SISTEM ENDOKRIN

PATOLOGI ANATOMI
FK UNIMAL
BANDAR LAMPUNG
NORMAL
Manifestasi Kelainan Hipofisis
Hyperpituitarism
Hypoppituitarism
Efek masa lokal
Penyakit hipofisis posterior
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
Pituitary Adenomas and
Hyperpituitarism
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
GROWTH HORMONE
(SOMATOTROPH CELL) ADENOMAS
Somatotropic adenoma with hypersecretion of growth hormone
- 2
nd
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
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

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
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

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
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
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

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

THYROID
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
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).
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
GENETIC FACTORS
GENDER
EMOTIONAL
INFLUENCES
SMOKING
OPHTHALMOPATHY
Major clinical manifestations of Graves disease
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

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
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
Dominant clinical manifestations of hypothyroidism
Thyroiditis
Thyroiditis describes a heterogeneous
group of inflammatory disorders of the
thyroid gland, including those that are
caused by autoimmune mechanisms
and infectious agents.
HASHIMOTO THYROIDITIS
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

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
Parathyroid Glands
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%

Secondary Hyperparathyroidism
Renal failure
inadequate dietary intake of calcium,
steatorrhea, and vitamin D deficiency, may
also cause this disorder
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.
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
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.

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