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Hyper and Hypothyroidism Editing File Mnemonic File Endocrine Block Pharmacology team 438 Hyper and Hypothyroidism Objectives: By the end of the lecture , you should know: ● Describe different classes of drugs used in hyperthyroidism and hypothyroidism and their mechanism of action ● Understand their pharmacological effects, clinical uses and adverse effects ● Recognize treatment of special cases such as hyperthyroidism during pregnancy, Graves’ disease and Thyroid Storm and special cases of hypothyroidism such as myxedema coma Color index: Black : Main content Purple: Females’ slides only Red : Important Grey: Extra info or explanation Blue: Males’ slides only Green : Dr. notes Hyperthyroidism Thyroid Function ● Normal amount of thyroid hormones are essential for normal growth and development by maintaining the level of energy metabolism in the tissue. ● Either too little or too much thyroid hormones will bring disorders to the body. Important Functions CVS: increase Growth & Thermoregulation Helps maintain heart rate & development, increase basal metabolic cardiac output especially in the metabolic rate energy balance which increase embryo & brain (BMR) oxygen demand Iodine Importance ● Thyroid hormones are unique biological molecules in that they incorporate iodine1 in their structure ● Adequate iodine intake (diet, water) is required for normal thyroid hormone production ● Major sources of iodine are: iodized salt, iodated bread, dairy products, shellfish ● Minimum requirement: 75 micrograms/day Iodine Metabolism 1 2 3 Iodide taken up by the Dietary iodine is absorbed thyroid gland is oxidized in the GI tract, then taken by peroxidase in the Oxidized iodine can then up by the thyroid gland (or lumen of the follicle: be used in production of removed from the body by - thyroid hormones I the kidneys) I Peroxidase 2 Iodide Iodine Thyroid Hormones2 Tetraiodothyronine (T \ thyroxine) 4 Triiodothyronine (T3) Synthesis Oxidation of Iodine Formation of T Iodine trapping: iodine: organification: 4 and T from MIT uptake of iodine (to its active form) The iodination of 3 and DIT: by the thyroid thyroid tyrosyl groups of Thyroid gland peroxidase thyroglobulin into (key enzyme of the peroxidase synthesis) MIT and DIT 1: Cannot be synthesized by the body, has to be supplied by diet. 2: once produced, they can control their own levels by feedback mechanisms Thyroid Regulation 1. Hypothalamus secretes Thyrotropin-Releasing Hormone (TRH) which stimulates synthesis and release of thyrotropin (Thyroid Hypothalamus Stimulating Hormone or TSH) by the anterior pituitary. - TRH 2. TSH then stimulates the thyroid gland to uptake iodine, + synthesize and release T4&T3. Ant. pituitary 3. T4 & T3 levels feedback to both hypothalamus and pituitary - affecting the release of TRH & TSH. TSH + 4. Thyroid hormones exert negative feedback on TSH release at the level of the anterior pituitary: Thyroid gland a. Inhibition of TSH synthesis. b. Decrease in pituitary receptor for TRH. 5. TSH release is influenced by hypothalamic (TRH), and by thyroid hormones themselves T3 / T4 Thyroid Hormone Disorders Hypothyroidism: Thyroid Refers to disorders in which the thyroid neoplasia: gland secretes Benign enlargement decreased amounts of or malignancies of the hormones gland Thyrotoxicosis: Hyperthyroidism: Is a term for all Refers to disorders in disorders with which the thyroid increased levels of gland secretes circulating thyroid increased amounts of hormones1 hormones Also defined as: Hypermetabolic Also defined as: Increased thyroid state cause by thyroid hormone hormone synthesis and secretion excess at the tissue level Not all patients with thyrotoxicosis All patients with hyperthyroidism have hyperthyroidism have thyrotoxicosis Causes of Thyrotoxicosis2 ● Thyroiditis With High ● Graves’ disease (60-80%) RAIU ● Iodine-induced thyrotoxicosis: RAIU 3 ● Multinodular goitre (14%) ○ Drugs (e.g. amiodarone ) With low ○ Radiografic contrast ● Adenomas/ Carcinomas media 1: Regardless of the cause. Therefor we can consider hyperthyroidism is a type of thyrotoxicosis but not vise versa. 2: Tested by hyperactive iodine uptake. 3: a powerful anti arrhythmic drug that contains iodine. Features of Diseases Features of Graves’ Disease (diffuse toxic goiter) ● Cause by thyroid stimulating immunoglobulins that stimulate TSH receptor, resulting in sustained thyroid over activity. ● Mainly in young adults aged 20-25 ● 5 times more frequent in women Exophthalmos ● Swelling and soft tissues of hands and feet Normal Goiter ● Clubbing of fingers and toes pretibial myxedema ● Half of cases have Exophthalmos (not seen with other causes of hyperthyroidism) ● 5% have pretibial myxedemia (thyroid dermopathy) Features of Toxic Multinodular Goiter ● Second most common cause of hyperthyroidism ● Most cases in women in 5th to 7th decades ● Often have long-standing goiter (chronic) ● Symptoms usually develop slowly Thyrotoxicosis Symptoms: Signs: ● Irritability ● Arrhythmia ● Dysphoria ● 1 Thyroid enlargement ● Heat intolerance and sweating ● Palpitations ● Warm, moist skin ● Fatigue & weakness ● Exophthalmos 2 ● Weight loss ● Pretibial myxedema ● Diarrhea Treatment of Hyperthyroidism 01 02 03 04 05 Thioamides Iodides\ Radioactive β-blockers Surgery (Antithyroids) Iodine Iodine 1: Very typical presentation, characteristic for graves. 