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Spring 2018 Pharm Exam 2 > Lecture 1: Thyroid Pharmacology > Flashcards

Lecture 1: Thyroid Pharmacology Flashcards

1
Q

What is most circulating TH bound to?

what is result of this?

A

TBG (thyroxin binding globulin) = plasma protein

- results in longer t 1/2 and low amt free hormone

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2
Q

Does TBG bind to more T4 or T3? (which TH hormone has higher free levels)

A

TBG binds to more T4 –> more T3 is free

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3
Q

What type of hormones can the pituitary respond to?

A

FREE hormones only

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4
Q

What are 2 causes of incr thyroid binding proteins?

A
  1. Drugs (estrogen, methadone)

2. Pregnancy

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5
Q

What is the result on the levels of TH when incr thyroid binding proteins? (whole process)

A

TH levels incr
(less free hormone–> pituitary sees less–> incr TSH–> incr TH levels –> levels of TSH and free THs return to normal (euthyroid)

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6
Q

Which isomers of thyroid hormones are naturally occurring and have more activity?

A

L-isomers

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7
Q

Where is T4 best abosrbed from

A

duodenum and ileum

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8
Q

How does hyperthyroidism affect clearance of T4 & T3?

Hypothyroidism?

A

Hyperythyroidism–> incr clearance T4/3 (shorter half life)

HYPOthyroidism –> decr clearance T4/3 (longer half life)

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9
Q

T4 vs T3:

  • which has longer half life (only need once daily dosing)
  • which has more potency/affinity for receptors
A 
T4 = longer half life 
T3 = more potency & affinity for rec
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10
Q

What modifies the body’s secretion and degradation rates of basically ALL other hormones

A

thyroid status (hyper, hypo, eu)

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11
Q

what is the physiologic effect of TH in nervous system

Others:

  1. incr heart effect, carb abs, BMR, O2 consumption
  2. breakdowns fats/proteins
  3. promotes normal growth/skeletal devel
  4. forms LDL rec
A

promotes normal brain development

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12
Q

3 indications for TH replacement therapy

A
  1. Adult HYPOthyroidism
  2. Infantile HYPOthyroidism (cretinism)
  3. Endemic Goiter
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13
Q

MC type and cause of Adult HYPOthyroidism

A

MC type = primary (thyroid gland defective)

MC cause = Hashimoto’s thyroiditis

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14
Q

What is Hashimoto’s thyroiditis?

What is characteristically seen w/this d/o?

A

autoimmune destruction of thyroid gland

assoc w/Abs to thyroid gland proteins

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15
Q

3 main features of Infantile HYPOthyroidism

MC areas for this type of hypothyroidism?

A
  1. Neuro impairement
  2. deaf-mutism
  3. Developmental failures

MC in iodine defic areas (prev w/screening)

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16
Q

Why is Endemic goiter rare in developed countries

Tx for endemic goiter

How is full dose of TH benefical

A

b/c iodide added to salt

Dietary supplementation of iodide

Full dose TH–> may hasten regression of goiter

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17
Q

Which thyroid prep has greater risk of cardiac toxicity and is CI in pts w/heart dz

A

T3

- Liothyronine sodium, L-triiodothyronine

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18
Q

Which thyroid prep is ToC for replacement therapy in hypothyroidism?

A

T4

- levothyroid sodium, L-thyroxin

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19
Q

What are the cardiac Sxs assoc w/T4?

What population must you use caution in w/T4?

A

palpitations, angina

caution in elderly

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20
Q

what is the thyroid prep given at T4 to T3 ratio of 4:1

A

Liotrix

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21
Q

Why is Liotrix not necessary for most pts

Who may it be benefical in?

A

body converts T4–> T3

may be beneficial in pts w/genetic polymorphism in deiodinase enzyme (cant convert T4–> T3)

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22
Q

What 2 drugs interactions w/T4? their effects?

