Page 222 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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! In the adrenogenital syndrome (→ B3a) cor- The consequences of hypertension (→ E)
tisol formation in the adrenal cortex is most importantly result from atherosclerotic
blocked, and thus adrenocorticotropic hor- damage in arterial vessels (→ p. 236ff.), which
mone (ACTH) release is not inhibited. As a re- can be observed well by means of fundoscopy.
sult excessive amounts of mineralocorticoid- Because of the resulting increase in flow resis-
active precursors of cortisol and aldosterone, tance, every form of hypertension ultimately
for example, 11-deoxycorticosterone (DOC), creates a vicious circle. Vascular damage final-
are produced and released (→ p. 264ff.). This ly leads to ischemia of various organs and tis-
+
leads to Na retention, hence to an increase in sues (myocardium, brain, kidneys, mesenteric
extracellular volume (ECV) and thus to cardiac vessels, legs), renal ischemia accelerating the
output H. vicious circle. Damage to the vascular walls to-
! Primary hyperaldosteronism (Conn’s syn- gether with hypertension can, for example,
drome; → B3b). In this condition an adrenal lead to brain hemorrhage (stroke) and in the
cortical tumor releases large amounts of aldo-
large arteries (e.g., aorta) to the formation of
Heart and Circulation Na retention in the kidney leads to cardiac (→ p. 238). Life expectancy is therefore mark-
aneurysms
rupture
and
their
ultimately
sterone without regulation. Also in this case
+
edly reduced. American life insurance compa-
output H.
! Cushing’s syndrome (→ B3 c). Inadequate
nies, monitoring the fate of 1 million men
whose blood pressure had been normal, slight-
ACTH release (neurogenic cause; hypophyseal
tumor) or an autonomous adrenal cortical tu-
ly, or moderately elevated when aged 45 years
had normal blood pressure (ca. 132/85 mmHg)
tration, resulting in a raised catecholamine ef-
nearly 80% were still alive 20 years later, while
fect (cardiac output increased), and the miner-
7 mor increase plasma glucocorticoid concen- (→ D), found that of those men who definitely
alocorticoid action of high levels of cortisol of those with initially raised blood pressure
+
(Na retention) lead to H. (→ p. 264ff.). A simi- (ca. 162/100 mmHg) fewer than 50% had sur-
lar effect occurs from eating large amounts of vived.
liquorice, because the glycyrrhizinic acid con-
tained in it inhibits renal 11β-hydroxysteroid
dehydrogenase. As a result, cortisol in the kid-
neys is not metabolized to cortison but rather
has its full effect on the renal mineralcorticoid
receptor.
! Pheochromocytoma (→ B3 d) is an adreno-
medullary tumor that produces catechol-
amines, resulting in uncontrolled high epi-
nephrine and norepinephrine levels and thus
both cardiac output hypertension and resis-
tance hypertension.
+
! Contraceptive pills can cause Na retention
and thus cardiac output hypertension.
Neurogenic hypertension. Encephalitis, ce-
rebral edemas or hemorrhage, and brain tu-
mors may lead to a massive rise in blood pres-
sure via central nervous stimulation of the
sympathetic nervous system. An abnormally
high central stimulation of cardiac action as
part of the hyperkinetic heart syndrome may
also cause H.
212
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Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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