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DEMS Unit 4 > Thyroid Pharm > Flashcards

Thyroid Pharm Flashcards

1
Q

How commonly are thyroid drugs prescribed

A

thyroid hormones consistently in top 10 of most frequently prescribed drugs

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2
Q

What activates the hypothalamic-pituitary-thyroid axis

A

circadian rhythms, prolonged cold exposure, acute psychosis

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3
Q

what can suppress the hypothalamic-pituitary-thyroid axis

A

severe stress

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4
Q

what stimulates pituitary release of TSH

A

TRH

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5
Q

what inhibits pituitary release of TSH

A

somatostatin, dopamine, glucocorticoids

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6
Q

major regulated step of thyroid hormone biosynthesis

A

uptake of iodide into thyroid gland; stimulated by TSH via G-protein coupled receptor – increased cAMP

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7
Q

what blocks iodide uptake

A

anions of similar size, like SCN, ClO4, I- itself

  • high concentrations of iodide >6mg, autoregulatory action via decreased expression of transporter)
  • cAMP generation inhibited by Lithium, which can cause hypothyroid sxs in anti-manic therapy
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8
Q

Role of thyroid peroxidase

A

oxidize iodide and incorporate into tyrosine residues on TG

- couples precursors MIT and DIT

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9
Q

Thyrotropin releasing hormone

A
  • tripeptide, administered IV with halflife of 4-5 min
  • activates phospholipase C– increases IP3– increases intracellular Ca++
    • this stimulates TSH production (and prolactin), which stimulates thyroid to produce T4
  • TRH blocked by T3 and somatostatin; potentiated by lack of T3
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10
Q

use of thyrotropin releasing hormone

A

test for pituitary reserve of TSH in suspected hypothyroidism and for hyperthyroidism

  • Unlabeled- antisedative effect for phenobarbital, benzos, EtOH overdose; high dose TRH may improve spimal cord injury outcomes
  • orphan drug for prevention in infant respiratory distress syndrome
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11
Q

TRH side effects

A

duration only a few min: urge to urinate, metallic taste, nausea, light-headedness

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12
Q

Thyroid Stimulating Hormone (drug)

A
  • aka thyrotropin
  • glycoprotein of alpha/beta subunits; prepared rom bovine source
  • IM or SC, t1/2 about 1 hr
  • stimulates cAMP via adenylate cyclase – increased iodine uptake and producon of thyroid hormone
  • blocked by Lithium
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13
Q

Use of pharm TSH

A
  • metastatic thyroid carcinoma (enhances radioactive uptake of I-131
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14
Q

side effects of TSH administration

A

nausea/vomiting, thyroid tenderness, allergic sxs, hyperthyroid sxs

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15
Q

MOA of thyroid hormones

A

enter cell via active transport. T4 converted to T3 via deiodinase. T3 enters nucleus to bind receptor

  • most effects mediated by increase in RNA then protein synthesis– increased Na/K ATPase – increased ATP turnover and O2 consumption – calorigenic effect
  • also increases in myosin ATPase and sarcoplasmic reticulum Ca ATPase
  • get increased fat/carb/protein consumption and metabolism
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16
Q

effects of thyroid hormones

A
  • optimal growth, development, function, maintenance of all body tissue
  • development of nervous, skeletal, reproductive tissues. hypo can cause dwarfism and mental retardation
  • influence secretion /degradation of other hormones
  • increased symp activity via thyroid hyperactivity– especially cardiovascular due to increased beta adrenergic receptors and adenylyl cyclase activity
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17
Q

causes of hypothyroid

A

Hashimoto’s most common; radiation exposure, surgery, iodine deficient, enzyme defects, pituitary disease (low TSH), rare hypothalamic disease (low TRH, low TSH)

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18
Q

treatment for hypothyroid

A

replacement therapy with levothyroxine (T4)

  • children need more per kilogram of body weight
  • require 6-8 wks for steady state; look at TSH 6-8 wks post dose adjustment and every 6-12 months after euthyroid state
  • may need increased dose for pregnancy due to increased TBG and increased placental metabolism of T4-T3– check every 1-3 months
  • use caution if underlying cardiac disease
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19
Q

how often to monitor pts with hypothyroid

A

check TSH 6-8 weeks post dose adjustment and every 6-12 months once in euthyroid state obtained

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20
Q

myxedema coma

A

(end state of untreated hypothyroidism)

  • acute medical emergency
  • hyponatremia, hypoglycemia, hypothermia, shock, death possible
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21
Q

how to treat myxedema coma

A

large doses with IV loading dose of T4 then daily dosing- can do T4/T3 combo or just T3 too
- may need hydrocortisone to prevent adrenal crisis as thyroid hormone may increase its metabolism (get low cortisol)

