C H A P T E R 3 6
Adrenocortical agents
539
ADRENOCORTICAL AGENTS
There are three types of corticosteroids: androgens
(discussed in Chapter 41), glucocorticoids and mineralo-
corticoids. Not all adrenocortical agents are classified as
only glucocorticoids or mineralocorticoids. Hydrocortis
one, cortisone and prednisone also have glucocorticoid
and some mineralocorticoid activity and affect potas-
sium, sodium and water levels in the body when present
in high levels (Table 36.2). Box 36.2 discusses their use
in different age groups. Figure 36.2 displays the sites of
action of the glucocorticoids and the mineralocorticoids.
G
lucocorticoids
Glucocorticoids
(Table 36.3) are so named because they
stimulate an increase in glucose levels for energy. They
also increase the rate of protein breakdown and decrease
the rate of protein formation from amino acids, another
way of preserving energy. Glucocorticoids also cause
lipogenesis, or the formation and storage of fat in the
body. This stored fat will then be available to be broken
down for energy when needed.
Several glucocorticoids are available for phar-
macological use. They differ mainly by route of
administration and duration of action. Glucocorticoids
include beclomethasone (
Beconase, Qvar
), betameth-
asone (
Celestone
,
Diprosone
and others), budesonide
(
Entocort
,
Pulmicort
,
Rhinocort
,
Symbicort
and others),
cortisone (
Cortate
), dexamethasone (
Dexmethsone
and
others), hydrocortisone (
Sigmacort, Solu-Cortef
,
and
others), methylprednisolone (
Advantan
,
Depo-Medrol
,
Depo-Nisolone
), prednisolone (
Panafcortelone
,
Predsol
,
Redipred
and others), prednisone (
Lodotra
,
Panafcort
,
Sone
) and triamcinolone (
Aristocort
,
Kenacomb
,
Tri-
cortone
and others).
Adrenal
cortex
Anterior pituitary
Exogenous
corticosteroids
No stimulation
to adrenal glands
Gland atrophies
and does not produce
corticosteroids
Adrenocortical
steroids
Inhibitory
Inhibitory
A
B
HPA
CRH
ACTH
Block CRH
and ACTH
release
Hypothalamus
FIGURE 36.1
A.
Normal controls of
adrenal gland. The hypothalamus
releases corticotropin-releasing
hormone (CRH), which causes release
of corticotropin (ACTH) from the
anterior pituitary. ACTH stimulates
the adrenal cortex to produce and
release corticosteroids. Increasing levels
of corticosteroids inhibit the release
of CRH and ACTH.
B.
Exogenous
corticosteroids act to inhibit CRH and
ACTH release; the adrenal cortex is
no longer stimulated and atrophies.
Sudden stopping of steroids results in
a crisis of adrenal hypofunction until
hypothalamic–pituitary axis (HPA)
controls stimulate the adrenal gland
again.
■■
TABLE 36.2 Selected corticosteroids: equivalent strength, glucocorticoid and mineralocorticoid effects
and duration of effects
Drug
Equivalent dose (mg)
Glucocorticoid effects
Mineralocorticoid effects
Duration of effects (hours)
Short-acting corticosteroids
cortisone
25
+
++++
8–12
hydrocortisone
20
+
++++
8–12
Intermediate-acting corticosteroids
prednisone
5
++++
++
18–36
prednisolone
5
++++
++
18–36
triamcinolone
4
+++++
—
18–36
methylprednisolone
4
+++++
—
18–36
Long-acting corticosteroids
dexamethasone
0.75
+++++++++
—
36–54
betamethasone
0.75
+++++++++
—
35–54
