Chris Thompson  

Anterior Pituitary

1) Cell Types

Chromophobes (50%) - Corticicotrophes (ACTH, β-LPH, MSH, all from pro-opiocortin)

Acidophils (40%) - Somatotrophes (GH), Mammotrophes (PL)

Basophils (10%) - Thyrotropes (TSH), Gonadotropes (LH, FSH) - share similar alpha subunits with different beta subunits for specificity.

2) Tumours

MACROADENOMAS are >1 cm and usually are acidophilic, secreting Growth hormone (70%) or Prolactin. Cause visual field defects or pituitary failure, and show as pituitary fossa enlargement or inhomogeneity on CT. Usually treated medically or with radiotherapy prior to trans-sphenoidal hypophysectomy, under steroid cover. Diabetes insipidus postoperatively is common.

MICROADENOMAS include Cushings disease (small corticotrophe tumour) and most prolactinomas.

a) Prolactinomas

In women cause menstrual irregularities, oligo-amennorrhoea, galactorrhoea, and occasionally hirsutism, and are usually microadenomas. In men symptoms are few (impotence) until large tumours cause signs. Treat with Bromocryptine. NB Prolactin release is controlled by Prolactin Release Inhibitory Factor, the only anterior pituitary hormone with an inhibitory releasing factor.

b) Acromegaly

Large hands, feet, tongue, protruding jaw, redundant facial skin cause characteristic facies. Cardiomegaly, cardiomyopathy, diabetes, hypertension, prolactin secretion, blindness, and occasionally a peripheral myopathy may occur. Occasionally burns out of its own accord, or else is treated with DXRT or surgery.

c) Cushings disease

Cushings disease is pituitary dependent inc ACTH (70% of cases of Cushings syndrome). Secretion of CRF, by cells in the median eminence of the hypothalamus, into the pituitary portal system, causes ACTH release in response to stress and diurnal rhythmn. ACTH is a 39 AA polypeptide with half-life of 15 minutes and MW of 49,000. Via a surface receptor on the zona reticularis, c-AMP is increased, causing inc uptake of cholesterol and inc glucocorticoid synthesis. Cushings sydrome is the clinical syndrome with features of prolonged high glucocorticoid levels, ie:

  • Central obesity, buffalo hump, round face
  • Striae, thinning and bruising of skin, hirsutism, acne
  • Osteoporosis, muscle wasting, catabolism
  • Psychiatric disturbances
  • Hyperglycaemia, high aminoacid and FFA levels
  • Mild hypertension with Na retention, enhanced responsiveness to circulating catecholamines, CCF

Treatment includes Radiotherapy, hypophysectomy, or Aminoglutethimide or Metapyrone, which decrease steroid production.

For surgery, treatment of diabetes, cardiac failure, and hypertension are required. Intubation, posturing, and IV access difficulties may arise. Steroid supplementation postop is essential and 300 mg Hydrocortisone per day is adequate.

Nelsons sydrome is the development of an ACTH producing Adenoma following bilateral Arenalectomy; pigmentation is pronounced.

3) Panhypopituitarism

Classically a person with cool, pale, dry skin, mental dullness, hypogonadism, amennorrhoea, postural hypotension, etc. Sheeehan's syndrome is absent lactation and panhypopituitarism following a PPH.

Rx with Glucocorticoids, thyroxine, and sex hormones.

4) Posterior pituitary

Cell bodies in the Supraoptic Nucleii secrete Vasopressin (ADH) into the systemic circulation in the Posterior pituitary. Oxytocin is similar.

a) Disorders of Vasopressin

i) Diabetes insipidus

Absence of ADH results in impermeable collecting tubules causing polyuria, free water loss, and hypernatraemia. Common after pituitary surgery, but usually resolves.

Management:

  • Frequent checks of serum and urine electrolytes, osmolarity, CVP
  • Replace urinary losses with similar fluid and correct existing defcicts.
  • Aqueous Pitressin 2-5 U s/c useful short-term
  • Pitressin Tannate or DDAVP for longterm use.

ii) Excessive ADH

Free water retention causes hyopnatraemia and eventual cerebral oedema.

5) Disorders of Adrenocortical function

a) Addisons disease

Primary adrenal failure, including both gluco- and mineralo-corticoid deficiency, with clinical features of:

  • Anorexia, nausea, vomiting.
  • Weakness, lethargy, somnolence.
  • Pigmentation (MSH)
  • Hypotension, hypovolaemia, especially under stress
  • HyperKalaemia, hypoNatraemia

Addisons disease is rare, but Addisonian crises in adrenocortically suppressed patients undergoing anaesthesia are more common.

Plasma cortisol and ACTH rises rapidy after induction of anaesthesia and commencement of surgery, and remains elevated for a variable period postop, in relation to the magnitude of the surgical stress. Apprehension, ether, and cyclopropane may elevate cortisol while etomidate can abolish any rise. The role of perioperative increases in steroid levels is uncertain as their abolition with high-dose narcotics, epidurals, and etomidate seems to have no adverse effects in normal people.

he situation may be different in Addisonian patients, where numerous reports describe hypotensive episodes in adrenally supressed patients undergoing major surgery or trauma. A variety of replacement strategies recommending from 25-600 mg Hydrocortisone/day have been described. Insulin-hypoglycaemia and Synacthen tests can demonstrate the magnitude of the adrenal suppression, but clinically it is impossible.

Current recommendations are:

  • 25 mg Hydrocortisone IV on induction for minor surgery
  • 100-300 mg Hydrocortisone/day by IV infusion for major surgery.

These low-dose regimes are intended to reduce sequelae such as retardation of healing, increased infection, and GIT haemmorrhage.

 


Last updated Tuesday, April 13, 2010
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