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Pituitary gland
Anatomy
Hypothalamus-functions
Midsagital view
illustrates parvicellular
neurosecretory cells
secrete releasing factors
into capillaries which are
then transported to the
anterior pituitary gland
to regulate the secretion
of pituitary hormones
Effect on pituitary
Stimulates ACTH
secretion
Stimulates TSH and
Prolactin secretion
Stimulates GH secretion
Inhibits GH (and other
hormone) secretion
Stimulates LH and FSH
secretion
Stimulates PRL secretion
Inhibits PRL secretion
Pituitary Gland
Pituitary
population
Product
Target
Corticotroph
15-20%
ACTH
Adrenal gland
-lipotropin Adipocytes
Melanocytes
Thyrotroph
Gonadotroph
Somatotroph
Lactotroph
3-5%
10-15%
40-50%
10-15%
TSH
LH, FSH
GH
PRL
Thyroid gland
Gonads
All tissues, liver
Breasts
gonads
ANTERIOR PITUITARY
(Adenohypophysis)
ACTH
ANTERIOR
PITUITARY(adenohypophysis)
- TSH
Stimulates the thyroid
gland
metabolic rate
- GH (Growth Hormone)
stimulates growth of
bone/tissue
glucose usage
consumption of fats as
an energy source
Anterior pituitary
Posterior Pituitary
Oxytocin
stimulates gravid uterus
causes let down of milk from the breast
ADH (vasopressin)
causes the kidney to retain water.
Pituitary Tumors
PITUITARY TUMORS
Hypopituitarism
Pituitary adenomas most common cause
Sequence of function loss from mass
effect:
Growth hormone GH deficiency
Gonadotropins
hypogonadism
ACTH
hypoadrenalism
TSH
hypothyroidism
Hypopituitarism
Hypopituitarism
Hypersecretion of Pituitary
Hormones
- Hyperprolactinemia
- Acromegaly
- Cushings Disease
Hypersecretion of Pituitary
Hormones
Hypersecretion of Pituitary
Hormones
Acromegaly
http://www.endotext.com/neuroendo/neuroendo5e/neuroendoframe5e.htm
Cushings Disease
Williams Textbook of Endocrinology. 8th Ed. Foster, DW, Wilson, JD (Eds), WB Saunders, Philadelphia, 1996
Hypercorticolism
terti
er
secund
er
prime
r
Cushings Syndrome
Moon facies
Facial plethora
Supraclavicular
fat pads
Buffalo hump
Truncal obesity
Weight gain
Purple striae
Proximal muscle
weakness
Easy bruising
Hirsutism
Hypertension
Osteopenia
Diabetes
mellitus/IGT
Impaired immune
function/poor
wound
healing
Williams Textbook of Endocrinology. 8th Ed. Foster, DW, Wilson, JD (Eds), WB Saunders, Philadelphia, 1996
Age 6
Age 7
Age 8
Williams Textbook of Endocrinology. 8th Ed. Foster, DW, Wilson, JD (Eds), WB Saunders, Philadelphia, 1996
Age 9
Age
Orth, D. UpToDate
Orth, D. UpToDate
Clinical Evaluation
Hormonal Evaluation
Radiologic Evaluation
Clinical Evaluation
Hormonal Evaluation
Basal hormone measurement and
dynamic stimulation testing.
Screening basal hormone
measurements :
Prolactin
TSH, FT4
ACTH, AM cortisol, midnight salivary cortisol
LH, FSH, estradiol or testosterone
Insulin-like growth factor-1 (IGF-1)
Hormonal Evaluation
Dynamic stimulation/suppression testing :
may be useful in select cases to further
evaluate pituitary reserve and/or for
pituitary hyperfunction
Dexametason test
Low dose : 2 mg
High dose : 8 mg
GHRH
TRH Stimulating
N
N/
CRH Stimulating
GnRH stimulation
Radiologic Evaluation
MRI
Preferred imaging study for the pituitary
Better visualization of soft tissues and vascular
structures than CT
Structures such as fatty marrow and orbital fat
show up as bright images.
high-intensity signals of structures with high
water content, such as cerebrospinal fluid and
cystic lesions
Radiologic Evaluation
CT-scan
Diagnosis
Usually delayed non specific nature of
symptoms
MRI imaging modality of choice
Tests can reveal whether adenoma is
hypo- or hyperfunctional
DIAGNOSIS -- deficiency
DIAGNOSIS - excess
Dexametason test
TREATMENT
DIABETES INSIPIDUS
Diabetes insipidus is a disorder of the
posterior lobe of the pituitary gland
characterized by a deficiency of antidiuretic
hormone (ADH), or vasopressin. Great
thirst (polydipsia) and large volumes of
dilute urine characterize the disorder.
T
Y
P
E
Pathophysiology
Central DI :
Loss of vasopressinproducing cells,
Causing deficiency in
antidiuretic hormone
(ADH) synthesis or
release;
Deficiency in ADH,
resulting in an inability
to conserve water,
leading to extreme
polyuria and polydipsia
Pathophysiology
Nefrogenic DI
Depression of
aldosterone release
or inability of the
nephrons to respond
to ADH,
causing extreme
polyuria and
polydipsia
Goals of 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 cause
Treatments
Replacement vasopressin therapy
with intranasal or I.V. DDAVP
(desmopressin acetate)
Correction of dehydration and
electrolyte imbalances
Treatment
A thiazide diuretic to deplete sodium
and increase renal water
reabsorption
Restriction of salt and protein intake