A
  1. Rifampin (incr clearance of T4)

2. Cholestyramine (decr GI abs of T4)

23
Q

indication for ANTIthyroid therapy

A

hyperthyroidism

24
Q

What is MC form of hyperthyroidism

A

Graves dz

25
Q

What type of d/o is Grave’s dz and what is characteristicially seen w/it

A

autoimmune d/o –> IgG antibodies

26
Q

Role of IgG antibodies in Grave’s dz

A

IgG antibodies that bind to TSH rec/mimics its effects and stim thyroid–> incr TH levels

27
Q

Hyperthyroidism looks like sympathetic NS overactivity but how do you know its not?

A

Catecholamine levels are NOT increased

28
Q

What are the 4 main classes/types of drugs for Hyperthyroidism

A
  1. Thioamide class
  2. Anion inhibitors
  3. Iodides
  4. Radioactive Iodide
29
Q

What are the 2 drug prototypes for the Thioamide class?

MOA for both?

A
  1. MMI (Methimazole)
  2. PTU (Propylthiouracil)

MOA = blocks iodide organification (TH production) and blocks coupling of iodotyrosines

30
Q

What is the additional MOA for PTU

A

Acts peripherally to block conversion of T4 –> T3

31
Q

Why do PTU and MMI have a slow onset of action

A

mechanism = inhibit hormone synthesis –> takes 3-4 wks to deplete hormone

32
Q

3 major AEs a/w MMI and PTU

Others: skin rash, joint pain

A
  1. Agranulocytosis
  2. Hepatotoxicity (worse w/PTU)
  3. Birth defects (more w/MMI)
33
Q

Recommendation for pregnant women on taking MMI vs PTU

A

PTU in 1st trimester –> then MMI

34
Q

What dz is MMI and PTU the major drugs of Tx for?

A

Thyrotoxicosis

35
Q

What is benefit of giving high enough conc to suppress gland for 2 yrs w/MMI or PTU

A

possible permanent remission

36
Q

3 types of Anion inhibitors for Txing hyperthyroidism

A
  1. Perchlorate (ClO4-)
  2. Pertechnetate (TeO4-)
  3. Thiocyanate (SCN)
37
Q

MOA for potassium perchlorate

major use?

A

blocks thyroidal uptake of iodine

Txs iodine induced HYPERthyroidism

38
Q

common drug that causes iodine induced HYPERthyroidism

A

amiodarone (iodine rich)

39
Q

Major AE a/w Anion inhibitors?

A

Aplastic Anemia

40
Q

What 2 ways do iodides work to tx hyperthyroidism

A
  1. inhibit organification and hormone rel

2. decr size of hypertrophic gland

41
Q

What do iodides precipitate

A

Wolff-Chaikoff effect

42
Q

In what situation is the Wolff-Chaikoff reversed w/ time?

term for this reversal effect

A

effect reverses over time – if iodides used ALONE

escape

43
Q

When are iodides CI? why?

A

Pregnancy –> fetal goiter

44
Q

3 uncommon AEs that are usu reversible when iodides stopped?

A
  1. acneiform rash
  2. swollen salivary glands
  3. mucous mem ulcerations
45
Q

When are iodides used? w/what other drugs

rarely used today

A

used w/PTU and b-blockers for thyroid storm

46
Q

After radioactive iodide concentrates in thyroid follicle cells what is its MOA

A

Beta particles selectively destroy thyroid gland

w/out injury to adj cells

47
Q

What is common eventual AE of radioactive iodide in most pts?

2 CIs

A

HYPOthyroidism

CI = kids, preg

48
Q

What dz does radioactive iodide Tx

A

thyrotoxicosis

49
Q

2 benefits of radioactive iodide Tx

A
  1. euthyroid in 6-8 wks

2. no incr CA risk

50
Q

3 Things given for PREoperative Tx before subtotal thyroidectomy?

A
  1. Thioamide drug
  2. KI (potassium iodide)
  3. beta blocker
51
Q

How long give Thioamide drug for PREoperative Tx before subtotal thyroidectomy?

A

til euthyroid (~6 wks)

52
Q

When give Kl as PREoperative Tx before subtotal thyroidectomy? Why?

A

10 days before surg

- decr gland size/vascularity –> decr surgical risk

53
Q

Why give beta blocker as PREoperative Tx before subtotal thyroidectomy?

A

antagonize cathecholamine effects –> sx relief

Spring 2018 Pharm Exam 2 (6 decks)

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