Download 2-Ant Pituitary

For each hormone you should know the
following:
• Chemical Structure
• Source and mode of action
• Metabolic effects
• Clinical disorders
• Laboratory use
Growth Hormone
GH (22 KD) is synthesized in acidophilic cells of pituitary as a single
polypeptide chain
• The highest level occurs after severe exercise, deep
sleep, and hypoglycemia [factors used in lab to
estimate growth hormone stimulation test] to
diagnose growth hormone deficiency.
• Its growth function occurs through specific factors
called somatomedins (IGF I and IGF II) produced
from liver cells in response to GH. These factors
are also called sulphation factors because they
incorporate sulphate to cartilage. They promote
their growth effect on target tissues (bone and
cartilage) through specific cell membrane
receptors.
Other functions of GH are metabolic as In humans,
GH stimulates:
• protein synthesis and amino acid uptake by cells,
[positive nitrogen balance] as in growing children.
• lipolysis (results in increased FFA in blood to be
used as energy),
• blood glucose synthesis by gluconeogenesis and
inhibition of glucose uptake by peripheral cells,
therefore causing hyperglycaemia, (it acts as
antagonist of insulin), preventing insulin binding
to its receptors.
GH undergoes two important abnormalities.
These are
1. Excessive GH w is of 2 types:
 Before epiphyseal closure of the long
bones leads to gigantism [during
childhood]
 After closure, leads to acromegaly
[during adulthood]
2. GH dysfunctions: results in short- stature [dwarfism]
Is of 2 types;
 GH-deficiency dwarfs w is due to true deficiency of
GH (because of pituitary damage or hypothalamic
disease)


So both GH & IGF-1 levels are low
They respond well to GH therapy.
 GH insensitivity ( resistance) dwarfs caused by
deficiency of liver GH receptors [Laron dwarfs] or
loss of IGF-1 response to GH i.e. loss of postreceptor response [Pygmies dwarfs ]


These patients have low IGF-1 but normal or high serum
GH level.
They not respond to GH therapy.
• PRL is also a polypeptide H produced by acidophilic
cells of pituitary .
• It is the only tropic H of pituitary that is normally under
negative control by prolactin inhibiting H (PIH) or called also
dopamine.
• Decreased dopamine production, or damage to the hypophyseal
stalk, leads to elevation of PRL secretion [Hyper- prolactinemia].
TRH induce prolactin secretion; as a result, woman with
hypothyroidism also has hyperprolactinemia
As PRL important for normal lactation.
• So deficiency results in lactation failure (Sheehan’s syndrome)
• But elevation causes infertility in both males & females
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Defect in secretion of pituitary
hormones, which is of two types:
Isolated deficiency: only one or two
hormones are deficient. (usual are
gonadotropins and GH).
Panhypopituitarism: in which all
hormones of anterior pituitary are
deficient due to pituitary tumours or
infarction. In infarction, it may occur
due to post-partum haemorrhage
((Sheehan's syndrome)).
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the features are usually due to target gland failure
e.g. deficiency of LH or FSH causes secondary
hypogonadism, which results in amenorrhoea, infertility,
atrophy of secondary sex characters, impotence in male
and loss of libido.
Deficiency of GH and TSH causes growth retardation
(dwarfism).
Deficiency of ACTH causes secondary adrenocortical
hypo-function.
This type should be differentiated from the primary cause
that's called Addison's disease, in which the adrenal
gland itself is destroyed by bacterial infection or by autoimmune disease which means loss of adrenocortex
function (cortisol↓). I
•
•
In Addison's disease, there are low levels of
cortisol with a very high level of ACTH. In
contrast, in the secondary type, both of these
hormones (cortisol and ACTH) are on low levels.
The second difference is that in primary, there is
hyperpigmentation while in secondary there is no
pigmentation (why?); because the low level of
cortisol in Addison's there is loss of negative
feedback inhibition, which results in excessive
secretion of CRH and in turn ACTH. But this
latter is also stimulator of melanocytes (cells of
melanin) which are important for melanin
production that gives us dark pigmentation of
skin and mucous membranes.
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•
•
In Addison's disease, there are low levels of
cortisol with a very high level of ACTH. In
contrast, in the secondary type, both of these
hormones (cortisol and ACTH) are on low levels.
The second difference is that in primary, there is
hyperpigmentation while in secondary there is no
pigmentation (why?);
because the low level of cortisol in Addison's
there is loss of negative feedback inhibition,
which results in excessive secretion of CRH and
in turn ACTH. But this latter is also stimulator of
melanocytes which are important for melanin that
give us dark pigmentation of skin and mucous
membranes.