} Review of the Thyroid Gland

} Thyroid-Pituitary Relationships
} Biosynthesis of Thyroid Hormones
} Thyroid Hormones
} Clinical Conditions
} Drugs
§ TRIIODOTHYRONINE (T3) AND THYROXINE (T4)
§ To normalize growth and development, body temperature,
and energy levels
§ Contain 59% and 65% (respectively) of iodine
§ CALCITONIN
§ Second type of thyroid hormone
§ Important in the regulation of calcium metabolism
 SYSTEM EFFECT
Metabolism
Increase oxygen consumption and oxygen
Calorigenesis dissociation, incr. basal metabolic rate, incr.
temperature
Lipid decr. total cholesterol (hepatic LDL receptors)
Carbohydrate increase absorption from GIT
Cardiovascular Inotropic: beta-receptors up-regulated; incr.
heart rate, incr.cardiac output
Renal Fluid retention
Neurological Essential for nervous system development
Growth Essential for normal growth, including bone
1. Thyroid hormone deficiency: hypothyroidism
• Iodine deficiency
• Post-procedural
• Autoimmune
• Drug-induced
} Deficiency of thyroid hormones
} Manifested by reversible slowing of all body
functions
– Cold intolerance
– Increased sleeping time
– Decreased appetite but increase in body weight
– Myxedema coma
} Management:
◦ Thyroid hormones (not for drug-induced
hypothyroidism)
} Dextrothyroxine
◦ has approx. 4% of the biological activity of L-isomer
} Levothyroxine
◦ Preparation of choice for thyroid replacement and
suppression therapy
} Liothyronine
◦ 3-4X more potent than levothyroxine
} Thyrotoxicosis – tissues are exposed to high
levels of thyroid hormones
◦ increased T3 and T4 ; decreased TSH
} Grave’s disease (diffuse toxic goiter) is the
most common form
} May be also caused by:
◦ Solitary Hyperfunctioning Nodules
◦ Drug-induced
– Signs and Symptoms: Hypermetabolic and
Hypersympathetic
– Heat intolerance
– Episodes of nervousness
– Tachycardia
– Palpitations
– Tremors
– Increased sweating
– Increased appetite but decrease in weight
– Eye changes: ophthalmopathy
} Can be controlled by:
◦ Antithyroid therapy
◦ Surgical thyroidectomy
◦ Destruction of the gland with radioactive iodine
} THIOAMIDES
◦ Propylthiouracil (PTU), Methimazole, Carbimazole
} ANION INHIBITORS
◦ Perchlorate, pertechnetate, and thiocyanate
} IODIDES
◦ Lugol’s solution, potassium iodide
} RADIOACTIVE IODINE
} ADRENOCEPTOR-BLOCKING AGENTS
◦ Propranolol, metoprolol, and atenolol
} Methimazole and PTU are major drugs for
treatment of thyrotoxicosis

} Mechanisms of action
– Prevent hormone synthesis by blocking iodide
organification through inhibition of thyroid
peroxidase catalyzed reactions

– Block coupling of iodothyronines

ž Can cross placental barrier, risk of fetal hypothyroidism,
pregnancy category D (lesser with PTU)
ž PTU: faster onset, shorter DOA
ž Methimazole: slower onset, longer DOA
ž PTU more protein-bound
ž Methimazole 10x more potent than PTU
} Block uptake of iodide by the gland through
competitive inhibition of the iodide transport
mechanism

} Useful for iodide-induced hyperthyroidism

(amiodarone-induced hyperthyroidism)

} Rarely used due to its association with

aplastic anemia
} Major anti-thyroids before the introduction of
thioamides
} Preparations:
◦ strong iodine solution (Lugol’s)
◦ potassium iodide
◦ iodine
} Rarely used as sole therapy
} MECHANISMS OF ACTION
◦ Inhibit organification and hormone release
through possible inhibition of thyroglobulin
proteolysis
◦ Decrease the size and vascularity of the
hyperplastic gland
} Thyroid storm
} Pre-operative preparation for thyroid surgery
} Protection of thyroid against fallout in the
event of a nuclear accident
} Uncommon but includes;
◦ acneiform rash
◦ Rhinorrhea
◦ Conjunctivitis
◦ bleeding tendencies
◦ anaphylactoid reactions
◦ polyarteritis nodosa
◦ mucousal ulcers
◦ swollen salivary glands
} 131I is the only isotope used for treatment of
thyrotoxicosis

} MECHANISM OF ACTION
◦ Destruction of the thyroid gland

} EFFECTS
◦ After oral administration, it is rapidly absorbed,
concentrated by the thyroid and incorporated into
storage follicles
◦ Destruction of thyroid parenchyma occurred within
6- 12 weeks
} INDICATIONS: It is the preferred drug for:
◦ all patients above 21 years of age who are not
pregnant or breast-feeding;
◦ debilitated, cardiac or elderly patients who are poor
surgical risks
◦ patients failing to respond to drug therapy
◦ patients who had ADRs with other treatments
◦ patients with recurrence after thyroid surgery
} MECHANISM OF ACTION
◦ Block the peripheral effects of thyroid hormone
◦ block the peripheral conversion of T4 to T3

} Used adjuncts in the management of

thyrotoxicosis

} Can cause clinical improvement of

hyperthyroid symptoms but do not typically
alter thyroid hormone levels