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22
Q

Drugs for hypothyroid

A

Levothyroxine (T4) adn Tiiodothyronine (T3)

  • Levo– take on empty stomach
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23
Q

drugs increasing hormone protein binding

A

Estrogens, Selective estrogen receptor modulators, tamoxifen

  • methadone, clofibrate, 5 fluorouracil, heroin
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24
Q

drugs decreasing protein binding

A 
salicylates
antiseizure meds (phenytoin, carbamazepine)
glucocorticoids
androgens
furosemide
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25
Q

does pituitary respond to total or free hormone levels

A

free hormone levels

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26
Q

drugs inhibiting 5’-deiodinase

A

Glucocorticoids

  • beta-adrenergic receptor antagonists
  • propylthiouracil (higher doses)
  • amiodarone
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27
Q

conditions inhibiting 5’ deiodinase

A
  • acute/chronic illness
  • caloric deprivation
  • malnutrition
  • fetal/neonatal period
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28
Q

major factor accounting for pharmacokinetic differences in T3, T4

A

degree of protein binding

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29
Q

Levothyroxine

A

synthetic T4; preparation of choice for replacement

  • stable, lack of allergenic foreign protein, low cost and longer half life for daily dosing
  • oral or IV
  • technically can switch between products but advisable to use same product for individual pt– as much as 10% difference between “equivalent” products
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30
Q

Liothyronine

A

synthetic T3

  • well absorbed, rapid action but shorter duration– quicker dosage adjustments
  • NOT recommended for routine replacement; high cost
  • can add if sxs persist with levo
  • avoid n pts with cardiac disease
  • used in T3 suppression test!!
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31
Q

what drug used in T3 suppression test

A

Liothyronine

32
Q

Liotrix

A

4: 1 mix of T4 adn T3
- more expensive, no advantage since conversion in periphery; not recommended
- combo therapy may cause increased low TSH and increased markers of bone turnover

33
Q

Thyroid USP

A

porcine thyroid extract of thyroxine and liothyronine

  • variable T4/T3 ratio– unexpected toxicities
  • protein antigenicity
  • product instability
  • less desirable than levothyroxine
  • NOT RECOMMENDED IN HYPOTHYROIDISM
34
Q

Adverse rxns with thyroid hormone replacement

A
  • Toxicity with excess related to plasma levels and thus equal to signs/sxs
  • Children: restlessness, insomnia, accelerated bone maturation/growth
  • adults: anxious, heat intolerant, palpitation/tachycardia, tremors, weight loss, increased bowel movements; can precipitate cardiac arrhythmias, angina pectoris, or MI in those with Cardiac disease
35
Q

DDI with thyroid hormones

A

increased adrenergic effects with sympathomimetics (epi, decongestants–phenylephrine, pseudoephedrine)

36
Q

Graves’ Treatment

A
  • modify tissue response (beta blockers/corticosteroids)
  • interfere with production of hormone (thionamides, iodides)
  • glandular destruction (surgery, radioactive iodine)
37
Q

Thionamides

A

Methimazole, Propylthiouracil (PTU–declining use)

  • M: 100% absorbed
  • PTU more protein bound, so less crosses placenta/secreted into breast milk
  • short half lives (5-13 hrs) but drugs accumulated in thyroid and have longer duration of action (P: 12-24; M: 40)
38
Q

MOA of thionamides

A
  • only work in thyrotoxicosis, not thyroiditis
  • prevent T3/T4 synthesis by blocking iodine organification/coupling
  • high dose PTU also inhibits conversion of T4 to T3
  • synthesis inhibited not release, so need 3-4 weeks to deplete T4 stores
39
Q

toxicity of thionamide

A
  • adverse rxns: pruritic rash, gastric intolerance, arthralgias
  • agranulocytosis most dangerous so routine CBC controversial but do if sore through/fever
  • rare hepatotoxicity with PTU but severe enough that routine PTU use is concerning
40
Q

Iodide as treatment

A

SSKI (potasium iodide), Lugol’s solution

  • rarely used today as sole therapy
  • high doses inhibit hormone syntheses (via elevated intracellular I) and hormone release (via elevated plasma I) through inhibiting TG proteolysis
41
Q

clinical use of iodide

A

NOT alone

  • start AFTER onset of thionamide effects or it can delay thionamide therapy
  • used to decrease size/vascularity of hyperplastic gland before surgery (given for 10 days prior to surgery)
42
Q

Iodine toxicity

A

uncommon, reversible

  • acneiform rash, rhinorrhea, metallic taste, swollen salivary glands
  • selective accumulation in salivary glands
43
Q

