6.1 Pitutary Disorder
6.1 Pitutary Disorder
6.1 Pitutary Disorder
Problems
Pituitary Gland
· Size of a grape
· Hangs by a stalk from the hypothalamus
· Protected by the sphenoid bone
· Has two functional lobes
· Anterior pituitary – glandular tissue
· Posterior pituitary – nervous tissue
Hormones of the Anterior Pituitary
· Six anterior pituitary hormones
· Two affect non-endocrine targets
· Four stimulate other endocrine glands
(tropic hormones)
· Characteristics of all anterior pituitary
hormones
· Proteins (or peptides)
· Act through second-messenger systems
· Regulated by hormonal stimuli, mostly
negative feedback
Hormones of the Anterior
Pituitary
Growth Hormone (GH)
· Gonadotropic hormones
· Regulate hormonal activity of the gonads
· Follicle-stimulating hormone (FSH)
· Stimulates follicle development in
ovaries
· Stimulates sperm development in
testes
Functions of Other Anterior Pituitary
Hormones
· Gonadotropic hormones (continued)
· Luteinizing hormone (LH)
· Triggers ovulation
· Causes ruptured follicle to become the
corpus luteum
· Stimulates testosterone production in
males
· Referred to as interstitial cell-stimulating
hormone (ICSH)
Hormones of the Posterior Pituitary
Hormones of the Posterior Pituitary
· Oxytocin
· Stimulates contractions of the uterus during
labor
· Causes milk ejection
· Antidiuretic hormone (ADH)
· Can inhibit urine production
· In large amounts, causes vasoconstriction
leading to increased blood pressure
(vasopressin)
Disorders of the Anterior Pituitary Gland
• Target tissue
– Thyroid, adrenal cortex, ovary, testes, uterus,
mammary glands and kidney
• Either excess or deficiency due to any pathologic
condition within the gland or hypothalmic dysfunction
which leads to disorders of the Anterior pituitary gland
• Two to focus on:
– Hyper-pituitarism
– Hypo-pituitarism
Hypo-pituitarism
• Deficiency of one or more anterior pituitary
hormones results in metabolic problems and sexual
dysfunction.
• Panhypopituitarism—decreased production of all of
the anterior pituitary hormones.
• Most life-threatening deficiencies—ACTH and TSH.
• Deficiency of gonadotropins.
• Growth hormone
– Proportionate dwarfism
Causes:
• Benign or malignant tumors.
• Anorexia nervosa
• Shock or severe hypotension
• Head trauma
• Brain tumors or infection
• Congenital
• Total destruction of pituitary gland by trauma, tumor, or
vascular lesion removes all stimuli..
• complication of radiation therapy to the head and neck
area.
• Clinical manifestation:
• Headache , visual changes, anosmia (loss of sense of
smell), and seizure.
• Adult with GH deficiency: truncal obesity, decreased
muscle mass causing reduce strength, decreased energy,
reduced exercise capability,
• FSH & LH deficiency for women menstrual irregularity,
diminished libido and change secondary sex
characteristics.(breast)
• For men: testicular atrophy,, loss of libido, impotence,
decreased facial hair and muscle mass.
• A deficiency of ACTH: weakness , fatigue,
headache, dry and pale skin, diminished
auxiliary and pubic hair.
• Thyroid deficiency: cold intolerance,
constipation, fatigue, weight gain, lethargy
• Diagnostic test:
• History & physical examination
• MRI scan & CT scan
• Laboratory studies.
• Interventions include:
• Surgery or irradiation for tumor removal
followed by life long hormone replacement.
– Replacement of deficient hormones( GH,
corticosteroids, thyroid hormone and sex
hormones)
– Somatropin- GH hormone.
– Estrogens and progesterone – women
– Testosterone- for men gonadotropin
deficiency
Hyper-pituitarism
• Over production of the growth hormone (GH) is
usually caused by pituitary tumor (adenoma)
leading to the over growth of bones and soft tissues.
• Excessive secretion GH in adult results in
ACROMEGALY, a condition characterized by a
thickening of bones and soft tissues.
• Adult: The problem develops after epiphyseal
closure, so the bones are unable to grow longer.
• Children: the epiphyseal plates are not closed , so
excessive GH secretion results in gigantism. These
children may grow as tall as 8 feet.
