THE
NEUROHYPOPHYSIS
A. The
Oxytocin
Function of
oxytocin
1. Causes
the milk ejection from the lactating breast; regulated by positive feedback
mechanism; PRL cooperates with oxytocin.
2. Stimulates
contraction of uterine muscles that occurs during childbirth; regulated by
positive feedback mechanism.
3. Aids
in fertilization by promoting fertilization of the ovum causing uterine
propulsion of the male semen upward the fallopian tubes (escalator effects of
oxytocin)
Regulation of
secretion
1. Stimulation
of the nipple by the sucking infant–oxytocin release stimulates the
myoepithelium of the ductulas if the infant is unable to obtain milk by
sucking.
2. Dilatation
of the cervix and stimulation of other generative organs – oxytocin release
plays a role in the initiation and maintenance of uterine contractions during
labor. Uterine muscle is responsible to oxytocin only if it has previously been
exposed to estrogen.
B. The
Antidiuretic Hormone (ADH): Vasopressin
Function of
ADH
1. Increase
water permeability of the luminal membrane of the collecting duct epithelium.
2. The
V1 receptors mediate vascular smooth muscle contraction and
stimulate prostaglandin synthesis and liver glycogenolysis. Activation of these
receptors increases phosphatidylinositol breakdown, thus causing cellular
calcium mobilization.
3. The
V2 receptors, which produce the renal actions of vasopressin,
activate G proteins and stimulate the generation of cyclic AMP.
Regulation of
secretion
ADH
stimulation starts with its binding to the V2 receptor located on
the distal convoluted tubules and collecting ducts. Adenyl cyclase is
activated, and cAMP is generated. The second messenger (cAMP) probably
initiates a phosphorylation of a membrane protein or proteins, causing an
increase in the luminal membrane permeability to the water. In addition to
regulating water balance in the body, the action of ADH has a concentrating
effect on the urine. The primary stimulus for ADH secretion is an increase in
the plasma osmolality as detected by the osmoreceptors in the brain. Patients
with an ADH deficiency have a polydipsia (increased thirst) and polyuria
(increased urine output). The name arginine vasopressin is also
applied to this hormone, since it can cause generalized vasoconstriction and
may help in maintaining blood pressure during traumatic injuries.
Clinical
significance of ADH
1. Hypersecretion
a. Diabetes
insipidus (D.I.)
– a disorder resulting from deficient ADH action and is characterized by the
passage of copious amounts of very dilute urine. This disorder must be
distinguished from other polyuric states such as primary polydipsia
and osmotic diuresis.
Classification
of D.I.
(1) Central
or Neurogenic D.I. – cause by hypophysectomy (complete or partial),
surgical removal of suprasellar tumors, histiocytosis, granulomas, infections,
interruption of blood supply.
(2) Nephrogenic
D.I.
– cause by chronic renal disease (any renal disease that interferes with
collecting duct or medullary function, e.g. chronic pyelonephritis),
hypokalemia, protein starvation, hypercalcemia, sickle cell anemia, Sjogren’s
syndrome, drugs (e.g., lithium, fluoride, methoxyflurane anesthesia, demecycline,
colchicine), congenital effect.
b. Primary
polydipsia
– a disorder of thirst that is either due to psychogenic causes or to altered
osmotic and non–osmotic regulation of thirst, which involves greatly increased
drinking, usually in excess of 5L of water per day, leading to dilution of the
ECF, inhibition of vasopressin secretion and water diuresis.
2. Hyposecretion
a. Syndrome
of Inappropriate Secretion of Antidiuretic Hormone (SIADH)
Conditions
associated with SIADH
(1) Malignant
lung disease, particularly bronchogenic carcinoma.
(2) Non–malignant
lung disease, e.g. tuberculosis
(3) Tumors
at other sites (especially lymphoma, sarcoma), e.g., duodenum, pancreas, brain,
prostate, thymus.
(4) CNS
trauma and infections
(5) Drugs
that stimulate vasopressin release, e.g., clofibrate, chlorpropamide and other
drugs such as thiazides, carbamazepine, phenothiazine, vincristine,
cyclophosphamide.
(6) Endocrine
diseases: adrenal insufficiency, myxedema, anterior pituitary insufficiency.
Laboratory diagnosis of ADH
1.
Vasopressin
test
Give 5 units
of aqueous vasopressin subcutaneously or 1 ug of desmopressin acetate
intravenously, intramuscularly or subcutaneously and measure urine osmolality
after 1 hour.
Patients with
complete central diabetes insipidus will show an increase of >50% in urine
osmolality, while patients with nephrogenic diabetes insipidus show an increase
of <50%.
Patients with
partial central diabetes insipidus also show increases of <50% and patients
with primary polydipsia have responses <9%. In these cases, measurement of
ADH levels is particularly helpful.
CONCEPT OF
PANHYPOPITUITARISM
Panhypopituitarism is a generalized
hypofunction of the pituitary gland with resulting decreases in all pituitary
hormone levels. Generally, panhypopituitarism is seen after severe damage has
occurred in the pituitary. These patients have thyroid and adrenal insufficiency
as well as absence of gonadal function. Most often, the treatment for this
syndrome is replacement of the deficient hormone.
1.
Simmond’s
disease
– is a form of panhypopituitarism that develops after destruction of the
pituitary by surgery, infection, injury or tumor. The symptoms may vary in
intensity and include extreme weight loss, general debility, dry skin,
bradycardia, hypotension, atrophy of the genitalia and breasts and premature
senility.
2.
Sheehan’s
syndrome
– another form of panhypopituitarism, often with an insidious onset. This
syndrome is caused by a pituitary infarction after complications of postpartum
hemorrhage. It is thought that the infarction may be caused by vascular spasms
of the hypophyseal arteries, resulting in a decreased blood flow to the
pituitary, tissue hypoxia and necrosis.
During
pregnancy, the pituitary is slightly enlarged from an increased demand of hormones,
causing an increased need for nutrients and oxygen to the pituitary cells. This
may make it more susceptible to the hypoxia induced by the vascular spasms. The
first symptom of Sheehan’s syndrome is failure of lactation (decreased PRL) and
postpartum amenorrhea (decreased FSH and LH). The number of symptoms and the
severity depend on the actual amount of pituitary tissue destroyed. Decreased
TSH results in hypothyroidism (dry skin, coarse hair, bradycardia,
hypotension). Mineralocorticoids from the adrenal cortex are usually not
affected by decreased ACTH, so plasma sodium is generally normal. If the
posterior as well as the anterior pituitary is damaged, the patient may also
have diabetes insipidus. Sheehan’s syndrome is more likely to develop in women
with poor prenatal care. This syndrome is becoming a rare disorder largely
because of improved prenatal care.
No comments:
Post a Comment