Adrenal Gland

Dr.Sabri.S.Eltayeb

2 adrenal glands on the top of each

kidney.

Each gland consists of:

1- Adrenal medulla

Related to sympathetic nervous system

Secretes epinephrine and norepinephrine

2- Adrenal cortex

Secretes Corticosteroids

All from cholesterol

Layers of the
Adrenal Cortex

Divided into three layers

1.

Zona Glomerulosa
(underneath the capsule)

2.

Zona Fasciculata (middle

and widest layer)

3.

Zona Reticularis
(deepest layer)

Different hormones are

produced in each layer.

Layers of the Adrenal

Cortex

1.

Zona Glomerulosa

15% of the adrenal cortex

Secretes Mineralocorticoids like

Aldesterone

2.

Zona Fasciculata

75% of the adrenal cortex

Secretes Glucocorticoids like cortisol,

corticosterone,
Controlled mainly via ACTH (hypothalamicpituitary axis)

3.

Controlled by angiotensin II, and K+

Zona Reticularis

CORTEX

ZONA
GLOMERULOSA

MINERALOCORTICOIDS
(ALDOSTERONE)

ZONA
FASICULATA

GLUCOCORTICOIDS
(CORTISOL)

ZONA
RETICULARIS

ANDROGENS

MEDULLA

CATECHOLAMINES
(EPINEPHRINE AND
NOREPINEPHRINE)

Actions of Adrenocortical
Hormones

Major Corticosteroids hormones:

1- Mineralocorticoids like
Aldosterone

affect extracellualar electrolytes Na+

& K+

2- Glucocorticoids like cortisol

important effects on carbohydrate

metabolism

3- Sex hormones or androgen

secreted in small amounts in both

Adrenocortical hormones

Adrenal steroid hormones

degraded in the liver conjugated with
glucuronic acid
excreted in bile & feces

cortisol
90-95% is bound to cortisol-binding
globulin (transcortin)
life of 60- 90 minutes

Aldosterone
60% is protein bound
life of 20 minutes

MECHANISM OF ACTION

Bind to DNA

Receptor hormone complex

mRNA
mRNA
Protein

EFFECTS

Glucocorticoids

ACTION

EFFECTS ON METABOLISM

Catabolic proteolytic action:

Mobilization of amino acids from
extrahepatic tissues: These serve as
substrates for gluconeogenesis

Gluconeogenesis, Glycogenolysis and

Anti Insulin Action Inhibition of glucose

FAT metabolism:

Mobilize fat from adipose tissue and

decrease hepatic lipogensis the
plasma level of free fatty acid which
good source of energy

Hormone also affect the distribution

of fat in the body.

Permissive action:

Presence of glucocorticoids is
important for some other hormone
to exert their effects, specially for
catecholamine's functions

Weak Mineralocorticoid effect at

Effects on CNS:
-increase excitability of neural
tissues (mood changes)

Effects on Bone:
-inhibits bone formation

Effects on Blood and Lymphoid

Tissue:

RBC and total hemoglobin,

platelet, monocyte and neutrophil

the number of eosinophils,

basophile and lymphocytes

Resistance to stress:

Stress lead to increase secretion of

ACTH leading to rise in the plasma
glucocorticoid level

This is essential for survival in these

condition by unknown mechanism

The role of cortisol in stress may be

through provide extra-supply of

Effects on inflammation and allergy

Glucocorticoids suppress the

inflammatory reaction by formation of
IL and inhibition release of lysosomal
enzyme.

Suppress all manifestation of reaction

by prevent release of histamine

Other effects of
Glucocorticoids
Glucocorticoids

have multiple effects

on FETAL DEVELOPMENT (maturation

of the lung and production of the
surfactant necessary for extra
uterine lung function)

DIURNAL VARIATION

Cortisol Secretion &

Feedback Loops

Trauma
Pain

Physical
Stress

Mental
stress

Emotion

CRH

ACTH

+
CORTISOL

LIVER
FATS
MUSCLE
BLOOD CELLS

FEEDBACK
CONTROL
OF CORTSOL
SECRETION

Mineralocorticoid

Include mainly aldosterone and

deoxycorticosterone (DOC) both
are secreted only from zona
glomerulosa in equal amount but
DOC has only 3% of aldosterone
activity

Action

Kidney are the major site of action of

hormone which act mainly in DCT &
CD Na+ reabsorption in exchange
with secretion of either K + or H +

Mineralocorticoid Na+ absorption

from saliva and sweet gland as well as
from GIT mucosa specially the colon

MECHANISM OF ACTION

Bind to DNA

mRNA
mRNA
Protein

ENaCs
Na K Adenosine Triphosphatase

Principal cells & aldosterone

control
1.

