Page 266 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

9 Hormones F. Lang

General Pathophysiology of Hormones
Hormones serve to regulate and to control or- their effect; on the other hand, they escape
gan functions. Their release is dependent on being broken down or being excreted by the
stimulation (or inhibition) through specific kidney.
factors. Hormones act upon hormone-produc- Some hormones must first be converted
ing cells themselves (autocrine), they influ- into their effective form at the site of their ac-
ence neighboring cells (paracrine), or they tion (→ A8). However, if this conversion is not
reach target cells in other organs via the blood possible, for example, due to enzyme defects,
(endocrine). In a stricter sense, hormones the hormone will have no effect. Hormonal ac-
achieve their effects predominantly via an en- tion may also not occur because the target or-
docrine path. For endocrine action to be effec- gan is unresponsive (e.g., due to defective hor-
tive the hormones must not be inactivated be- mone receptors or faulty intracellular trans-
fore reaching their target cells. Some hor- mission) or functional incapacity of the target
mones require activation (see below). The cells or organs (→ A9).
transition from endocrine hormones to para- Causes of increased hormone effects (violet
crine mediators and transmitters is a fluid one. arrows) include, first of all, increased hormonal
At the target cells the hormones bind to re- release. This may be due to an excessive influ-
ceptors and exert their effects via various ence of individual stimuli (→ A1), increased
mechanisms of cellular signal transduction. It sensitivity (→ A4), or too large a number of
is usually through a reduction of stimulating hormone-producing cells (hyperplasia, adeno-
factors that these effects lead to a reduced re- ma; → A2). Hormonal excess can also be
lease of the particular hormone, i.e., there is a caused by the production of hormones in un-
regulating cycle with negative feedback differentiated tumor cells outside of hormonal
(→ A6). In a few cases there is positive feed- glands (ectopic hormonal production; → A3).
back (of limited duration), i.e., the hormones The small-cell bronchial carcinoma is particu-
cause an increased activity of stimuli and thus larly frequently active endocrinally.
promote their own release. The term control- Raised hormonal action is also to be expect-
ing (→ A1) is used when hormone release is ed if a hormone is broken down or inactivated
influenced independently of hormonal effects. too slowly (→ A7; e.g., in dysfunction of the in-
Several independent controling and regulating activating organ [kidney or liver]). The break-
stimuli can act on the hormone-producing ing down can be delayed by binding to plasma
glands. proteins, but the protein-bound proportion
A reduced hormone effect (blue arrows) would not be exerting any action either (see
can be due to abnormal hormone synthesis and above).
storage. Other causes can be abnormalities of Finally, hormonal effects can be increased
transport within the synthesizing cells or ab- by hypersensitivity of the target organ (too
normalities of release (→ A5). Hormone defi- many hormone receptors or ones that are too
ciency may also arise when the hormonal sensitive), by increased intracellular transmis-
glands are not stimulated sufficiently to meet sion, or hyperfunction of the hormone-sensi-
the needs of the organism (→ A1), when the tive cells (→ A9).
hormone-producing cells do not react sensi- The clinical features, i.e., the sum of the
tively enough to the stimuli (→ A4), or when pathophysiological changes in the organism,
there are not enough hormone-producing cells are the result of reduced or increased hor-
(hypoplasia, aplasia; → A2). mone-specific effects.
Other possible causes are too rapid inactiva-
tion or accelerated breakdown of hormones. In
the case of hormones that are bound to plasma
proteins (→ A7) the duration of action de-
256 pends on the proportion of bound hormones.
In their bound form hormones cannot exert
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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