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Pituitary Gland (hypophysis)
 1 cm in diameter and 0.5 to 1 gm in weight
 Lies in sella turcica (bony cavity at the base of brain
 Connected to hypothalamus by pituitary stalk
 Physiologically it is divided into two parts
 Anterior pituitary (adenohypophysis)
 Posterior pituitary (neurohypophysis)
Pars intermedia is small avascular zone between the two.
 Embryologically the two parts develop from different
sources
 Anterior pituitary from Rathke’s pouch (invagination of
pharyngeal epithelium)
 Posterior pituitary from neural tissue outgrowth from
hypothalamus
Anterior Pituitary Hormones
Cell Types in the Anterior Pituitary
 Somatotropes (acidophils) (30-40%)
 Corticotropes (20%)
 Thyrotropes
 Gonadotropes
 Lactotropes
Posterior Pituitary Hormones
 Antidiuretic Hormone
 Oxytocin
These hormones are secreted by magnocellular neurons
located in the supraoptic and paraventricular nucleus of
hypothalamus
 Hypothalamus controls pituitary secretion
 There are neural connections between the hypothalamus
and the posterior pituitary and vascular connections
between the hypothalamus and anterior pituitary
Hypothalamic Releasing and
Inhibitory Hormones
 Thyrotropin-releasing hormone
 Corticotropin-releasing hormone
 Growth hormone-releasing hormone
 Growth hormone-inhibitory hormone
 Gonadotropin-releasing hormone
 Prolactin inhibitory hormone
 These hypothalamic releasing and inhibitory hormones are
conducted through minute blood vessels called
hypothalamic-hypophysial portal vessels to the anterior
pituitary gland
 The hypothalamic-hypophysial portal vessels form a
direct vascular link between hypothalamus and the
anterior pituitary
Hypothalamic- Hypophysial Portal
Blood Vessels
 Hypothalamic releasing and inhibitory hormones are
secreted into median eminence
 The neurons secreting these factors are present in different
parts of hypothalamus
 Their endings secrete these factors into the tissue fluid
from where theses hormones are absorbed into
hypothalamic-hypophysial portal system
Growth Hormone (somatotropic
hormone or somatotropin)
 Protein hormone (191 amino acids), molecular weight
22,005
 Approximately 50% of the circulating pool of growth
hormone is in the bound form providing reservoir to
prevent fluctuations
 The half life of circulating growth hormone in humans is
6-20 min and daily growth hormone output is 0.2-1.0
mg/dl
 The plasma growth hormone level is less than 3 ng/ml
Physiological Functions of Growth
Hormone
 Growth hormone promotes growth of almost all the
body tissues
 It promotes increase in size of cells, increased mitosis
and differentiation of certain type of cells such as
bone growth cells, muscle cells
.
Effect of Growth hormone on
Skeletal frame work
 Increased deposition of protein by chondrocytic and
osteogenic cells
 Increased rate of reproduction of these cells
 Conversion of chondrocytes into osteogenic cells causing
bone deposition
 Long bones grow in length at the epiphysial cartilages
where epiphysis at the ends of long bones are separated
from shaft.
