Thyroid Gland Pathology: Functional Disorders and Diagnosis PDF

Thyroid gland functional pathology by Dr. Husam-eldin Omer  Introduction The thyroid gland weighing 17-27 g in adults. It composed of follicles contain a proteinaceous stored secretion (colloid). Follicles are lined by cuboidal epithelial cells. The main function of th...

Thyroid gland functional pathology by Dr. Husam-eldin Omer  Introduction The thyroid gland weighing 17-27 g in adults. It composed of follicles contain a proteinaceous stored secretion (colloid). Follicles are lined by cuboidal epithelial cells. The main function of these cells is the synthesis of thyroid hormones, thyroxine (T4) & tri- iodothyroxine (T3) using iodine that merging in the colloid material. The thyroid also contains a population of cells known as C-cells. These cells sparsely scattered throughout the gland and secrete calcitonin hormone. This peptide hormone is involved in calcium metabolism and acts opposite to the action of parathyroid hormone.  Classification of thyroid functional pathology (a) Hyperthyroidism or thyrotoxicosis with excess T3 and T4 hormones. The over all result is an increased metabolic rate. There is weight loss but increase of appetite. The patient is tired but hyperkinetic. There is heat intolerance, excessive sweating and hot moist palms. The patient is usually nervous, irritable and emotionally labile. There is an increase in cardiac output, tachycardia, and palpitation. In older patients atrial fibrillation is often present and cardiac failure may be the presenting feature. Lid retraction, lid lag and the infrequent blinking are due to abnormal contraction of levator palpebrae superioris This muscle shows an increased sensitivity to adrenaline as a result of enhanced beta receptors responsiveness This hormone / hormone interaction explain many other clinical features of thyrotoxicosis. Most of the patients with out stretching hands show a fine tremor and have recurrent diarrhea. Women develop menorrhagia. In advanced severe cases, exophthalmos and pretibial myxedema may occur. The last sign is due to accumulation of mucopolysaccharides in the deep dermis. Exophthalmos is due to infiltration of orbital tissue by mucopolysaccharides, & lymphocytes. Thyrotoxicosis with exophthalmos + lid retraction The most common underlying pathological cause is Grave's disease ( 80% of cases). Toxic nodular goiter is implicated in about 10% and the toxic nodule accounts for another5- 10%. The disease may also be seen in early Hashimoto`s thyroiditis (Hashitoxicosis). Other rare causes include TSH over secretion from a pituitary adenoma and hyper doses of thyroid hormones.  Grave’s disease (Pretibial myxoedema) (b) Hypothyroidism which is called myxoedema in adults and cretinism in children. In myxoedema the patient gains weight. She or he is tired and lethargic. The intellectual function may be impaired and moreover there may be frank psychosis ( myxoedema madness). The hair is dry. The skin is dry, cold and shows coarse features due to accumulation of mucopoly-saccharides in the dermis. Similar deposits around nerves may cause pain and paraesthesia, while involvement of the larynx and tongue results in hoarse voice and large tongue. The patient feels cold and may develop hypothermia. The blood cholesterol levels are often increased. The commonest cause of myxoedema is autoimmune thyroiditis, either primary myxoedema or Hashimoto`s disease. It also occurs late in cases of severe iodine deficiency or in patients with severe dyshormonogenesis (e.g. drugs) Cretinism Is the form of severe hypothyroidism in infancy. The baby often appears normal at birth. Soon he starts to show signs of mental and growth retardation, neuromuscular abnormalities and deafness.There is a typical facial appearance, with coarse features & large protruding tongue.  Primary myxedema (coarse skin and face, no goiter)  Cretinism(mental retardation appearance+ coarse face + large protruding tongue) Cretinism may occur due to thyroid hypoplasia or agenesis with absence of goiter or it develops in areas of endemic goiter due to lactating mother iodine deficiency and this causes cretinism with nodular goitre. The congenital abnormality of one of the enzymes that involved in the biosynthesis of thyroxine may also be a cause.  Thyroid gland autoimmune diseases Grave's thyroiditis The commonest form of thyrotoxicosis. It is five times more common in females. The pathogenesis is the production of an autoantibody which binds to the acinar epithelial cells and acts like TSH. These thyroid stimulating immunoglobins (TSI) cause selective stimulatory hyperplasia & there is a diffuse uniform moderately enlarge goiter. TSH is markedly low. Hashimoto`s thyroiditis Thyroid growth immunoglobulins are thought to be the main cause. The growth stimulatory hyperplasia is not selective and involves also stimulation of inflammatory cells and fibrosis. Often there is an initial goitre, but sooner or later there will be marked fibrosis and gland atrophy. The disease occurs mainly in middle-aged women. Female to male ratio 20:1. Most of patients are euthyroid in the early stages and present with a painless small to middle size, not uniform goitre. Then, in majority  of cases the features of hypothyroidism start to appear and the TSH becomes high. Occasionally, patients present firstly with hyperthyroidism (Hashitoxicosis). Lymphocytic thyroiditis is considered as mild form of Hashimoto’s thyroiditis. Primary myxoedema The auto immune reaction is severe and it is neither stimulatory for thyroid function, nor for follicular epithelium hyperplasia. There is almost pure stimulation for inflammation and fibrosis so there is severe fibrosis and atrophy. It occurs mainly in elderly women. Hypothyroid features are severe and the TSH is very high.  Differentiation of Thyroid hyperplasia Generally the different types of thyroid hyperplasia leads to what is called clinically thyroid goitre. Main three types of thyroid hyperplasia; 1- Hyperplasia which due to thyroid stimulating Igs (TSI). The goitre is smooth or uniform (not nodular) and not large. This typically seen in Grave's autoimmune thyroiditis. 2-Hyperplasia that is due to thyroid growth stimulatory Igs (TGI) Hashimoto’s and lymphocytic auto thyroiditis are examples. The goitre is a little pit nodular as the stimulation is not selective, but it still not that large 3-Compensatory thyroid hyperplasia Usually here is a large nodular goitre. This type has three clinical forms;- a- endemic colloid multinodular goiter is the most common of all thyroid diseases. The patient is often euthyroid, hence the term simple or non-toxic nodular ` goiter. It occurs in areas deficient in iodine and it can affect all ages. The follicles are rich in the unused colloid material which is deficient in iodine. It also involves babies of iodine deficient lactating mothers. b -The sporadic goitre The main cause is the inherited defect in biosynthesis of thyoroxine so the affected child end with cretinism with goitre. It also may occur in elderly patients due to poor dietary in take. Other rare causes like drugs or chemicals which interfere with thyroxin synthesis (dyshormonogenesis) or the newborns for mothers who were using antithyroid drugs. C - toxic nodular goitre It is an especial rare form of nodular goitres in which one or few nodules after long time of the compensatory stimulation start to develop autonomous hyper secretary activities leading to thyrotoxic state. Here TSH will change from high to low THYROID MULTI-NODULAR GOITRE Multinodular colloid goitre (Follicles rich in unused colloid+flatten acinar cells)