Clinical manifestation:
• Changes in physical appearance.
• Enlargement of tongue that leads to speech
difficulties.
• Sleep apnea due to obstruct airway result from
increased amount of pharyngeal soft tissues.
• Skin become thick, leathery, & oily.
• Women- menstrual disturbances.
• Diagnostic test:
• History, physical examination, CT & MRI scan,
• Evaluation of plasma insulin like growth factors –I
levels, IGF binding protein -3 levels(peripheral action of GH
is mediated by IGF)
Gigantism
• Gigantism is the onset of growth hormone
hypersecretion before puberty.
Patient-Centered Collaborative Care
• Assessment
• Nonsurgical management:
– Drug therapy- to reduce GH secretion or the effects on
tissues
• Somatostatin analogues
• Dopamine agonists
• Growth hormone antagonist
– Radiation
– Gamma knife procedure
• Usually one time treatment
Surgical Management
Surgical treatment
• Hypophysectomy (removal of pitutary gland)
through transsphenoidal approach
• Surgery produce an immediate reduction in GH
levels.
• Life long hormone replacement therapy.
• Radiation therapy.
• Drug therapy: sandostatin to reduce GH
Posterior
Pituitary
Disorders
DIABETES INSIPIDUS
• Water metabolism problem caused by an antidiuretic
hormone deficiency (either a decrease in ADH or
vasopressin synthesis or an inability of the kidneys to
respond to ADH).
• Great thirst (polydipsia) and large volumes of dilute urine
characterize the disorder
• Diabetes insipidus is classified as:
– Nephrogenic
– Neurogenic
– Psychogenic
– Neurogenic DI occurs when a lesion of the
hypothalamus, infundibular stem or posterior
pituitary interferes with ADH synthesis, transport or
release.
– Causes:
• Interference with ADH synthesis or release
• Multiple causes include brain tumor, head
injury, brain surgery CNS infections.
– Nephrogenic DI is a condition in which there is
adequate ADH, but there is a decreased response to
ADH in the kidney.
– Causes:
– Lithium drugs
– Hypokalemia
– Hypercalcemia
• Psychogenic or primary DI:
– Problem results from excessive water intake
CAUSES
– Structural lesion in thirst center
– Psychological disorder
Causes:
• Secondary to head trauma, brain tumor, or surgical
ablation or irradiation of the pituitary gland.
• It may also occur with infections of the central
nervous system (meningitis, encephalitis,
tuberculosis) or tumors (eg, metastatic disease,
lymphoma of the breast or lung).
• Failure of the renal tubules to respond to ADH
Clinical manifestation:
• very dilute, water-like urine with a specific gravity of
1.001 to 1.005 occurs.
• Intense thirst- patient tends to drink 2 to 20 liters of
fluid
• Polyuria
• Polydipsia
• Fatigue due to nocturia
• Chance to get severe fluid loss, weight loss,
constipation, poor tissue turgor, hypotension,
tachycardia and shock
• CNS involvement leads to mental dullness
irritability, coma
Diagnostic test:
• History and physical examination.
• Plasma and urine osmolality study. Find specific
gravity level.
• CT scan , MRI scan- to find the cause tumor or
injury in head
Management:
The objectives of therapy are
(1)to replace ADH (which is usually a long-term
therapeutic program),
(2)to ensure adequate fluid replacement, and
(3)to identify and correct the underlying intracranial
pathology
PHARMACOLOGIC THERAPY
• Desmopressin (DDAVP), a synthetic vasopressin without
the vascular effects of natural ADH,- It is administered
intranasally; the patient sprays the solution into the nose
through a flexible calibrated plastic tube. One or two
administrations daily or every 12 to 24 hours usually
control the symptoms
• Intramuscular administration of ADH, or vasopressin
tannate in oil, which is used when the intranasal route is
not possible. It is administered every 24 to 96 hours. The
vial of medication should be warmed or shaken vigorously
before administration. The injection is administered in the
evening so that maximum results are obtained during sleep.
For nephrogenic DI
• Thiazide diuretics, mild salt depletion, and
prostaglandin inhibitors (ibuprofen,
indomethacin, and aspirin) are used to treat
the nephrogenic form of diabetes insipidus.