is the decreases in both anterior and posterior pituitary gland.

1. FRONT E
I R
Lecture 2.
Hypopituitarism:

2. Overview:
• There is usually deficiency of one or more of the
pituitary hormones affecting either anterior pituitary,
or posterior pituitary and hypothalamus.
• The clinical features depend on the:
1. Patient’s age.
2. Type and severity of the hormone deficiencies.
3. One of the manifestations of hypopituitarism is
pallor of skin.
• Causes of hypopituitarism:
a) Congenital ‘rare’.
b) Acquired.

6. • Adenohypophyseal hypofunction is invariably due to
destruction of the anterior lobe of more than 75%
because the anterior pituitary possesses a large
functional reserve.
• Lesions of the anterior pituitary include:
A. Nonsecretory (chromophobe) adenoma.
B. Metastatic carcinoma.
C. Craniopharyngioma.
D. Trauma.
E. Postpartum ischemic necrosis (Sheehan's syndrome).
F. Empty-sella syndrome.
G. Rarely, tuberculosis.

7. • Two syndrome associated with hypopituitarism are:
1. Panhypopituitarism.
2. Pituitary Dwarfism.

8. PANHYPOPITUITARISM:
• The classical clinical condition of major anterior
pituitary insufficiency is called panhypopituitarism.
• Three most common causes of panhypopituitarism
are:
A. Sheehan’s syndrome and simmond’s disease.
B. Empty - sella syndrome.
C. Non-secretory (chromophobe) adenoma.

9. A. Sheehan’s syndrome and
simmond’s disease:
• Pituitary insufficiency occurring due to postpartum
pituitary (Sheehan’s) necrosis is called Sheehan’s
syndrome.
• Whereas occurrence of similar process without
preceding pregnancy as well as its occurrence in males
is termed Simmond’s disease.
• Pathogenesis mechanism:
Enlargement of the pituitary occurring during
pregnancy which may be followed by hypotensive
shock precipitating ischemic necrosis of the pituitary.
DIC following delivery.
Traumatic injury to vessels.
Excessive hemorrhage.

12. • Patients with long-standing diabetes mellitus
appear to be at greater risk of developing this
complication.
• Clinical features:
1. Failure of lactation following delivery.
2. Loss of axillary and pubic hair.
3. Amenorrhoea.
4. Sterility and loss of libido.
5. Hypothyroidism and adrenocortical insufficiency.
• Microscopic examination:
• Early stage are ischaemic necrosis and
haemorrhage, while later necrotic tissue is replaced
by fibrous tissue.

14. • Diagnosis:
• History taking and physical examination.
• MRI; shrinkage of pituitary gland.
• Treatment:
• Hormone replacement therapy.

16. B. Empty-sella syndrome:
• Is characterized by the appearance of an empty sella
and features of panhypopituitarism.
• The pituitary is usually present in a compressed state.
• It may be partial or total empty.
• Causes:
1. Most commonly, herniation of subarachnoid space
into the sella turcica due to an incomplete
diaphragma sella.
2. Sheehan’s syndrome.
3. Infarction and scarring in an adenoma.
4. Irradiation damage.
5. Surgical removal of the gland.

18. • Diagnosis:
• Computed tomography (CT) scan of the head shows
an empty sella turcica.
• Treatment:
• Hormonal replacement therapy.

19. C. Null cell ‘Nonsecretory
(chromophobe) pituitary adenoma:
• Mechanism is the growth of a non secreting tumor
that causes destruction of the adjacent normal
gland.
• The commonest tumour is one derived from
apparently inactive cells.
• Absent hormonal manifestation.
• Prolactin may be high and the clinical effects may
thus be limited to infertility and be discovered only
because of failed conception in the female.

20. PITUITARY DWARFISM:
• Severe deficiency of GH in children before growth is
completed results in retarded growth and pituitary
dwarfism.
• Pituitary dwarfism appear after one year of age.
• Cuases:
1. Most commonly, inherited autosomal recessive
disorder.
2. Pituitary adenoma.
3. Craniopharyngioma.
4. Infarction.
5. Trauma to the pituitary.

