1. Pathology of pituitary gland
By: Shifaa’ Qa’qa’

2. Sella turcica
Adenohypophysis (80%):
- epithelial cells
- acidophil , basophil , chromophobe
Somatotrophs, Mammosomatotrophs, Corticotrophs, Thyrotrophs, Gonadotrophs
blood supply from the low-pressure portal venous system.

5. Neurohypophysis:
- modified glial cells, axonal processes, axon terminals (from nerve cell bodies in the supraoptic
and paraventricular nuclei of the hypothalamus)
Oxytocin, antidiuretic hormone (ADH) /vasopressin
Receives its blood directly from arterial branches

6. pituitary disease:
Hyperpituitarism ---- anterior pituitary adenoma
Hypopituitarism ---- ischemic injury, surgery, radiation, inflammatory reactions, nonfunctional pituitary adenomas

7. Local mass effects:
radiographic abnormalities of the sella turcica
bitemporal hemianopsia
headache, nausea, and vomiting (+ICP)
Seizures, obstructive hydrocephalus
cranial nerve palsy

8. pituitary apoplexy:
rapid enlargement of the lesion
acute hemorrhage into an adenoma
depression of consciousness, sudden headache, neusea , vomitting, vision loss---hypopituitarism
neurosurgical emergency

9. HYPERPITUITARISM AND PITUITARY ADENOMAS
The most common cause of hyperpituitarism is an adenoma arising in the anterior lobe. Hyperplasia of the anterior pituitary, Carcinomas of the anterior pituitary (rare) extrapituitary tumors, hypothalamic disorders

11. Pituitary adenomas:
Functional
Nonfunctioning IHC stain
hormone negative IHC stain / null cell
Sporadic ---- G protein mutation
Inherited (5%)---- MEN1, CDKN1B, PRKAR1A, and AIP
Microadenomas less than 1 cm
Macroadenomas exceed 1 cm
Nonfunctioning
----- hypopituitarism

13. Gsα
G-protein mutations
Mutation in the α-subunit/ GNAS mutations
Interferes with GTPase activity

14. TP53 mutaion

15. pituitary adenoma:
well-circumscribed
cellular monomorphism
absence of a significant reticulin network
Atypical adenomas: brisk mitotic activity, P53 mutation, aggressive behavior (invasion and recurrence)

18. Prolactinomas
M.c hyperfunctioning pituitary adenoma
Microadenomas / macroadenomas
Hyperprolactinemia (amenorrhea, galactorrhea, loss of libido, and infertility). subtle in men and older women

19. Hyperprolactinemia:
prolactin-secreting pituitary adenomas
pregnancy,
high-dose estrogen therapy
renal failure
hypothyroidism,
hypothalamic lesions
dopamine-inhibiting drugs (e.g., reserpine)
any mass in the suprasellar compartment may disturb the normal inhibitory influence of hypothalamus on prolactin secretion

20. Growth Hormone–Producing (Somatotroph Cell) Adenomas:
2nd m.c
insulin-like growth factor I (somatomedin C) liver
Gigantism---- increase in body size,long arms and legs---- before the epiphyses close
Acromegaly ---- soft tissues, skin, and viscera bones after closure of the epiphyses

23. abnormal glucose tolerance and diabetes mellitus,
generalized muscle weakness,
hypertension,
arthritis,
osteoporosis,
and congestive heart failure.

24. Adrenocorticotropic Hormone–Producing (Corticotroph Cell) Adenomas:
Hypercortisolism Cushing disease
Cushing syndrome
Hyperpigmentation /MSH
Nelson syndrome ---- hypercortisolism does not develop ---- No adrenals

26. Gonadotroph (luteinizing hormone [LH]–producing and follicle-stimulating hormone [FSH]–producing) adenomas:
Mass effect
Thyrotroph (thyroid-stimulating hormone [TSH]–producing) adenomas: 1%
rare cause of hyperthyroidism

27. HYPOPITUITARISM
Loss or absence of 75% or more of the anterior pituitary parenchyma.

28. Causes:
Nonfunctioning pituitary adenomas
Ischemic necrosis(Sheehan syndrome, DIC, sickle cell anemia, elevated intracranial pressure, traumatic injury, and shock of any origin)
surgery or irradiation
sarcoidosis
Tuberculosis
Trauma
metastatic neoplasms

29. Hypopituitarism accompanied by evidence of posterior pituitary dysfunction in the form of diabetes insipidus is almost always of hypothalamic origin

30. Manifestations:
Children--- growth failure (pituitary dwarfism) ---- growth hormone deficiency
Gonadotropin deficiency (amenorrhea and infertility in women and to decreased libido, impotence, and loss of pubic and axillary hair in men)
TSH---- Hypothyroidism
ACTH----- hypoadrenalism
Prolactin deficiency---- failure of postpartum lactation.
MSH deficiency pallor

31. POSTERIOR PITUITARY SYNDROMES
Oxytocin:
stimulates the contraction of smooth muscle in the pregnant uterus and of muscle surrounding the lactiferous ducts of the mammary glands.
Impairment of oxytocin synthesis and release has not been associated with significant clinical abnormalities.

32. ADH:
Released in response to:
- increased plasma oncotic pressure,
- left atrial distention
- Exercise
certain emotional states,
----- collecting tubules of the kidney to promote the
resorption of free water

33. ADH deficiency causes diabetes insipidus, a condition characterized by excessive urination (polyuria)
Causes:
- head trauma,
- neoplasms,
- inflammatory disorders of the hypothalamus and pituitary,
- surgical procedures involving the hypothalamus or pituitary
- spontaneously (idiopathic)

34. Central diabetes insipidus (ADH deficiency)
Nephrogenic diabetes insipidus

35. Large volumes of dilute urine with an inappropriately low specific gravity.
Serum sodium and osmolality are increased as a result of excessive renal loss of free water,
Resulting in thirst and polydipsia.
Dehydration

36. syndrome of inappropriate ADH (SIADH) secretion:
ADH excess
resorption of excessive amounts of free water, hyponatremia

37. The most common causes of SIADH
- secretion of ectopic ADH by malignant neoplasms (particularly small cell carcinomas of the lung)
- non-neoplastic diseases of the lung
- local injury to the hypothalamus or neurohypophysis.

38. - hyponatremia,
- cerebral edema, and resultant neurologic dysfunction.
Although total body water is increased, blood volume remains normal, and peripheral edema does not develop.