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 a nd 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 post- receptor 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

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)).

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 auto- immune 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.

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.