Page 278 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Excess Adrenocorticoid Hormones: Cushing’s Disease
Glucocorticoids (especially cortisol) stimulate density lipoproteins (VLDL) which are passed
gluconeogenesis in the liver and inhibit glucose into the blood (→ A3). In addition, the liver
uptake in peripheral cells. They also stimulate forms ketone bodies from fatty acids. A redis-
lipolysis, the breakdown of proteins in the pe- tribution of fat tissue occurs due to differing
riphery, and the formation of plasma proteins sensitivities of peripheral fatty tissue for glu-
(e.g., angiotensinogen) in the liver. They pro- cocorticoids and insulin. This results in cen-
mote the formation of erythrocytes, thrombo- tripetal fat stores, rounded or moon faces and
cytes, and neutrophil granulocytes (neutro- fat deposits in the neck (“buffalo” hump),
phils). At the same time they reduce the num- while the limbs are noticeably thin. Peripheral
ber of eosinophil granulocytes (eosinophils) protein breakdown (→ A5) leads to muscle
and basophil granulocytes (basophils), lym- wasting, osteoporosis (loss of bone matrix),
phocytes, and monocytes. They also, via the striae (breakdown of subcutaneous connective
formation of the proteins lipocortin and vaso- tissue), and purpura (increased vascular fragil-
cortin, suppress the release of histamine, inter- ity). Because repair is impeded, wound healing
leukins, and lymphokines. By inhibiting phos- is delayed. The effect on bone is aggravated by
pholipase A 2 they suppress the formation of CaHPO 4 deficiency and in children results in
Hormones ish antibody formation and thus act as immu- polycythemia (→ A1), thrombocytosis, and
prostaglandins and leukotrienes. They dimin-
delayed growth. The effects on blood lead to
raised coagulability (→ A6). Weakened im-
nosuppressives. Glucocorticoids suppress in-
Sensitization of the circulation to catechol-
proliferation, but at the same time impede col-
9 flammation by inhibiting connective tissue mune defenses encourage infections (→ A4).
lagen synthesis and repair. They stimulate the amines causes, among other things, an in-
secretion of acids and pepsin in the stomach crease in cardiac contractility as well as pe-
and slow down mucus production. In addition, ripheral vasoconstriction, and thus leads to hy-
they decrease the plasma levels of calcium and pertension (→ A7), which, together with hy-
phosphate, in part by inhibiting calcitriol for- perlipidemia and raised coagulability of blood,
mation. They also sensitize blood vessels and promotes the development of atherosclerosis,
the heart to catecholamines, partly by inhibit- thrombosis, and vascular occlusions (→ A6).
ing prostaglandin synthesis, stimulate the re- Due to stimulation of hydrochloric acid and
lease of norepinephrine, and increase the ex- pepsin secretion and the inhibition of mucus
citability of the nervous system. secretion in the stomach, gastric and/or duo-
Mineralocorticoids (especially aldosterone) denal (peptic) ulcers develop (→ A8). The ef-
+
further renal retention of Na and water. They fects on the nervous system can trigger an en-
thus facilitate a rise in blood pressure. They docrine psychogenic syndrome.
2+
+
also stimulate renal elimination of K , Mg , An increased mineralcorticoid effect causes
+
and H and simultaneously the intracellular hypervolemia, which in turn leads to hyperten-
uptake of potassium. However, at high plasma sion; it also causes hypokalemia, hypomagne-
levels cortisol also exerts a significant mineral- semia, and alkalosis, which in turn lead to in-
ocorticoid effect, even though it is largely in- creased neuromuscular excitability (→ A10).
activated in the target cells of the mineralocor- The effects are, among others, abnormal action
ticoids (→ p. 266). Dehydro-epiandrosterone potential formation and conduction in the
(DHEA), the precursor of the steroid sex hor- heart.
mones, is also formed in the adrenals, in addi- An excess of androgens (→ A9) can lead to
tion to mineralocorticoids and glucocorticoids. masculinization and amenorrhea (virilism) in
The metabolic effects of glucocorticoid ex- women, and to an accelerated onset of sexual
cess favor the development of diabetes melli- characteristics in male children (incomplete
tus (→ p. 286ff.), i.e., steroid diabetes, in which precocious puberty; → p. 272).
the release of insulin is increased (→ A2). The
268 free fatty acids formed by stimulated lipolysis
are utilized in the liver to generate very low
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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