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The endocrine system Pituitary gland Anterior lobe Posterior lobe Endocrine abnormalities Local mass effect Hyperpituarism Caused by adenomas: Growth hormone Adrenocorticotropic hormone Prolactin Rare – thyroid stimulating hormone, gonadortropin 25% adenomas – non-functional (causes HYPOpituarism by compression) Microadenomas, macroadenomas (10mm) Nuclear atypia is NOT sign of malignancy Ultrastructurally – secretory granules Somatotropic adenomas Acromegaly – in adults Gigantism – prior to closure of epiphyses Granulated, eosinophilic cells – eosinophilic adenoma Prolactinomas Hypogonadism Galactorrhea Granulated acidophilic or chromophobic cells – chromophobic adenoma Corticotroph tumors Cushing’s syndrome Basophilic cells – basophilic adenoma Hypopituarism Caused by 1) hypothalamic lesions: Craniopharyngioma Glioma Germinoma 2) pituitary lesions: Nonsecretory adenomas Sheehan’s syndrome Empty sella syndrome Clinically – variable Hypogonadotropism Hypothyroidism, etc. Hypothalamic lesions – craniopharyngioma Benign cystic tumor Calcifications Squamous epithelial cells and reticular stroma Nonsecretory chromophobe pituitary adenoma Mass effect (visual problems, headache) Chromophobic or oncocytic forms exists Sheehan’s syndrome Associated with obstetric haemorrhage or shock Caused by infarction of anterior pituitary Gonadal failure – inability to lactate ACTH, TSH deficiency Healing of necrosis – fibrous tissue Posterior pituitary syndrome Excess or deficiency of antidiuretic hormone – ADH Caused by suprasellar/hypothalamic lesions Posterior pituitary syndrome Excess of ADH Abnormal resorption of water, hyponatremia and inability to excrete diluted urine Caused by ectopic ADH secretion: Non-endocrine neoplasms (small cell carcinoma of the lung) Non-neoplastic pulmonary diseases (TBC, pneumonia) Primary CNS lesions (infarcts, meningitis, haemorrhage) Posterior pituitary syndrome ADH deficiency (Diabetes insipidus) Inability to concentrate urine: Polyuria Polydipsia Hypernatremia Thyroid gland Hyperthyroidism Hypothyroidism Goitre – focal, diffuse Hyperthyroidism (thyrotoxicosis) Increased levels of triodothyronine (T3), thyroxine (T4) Clinically: wide-eyed gaze, tachycardia, palpitations, nervouseness, weight loss (increased appetite), moist hand, tremor, peripheral vasodilatation Associated with diffuse hyperplasia (Graves’ disease) or with toxic multinodular goitre or toxic adenoma May be associated with struma ovarii (teratoma)!! Graves’ disease Autoimmune process Presence of thyroid stimulating antibody (TSAb) and thyrotropin binding inhibitor immunoglobulin (TBII) Associated with other autoimmune diseases Presence of hyperplasia of foIlicular epithelium , depletion of colloid and lymphoid aggregates Hypothyroidism Cretinism (during infancy) Endemic form Sporadic form Physical an mental retardation Myxoedema (in adults) Slowing of physical and mental activity, fatigue and apathy Signs - periorbital oedema, coarsening of skin, cardiomegaly, accumulation of mucopolysaccharides in dermis Various causes - idiopathic primary, inflammation – Hashimoto thyroiditis, etc. Thyroiditis Hashimoto’s thyroiditis De Quervain’s thyroiditis Riedel’s fibrosing thyroiditis Lymphocytic thyroiditis Infectious thyroiditis Hashimoto’s thyroiditis Autoimmune disorder Female predominance Defect in suppressor T cells, production of autoantibodies Associated with other autoimmune disease (SLE, Sjögren sy, rheumatoid arthritis…) Microscopically – dense lymphocytic infiltrate, germinal centers, abundant eosinophilic oncocytes (Hürtle cells) De Quervain’s subacute granulomatous thyroiditis Also known as giant cell thyroiditis Probably viral etiology Destruction of follicles, neutrophil infiltrate, multinucleate giant cells Recovery in 6-8 weeks Subacute lymphocytic thyroiditis Nonspecific lymphoid infiltration