Thyroid Gland Disorders New Lecture PDF

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BUC

Dr/Gena Mahmoud Elmakromy

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thyroid disorders hyperthyroidism hypothyroidism endocrinology

Summary

This lecture covers thyroid gland disorders. It details the physiology, causes, symptoms, and management of hyperthyroidism and hypothyroidism. It also discusses Grave's disease and other related conditions.

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Thyroid gland disorders BY Dr/Gena Mahmoud Elmakromy Lecturer of internal medicine and endocrinology BUC Thyroid gland Intended Learning Objectives: Physiology of thyroid hormone secretion. the definition and clinical picture of thyroid...

Thyroid gland disorders BY Dr/Gena Mahmoud Elmakromy Lecturer of internal medicine and endocrinology BUC Thyroid gland Intended Learning Objectives: Physiology of thyroid hormone secretion. the definition and clinical picture of thyroid gland disorder. Classify types of hyper and hypothyroidism. Grave’s disease clinical picture and management. The definition, symptoms and signs of subclinical hyperthyroidism and hypothyroidism thyroid storm definition, clinical picture and management. Physiology: Hyperthyroidism is the clinical effect of excess thyroid hormone secretion usually from gland hyperfunction. A wide range of conditions can cause hyperthyroidism, although Graves’ disease is the most common. Graves’ disease constituites ⅔ of cases of hyperthyroidism. Causes: Graves’disease, an autoimmune disorder, causes the production of antibodies (thyroid stimulating immunoglobulin [TSI]) (TSH receptor antibody), which stimulate the thyroid to secrete T4 and T3. Intrinsic thyroid autonomy can be caused by the following: - Toxic solitary adenoma. - Toxic multinodular goiter (Plummer disease), a non-autoimmune disease of the elderly associated commonly with arrhythmia and CHF. Causes (cont.): Transient hyperthyroidism results from subacute thyroiditis (painful) or lymphocytic thyroiditis (painless, postpartum). Drugs such as amiodarone, alpha interferon, and lithium can induce thyrotoxicosis. Excess iodine, as may occur in people taking certain expectorants or iodine-containing contrast agents for imaging studies, may cause hyperthyroidism. Causes (cont.): Extrathyroid source of hormones include: - Thyrotoxicosis factitia (excess exogenous L- thyroxine) - Ectopic thyroid tissue (struma ovarii i.e. ovarian teratoma with thyroid tissue, metastatic follicular thyroid carcinoma). Rarely, hyperthyroidism can result from excess production of TSH from pituitary adenoma (secondary hyperthyroidism). ` Symptoms: Diarrhoea; weight loss; appetite increase; over-active; sweats; heat intolerance; palpitations; tremor; irritability; labile emotions; oligo menorrhoea ± infertility. Rarely psychosis; chorea; panic; itch; alopecia; urticaria. Signs: Pulse fast/irregular (AF or SVT; VT rare); warm moist skin; fine tremor; palmar erythema; thin hair; lid lag; lid retraction. There may be goiter; thyroid nodules; or bruit depending on the cause. What is Graves’ disease? Graves’ disease (toxic diffuse goiter) is hyperthyroidism with diffuse goiter, exophthalmos, and dermopathy. In Graves’, autoantibodies form and bind to the TSH receptor in thyroid cell membranes, stimulating the gland to hyperfunction (TSI). Commonly affects patients age men (9:1) Significant genetic component, i.e., a person is more likely to be affected if they have family member with the disease Commonly triggered by stress, infection, and pregnancy Patients with another autoimmune disease such as type 1 diabetes or pernicious anemia are more likely to be affected Clinical Findings Graves’ is associated clinically with diffuse painless enlargement of the thyroid (goiter). Additionally: Nervous manifestations (younger patients) Irritability, emotional lability, inability to sleep, tremors, proximal muscle weakness (prominent symptom in many patients, and the primary reason why they see a physician). Cardiovascular manifestations Dyspnea, palpitations, atrial fibrillation, angina, and possible cardiac failure. Pulse is usually with big volume and the blood pressure showing systolic hypertension. Cardiac examination : accentuated heart sound and functional to and fro high pitched sound usually over pulmonary area(Lerman scratch). Skin manifestations: Excessive sweating and heat intolerance Warm and moist skin Palmar erythema, hair loss along with fine and silky hair in hyperthyroidism Skin manifestation of hyperthyroidism Nail onycholysis (separation of finger nail from nail bed) plummer’s nails Ocular signs such as staring due to lid retraction, infrequent blinking, and lid lag Gastrointestinal manifestations: Frequent bowel movements and vomiting, Weight loss despite increased appetite Genital manifestations: - Menstrual irregularity such as oligomenorrhea, and infertility in women. - Decreased libido and erectile dysfunction in men. Osteoporosis and hypercalcemia, as a result of increases in osteoclast activity Signs of Graves’ disease: 1- Eye disease (‘Thyroid eye disease’):exophthalmos, ophthalmoplegia. 