Page 280 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Deficiency of Adrenocorticoid Hormones: Addison’s Disease
For the effects of the adrenocorticoid hor- tex. If both adrenals are absent, ACTH can
mones, see p. 268. even cause the ectopic formation of adreno-
Glucocorticoid deficiency frequently leads corticoid hormones, but this is usually inade-
to hypoglycemia as a result of disinhibited gly- quate. In secondary adrenocorticoid insuffi-
colysis and reduced gluconeogenesis (→ A1). ciency skin pigmentation is decreased because
This is especially marked in secondary deficien- of a lack of α-MSH and ACTH.
cy of adrenocorticoid hormones due to pitui- Mineralocorticoid deficiency leads to renal
2+
+
tary insufficiency, because it is associated salt loss and renal retention of K , Mg , and
with decreased somatotropin secretion, the H + (→ A5). Na + reabsorption in the sweat
hyperglycemic effect of which will be absent glands and gut is also impaired. This results in
(→ p. 262). The hypoglycemia activates the salt deficiency, hypotonic dehydration, hypo-
sympathetic nervous system and inhibits the volemia, drop in blood pressure, and in the in-
release of insulin, and thus also of its influence crease of intracellular volume (→ p.122ff.).
on lipolysis and protein breakdown. The re- This can lead to a decrease in renal perfusion
duced lipolytic and proteolytic action of corti- and glomerular filtration rate, causing an in-
sol is more than compensated by a decreased crease of plasma creatinine concentration.
Hormones polysis and protein breakdown are thus stimu- release of renin and angiotensin I–II will be
Also, due to the impaired renal perfusion the
insulin and an increased epinephrine effect. Li-
raised. As angiotensin II stimulates ADH re-
lated. Further effects of the raised epinephrine
the release of angiotensin II contributes to hy-
The reduced sensitivity to catecholamines of
9 release are tachycardia and sweating (→ A2). lease and ADH leads to renal water retention
2+
+
the heart and blood vessels leads to a fall in poosmolarity. The retention of K , Mg , and
+
blood pressure despite the release of epineph- H leads to reduced neuromuscular excitabil-
rine. Due to the diminished secretion of hydro- ity as well as abnormalities of action potential
chloric acid, pathogens that have been swal- formation and conduction in the heart due to
lowed will be less effectively killed in the hyperkalemia, hypermagnesemia, and acidosis
stomach and more commonly cause gastroin- (→ A8 and p.124ff.). In combined mineralo-
testinal infections (→ A6). Diarrhea and vom- corticoid and glucocorticoid deficiency, the in-
iting occur with corresponding loss of water creased fat and protein breakdown and loss of
and electrolytes. The lack in glucocorticoid ef- fluid cause weight loss, and arterial hypoten-
fect on blood-forming cells results in anemia, sion and anemia reduce physical fitness.
neutropenia, eosinophilia, and lymphocytosis A lack of androgens manifests itself espe-
(→ A4). Other symptoms are fatigue and cially in sparse pubic hair as well as muscle
weakness. Furthermore, depression is caused wasting and loss of libido (→ A7). However,
by the lack of glucocorticoid action on the lack of adrenal androgens is of no consequence
brain. However, while cortisol deficiency per- in men, as long as testosterone production in
sists, sensitivity of the target cells is raised the testes is normal.
and they thus delay the onset of symptoms. Acute worsening of the symptoms leads to
In primary adrenocorticoid insufficiency Addisonian crisis with extreme weakness, fall
(Addison’s disease) the diminished negative in blood pressure, tachycardia, diarrhea, hypo-
feedback from cortisol leads to a massive rise glycemia, hyponatremia, hyperkalemia, and
in the synthesis of pro-opiomelanocortin oliguria. It is frequently the consequence of an
(POMC), the precursor of ACTH. This increases infection that normally, but not in patients
formation not only of ACTH, but also of α-me- with Addison’s disease, leads to an increase in
lanotropin (α-MSH or melanocortin). α-MSH cortisol release.
as well as ACTH itself cause brown discolor-
ation of the skin (→ A3), because of which Ad-
dison’s disease has been called “bronze dis-
270 ease”. If one adrenal cortex is absent, ACTH
causes hypertrophy of the intact adrenal cor-
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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