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  1. 1. Hypothyroidism DR. S. ASWINI KUMAR. MD Professor of Medicine Medical College Hospital Thiruvananthapuram Learning objectives: • Understand thyroid hormone function • Narrate the causes of hypothyroidism • Describe the pathophysiology of hypothyroidism • Identify risk factors for hypothyroidism • Describe optimal approaches to treatment • Understand side effects relevant to the treatment • Describe consequences of minor deficiency of hormones • Know effects of excess thyroxin dosage in clinical practice Thyroid Hormone Physiology: • Thyroid hormones are necessary for the normal metabolism of human body • They have an important role to play in acceleration of growth and development • They have a role in increasing body’s calorie production as per requirement • Every tissue of body is affected directly or indirectly by the actions of the hormones • The functions of thyroid hormones include: • regulation of basal metabolic rate and adjustments of resting oxygen consumption • increased uptake, synthesis and utilization of glucose and heat production • sympathomimetic effects including increased heart rate and force of contraction Thyroid Hormone Control: • Hypothalamic-pituitary-thyroid axis controls synthesis and release of thyroid hormones • The hypothalamus synthesizes a peptide thyrotropin releasing hormone (TRH) • TRH stimulates pituitary thyrotrophs to produce thyroid stimulating hormone (TSH) • TSH travels to and stimulates the thyroid gland, trophically to produce T4 and T3 T4 - T3 conversion: • The major product of thyroid gland is T4. It accounts for 85% of thyroid hormone output • T4 is metabolized by mono-deiodination to T3 , the more potent, biologically active form • Circulating T4 has a half-life of seven days, whereas T3 has a half life of only one day Thyroid Hormone Receptors: • 3 receptors mediate the primary actions of thyroid hormone • These are named as TRa1, TRß1, and TRß2 • Interaction of T3 with its receptor promotes binding of cofactors • These cofactors regulate expression of thyroid-hormone-responsive genes • They act either through activation or repression of transcription Hypothyroidism: • Definition: It is the manifestation of effects of reduced thyroid hormones in human tissues • 1.8% of total population affected and 2nd only to DM as commonest endocrine disorder • Incidence increases with age and it is more common in females - 2-3% of older women Classification of Hypothyroidism: • Clinical Hypothyroidism (Overt Hypothyroidism) • Symptoms are manifest - TSH is high and serumT3 and T4 are low • Subclinical Hypothyroidism (Mild Hypothyroidism) • No symptoms - Mild TSH and Normal T3 & T4 • Euthyroid individual – • Normal thyroid function Normal TSH – Normal T4 and T3
  2. 2. Etiology: • PRIMARY HYPOTHYROIDISM - 99% • Hoshimoto’s thyroiditis is the most common cause • Idiopathic hypothyroidism is also probably cases of old Hoshimoto’s Thyroiditis • Irradiation or Surgical removal of thyroid or Drug therapy • Iodine deficiency is still the most common cause of hypothyroidism • Infiltrative Diseases: Sarcoidosis, Amyloidosis • SECONDARY HYPOTHYROIDISM [1%] • Decreased TSH production and resultant reduction in T4 • Pituitary neoplasm, Pituitary necrosis (Sheehan’s syndrome) • Congenital hypopituitarism • Hypothalmic dysfunction (Teritiary Hypothyroidism) Hashimoto’s Thyroiditis: • Dr. Hakaro Hashimoto was born in Iga-Ueno in Japan in the year 1881 • He graduated in Medicine form Kyushu Imperial Medical University • In 1912, he described the chronic thyroid disorder • He termed it as Struma Lymphamatosa; but now called as Chronic Lymphocytic Thyroiditis • It is characterized by diffuse lymphocytic infiltration, fibrosis and parenchymal atrophy Pathogenesis: • Reduced metabolic rate causes reduced performance • Hence weight gain occurs despite a poor appetite • The pathology is deposition of Glycos-Amino Glycans(GAG) in tissues • GAG is hygroscopic and causes mucinous edema • Hence this results in a boggy non-pitting edema in tissues which are lax • Skin and hair effects: • Skin has reduced sweating and sebaceous secretions • And there is thinning of epidermis, hyperkeratosis of stratum corneum • Hence the skin is pale, cool, dry and coarse • Capillary fragility causes easy bruisability • Scalp and body hair as well as the nails are dry and brittle • Cardiovascular effects: • Decrease in heart rate, pulse pressure and ↓ in the cardiac output • ↓ blood supply and vasoconstriction of skin – results in cold intolerance • Increased systemic vascular resistance – leads to increase in DBP • Flabby myocardium and pericardial effusions are common • ECG changes – sinus bradycardia, low voltage, ST & T changes • Respiratory and GIT effects: • Hoarseness of voice – due to GAG deposition in larynx • Obstructive sleep apnoea to a thick tongue falling back • Constipation due to reduced gut peristalsis • Myxedema megacolon and Myxedema ileus are uncommon • Neuromuscular effects: • Slowed physical and mental functions leads to lethargy and increased somnolence • Carpel tunnel syndrome due to deposition of GAG • Delayed relaxation of ankle jerk is a useful bed side clinical finding • Deafness and depression and rarely Myxedema madness may occur Signs and Symptoms: • These are non-specific and gradual in onset • May be confused with other conditions like postpartum depression and Alzheimer’s • One must maintain high index of suspicion
  3. 3. Common signs and symptoms: Laboratory values Additional Tests: • Once diagnosis of primary hypothyroidism is made, • Additional imaging or serologic testing are unnecessary if gland is WNL • In secondary cases, further testing with pituitary provocative testing • imaging with CT scan annd or MRI to rule out microadenoma • Evidence of ↓ of >1pituitary hormone indicates a panhypopituitary problem • Serum cholesterol may be elevated. Complete lipid profile and ECG studies • Prolactin levels are elevated in Secondary Hypopiuitarism • Blood Haemoglobin and ferritin testing for anaemia are indicated in most cases Antibodies in hypothyroidism: • Anti Thyroid Per-Oxidase [anti microsomal] antibodies – Anti-TPO in most cases • Anti thyroglobulin antibodies – Anti TG. Also found elevated in Hashimoto’s Thyroiditis • Anti bodies against T3 and T4 in auto immune disease. • Anti TSH Receptor and Anti-T3 T4 Receptor antibodies are also sometimes seen • Anti gastric parietal cell antibodies are seen in 10% and this may lead to Pernicious Anemia Thyroid Hormone Replacement: • Most healthy adults require 1.7 ugm/kg/day – 100-150ug/day • Levothyroxine cause increases in resting heart rate and BP • Start at low doses in older and if cardiovascular compromise • Elderly, dosage falls down to – 1.0 ugm/kg/day -50-100ug/day • For full replacement children need up to 4ugm /kg/day
  4. 4. Monitoring thyroid function: • Followed by serial TSH measurements • Changes in TSH levels lag behind serum T3 T4 • Resetting pituitary gland takes about 1 month • So TSH not be checked sooner than 4 weeks • Goal to keep TSH in lower half of normal range • No need to monitor the T3 T4 levels normally • In pituitary insufficiency T3 & T4 are followed • Goal to keep T3 T4 in upper range of normal • Once stable TSH or Free T4 monitored yearly • Once stable it remains stable until 60-70 yrs Pregnancy and Thyroid: • During pregnancy the requirement for FT4 increases by 25-50% • Estrogens → TBG → ↓FT4 → TSH + TPO Ab →Hypothyroidism • Miscarriage, preterm delivery, preeclampsia & placental abruption • Can lead to ↓intellectual capacity & developmental delay in children • (AACE) recommend universal thyroid testing for pregnant women Myxedema coma: • High mortality rate, despite intensive treatment • Myxedema coma almost always occurs in the elderly • Reduced consciousness, seizures + other features of hypothyroidism • Precipitated by factors that impair respiration like sedatives • Other precipitating factors - MI, CCF, CVA, UGIB and Pneumonia • Myxedema coma-Treatment: • Levothyroxine A single IV bolus of 500 g loading dose • Levothyroxine is continued at a dose of 50 to 100 g/day • If IV is not available the same initial dose by NG tube • Supportive therapy: • Correct metabolic disturbances & precipitating factors • Hydrocortisone 50mg q6h should be administered • Early use of broad-spectrum antibiotics for infection • Space blankets should be used to prevent heat loss • External warming for <300C, otherwise CV collapse • Hypertonic saline if there is hyponatremia • Hypotonic IV fluids avoided because water retention • Intravenous glucose if there is hypoglycemia • Sedatives avoided and blood levels monitored • Ventilator support with regular blood gas analysis Subclinical Hypothyroidism • Definition: Biochemical evidence but no clinical evidence • No universal consensus in treatment of mildly elevated TSH • Little risk if excessive treatment is avoided and clinical benefits • Patients will progress to overt HYPO if TSH is >6mU/l • Start with low dose 25-50 ug/day and slowly titrate upwards Risk of over treatment • Over treatment may result in atrial fibrillation • Otherwise there is a risk of development of osteoporosis • Then there is a possibility of inducing frank hyperthyroidism • Emotional lability, nervousness, irritability, poor concentration • Start with low dose 25-50 ug/day and slowly titrate upwards