2 – Pretibial myxoedema: oedematous swellings above lateral malleoli: the term myxoedema is confusing here. 3- Thyroid acropachy: extreme manifestation, with clubbing, painful finger and toe swelling, and periosteal Pretibial myxedema in Grave’s disease Thyroid acropachy Diagnosis Diagnosis of Graves’ is made on history and physical exam. Lab studies include the following: Decreased TSH (but elevated TSH in secondary hyperthyroidism) High serum free T4 and T3 Elevated RAIU (but decreased RAIU in subacute thyroiditis and factitious hyperthyroidism) Elevated TSI( TSH receptor antibody) , antithyroglobulin, and antimicrosomal antibodies There may be mild normocytic anaemia, mild neutropenia (in Graves’), elevated ESR, elevated Ca2+, elevated LFT. Treatment 1-Drugs: B-blockers (eg propranolol 40mg/6h) for rapid control of symptoms. Antithyroid medications (methimazole (carbimazole) or propylthiouracil), which blocks the synthesis of thyroid hormones resulting in control of high thyroid hormones. Methimazole has a longer half-life, reverses hyperthyroidism more quickly, and has fewer side effects than propylthiouracil. Methimazole requires an average of 6 weeks to lower T4 levels to normal and is often given before radioactive iodine treatment; it can be taken 1x/ day. Use propylthiouracil only when methimazole is not appropriate because of its potential for liver Two strategies (equally effective): A-Titration, eg carbimazole 20– 40mg/24h PO for 4wks, reduce according to TFTs every 1–2 months. B-Block-replace: Give carbimazole + levothyroxine simultaneously (less risk of iatrogenic hypothyroidism). In Graves’, maintain on either regimen for 12–18 months then withdraw. >50% will relapse, requiring radioiodine or For years propylthiouracil was the traditional drug of choice during pregnancy because it causes fewer severe birth defects than methimazole. However, experts now recommend that propylthiouracil be given during the first trimester only. This is because there have been rare cases of liver damage in people taking propylthiouracil. After the first trimester, women should switch to methimazole for the rest of the pregnancy. For women who are nursing, methimazole is probably a better choice than propylthiouracil (to avoid liver side effects). Both drugs can cause agranulocytosis. Carbimazole SE: agranulocytosis (decreased neutrophils, can lead to dangerous sepsis; rare (0.03%)); warn to stop and get an urgent FBC if signs of infection, eg fever, sore throat/mouth ulcers. 2- Radioiodine ( 131I): Most become hypothyroid post-treatment. There is no evidence for increased cancer, birth defects, or infertility in women. CI: pregnancy, lactation. Caution in active hyperthyroidism as risk of thyroid storm. Indications include: Large thyroid gland Multiple symptoms of thyrotoxicosis High levels of thyroxine High titers of TSI Because of the high relapse rate (>50%) associated with antithyroid therapy, many physicians in the United States prefer to use radioactive iodine as first- line therapy. With radioactive iodine, the desired result is hypothyroidism due to destruction of the gland, which usually occurs 2-3 months post administration, after which hormone replacement treatment is indicated. 3-Thyroidectomy (usually total): Carries a risk of damage to recurrent laryngeal nerve (hoarse voice) and hypoparathyroidism. Patients will become hypothyroid, so thyroid replacement needed. Subtotal thyroidectomy (and rarely total thyroidectomy) is indicated only in pregnancy (second trimester), in children, and in cases when the thyroid is so large that there are compressive symptoms. Complications of thyrotoxicosis Heart failure (thyrotoxic cardiomyopathy, increase in elderly), angina, AF (seen in 10– 25%: control hyperthyroidism and warfarinize if no contraindication), Osteoporosis, Ophthalmopathy, Gynaecomastia. Increase thyroid storm What is Subclinical hyperthyroidism? Subclinical hyperthyroidism occurs when there is low TSH, with normal T4 and T3. There is a 41% increase in relative mortality from all causes versus euthyroid control subjects—e.g from AF and osteoporosis. Management: - Confirm that suppressed TSH is persistent (recheck in 2–4 months). - Check for a non-thyroidal cause: illness, pregnancy, pituitary or hypothalamic insufficiency (suspect if T4 or T3 are at the lower end of the reference range), use of TSH- suppressing medication, eg If TSH

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