2:Despite increased food uptake 1) Thioamides Methimazole\Carbimazole Drugs Propylthiouracil (PTU) Carbimazole: prodrug converted to the active metabolite methimazole ● Both PTU and Methimazole: Inhibits synthesis of thyroid hormones by inhibiting the peroxidase enzyme that catalyzes the iodination of tyrosine residues. MOA ★ Additional Mechanism for PTU ONLY: blocks the conversion of T4 to T3 in peripheral tissues ● Rapidly absorbed ● Rapidly absorbed ★ Protein binding: most of the drug ★ Protein binding: 80-90% 1 is free ● Accumulation: in thyroid ● Accumulation: in thyroid P.K ● Excreted by kidneys as inactive ● Excretion is slow, 60-70% of drug is metabolite within 24 hours 2 recovered in urine in 48 hours ● Half-life: 1.5 hours (short) 2 ● Half-life: 6 hours (long) ● Administered every 6-8 hours ● Administered every 8 hours ● Crosses placenta less readily as it is ● Concentrated in thyroid & crosses Pregnancy highly protein bound placenta ★ Recommended in pregnancy ★ Not recommended in pregnancy Breast ● Less secreted in breast milk ● Secreted feeding ★ Recommended ★ Not recommended ● Skin reactions (frequency: 4-6%): Urticarial or macular reaction3 ● Arthralgia (1-5%) ● GIT effects (1-5%): Gastric distress and nausea ● Polyarthritis (1-2%): So-called anti-thyroid arthritis4 ★ Agranulocytosis (0.1-0.5%): Seen in patients with Graves’ disease; occurs within ADRs 90 days of treatment ★ Immunoallergic hepatitis(0.1-0.5%) ● ANCA-positive vasculitis ● Abnormal sense of taste or smell (Anti-neutrophil cytoplasmic (rare) antibodies5) (rare) 2) Iodine\ Iodide 1- Organic iodides: iopanoic acid or ipodate Drug 2- Potassium iodide or lugol’s solution ● Inhibit thyroid hormone synthesis and release ★ MOA Block the peripheral conversion of T4 to T3 ★ The effect is not sustained6 (produce a temporary remission of symptoms) ★ Prior to thyroid surgery to decrease vascularity & the size of gland Uses ● Following radioactive iodine therapy ● Thyrotoxicosis ★ Should not be used as single therapy C.I ★ Should not be used in pregnancy7 ● May produce iodism8 (rare, as iodine isn’t much used now), Iodism symptoms: skin ADR rash, hypersalivation, oral ulcers, metallic taste, bad breath 1: More free drug = more drug available to induce its action 2: Long duration of action = less frequent administration. 3: most common side effect. 4: that is why when a patient comes complaining of arthritis always ask about medications. 5: test for ANCA levels when treating with PTU. 6: should not be given alone unless used for a short period of time. 7: cross the placenta 8: only if given in large amounts 2) Iodine\ Iodide 3) Radioactive Iodine (RAI) 1- Organic iodides: iopanoic acid or ipodate Drug 2- Potassium iodide or lugol’s solution Drug Radioactive Iodine (RAI) ● Inhibit thyroid hormone synthesis and release ● 131 I isotope (therapeutic effect due to emission of β rays1) ★ ★ MOA Block the peripheral conversion of T4 to T3 MOA Accumulates in the thyroid gland and destroys parenchymal cells, producing a ★ The effect is not sustained1 (produce a temporary remission of symptoms) long-term decrease in thyroid hormone levels. ★ Prior to thyroid surgery to decrease vascularity & the size of gland ● Clinical improvement may take 2-3 months Uses ● Following radioactive iodine therapy ● Half-life 5 days ● Thyrotoxicosis ★ Cross placenta & excreted in breast milk = C.I in pregnancy and breastfeeding ● Available as a solution or in capsules ★ Should not be used as single therapy ● C.I Advantages: ★ Should not be used in pregnancy2 ○ Easy to administer, effective, painless and less expensive P.K ○ safe if given within therapeutic dose, and less toxic than other drugs ● May produce iodism3 (rare, as iodine isn’t much used now), Iodism symptoms: skin ● ADR Disadvantages: rash, hypersalivation, oral ulcers, metallic taste, bad breath ○ High incidence of delayed hypothyroidism2 ★ Large doses have cytotoxic actions (necrosis3 of follicular cells followed by fibrosis) ○ May cause genetic damage ○ May cause leukemia & neoplasia induced by the genetic damage ● Hyperthyroidism mainly in old patients (above 40) ● Graves’ disease Uses4 ● Patients with toxic nodular goiter5 ● Can be used as a diagnostic method 4) β-blockers6 Drug
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