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abnormal the dexamethasone suppression test is of value. If dexamethasone produces some suppression of
cortisol production, this is suggestive of pituitary disease, while complete failure of suppression suggests
primary adrenal disease or ectopic ACTH production by tumour, e.g. small-cell bronchogenic carcinoma.
If there is any doubt, further tests using the response to exogenous corticotrophin releasing hormone may
be helpful.
Treatment
Transphenoidal hypophysectomy is the first line treatment for Cushing’s disease5 when caused by microadenoma
and is curative in over 80 per cent of patients. The pituitary is irradiated in the remaining 20 per
cent to prevent Nelson’s syndrome.6
Bilateral adrenalectomy remains a useful treatment for patients who are not cured by hypophysectomy,
but again pituitary irradiation must be given to limit the development of Nelson’s syndrome.
Radiotherapy alone has been shown to be curative in approximately 40 per cent of patients over the age of
18, and in approximately 80 per cent of those under 18. Pharmacotherapy has a limited role in Cushing’s
disease. The most commonly used drug is metyrapone which blocks 11-hydroxylase in the adrenal
glands. Side-effects include nausea, oedema, somnolence, and hypertension. It is useful to render patients
euadrenal before surgery. Other drugs such as ketoconazole, cyproheptadine, and aminoglutethimide have
only limited use.
Operational implications
Individuals with active Cushing’s disease are unfit and would remain so until hormone secretion returns
to normal.
Aeromedical considerations
After adequate treatment, it may take six months or more for symptoms and signs to subside and thus
medical certification should be denied for one year. The certification issue may be dependent on a
satisfactory report from and continuous supervision by an endocrinologist. It is possible that
recertification in any category may be feasible but continual surveillance with regular reports from the
endocrinologist must be mandatory.
The posterior pituitary (neurohypophysis)
The posterior lobe of the pituitary gland consists principally of terminal extensions of neurones which
arise in the pre-optic nucleus of the hypothalamus. The posterior pituitary secretes two principal peptides
vasopressin (anti-diuretic hormone - ADH) and oxytocin, together with their carrier proteins
(neurophysins).
DIABETES INSIPIDUS
Aetiology and pathogenesis
5 Cushing’s disease is a term applied to Cushing’s syndrome when of pituitary origin.
6 Nelson’s syndrome: hyperpigmentation, ACTH excess and pituitary expansion. Named after Donald H. Nelson,
American internist (1925- ).
ICAO Preliminary Unedited Version — March 2010 III-4-10
Diabetes insipidus (DI) may be idiopathic or caused by:
a) trauma (head injury and neurosurgery)
b) primary or secondary neoplasms of the hypothalamus
c) vascular cause such as haemorrhage and thrombosis, Sheehan’s syndrome7 and sickle cell
haemoglobinopathy
d) granulomatous disease such as sarcoid and histiocytosis
e) infections e.g. meningitis and encephalitis
Rarely DI may be genetically inherited. A primary form of neurogenic DI is the DIDMOAD syndrome
(diabetes insipidus, diabetes mellitus, optic atrophy and nerve deafness), which is inherited as an
autosomal recessive condition. The vast majority of cases may be idiopathic; an autoimmune mechanism
has been postulated.
Signs and symptoms
The most marked features are polydypsia and polyuria reaching 10 to 20 litres per 24 hours. The urine is
of low specific gravity (< 1.003) and osmolality (50-100 mosmol/kg).
The major differential diagnosis is psychogenic polydypsia, which is more common than true DI. The
plasma osmolality in true diabetes insipidus is usually greater than 290 mosmol/kg on a background of
the urinary findings above. To confirm the diagnosis, a water deprivation test (under close supervision) is
carried out. If the urine is not concentrated after eight hours, an injection of 2 μg of the ADH analogue
DDAVP (desmopressin) is given and in the patient with true diabetes insipidus this produces a rapid
concentration of the urine.
Treatment
The long acting vasopressin analogue, desamimo-D-arginine vasopressin (DDAVP) acts almost solely on
the type I receptors in the renal tubule and is the mainstay of treatment.
It is usually given by intra-nasal spray (10-20 μg twice daily). Recently an oral formulation has become
available and is used in a dose of 100-200 μg three times a day. The sulphonylurea chlorpropamide
enhances the renal response to ADH, but is only used in partial forms of DI and carries a risk of
hypoglycaemia.
　
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