DEMS Unit 4 > Thyroid Pharm > Flashcards

Thyroid Pharm Flashcards

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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
does pituitary respond to total or free hormone levels
free hormone levels
26
drugs inhibiting 5'-deiodinase
Glucocorticoids - beta-adrenergic receptor antagonists - propylthiouracil (higher doses) - amiodarone
27
conditions inhibiting 5' deiodinase
- acute/chronic illness - caloric deprivation - malnutrition - fetal/neonatal period
28
major factor accounting for pharmacokinetic differences in T3, T4
degree of protein binding
29
Levothyroxine
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
30
Liothyronine
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!!
31
what drug used in T3 suppression test
Liothyronine
32
Liotrix
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
Thyroid USP
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
Adverse rxns with thyroid hormone replacement
- 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
DDI with thyroid hormones
increased adrenergic effects with sympathomimetics (epi, decongestants--phenylephrine, pseudoephedrine)
36
Graves' Treatment
- modify tissue response (beta blockers/corticosteroids) - interfere with production of hormone (thionamides, iodides) - glandular destruction (surgery, radioactive iodine)
37
Thionamides
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
MOA of thionamides
* 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
toxicity of thionamide
- 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
Iodide as treatment
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
clinical use of iodide
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
Iodine toxicity
uncommon, reversible - acneiform rash, rhinorrhea, metallic taste, swollen salivary glands - selective accumulation in salivary glands
43
Radioactive iodine
- I-131 - oral, rapid absorbtion, concentrated in thyroid to cause slow inflammatory process that destroys parenchyma of gland over weeks to months
44
advantages of radioactive iodine
easy admin, effective, low expense, not painful | - permanent resolution of hyperthyroidism
45
disadvantages of radioactive iodine
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
Thyroidectomy
- 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
Thyroid storm
sudden, acute exacerbation of thyrotoxicosis - may occur in noncompliant, incompletely treated, or undiagnosed pt with hyperthyroidism who has acute stress (infection, surgery, trauma)
48
Thyroid storm sxs
fever, flushing, sweating, tachycardia/a fib, high output heart failure, delirium, coma - hypermetabolism and excessive adrenergic activity
49
Thyroid storm treatment
- 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
is levothyroxine narrow or wide therapeutic index
narrow!
51
where is exogenous thyroid hormone absorbed
ileum/colon; impaired absorption in severe myxedema
52
drugs impairng absorption of levothyroxine
``` metal ions (antacids, calcium and levothyroxine) - cipro, bile acid sequestrants, raloxifene, sucralfate ```
53
how to take levothyroxine
empty stomach with water; space dose 3 hrs before or 4-6 hrs after interacting drug
54
formula to calculate fluctuation in drug concentration
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
how long til you reach steady state after starting dose
4-5 weeks
56
how long after changing dose will you reach new steady state for T4
4-5 weeks
57
how long until resolution of hypothyroid sxs with drugs
resolution begins within 2-3 weeks
58
Does levothyroxine or triiodothyronine have greater oral bioavailability
Triiodothyronine
59
Does levothyroxine or triiodothyronine have greater affinity for thyroid hormone receptors
Triiodothyronine (T3)
60
Does levothyroxine or triiodothyronine have greater potential for CV side effects durign therapy initiation
T3-triiodothyronine
61
Is levothyroxine or triiodothyronine more expenxive
triiodothyronine
62
Does levothyroxine or triiodothyronine have longer duration of action
T4
63
increased risk of osteoporosis
Liothyronine
64
which drug is porcine thyroid extract
Thyroid USP -- contains T3 and T4
65
which hyperthyroid drugs are synthesis inhibitors
thionamides, iodides
66
which hyperthyroid drugs are modifying tissue response
Beta blockers, corticosteroids symptomatic improvement!
67
which Graves' treatment is mainly glandular destruction
radioactive iodine and surgery
68
why do we have lag in thyroid drug response
since we have stores of thyroid hormone in colloid
69
which beta blocker used in Graves
propanolol (beta 1 and 2 action) blocks conversion but Metoprolol-atenolol are beta1 selective, longer T1/2
70
is graves causing excessive release or production
excessive production
71
is thyroiditis causing excessive release or production of hormone
release
72
Major side effect with tionamides
agranulocytosis
73
Methimazole or PTU have faster achievement of euthyroid state
Methimazole
74
what do we use to control CV sxs in graves'
Beta blockers
75
Does PTU or methimazole have risk of hepatotoxicity
PTU
DEMS Unit 4
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