sistem endokrin
DESCRIPTION
NMBHGFDFXFTRANSCRIPT
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SISTEM ENDOKRIN
PATOLOGI ANATOMIFK UNIMAL
BANDAR LAMPUNG
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NORMAL
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Manifestasi Kelainan Hipofisis
Hyperpituitarism Hypoppituitarism Efek masa lokal Penyakit hipofisis posterior
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Pituitary Adenomas and Hyperpituitarism
functional silent Pituitary adenomas are classified
on the basis of hormone(s) produced by the neoplastic cells detected by immunohistochemical stains performed on tissue sections
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Pituitary Adenomas and Hyperpituitarism
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PROLACTINOMAS
Prolactinoma with hyperprolactinemia - is most common/30% pituitary tumor - staining chromophobe - in women amenorrhea & galactorrhea - caused by hypothalamic lesions or medications methyl dopa, reserpine interfere with dopamine (prolactin-inhibitory factors) secretion - can also be associated with estrogen therapy
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GROWTH HORMONE (SOMATOTROPH CELL) ADENOMAS Somatotropic adenoma with hypersecretion of growth hormone - 2nd most common pituitary tumor - staining acidophyl - causes secondary hyperfunction of somatomedins by the liver. End organ effects are caused by both growth hormone and somatomedins, especially somatomedin C (insulin-like growth factor 1/IGF-1) - results gigantism if adenoma develops before epiphyseal closure and acromegaly if adenoma develops after epiphyseal closure - acromegaly overgrowth of jaws, face, hands and feet, and general enlargement of viscera with hyperglycemia, osteoporosis and hypertension - can also result in local compression effects due to expansion of the tumor within the sella tursica
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CORTICOTROPH CELL ADENOMAS
Corticotropic adenoma and hypersecretion of ACTH - results in increased production of ACTH / hypercorticism - is called Cushing syndrome or Cushing disease 1. Cushing disease hypercorticism adenoma most often a basophilic adenoma basophilic microadenoma 2. Cushing syndrome hypercorticism regardless of cause, is most often of pituitary and less often of adrenal origin may be due to ectopic ACTH production by various tumors especially small cell carcinoma of lung
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Hypopituitarism
Tumors and other mass lesions Pituitary surgery or radiation Ischemic necrosis of the pituitary
and Sheehan syndrome Rathke cleft cyst Empty sella syndrome Genetic defects
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Selective deficiency of one or more pituitary hormones (1) deficiency of growth hormone - in children, result in growth retardation (pituitary dwarfism) - in adults, may result in increased insulin sensitivity with hypocalcemia, decreased muscle strength and anemia (2) deficiency of gonadotropins - in preadolescent children, results in retarded sexual maturation - in adults, results in loss of libido, impotence, loss of muscular mass, and decreased hair in men, and amenorrhea and vaginal atrophy in women (3) deficiency of TSH - result in secondary hypothyroidism (4) deficiency of ACTH - results in secondary adrenal failure - does not result in hyperpigmentation of the skin, probably because of lack of both ACTH and -MSH; this is in contrast to primary adrenal failure (Addison disease), in which ACTH is increased and hyperpigmentation is the rule
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POSTERIOR HYPOPHYSIS (NEUROHYPOPHYSIS) HORMONES - are synthesized in the hypothalamus and transported via axons to the posterior pituitary a. Oxytocin : induces uterine contarction during labor and ejection of milk from mammary alveoli b. Anti diuretic hormone (ADH, vasopressin) - promotes water retention through
action on the renal collecting ducts
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Syndrome of inappropriate ADH(SIADH) secretion is most commonly caused by ectopic production of ADH by various tumors, especially small cell carcinoma of lung. Results in retention of water with consequent dilutional hyponatremia, reduced serum osmolality, and inability to dilute urine Deficiency of ADH: results in diabetes insipidus; characterized by polyuria, with consequent dehydration and insatiable thirst - can be caused by tumors, trauma, inflammatory processes, lipid storage disorders, and other conditions characterized by damage of the neurohypophysis or hypothalamus
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C. NON FUNCTIONING PITUITARY TUMORS
Non secreting pituitary adenomas - are most often chromophobe - result in dysfunction because of local pressure phenomena - are clinically variable ;manifestations include hypopituitarism, headache,visual disturbance (bilateral hemianopsia / loss of peripheral visual fields due to pressure on optic chiasm), and palsies caused by cranial nerve damage
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Craniopharyngioma - is benign childhood tumor derived from remnants of the Rathke pouch - is not a true pituitary tumors - similar to ameloblastoma of the jaw - is characterized by nests and cords of squamous or
columnar cells in loose stroma, closely resembling the appearance of the embryonic tooth bud enamel organ
- is often cystic; lining epithelium of flat or columnar cells often expands into papillary projections
- is often detected radiographically because of calcification
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THYROID
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Hyperthyroidism Thyrotoxicosis is a hypermetabolic state caused
by elevated circulating levels of free T3 and T4 The three most common causes of thyrotoxicosis
are also associated with hyperfunction of the gland and include the following: • Diffuse hyperplasia of the thyroid associated
with Graves disease (accounts for 85% of cases)
• Hyperfunctional multinodular goiter • Hyperfunctional adenoma of the thyroid
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Prolonged hypersecretion of thyroid hormone can result from (1) abnormal thyroid stimulator (Graves
disease), (2) intrinsic disease of the thyroid gland
(toxic multinodular goiter or functional adenoma), and
(3) excess TSH production by a pituitary adenoma (rare).
