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7/28/2019 pendahuluan blok endokrin

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SISTEM ENDOKRIN

PATOLOGI ANATOMI

FK UNIMALBANDAR 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 thebasis of hormone(s) produced by theneoplastic cells detected by

immunohistochemical stains performedon tissue sections


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Pituitary Adenomas and

Hyperpituitarism


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PROLACTINOMASProlactinoma with hyperprolactinemia

- is most common/30% pituitary tumor

- staining

chromophobe- in women amenorrhea &

galactorrhea

- caused by hypothalamic lesions or

medications

methyl dopa, reserpineinterfere 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 growthhormone 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 andSheehan 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, inflammatoryprocesses, 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 localpressure phenomena

- are clinically variable ;manifestations

include hypopituitarism, headache,visual

disturbance (bilateral hemianopsia / loss ofperipheral 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 orcolumnar cells in loose stroma, closely resembling the

appearance of the embryonic tooth bud enamel organ- is often cystic; lining epithelium of flat or columnar cellsoften expands into papillary projections

- is often detected radiographically because of calcification


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THYROID


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Hyperthyroidism

Thyrotoxicosisis a hypermetabolic state caused byelevated circulating levels of free T3 and T4

The three most common causes of thyrotoxicosis are

also associated with hyperfunction of the gland andinclude the following: Diffuse hyperplasiaof the thyroid associated

with Graves disease (accounts for 85% of

cases) Hyperfunctional multinodular goiter Hyperfunctional adenomaof the thyroid


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Prolonged hypersecretion of thyroidhormone can result from

(1) abnormal thyroid stimulator (Gravesdisease),

(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 activatingadenylyl cyclase and increasing thyroidhormone secretion thyroid becomes

diffusely hyperplastic and excessively vascular


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GENETIC FACTORS

GENDER

EMOTIONALINFLUENCES

SMOKING

OPHTHALMOPATHY


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Major clinical manifestations of Graves disease


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Hypothyroidism

Hypothyroidism refers to the clinical manifestationsof thyroid hormone deficiency

It can be the consequence of three generalprocesses:

Defective thyroid hormone synthesis, with compensatorygoitrogenesis (goitrous hypothyroidism)

Inadequate thyroid parenchyma function, usually due tothyroiditis, surgical resection of the gland, or therapeuticadministration 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 OftenAutoimmune

antibodies that block TSH or TSH receptorswithout activating the thyroid

Goitrous Hypothyroidism ReflectsInadequate Secretion of Thyroid Hormone The etiology of goitrous hypothyroidism includes

iodine deficiency, antithyroid agents (drugs ordietary goitrogens), long-term iodide intake, anda number of hereditary defects in thyroidhormone synthesis


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Endemic Goiter

Endemic goiter is goitrous hypothyroidism

due to dietary iodine deficiency in localeswith 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 heterogeneousgroup of inflammatory disorders of the

thyroid gland, including those that arecaused by autoimmune mechanismsand infectious agents.


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HASHIMOTO THYROIDITIS


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SUBACUTE (GRANULOMATOUS)THYROIDITIS

caused by a viral infectionor a postviralinflammatory process

majority of patients have a history of anupper respiratory infection just beforethe 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% ofcases)

Medullary carcinoma (5% of cases) Anaplastic carcinoma (


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Parathyroid Glands


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Hyperparathyroidism

PRIMARY HYPERPARATHYROIDISM

Primary hyperparathyroidism is one of the

most common endocrine disorders, and itis an important cause ofhypercalcemia

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, mayalso 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. Thedisease is clinically characterized byhypocalcemia and hyperphosphatemia.


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Hypoparathyroidism

There are many possible causes of deficientPTH secretion resulting in

hypoparathyroidism: Surgically inducedhypoparathyroidism

Congenital absenceof all glands

Familial hypoparathyroidism Idiopathic hypoparathyroidism


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Hypoparathyroidism

The major clinical manifestations ofhypoparathyroidism are referable to

hypocalcemia and are related to the severityand chronicity of the hypocalcemia

The hallmark of hypocalcemia is tetany

Mental status changescan include emotionalinstability, anxiety and depression, confusionalstates, hallucinations, and frank psychosis.


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Hypoparathyroidism

Intracranial manifestationsincludecalcifications of the basal ganglia,

parkinsonian-like movement disorders. Ocular diseaseresults in calcification of the

lens leading to cataract formation.

Cardiovascular manifestationsinclude aconduction defect

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