Description
This comprehensive lecture on hypothyroidism, authored by Dr. B. C. Kamanga, MD, from the University of Zambia (UNZA), provides an authoritative review of the etiology, clinical features, and management of thyroid hormone deficiency. The presentation details the classification of hypothyroidism into primary, secondary, and tertiary causes, with a focus on Hashimoto's thyroiditis as a common autoimmune etiology. It systematically outlines the multi-system clinical manifestations, including dermatological findings like cool, dry skin and myxedema, cardiovascular effects such as bradycardia and pericardial effusion, gastrointestinal issues like constipation, hematologic abnormalities including anemia, and neuropsychiatric symptoms ranging from fatigue and depression to 'myxedema madness'. The lecture explains the pathophysiology involving glycosaminoglycan accumulation and provides clear guidance on the interpretation of thyroid function tests. The core of the presentation is dedicated to the principles of treatment, emphasizing levothyroxine (T4) replacement therapy, appropriate dosing strategies across different age groups including during pregnancy, and the critical monitoring of serum TSH and T4 levels. It also reviews important drug interactions that can affect thyroid hormone absorption or metabolism. This resource is essential for medical students, postgraduate trainees in internal medicine and endocrinology, and practicing clinicians seeking to solidify their understanding of the diagnosis and evidence-based management of hypothyroidism. It serves as a valuable study and reference tool for both exam preparation and clinical practice. Review this detailed presentation to enhance your diagnostic and therapeutic approach to this common endocrine disorder.
What's inside
Management of Hypothyroidism B. C. Kamanga, MD UNZA Definition A clinical syndrome resulting from a deficiency of thyroid hormones. Etiology Primary – thyroid failure Secondary Hypothyroidism results from TSH deficit, which may be due to hypopituitarism caused by a pituitary adenoma, apoplexy, infiltrative disease-sarcoidosis Tertiary Hypothyroidism results from hypothalamic deficiency, rarely of TRH deficiency Peripheral resistance to the action of thyroid hormone Hashimoto’s Thyroiditis Chronic lymphocytic thyroiditis Leads destruction of the Thyroid by the immunologic process Antibodies against Thyroglobulin and Thyroperoxidase are diagnostic of this disease Clinical Features Skin feels cool and looks pale, due to reduced blood flow in it Dry roughness skin: the epidermis has an atrophied cellular layer and hyperkeratosis Decreased sweating: Generalized nonpitting edema (myxedema) in severe hypothyroidism, due to infiltration of the skin with glycosaminoglycans and associated water retention Clinical Features Periorbital edema; a manifestation of generalized nonpitting edema as in Graves’s hypothyroidism Graves' ophthalmopathy may persist or worsen when hypothyroidism in Graves' hyperthyroidism. Bradycardia Impaired cardiac contraction, leading to reduced cardiac output Decreased exercise capacity and shortness of breath during exercise low voltage of QRS complexes and P and T waves Clinical Features Cardiomegaly on CXR, due to increased interstitial edema, myofibrillary swelling, LV dilatation, pericardial effusion Myxedema induces coronary artery disease Hypertension, due to increased peripheral vascular resistance Fatigue, shortness of breath on exertion, and decreased exercise capacity as a result of impaired respiratory function + cardiovascular disease Hypoventilation (shallow and slow respirations), due to respiratory muscle weakness + reduced pulmonary responses to hypoxia and hypercapnia Obstructive sleep apnea may be due to macroglossia Clinical Features Constipation, even ileus as a result of reduced gut motility Decreased taste sensation Gastric atrophy, if antiparietal cell antibodies present Pernicious anemia, resulting from chronic atrophic gastritis Weight gain, due to decreased metabolic rate + accumulation of fluid (nonpitting edema Decreased glomerular filtration rate Impaired ability to excrete a water load Clinical Features Anemia, due to impaired hemoglobin synthesis Iron deficiency, due to increased iron loss with menorrhagia + impaired intestinal absorption of iron Folate deficiency, due to impaired intestinal absorption of folic acid Pernicious anemia, due to vitamin B12 –deficiency (megaloblastic anemia) Clinical Features Women with hypothyroidism may have either oligo- or amenorrhea or hypermenorrhea-menorrhagia Decreased fertility Increased likelihood for early abortion Hyperprolactinemia (in PRIMARY hypothyroidism), leading to gynaecomastia/ galactorrhoea and amenorrhoea Reduced Serum sex hormone-binding globulin concentration, WHICH may lower serum total SEX hormone concentrations. Clinical Features General depression of central nervous system function Sleepiness, inability to concentrate Sluggish thought processes Respond slowly to questions Less able to retrieve information from memory Agitated (“myxedema madness”) PET: 23% reduction in cerebral blood flow and a 12% reduction in cerebral glucose metabolism Clinical Features Delayed relaxation phase of deep tendon reflexes Carpal tunnel syndrome Paresthesia Elevation in serum CPK level Muscle cramps, proximal muscle weakness hyponatremia , due to reduced free water clearance Decreased lipid clearance may cause an elevation in the serum free fatty acids levels and Total as well as LDL cholesterol Plasma homocysteine concentrations may rise Clinical Features Generalized slowing down of metabolic processes Cretinism in newborn infants Short stature, mental retardation, precocious puberty in adolescents Pathogenesis of Hypothyroidism Accumulation of glycosaminoglycans (a hydrophilic) in interstitial and increased capillary permeability to albumin leads to interstitial edema in the skin, heart muscle, and striated muscle. Interpretation of Thyroid Function Tests Treatment Replacement of Triiodothyroxine (T3): unsatisfactory due to rapid absorption, short half-life, and transient effect Levothyroxine (T4) is converted to T3 intracellularly Taken Once daily, half-life: 7 days Treatment monitored with serum TSH and T4 levels in Primary hypothyroidism, but Free T4 in secondary hypothyroidism Treatment Replacement doses of levothyroxine in adults range from 0.05 to 0.2 mcg/d. In young children: 4-5 ug/kg/d ■ In adults: average 1.7 ug/kg/d In elders, start with lower dose;25mcg daily, increase the dose at 4- to 6-week intervals based on serum FT4 and TSH levels Dose should be increased about 25% during pregnancy Treatment Drugs that reduce thyroid hormone production (Lithium and Iodine-containing medications (Amiodarone)) Drugs that reduce thyroid hormone absorption (Sucralfate, Ferrous sulfate, Cholestyramine, Colestipol, Aluminum-containing antacids, Calcium products Drugs that increase metabolism of thyroxine (Rifampin, Phenobarbital, Carbamazepine, Warfarin Oral hypoglycemic agents Increase thyroxine availability and may decrease …
An extract of the text. Open the file below to read the full document.