ACROMEGALY AND GIGANTISM

Professor Nunu Beridze

 DETERMINATION OF ACROMEGALY(AM)
AND GIGANTISM
 Asa pathologic condition when eosinophilic adenoma of anterior
pituitary is accompanied byHypersecretion of GH alog with
abnormal growth of different tissues.

 GIGANTISMis the same disease, developed in childehood and

accompanied with abnormally accelerated growth of the body.
 ETIOLOGY AND PATHGENESIS
 PITUITARY ADENAMAS are present in all cases and are about one cm in
diameter.
 Excessive GH secretion is a primary pituitary disorder
 GHsecretion increment it is episodi cand the number, duration and
amplitude of episodes are increased and occur randomly during 24 hour
 Most of effects of GH elevation are caused by its’ stimulatory effect on
liver production of IGF-1.
 IGF-1 causes characteristic proliferation of bone cartilage,soft tissues ,
 Organomegaly.
 THE insulin resistance and decreased glucose tolerance are due to
direct effect of GH, but not IGF-1
 CLINICAL PICTURE

In cases of adult onset of the disease disproportional growth of the skeleton and soft tissues and inner organs
occures.
When the disease develops in childhood the development is
proportional with high for age height GIGANTISM.
Hypertrophia and hyperplasia of other endocrine organs with increase of their function at early stages of the
disease.
In patients with gigantism enlargement of inner organs is proportional to height whitought functional changes.
Newropathia myopathia, due to stimulatory effect of GH on protein synthesis
Patients are complaining on headache, paresthesia. Nausea, vomitimg, seasors
In severe cases.
Hyperprolactinemia with its’ simpthoms often coexists
Heart left ventricular hypertrophy, followed by the dilatation and progressive cardial insufficiency develops
Hydh BP and early development of atherosclerosis, tendency to bronchopneumonia and amphisema, in some
patinets gastric ulcer biliar stones and gastric neoplasia .


 DIAGNOSIS
 Bloodclinical analysis at the beginning of the disease is usually
normal;
 Decreased glucose tolerance and DM in some cases(15-20%);
 Hypoalbuminemia. Hyperglobulinemia, hyperfibrinogenemia,
hyperprolactinemia, may be also thyrois dysfunction, increased
PTH level.
 X-ray examination, CT and MRI reveal enlarged SELLA TURCICA,
thickening of bones, increased pneumatization of paranasal
synuses.
 Incontrast to healthy persons GH level aftae the insulin
challenge remains increased throught the test.
 TREATMENT
 MOR OFTEN RENTGENOTHER,GAMMA- THERAPY of the hypothalamo-pituitary region
 Drug therapy PARLODEL or BROmocriptin depending on the sevetiry of the disease.
 SHIHANS’ SYNDROME
 This is the syndrome, accompanying destructive changes in anterior
pituitary with theWhithdrowel of all anterior pituitary hormones and is
more prevalante in30-40 years old women.
 ETIOLOGY; destruction of the gland by the tumor, viral and bacterial
agents, hemorrhage, ischemia of different origin, massive postpartum
bleeding.
 In such cases all sypthoms of secondary hypofunction of peripheral encrine
organs are present.
 Anorexia end progressive weight loss even up to kachexia develops.
 TREATMENT- substitution with hormone required.

 HIPOPHISAL NANISM
 HN is genetic disease due to development of absolute or
relative GH deficiency.
 HYPOPHISAL NANISM (HN)

 HN is genetic disease due to absolute or relative deficiency of GH that

leads to growth retardation and very low height,no more than120 cm in
females and 130cm in males with normal body proportion.
 SOMEtimes the deficiency of all anterior pituitary hormones may also
coexist.
 Nanism may alsow develop when peripheral tissues are insensitive to N
level of GH and somatomedin level is low.
 Differential
diagnosis with: thyreogenic nanism, corticogenic, exogenic,
thymogenic and others.
 Treatment whith anabolic steroids.
 DIABETUS INSIPIDUS
 This is a pathologic state caused by the deficiency of posterior pituitary hormole ADH

 Three types of ADH deficiency are known:

 ABSOLUTE DEFICIENCY of ADH due to the damage of the gland, idiopathic and renal form.
 CLINICAL manifestations:
 Sudden onset: permanent thirst, massive urination up to 40l, decreased uppetite,headache, dry skin ,
 In children is accompanied by growth and sexual development retardation;
 Laboratory findings: low density urine 1001 – 1005
 TREATMENT: diet reach in vegetables, fruits. Etiologic treatment as wellas substitution with synthetic ADG:
 Adiurecrin intranasally and pituitrin subkutaneously