 Lengthening does not occur if epiphysis are united with
the shaft
 Growth hormone strongly stimulates osteoblasts so bones
can become thicker under the influence of growth
hormone through out life
Growth Hormone is Potent Protein Sparer
 Growth hormone promotes protein deposition in tissues by
increasing amino acid transport through cell membrane
 Enhancement of mRNA Translation
 Increased nuclear transcription of DNA to mRNA (over
prolonged periods)
 Decreased catabolism of proteins and amino acids
Growth hormone enhances Fat utilization for
energy
 Fats are used for energy in preference to the use of
carbohydrates and proteins
 Release of fatty acids from adipose tissue
 Conversion of fatty acids to acetyl-CoA
Mobilization of fat by growth hormone requires several
hours whereas enhancement of protein synthesis can begin
in minutes
Ketogenic Effect of Excess Growth
Hormone
 The growth hormone increases free fatty acid levels in the
blood which are utilized for providing energy. When
excess quantities of growth hormone are present large
quantities of acetoacetic acid formed by liver are released
into body fluids causing Ketosis
Growth Hormone Decreases
Carbohydrate Utilization
 Growth hormone increases blood glucose levels
 Decreased glucose uptake in tissues such as muscle and
fat
 Increased glucose production by the liver
 Increased Insulin secretion (causes insulin resistance)
Growth Hormone Effects are
Diabetogenic
 Growth hormone causes insulin resistance
 Decreased glucose utilization by the cells
Raising blood levels of fatty acids above normal decreases
the sensitivity of liver and skeletal muscle to Insulin’s
effects
 Insulin and carbohydrates are necessary for growth
hormone to exert its growth promoting action (insulin has
also protein anabolic effect)
 Growth hormone increases the ability of pancreas to
respond to insulinogenic stimuli such as glucose
Growth Harmone effect on
electrolytes
 Growth hormone increases intestinal absorption of
calcium
 Growth hormone reduces excretion of sodium and
potassium
Somatomedins(insulin like growth factors)
 The effects of growth hormone on growth, cartilage and
protein metabolism depend on interaction between growth
hormone and somatomedins which are polypeptide growth
factors secreted by liver and other tissues
IGF-I (somatomedin-C)
 Secretion of IGF-I before birth is independent of growth
hormone but is stimulated by growth hormone after birth
 It has pronounced growth promoting activity
 Its concentration in plasma rises during childhood, peaks
at the time of puberty and declines in the old age.
 The IGF-I receptor is very similar to Insulin receptor
Duration of Action of
Somatomedin C
 Half life of somatomedin C is 20 hrs whereas that of
growth hormone is 20 minutes
 Somatomedin C is strongly attached to plasma protein and
released slowly
 Growth hormone is bound loosely
IGF-II
 IGF-II plays important role in the growth of fetus and its
secretion is independent of growth hormone
 Growth hormone and somatomedins can act both in
cooperation and independently to stimulate pathways that
lead to growth
Diurnal variations in Growth
hormone Secretion
 The levels of Growth hormone are low during the day
 During sleep large pulsatile bursts of Growth hormone
secretion occur (specially in first two hours of deep sleep)
 Secretion of Growth hormone is under Hypothalamic
control
Regulation of Growth Hormone
Secretion
 GHRH
 GHIH (somatostatin)
 Ghrelin (it is mainly secreted in stomach but also
produced in hypothalamus and it has marked growthhormone stimulating activity)
The balance between the effects of these hypothalamic
factors on pituitary will determine the level of growth
hormone release
Panhypopituitarism
 Decreased secretion of all the anterior pituitary
hormones. It may be
Congenital
Acquired (tumor destroying the gland)
Dwarfism
 Causes
Panhypopituitarism during childhood
 All body parts develop in appropriate proportion but the
rate of development is slow
 The child does not pass through puberty
 If there is only growth hormone deficiency the sexual
maturity occurs
African pygmy (Levi-Lorain dwarf)
 Rate of growth hormone secretion is normal or high
 There is growth hormone insensitivity and there is
hereditary inability to form somatomedin C
Treatment
 Human Growth hormone preparation
Panhypopituitarsm in Adults
 Tumors (craniopharyngiomas, chromophobe tumors)
 Thrombosis of pituitary vessels, infarction of the gland
due to shock after delivery in women
Effects
 Hypothyroidism
 Decreased secretion of adrenal hormones
 Decreased secretion of gonadotropic hormones
(sexual functions are lost)
Gigantism
 Cause
Acidophilic tumors of anterior pituitary before
puberty
 All the body tissues grow very rapidly
 If the condition develops before the union of shaft and
epiphysis the person becomes giant
 There is hyperglycemia
Treatment
 Surgical removal of tumor or irradiation
Acromegaly
 Cause

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

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Acidophilic tumor after puberty
The bones continue to become thicker
Soft tissues also become thicker
There is enlargement of viscera specially kidneys, liver,
tongue
The bone enlargement is specially marked in
membranous bones
There is kyphosis