Adrenal gland

6/6/2013

The Adrenals
Mammals have an adrenal gland above each
kidney.
Adrenal medulla is the inner core which
produces adrenaline (epinephrine) and
norepinephrine.
Adrenal cortex is the outer shell that produces
the steroid hormones cortisol and aldosterone.

Adrenal Medulla
The adrenal medulla releases adrenalin
(epinephrine) and norepinephrine in times of
stress.
Identical to the effects of the sympathetic nervous system,
but longer lasting.
Accelerated heartbeat, increased blood pressure, higher levels of
blood sugar and increased blood flow to heart and lungs.

Catecholamine Degradation:
All catecholamines are rapidly eliminated from
targetcells and the circulation by three mechanisms:
1. Reuptake into secretory vesicles
2. Uptake in nonneuronal cells (mostly liver)
3. Degradation

Adrenal Cortex
The adrenal cortex produces the
steroid hormone cortisol
(hydrocortisone).
Reduces inflammation.
Synthetic derivatives such as prednisone are
used as anti-inflammatory agents.

Stimulates carbohydrate metabolism.

Adrenal Cortex
The adrenal cortex also produces
aldosterone.
Aldosterone acts in the kidney to
promote the uptake of sodium &
other salts from the urine.
These salts are important in nerve
conduction.
With ACTH, aldosterone production is
also controlled by angiotensin11

Aldosterone and PTH are the

only two hormones essential for

adrenal cortical disorders

Adrenal gland:
Upper pole of each kidney
Adrenal Cortex: secretes three major
steroid hormones ( synthesized primarily
frm cholesterol)
Glucocorticoids (Cortisol)
Mineralocorticoids (aldosterone)
Adrenal androgen

glucocorticoids
Cortisol is main glucocorticoids
Secreted at rate of 25mg/day
Transport binding to corticosteroid-binding
globulin (CBG) 5 ~ 10% free (active)

Major effect:
CHO , protein and lipid metabolism
Lipolysis and release of FFAs
Have anti-inflammatory effect and suppress
immune system (used to treat inflammations)

 cortisol
Controlled by HPA axis
Hypothalamus CRH (corticotrpin
releasing hormone) and in circadian
rhythm (max 2-4am)
Anterior Pituitary ACTH
(adrenocortictropin hormone)
Adrenal cortex cortisol
Peak @ 8am; declines throughout day

 Mineralocorticoids:
Regulate salt homeostasis
Aldosterone
Other: deoxycorticosterone (DOC) , 18
hydroxy DOC, corticosterone and
cortisol

 Adrenal androgens:
Androgens, progesterone , estrogen

Adrenal insufficiency
Primary adrenal
insufficiency:
Addisons disease:
Progressive destruction or
dysfunction of adrenal
cortex
Most commonly is of an
autoimmune etiology,
resulting from chronic
destruction of the adrenal
cortex
All adrenal steroids are
deficient

Primary Adrenal Insufficiency

Several Other Mechanisms Exist:

Bilateral adrenal hemorrhage

Infection: Tuberculosis, CMV, Histoplasmosis
Metastatic Disease
Deposition Diseases: Hemochromatosis, Amyloidosis,
Sarcoidosis
Drug Induced: Ketoconazole, Etomidate, Rifampin,
Anticonvulsants
Congenital Adrenal Hyperplasias

Symptoms of Addisons
disease

Fatique
Weakness
GI disturbance
Weight loss
Postprandial hypoglycemia
Dehydration
Hypotension
Hyponatremia
Hyperkalemia
Acidosis
Increased skin pigmentation can be seen with primary adrenal
insufficiency secondary to melanocyte stimulating activity
associated with ACTH

Addisons disease
Diagnosis
Measurement of basal ACTH & cortisol
ACTH > 150pg/ml with serum cortisol
<10ug/dl is diagnostic

ACTH stimulation test (recommended):

Cortisol level will not increase over baseline
concentration.

Secondary adrenal insufficiency

(lack of ACTH)
Secondary hypocortisolism
Symptoms as primary except
absence of skin pigmentation
Caused by :
Pituitary disease
Long term glucocorticoid treatment

Secondary adrenal insufficiency

(lack of ACTH)
Laboratory assessment:
Baseline:
Cortisol: low
Urine free cortisol: low
ACTH: Low

ACTH stimulation test:

Cortisol response to stimulation

Primary adrenal
hyperfunction
Known as Cushings syndrome
High cortisol and low ACTH
Caused by :
Adrenal tumor
Nodular adrenal hyperplasia

Primary adrenal
hyperfunction
Symptoms:
Physical appearance due to mobilization
of fat stores: truncal obesity, moon face,
Muscle weakness
Hypertension
Hyperglycemia
Hirsutism
Menstrual disturbance
Psychiatric disturbance

Primary adrenal
hyperfunction
Laboratory assessment:
Baseline levels :
cortisol high
Free urine cortisol : high
ACTH: Low

Lack of diurnal variation

High dose dexamethasone suppression
test:
No suppression of cortisol

Reproductive system
hormones
Reproductive endocrinology:
Hypothalamus pituitary gonadal axis

Gonadotropin release hormone (GnRH)

LH
FSH
Sex steriod hormones
Ovaries , Tests and adrenal glands

Hypothalamus pituitary gonadal axis