  • what kind of drug?
  • what MOA?
  • clinical uses?
  • PK - onset / potency / half life
  • AEs/CIs?
A
  • is a thioamide (antithyroid drug)
  • MOA: inhibits TH synthesis by i_nhibiting thyroperoxidase_
  • clinical uses: first line drug for hyperthyroidism
  • PK:
    • onset - rapid
    • highly potent (> PTU)
    • t1/2 = 6 hrs (> PTU)
  • AE:
    • hepatoxic: hepatic failure / hepatitis / jaundice (< PTU)
    • teratogenic (> PTU)
    • agranulocytosis
    • common - GI/rash/fever
  • CI: 1st trimester of pregnancy
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11
Q

propylthiouracil (PTU)

  • what kind of drug?
  • what MOA?
  • clinical uses?
  • PK - onset / potency / half life
A
  • thioamine (antithyroid drug)
  • MOA:
    1. inhibits TH synthesis by inhibiting thyroperoxidase
    2. inhibits T4–>T3 synthesis by inhibiting D1 5’-diodinase
  • clinical:
    • hyperthyroidism in 1st trimester of pregnancy
    • thyroid storm
    • if pt has AEs to methimazole
  • PK
    • onset - slow
    • potency - low (< PTU)
    • t1/2 = 1.5 ( < PTU)
  • AEs:
    • hepatoxic: hepatic failure / hepatitis / jaundice (> methimazole)
    • teratogenic (< PTU)
    • agranulocytosis
    • common - GI/rash/fever
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12
Q

when is PTU preferred over methimazole?

A
  • for pt in 1st trimester of pregnancy
  • for a “thyroid storm” - inhibits T3/T4 conversion
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13
Q

how does propylthiouracil (PTU) differ from methiomazole pharmokinetically

A

PTU has

  • < potency
  • < half life
  • slower onset of action (3-4 wks)
  • more toxic - i.e., hepatotoxic
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14
Q

potassium iodide (KI)

  • what kind of drug?
  • what MOA?
  • what cinical uses?
  • AEs?
  • CIs?
A
  • antithyroid drug
  • MOA:
    • 150 mg (recommended dose): of proteolysis
    • > 6 mg: inhibits t_hyroperoxidase enzyme_
  • clinical uses:
    • decrease size/vascularity of thyroid gland prior to surgery
    • inhibit uptake of radioactive iodine after exposure - likely following a nuclear accident
  • AEs:
    • GI: unpleasant taste / salivary gland inflammation / gastritis
    • immune: anaphyolaxis / angioedema / thormbocytopenia
    • skin lesion
  • C/I:
    • within 3 weeks prior to 131iodine radioation therapy
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15
Q

in what form is KI given?

A

lugol’s solution

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16
Q

anion inhibitors

  • include what drugs?
  • are what kind of drugs?
  • have what MOA?
  • have what clinical uses?
A

ate- perchlorate, pertechnetate, thiocynate

  • antithyroid drugs
  • MOA: competitive inhibition of I- uptake by Na/I symptorter on follicular cell
  • clinical use: tx of hyperthyroidism due to excess iodine consumption
    • ​(ex - amiodarone-indued)
  • AE:
    • aplastic anemia
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17
Q

perchlorate

  • what kind of drug
  • MOA
  • clinical uses
  • AE
A
  • antithyroid drugs
  • MOA: competitive inhibition of I- uptake by Na/I symptorter (NIS) on follicular cell
  • clinical use: tx of hyperthyroidism due to excess iodine consumption
    • ​(ex - amiodarone)
  • AE:
    • aplastic anemia
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18
Q

pertechenate

  • what kind of drug
  • MOA
  • clinical uses
  • AEs
A
  • antithyroid drugs
  • MOA: competitive inhibition of I- uptake by Na/I symptorter on follicular cell
  • clinical use: tx of hyperthyroidism due to excess iodine consumption
    • ​(ex - amiodarone-indued)
  • AE:
    • aplastic anemia
19
Q

thiocynate

  • what type of drug
  • MOA
  • clinical uses
  • AEs
A
  • antithyroid drugs
  • MOA: competitive inhibition of I- uptake by Na/I symptorter on follicular cell
  • clinical use: tx of hyperthyroidism due to excess iodine consumption
    • ​(ex - amiodarone-indued)
  • AE:
    • aplastic anemia
20
Q

I131

  • what kind of drug?
  • MOA?
  • PK
  • clinical uses?
  • AEs?
A
  • radioactive iodine
  • MOA: taken up and concentrated in thyroid gland then –> destroys parenchymal cells
  • PK - slow onset
  • clinical uses: hyperplasia (Grave’s disease)
    • ​(untrolled hyperparathyoidism)
  • AE:
    • permanent hyperthyroidism (almost inevitable)
    • radiation thyroiditis - tho not to the degree to cause cancer
    • sore throat
    • opthalmopathy exacerbation (presents in grave’s pts)
21
Q

which thyroid drug can cause permanent hypothyroidism?

what is the tx in this situation?

A

radioactive iodine (I131) - used to tx Grave’s

treatment: levothyroxine

22
Q

wat is the only “definitive” therpay for hyperthyroidism?

A

radioactive iodine (I131) - destroys parencymal cells

23
Q

what drug is given for exposure to a nuclear event?

A

KI (Lugol’s Solution)

24
Q

what drug can be given to decrease size and vascularity of thyroid gland pre-surgery?