21. • Clinical features:
o In children:
1. Retardation in growth of bones.
2. Normal mental state for age.
3. Poorly-developed genitalia.
4. Delayed puberty.
o In adults:
1. Episodes of hypoglycaemia ‘result in increased
insulin sensitivity’.
2. Decreased muscle strength.
3. Anemia.

23. • Diagnosis:
• Limbs disproportionate to the trunk are noted.
• Test level of growth hormone.
• Physical examination.
• Radiological measurement.
• Treatment:
• Regular injection of synthetic human GH.

25. • Insufficiency of the posterior pituitary and
hypothalamus is uncommon.
• The only significant clinical syndrome due to
hypofunction of the neurohypophysis and
hypothalamus is diabetes insipidus

26. DIABETES INSIPIDUS:
• Is a deficient in secretion of ADH.
• Causes:
1. Inflammatory lesion.
2. Neoplastic lesions of the hypothalamo-
hypophyseal axis.
3. Surgery.
4. Radiation.
5. Head injury.
6. Idiopathic.

27. • Types of diabetes insipidus:
• Central diabetes insipidus: Due to decreased
production of ADH.
• Nephrogenic insipidus: Due to decreased renal
responsiveness to ADH.
• Causes of diabetes insipidus:
• Central diabetes insipidus: Head trauma,
neoplasms, Langerhans cell histiocytosis, infectious
processes, surgical procedures, autoimmune
diseases.
• Nephrogenic diabetes insipidus: Chronic renal
disease; sickle cell anemia.

31. • Clinical features:
• Excretion of a very large volume of dilute urine.
• Polyuria and polydipsia.
• Diagnosis:
• Low specific gravity (below 1.010).
• Urine osmolality is < 200 mOsm/kg.
• Serum osmolality is increased.
• Water deprivation test = to rule in or out conditions
that may exhibit an osmotic imbalance in either the
plasma or urinary tubular compartment.
• ADH Challenge: Performed after water deprivation test.
• In both central and nephrogenic DI, the plasma
osmolarity in the presenting patient will be increased
to approximately >295 mOsm/kg.

32. oCentral:
Responds to ADH.
Urine output decreases.
Urine osmolality increases.
oNephrogenic:
Does not respond to ADH because kidneys are resistant
to ADH.
Administration of ADH does not change urine
osmolality.
• Treatment:
• In mild DI water intake are increased.
• In central DI, Administration of ADH ‘desmopressin’.
• In nephrogenic DI, thiazide diuretics, producing a
decrease in urine volume by approximately 50%.

34. Pituitary apoplexy:
• Hemorrhage into the pituitary gland, usually into an
adenoma.
• Causes:
1. Pituaitry adenomas.
2. Hypertension.
3. Disturbed in blood coagulation.
4. Radiation.
5. Pregnancy.
6. Dopamine agonists.
• Clinical features:
• Rapid onset headache.
• Rapid onset diplopia.

37. • Complications:
• Hypopituitarism and diabetes insipidus.
• Potentially cardiovascular collapse and death.
• Diagnosis:
• MRI ‘infraction or hemorrhage’
• Blood test for hormones, electrolyte, CBC,
coagulation test, and IGF-1.
• Visual field testing.
• Treatment:
oTime.
oSurgical decompression.
oLong term hormone supplementation

38. Nelson syndrome:
• Is a disorder charecerized by abnormal hormone
secretion, enlargement of the pituitary gland and the
development of large and invasive growths known as
adenomas.
• 15-25% of people undergo surgical removal of
ADRENAL GLAND.
• Causes:
• Removal of both adrenal gland.
• Clinical feature:
• Intense skin pigmentation.
• Headache.
• Visual field disturbance.
• Amenorrhea.

40. • Treatment:
• Transsphenoidal surgery