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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

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pituitary gland
Pituitary gland
  • Anterior lobe
  • Posterior lobe
  • Endocrine abnormalities
  • Local mass effect
hyperpituarism
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
Somatotropic adenomas
  • Acromegaly – in adults
  • Gigantism – prior to closure of epiphyses
  • Granulated, eosinophilic cells – eosinophilic adenoma
prolactinomas
Prolactinomas
  • Hypogonadism
  • Galactorrhea
  • Granulated acidophilic or chromophobic cells – chromophobicadenoma
corticotroph tumors
Corticotroph tumors
  • Cushing’s syndrome
  • Basophilic cells – basophilic adenoma
hyp o pituarism
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
Hypothalamic lesions – craniopharyngioma
  • Benign cystic tumor
  • Calcifications
  • Squamous epithelial cells and reticular stroma
nonsecretory chromophobe pituitary adenoma
Nonsecretory chromophobe pituitary adenoma
  • Mass effect (visual problems, headache)
  • Chromophobic or oncocytic forms exists
sheehan s syndrome
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
Posterior pituitary syndrome
  • Excess or deficiency of antidiuretic hormone – ADH
  • Caused by suprasellar/hypothalamic lesions
posterior pituitary syndrome12
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 syndrome13
Posterior pituitary syndrome

ADH deficiency (Diabetes insipidus)

Inability to concentrate urine:

  • Polyuria
  • Polydipsia
  • Hypernatremia
thyroid gland
Thyroid gland
  • Hyperthyroidism
  • Hypothyroidism
  • Goitre – focal, diffuse
hyperthyroidism thyrotoxicosis
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
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
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
Thyroiditis
  • Hashimoto’s thyroiditis
  • De Quervain’s thyroiditis
  • Riedel’s fibrosing thyroiditis
  • Lymphocytic thyroiditis
  • Infectious thyroiditis
hashimoto s 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
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
Subacute lymphocytic thyroiditis
  • Nonspecific lymphoid infiltration
  • Without germinal centre
  • In women in postpartum period
riedel s fibrosing thyroiditis
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
Tumors

Benign – adenomas

  • Well demarcated
  • Fibrosis
  • Haemorrhage
  • Calcifications
  • Hürtle cell adenoma - oncocytic
  • Usually „cold“

Malignant - carcinomas

  • See transparency
parathyroid gland
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
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, 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
Adrenal cortex - hyperfunction

Three syndromes:

  • Cushing’s syndrome
  • Hyperaldosteronism
  • Adrenogenital syndromes
cushing s syndrome
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
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
Adrenogenital syndromes
  • Variable manifestation (virilization, pubertax praecox, hermaphroditism, pseudohermaphroditism)
  • Autosomal recessive trait
  • Most often – deficiency of 21-hydroxylase - virilization
hypofunction of adrenal cortex
Hypofunction of adrenal cortex
  • Adrenal crisis
  • Addison’s disease
  • Secondary insufficiency
primary acute adrenocortical insufficiency
Primary acute adrenocortical insufficiency
  • Rapid withdrawal of steroids
  • Massive destruction of steroids – Waterhouse-Friderichsen syndrome:
  • During septic meningococcal infection
  • Massive hemorrhage
  • Hypotension
  • Shock
  • DIC
addison s disease chronic adrenocortical insufficiency
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
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
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