Without germinal centre In women in postpartum period Riedel’s fibrosing thyroiditis Thyroid replaced by fibrous tissue Fibrous tissue extends and penetrate into the surrounding neck structures May be mistaken for infiltrating neoplasm Tumors Benign – adenomas Well demarcated Fibrosis Haemorrhage Calcifications Hürtle cell adenoma - oncocytic Usually „cold“ Malignant - carcinomas See transparency Parathyroid gland Primary hyperparathyroidism Hypersecretion of parathormone Caused by adenoma (80%), hyperplasia (15%), carcinoma (5%) Bone resorption, hypercalcemia – osteoporosis, muscle weaknes, nephrolithiasis, ulcers, pancreatitis, headache, depression Secondary hyperparathyroidism In patients with renal failure Compensatory hypersecretion of parathormone (reaction to phosphate retention and hypocalcemia) Parathyroid gland - tumors Adenoma Solitary, encapsulated – compression of adjacent gland No stromal fat Composed predominatly of chief cells Part of MEN I, MEN II Carcinoma Rare Invasion, metastases Hyperplasia All glands Fat cells interspersed Hypoparathyroidism, pseudohypoparathyroidism Hypoparathyroidism Multiple etiology (surgical removal, autoimunne destruction, congenital…) Tetany, neuromuscular excitability, paraesthesiae psychosis Pseudohypoparathyroidism Rare Abnormality PTH receptors, loss of responsiveness, hypocalcemia Compensatory parathyroid hyperfunction Adrenal cortex - hyperfunction Three syndromes: Cushing’s syndrome Hyperaldosteronism Adrenogenital syndromes Cushing’s syndrome Causes: Administration of exogenous glucocorticoids – most common Pituitary hypersecretion of ACTH (Cushing’s disease) – adenoma Ectopic ACTH secretion – small cell carcinoma !! Histology: Crooke’s hyaline changes within pituitary basophils Clinically: Central obesity, moon facies, fatigability, hirsutism, hypertension, osteoporosis, cutaneous striae Hyperaldosteronism Conn’s syndrome: Adenoma/hyperplasia Excessive production of aldosterone – low plasma renin, sodium retention, hypertension, loss of potassium, muscular weakness, cardiac arrhytmias, metabolic alkalosis, tetany Secondary: Reduced glomerular perfusion (fail in blood volume) – activation of renin angiotensin system – stimulation of aldosterone secretion Most common Adrenogenital syndromes Variable manifestation (virilization, pubertax praecox, hermaphroditism, pseudohermaphroditism) Autosomal recessive trait Most often – deficiency of 21-hydroxylase - virilization Hypofunction of adrenal cortex Adrenal crisis Addison’s disease Secondary insufficiency Primary acute adrenocortical insufficiency Rapid withdrawal of steroids Massive destruction of steroids – WaterhouseFriderichsen syndrome: • • • • • During septic meningococcal infection Massive hemorrhage Hypotension Shock DIC Addison’s disease (chronic adrenocortical insufficiency) Autoimunne Infection (TBC, fungi, etc.) Metastatic cancer (lung, stomach, etc.) Clinically: • • • • Anorexia Weakness Cutaneous hyperpigmentation ACTH elevation (in primary insufficiency) Secondary insufficiency decreased production of ACTH, absence of hyperpigmentation, normal aldosterone levels Adrenal medulla Phaeochromocytoma Catecholamine production – hypertension 85% in medulla (extra-adrenal tumors designated paragangliomas) Sporadic (90%) or associated with familial syndromes (MEN, von Hippel-Lindau, von Recklinghausen) Histologically – pleomorphism, mitotic activity - however there are no reliable histological predictors of malignancy!! Only criterion of malignancy – metastasis Other tumors – neuroblastoma, ganglioneuroma Multiple Endocrine Neoplasia MEN MEN I (Wermer’s syndrome) Parathyroid (hyperplasia, adenoma) Pancreas (islet cell tumors) Pituitary (adenoma) MEN II (Sipple’s syndrome) Medullary thyroid carcinoma Phaeochromocytoma Parathyroid adenoma/hyperplasia MEN III MEN II and neuroma/ganglioneuroma All MENs – autosomal dominant trait