PRIMARY ACUTE ADRENOCORTICAL INSUFFICIENCY

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					            PRIMARY ACUTE ADRENOCORTICAL INSUFFICIENCY:
       (1) as a "crisis" in patients with chronic adrenocortical insufficiency
precipitated by any form of stress that requires an immediate increase in steroid
output from glands incapable of responding.
       (2) from too rapid with drawal of steroids from patients whose adrenals have
been sup-presed by long - term steroid administration;
       (3) as aresult of some massive destruction of the adrenals (a) in neonates,
following prolonged and difficult delivery, with considerable trauma and hypoxia,
leading to extensive adrenal hemorrhages beginning in the medulla and extending
into the cortex. Newborns are particularly vulneable because they are often
deficient in prothrombin for at least several days aftdr birth.
       (b) in possurgical patients who develop disseminated intravascular
coagulation ( DIG ) with consequent hemorrhagic infarction of the adrenals,
potentiated by anticoagulation therapy
       (c) when massive adrenal hemorrhage complicates a bacteremic infection, in
this setting called the Waterhouse-Friderichsen (W-F) syndrome.
       This uncommon but catastrophic syndrome is characterized by the
following:
       1)     An overwhelming septicemic infection most often caused by
meningococci but occasionally other highly virulet organisms, such as gonococci,
pneumococci, or staphy-lococci;
       2) Rapidly progressive hypotension leading to shock;
       3) DIG;
       4) Rapidly developing adrenocortical insufficiency.

       Chronic hypoadrenalism - Addison"s disease - results from failure of the
adrenal cortices to produce adrenocortical hormones. ( primary ). Etiology :
       1. primary atrophy of the adrenal cortices, resulting in about 80 per sent of
the cases from autoimmunity against the cortices;
       2. tuberculous destruction of the adrenal glands;
       3. invasion of the adrenal cortices by cancer .
       Basically, the disturbances in Addison"s disease are as follows :
       fa) mineralocorticoid deficiency : lack of aldosterone secretion decrease in
sodium re-absorption loss of sodium ions, chloride ions, and water decrease in
extracellular fluid volume and plasma volume in the untreated patient death usually
occurs 4 days to weeks after complete cessation of mineralocorticoid secretion lack
of aldosterone hyperkalemia and mild acidosis decreasae in cardiac output.
       (b) Glucocorticoid deficiency, loss of cortisol secretion impossibility for the
patient to maintain normal blood glucose concentration between meals; reduction
of protein and fat mobilization from the tissues depression of many other metabolic
functions of the body.
       (c) high susceptabiliy to the deteriorating effects of different types of stress
( even a mild respiratory infection can sometimes cause death ).
       (d) melanin pigmentation of the mucous membranes and skin. The
mechenism : lack of cortisol depression of normal negative feedback to the
hypothalamus and anterior pituitary tremendous rates of ACTH and MSH secretion
increased formation of melanin by melano-cytes.
        Secondary.
        Any disorder of the hypothalamus and pituitary, such as metastatic cancer,
infection, infarction, or irradiation, that reduces the output of ACTH leads to a
syndrome of hypoadrenalism having many similarites to Addison"s desease.
        However, administration of adrenalin in Addisons disease is not particularly
effective, whereas administration of preparations of the cortical part of the
adrenals, especially al-dosterone, produces a favourable effect; adynamia
disappears, the pathologic phenomena in the gastrointestinal tra
				
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