Angiotensin II:

Rennin-Angiotensin-Aldosterone System
Fall in Na+, extracellular fluid volume, arterial blood pressure
Adrenal
Cortex

Juxtaglomerular
Apparatus

Liver

Lungs

Renin
+

Angiotensinogen

Helps
Correct

Angiotensin I

Converting
Enzyme

Angiotensin II

Aldosterone

Increased
Sodium
Reabsorption

2. ACTH
3. Na+ and K + serum level
4. Other factors:
a.

ANP

b.

Circadian rhythm

Abnorma
lities

Adrenocortical
Insufficiency

1.

2.
3.

Failure of adrenal cortex to

produce adrenocortical hormones
Primiary Adrenal Insufficiency
(Addisons disease)
autoimmune-mediated destruction
of the adrenal glands (80%)
mainly due to tuberculosis (19%)
chronic fungal infection( rare)

Adrenocortical
Insufficiency

Secondary Adrenal
Insufficiency:

1.

Inadequate secretion of ACTH by

the pituitary gland

2.

may arise due to the prolonged or

improper use of glucocorticoid
hormones

Addisons Disease
Failure of adrenal cortex to produce
adrenocortical hormones
1/ Mineralocorticoid deficiency or Lack of
aldosterone
1.

Hyperkalemia, mild acidosis

2.

Decrease renal Na+ absorption,

Hyponatremia,

3.

Decrease extracellular fluid volume

Addisons Disease cont

2/ Glucocorticoid deficiency

decrease cortisol glucose imbalance

Muscle weakness due to lack of

mobilization of energy substrate (FFAs)

Decrease resistance to stress (infection)

3/ Melanin pigmentation

Mucus membranes and skin Lips and

nipples

Disorders of the Adrenal

Gland

Cushings

Syndrome

a disease caused by excess of cortisol

production or by excessive use of
cortisol or other similar steroid
(Glucocorticoids) hormones

Cushings
Syndrome

Adrenal cortex tumors that make

cortisol

Secondary to an excess of ACTH:

Pituitary tumor producing too much

ACTH, stimulating the adrenals to
grow (hyperplasia) and to produce
too much cortisol

Characteristics

Increase protein catabolism: lead to

Poorly developed muscles result

muscle weakness

Thin skin and subcutaneous tissues,

wound heal poorly

Bone resorption lead to osteoporosis

Central obesity:

Body fat redistributed, fat collect

mainly in face, abdominal wall and
upper part of the back (producing
buffalo hump)

Thin and weak limb

As thin abdominal skin is stretched,

the abdominal skin tissue rupture

Hypertension and hypervolemia due

to Na+ and water retention

Impaired glucose tolerance:

gluconeogenesis produced by
Glucocorticoids lead to hyperglycemia
with peripheral utilization of
glucose

Produce type of secondary diabetes

Nervous symptoms:

Accelerate the basic EEG rhythm

and mental abnormalities (e.g.
irritability, anxiety, depression and
emotional disturbances) which more
severe than those occurring in
Addison's disease

Blood changes:

Mild polycythemia and lymphopenia

Increase susceptibility to infections

as result of depression of immune
system

Adrenocortical
Insufficiency

Cushings
syndrome

CUSHINGS SYNDROME

Moon face

Actions of glucocorticoids

Central
Obesity

:HYPERALDOSTERONISM
Excessive levels of aldosterone cause sodium
retention and potassium excretion, with
resultant hypertension and hypokalemia.
1. primary:
Indicates a primary, autonomous
overproduction of aldosterone, with resultant
suppression of the renin-angiotensin system
and decreased plasma renin activity.

: CAUSES
1.Aldosterone-producing
adrenocortical neoplasm, usually an
adenoma (Conns syndrome).
2.Primary adrenocortical
hyperplasia.
3. renal ischemia ( secondary to
hyper secretion of rennin )

:MANIFESTATIONS
1. Hypertension
2. Hypokalemia.
3. Serum renin levels , are low ( in
primary ) high in secondary .
4.Conns syndrome occurs most frequently
in middle adult life and is more common in
females than in males (2 : 1).

THANKS