A

KI (lugol’s solution)

25
Q

what cardiac manifestations are associated with thyrotoxicosis / hyperthyroidism?

how are they managed?

A

tachycardia / tachyarrythmia (a-fib) / heart faiure

can be treated with:

  • beta blockers: metoprolol, esmolol, propanolol - rapid symptomatic relief
  • CCBs: diltiazem, verapamil - given if beta blockers C/I (asthma)
  • corticosteroids: given to prevent shock from cardiac event
26
Q

what are the AEs of I131?

A
  • permanent hyperthyroidism (almost inevitable)
  • radiation thyroiditis - tho not to the degree to cause cancer
  • sore throat
  • opthalmopathy exacerbation (presents in grave’s pts)
27
Q

what is the role of corticosteroids in the thyroid hormone metabolism?

A
  • endogenous role: inhibits TSH secretion & T4-T3 conversion
  • tx role: given in hyperthyroidism / thyrotoxicosis: to manage cardiac manifestations - tachy / arrythmias / HF
    • protects patient from shock
28
Q

amiodarone has what effects on thyroid metabolism?

A
  • is highly iodine rich can cause hyperthyroidism or hypothyoirism
    • hyper: tx = perchlorate. pertechenate, thiocynate
29
Q

what is the role of lithium in thyroid hormone metabolism?

A

causes hypothyroidism

30
Q

hypothyroidism

  • defintion?
  • major causes?
A

hypo-metabolic state due to low cirulating T3 & T3 (< 0.5 mlu/L)

causes:

  • hashiomoto’s disease
  • congenital cretinism
  • surgical removal of part/all of thyroid
  • thyroiditis* can also cause hyper
31
Q

what is congenital cretinism & how does it present?

A

hypothyroidism present at birth

presentation: dwarfism, mental retardation

32
Q

what are the manifestations of hypothyroidism?

A

hypometabolic state

  • cold intolerance
  • weight gain (decreased metabolic rate)
  • bradycarda
  • decreased drug metabolism
  • lethargy / faituge / weakness
33
Q

what are the classes of drugs used to treat hypothyroidism?

list the drugs in each class?

A

hypothyoidism is treated by giving supplemental thyroid hormone - either synthetic or natural

  • synthetic TH
    • levothyoxine (T4)
    • liothyronine (T3)
    • liotrix (T3 + T4)
  • natural TH
    • dessicated thyroid (T3 + T4)
34
Q

biologically, what converts T4 into T3?

where does this conversion occur?

A

T4 –> T3 (more potent)

  • by 5’-deiodinases in the peripheral tissues
    • D1 5’-diodinases: in most of periphery
    • D2 5’-diodinases: in brain specifically
35
Q

contrast T4 and T3 in terms of

  • half life
  • potency
  • receptor binding affinity
  • what synthetic thyroid hormone drugs they’re found in
A
  • half life: T3 (1 day) < T4 (7 days)
  • potency: T3 > T4 (4x more)
  • receptor binding affinity: T3 > T4 (10x more)
  • drugs:
    • T4 - levothyoxine
    • T3 - liothyronine
36
Q

thyroid hormones - MOA & physiological effects

A
  • if drug if T4 (levothyroxine), its converted to T3 by 5’-dionidase
  • T3 binds to nuclear (Subclass II) receptors and modulate gene transcription
    • two tissue specific receptor types: THR-alpha and THR-beta:
      • TRH alpha receptors regulate HR /body temp / skeleletal muscle function / bone development
37
Q

thyroid hormones PK (onset and half life)

A
  • onset: slow (3-5 days)
  • half life:
    • T3 = 1 day
    • T4 = 7 days
38
Q

what are the physiologic effects of thyroid hormones?

A
  • normal macromolecule developemnt
  • promotion of growth & development
  • cardiovascular stimulation
  • feedback inhibition of TRH & TSH
39
Q

thyroid hormone clinical uses? what is the goal of thyroid hornone therapy in each condidition?

A

hypothyroidism - goal to maintain normal TSH

cretinism - given in newborns to prevent irreversible mental retardation

myxedoma coma (coma due to severe hypothyroidism) - give T3 + T4

prevention of tumor-growth nodule following cancer surgery goal to keep below normal TSH (TSH suppression therapy)

40
Q

thyroid hormone AE

A
  • sx of hyperthyroidism: heat intolerance / weight loss / tachycardia / tachyarrythnias /
  • osteoporosis (if given long term, esp in post-menopausal women)
41
Q

thyroid hormones should be given in caution with patients with?

which of these patient should be started on a low dose?

A
  • adrenal insufficiency
  • diabetes
  • osteoporosis

start on a low dose:

  • long standing hypothroidism
  • CV disease
  • age > 60 yrs old
42
Q

what hypothyroid pts should be started on low-dose thyroid hormone?

A

pts

  • with long standing hypothyroidism
  • over age 60
  • with CV disease
43
Q

what is TSH suppression therapy?

when is it done and what drugs are used?

A
  • done in pts
    • with thyroid nodules
    • that are post thyroid-cancer surgery
  • done with thyroid hormones (levothyroxine, liothyronine, liotrix)
44
Q

how do we treat a myxedema coma?

A

with thyroid hormones: levothyroxine (T4), liothyronine (T3), liotrix

Pharmacology II (5 decks)

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