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Pathogenesis
IMMUNE MECHANISMS IgG antibodies that bind to the TSH
receptor on the plasma membrane of thyrocytes stimulate the TSH receptor activating adenylyl cyclase and increasing thyroid hormone secretion thyroid becomes diffusely hyperplastic and excessively vascular
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GENETIC FACTORS
GENDER EMOTIONAL
INFLUENCES SMOKING OPHTHALMOPATH
Y
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Major clinical manifestations of Graves disease
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Hypothyroidism Hypothyroidism refers to the clinical
manifestations of thyroid hormone deficiency It can be the consequence of three general
processes: Defective thyroid hormone synthesis, with
compensatory goitrogenesis (goitrous hypothyroidism) Inadequate thyroid parenchyma function, usually due
to thyroiditis, surgical resection of the gland, or therapeutic administration of radioiodine
Inadequate secretion of TSH by the pituitary or of thyroid-releasing hormone (TRH) by the hypothalamus
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Primary (Idiopathic) Hypothyroidism is Often Autoimmune antibodies that block TSH or TSH receptors
without activating the thyroid Goitrous Hypothyroidism Reflects
Inadequate Secretion of Thyroid Hormone
The etiology of goitrous hypothyroidism includes iodine deficiency, antithyroid agents (drugs or dietary goitrogens), long-term iodide intake, and a number of hereditary defects in thyroid hormone synthesis
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Endemic Goiter Endemic goiter is goitrous
hypothyroidism due to dietary iodine deficiency in locales with a high prevalence of the disease
Congenital Hypothyroidism is also Termed Cretinism
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Dominant clinical manifestations of hypothyroidism
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Thyroiditis
Thyroiditis describes a heterogeneous group of inflammatory disorders of the thyroid gland, including those that are caused by autoimmune mechanisms and infectious agents.
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HASHIMOTO THYROIDITIS
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SUBACUTE (GRANULOMATOUS) THYROIDITIS
caused by a viral infection or a postviral inflammatory process
majority of patients have a history of an upper respiratory infection just before the onset of thyroiditis
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Neoplasms of the Thyroid
ADENOMAS CARCINOMAS
Papillary carcinoma (75% to 85% of cases)
Follicular carcinoma (10% to 20% of cases)
Medullary carcinoma (5% of cases) Anaplastic carcinoma (<5% of cases
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Parathyroid Glands
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Hyperparathyroidism
PRIMARY HYPERPARATHYROIDISM Primary hyperparathyroidism is one of
the most common endocrine disorders, and it is an important cause of hypercalcemia
Adenoma: 75% to 80% Primary hyperplasia (diffuse or nodular):
10% to 15% Parathyroid carcinoma: less than 5%
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Secondary Hyperparathyroidism Renal failure inadequate dietary intake of calcium,
steatorrhea, and vitamin D deficiency, may also cause this disorder
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Hypoparathyroidism
Hypoparathyroidism results from decreased secretion of PTH or end-organ insensitivity (pseudohypoparathyroidism) due to congenital or acquired conditions. The disease is clinically characterized by hypocalcemia and hyperphosphatemia.
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Hypoparathyroidism
There are many possible causes of deficient PTH secretion resulting in hypoparathyroidism: Surgically induced hypoparathyroidism Congenital absence of all glands Familial hypoparathyroidism Idiopathic hypoparathyroidism
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Hypoparathyroidism
The major clinical manifestations of hypoparathyroidism are referable to hypocalcemia and are related to the severity and chronicity of the hypocalcemia The hallmark of hypocalcemia is tetany Mental status changes can include emotional
instability, anxiety and depression, confusional states, hallucinations, and frank psychosis.
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Hypoparathyroidism
Intracranial manifestations include calcifications of the basal ganglia, parkinsonian-like movement disorders.
Ocular disease results in calcification of the lens leading to cataract formation.
Cardiovascular manifestations include a conduction defect