Endocrine systems
In higher animals systemic homeostasis is the
responsibility of the endocrine glands. They are the
regulators and their hormones are the effector
signals. In contrast to the simplicity of the control
model shown in Figure 7.6, hormone systems may
produce multiple hormones, regulate multiple target
processes, and in turn be regulated by other tissues.
Additional complexity is found in the interdependent
networks of endocrine regulation. Consider, for
example, that the pituitary and the adrenal glands
produce hormones that act to counterbalance the
regulatory effects of insulin on plasma glucose. And
the pancreatic islets themselves are the source of the
most important counterregulatory hormone, gluca-
gon. Still, the physiology of most endocrine glands
is well represented by the comparatively simple
model shown in Figure 7.8. The control tissue for
many endocrine organs is the pituitary and for the
pituitary it is the hypothalamus. In the first case, the
control signal is the trophic hormone; in the second,
the control signal is a hormone-releasing factor or a
neurotransmitter.
Primary endocrine dysfunction resides in the
gland itself. Primary hypofunction is usually due to
a reduced number of functional cells but may also
arise from reduced functional capacity of the cells of
an intact organ as in the heritable disorders of
hormone synthesis or secretion. Primary hyperfunc-
tion usually results from neoplasia of the gland with
at least some degree of autonomy of hormone
production present in the neoplastic cells. Secon-
dary endocrine dysfunction occurs as a result of
either abnormal control tissue function or a disorder
in the effector tissue response to hormone.
Primary endocrine dysfunction produces disease
in which the clinical picture is consistent with the
gland's functional state, but so does secondary
endocrine dysfunction due to disordered control
tissue. Consequently, the level of the control signal,
i.e., the plasma concentration of the trophic
hormone, must be measured to separate these two
possibilities. In contrast, when secondary endocrine
dysfunction is attributable to an abnormal effector
tissue, the clinical findings referable to that effector
tissue are inconsistent with the endocrine functional
state. The diagnosis of this form of secondary
dysfunction is thereby readily made. Consistent
findings can be expected, however, for other effec-
tor tissues that are not abnormal.
Evaluation of endocrine function
The laboratory evaluation of endocrine gland
function proceeds in two steps. First, the functional
state of the gland, defined as the rate of secretion of
its hormone product, is assessed using function
markers, the most important of which is the steady-
state plasma concentration of the hormone itself.
Second, trophic hormones or feedback markers are
measured to compare the gland's functional state to
the level of physiologic stimulation or endocrine
function. Such an analysis makes possible the
distinction of primary from secondary dysfunction.
Because hormone clearance rates remain nearly
constant in primary endocrine disease, the secretory
rate of an endocrine gland, and hence its functional
state, is directly proportional to the plasma concen-
tration of the hormone,
synthetic rate =
clearance rate x plasma hormone concentration
where clearance rate is a constant. As will be
discussed later in this chapter, for hormones that
experience significant plasma protein binding, i.e.,
steroid and thyroid hormones, the concentration of
bioactive hormone must be measured rather than the
concentration of total hormone. Similarly, it is the
clearance rate of the bioactive hormone that remains
constant in endocrine disease, not the clearance rate
of total hormone. When circulating hormone
Organ Function
7-8
endocrine
gland
effector
tissue
target
process
feedback signals
effect
hormone
control
tissue
releasing
factor
trophic
hormone
accessory influences
Figure 7.8
A simple model of endocrine homeostasis.