Radioactive iodine

A
  • I-131
  • oral, rapid absorbtion, concentrated in thyroid to cause slow inflammatory process that destroys parenchyma of gland over weeks to months
44
Q

advantages of radioactive iodine

A

easy admin, effective, low expense, not painful

- permanent resolution of hyperthyroidism

45
Q

disadvantages of radioactive iodine

A

slow onset/time to peak, some need 2nd dose, can get radiation thyroiditis with CV complications in elderly or susceptible pts, may cause worsening opthalmopathy
- hypothyroidism: 80% require replacement therapy

  • DON’t GIVE TO PREGO OR NURSING WOMEN!!
46
Q

Thyroidectomy

A
  • treatment of choice if large gland
  • rare today due to radioactive iodine effetiveness– risks of general anesthesia and parthyroid/recurrent laryngeal nerve damage becomes relatively great
  • advantage of rapid, permanent cure of hypoerthyroidism
  • get antithyroid drugs until euthyroid (6 weeks) + iodine prior to surgery
  • 50-60% need thyroid supplementation post surgery (iatrogenic hypothyroidism)
  • can be used in 2nd trimester of pregnancy if needed
47
Q

Thyroid storm

A

sudden, acute exacerbation of thyrotoxicosis
- may occur in noncompliant, incompletely treated, or undiagnosed pt with hyperthyroidism who has acute stress (infection, surgery, trauma)

48
Q

Thyroid storm sxs

A

fever, flushing, sweating, tachycardia/a fib, high output heart failure, delirium, coma
- hypermetabolism and excessive adrenergic activity

49
Q

Thyroid storm treatment

A
  • try to control sxs, inhibit release of preformed thyroid hormone, block conversion of T4 to T3
  • Propanolol (control CV effects and blocks conversion)
  • sodium iodide IV, potassiumiodide drops – slow hormone release
  • PTU blocks synthesis and conversion
  • Hydorcortisone- protects against shock, blocks conversion, may modulate immune response that makes thyrotoxicosis worse
50
Q

is levothyroxine narrow or wide therapeutic index

A

narrow!

51
Q

where is exogenous thyroid hormone absorbed

A

ileum/colon; impaired absorption in severe myxedema

52
Q

drugs impairng absorption of levothyroxine

A 
metal ions (antacids, calcium and levothyroxine)
- cipro, bile acid sequestrants, raloxifene, sucralfate
53
Q

how to take levothyroxine

A

empty stomach with water; space dose 3 hrs before or 4-6 hrs after interacting drug

54
Q

formula to calculate fluctuation in drug concentration

A

2^x

  • x = number of half lives in dosing interval
    (eg. T4 half life is 7 days, so dosing once a day– 2^(1/7) = 1.1, so 10% fluctuation)
55
Q

how long til you reach steady state after starting dose

A

4-5 weeks

56
Q

how long after changing dose will you reach new steady state for T4

A

4-5 weeks

57
Q

how long until resolution of hypothyroid sxs with drugs

A

resolution begins within 2-3 weeks

58
Q

Does levothyroxine or triiodothyronine have greater oral bioavailability

A

Triiodothyronine

59
Q

Does levothyroxine or triiodothyronine have greater affinity for thyroid hormone receptors

A

Triiodothyronine (T3)

60
Q

Does levothyroxine or triiodothyronine have greater potential for CV side effects durign therapy initiation

A

T3-triiodothyronine

61
Q

Is levothyroxine or triiodothyronine more expenxive

A

triiodothyronine

62
Q

Does levothyroxine or triiodothyronine have longer duration of action

A

T4

63
Q

increased risk of osteoporosis

A

Liothyronine

64
Q

which drug is porcine thyroid extract

A

Thyroid USP – contains T3 and T4

65
Q

which hyperthyroid drugs are synthesis inhibitors

A

thionamides, iodides

66
Q

which hyperthyroid drugs are modifying tissue response

A

Beta blockers, corticosteroids

symptomatic improvement!

67
Q

which Graves’ treatment is mainly glandular destruction

A

radioactive iodine and surgery

68
Q

why do we have lag in thyroid drug response

A

since we have stores of thyroid hormone in colloid

69
Q

which beta blocker used in Graves

A

propanolol (beta 1 and 2 action) blocks conversion but Metoprolol-atenolol are beta1 selective, longer T1/2

70
Q

is graves causing excessive release or production

A

excessive production

71
Q

is thyroiditis causing excessive release or production of hormone

A

release

72
Q

Major side effect with tionamides

A

agranulocytosis

73
Q

Methimazole or PTU have faster achievement of euthyroid state

A

Methimazole

74
Q

what do we use to control CV sxs in graves’

A

Beta blockers

75
Q

Does PTU or methimazole have risk of hepatotoxicity

A

PTU

DEMS Unit 4 (16 decks)

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