THE ADRENAL GLAND

Anatomy, Embryology & Physiology

Sreeja Biswas
 INTRODUCTION
ADRENALS :
Two small yellow flattened bodies at the back of
abdomen, retroperitoneal
Above & in front of upper end of each kidneys
Size varies from 3-5 cm length
4-6 mm thickness
less in width
Average weight is about 1.5-2.5 gms each
Most highly perfused of all organs
(blood flow 2000 ml/kg/min)
 DEVELOPMENT
ADRENAL CORTEX :
Celomic mesoderm(near cephalic end of mesonephros)
Recognizable first at about 4th week of gestation(series of
buds at root of mesentery suprarenal ridge)

ADRENAL MEDULLA :
Sympatho-chromaffin tissue(ectoderm)
Recognizable first at about 5th to 6th week of gestation
SURGICAL RELEVANCE :
Extra-adrenal sites for cortex & medulla - usually along the
paths of migration during embryogenesis
 ANATOMY
RIGHT SUPRARENAL GLAND :
Triangular in shape
2 surfaces - anterior & posterior
Anterior surface - forward and laterally
Inferior Vena Cava – medially
Right lobe of liver – laterally
Posterior surface – upper part-diaphragm
lower part-right kidney
Base – downward
Hilum – below apex, suprarenal vein emerges from anterior
border
 ANATOMY (cont.)
LEFT SUPRARENAL GLAND :
Larger, crescentric – medial & lateral borders
anterior & posterior surfaces
Medial border – convex
Lateral border – concave(upper part of left kidney)
Anterior surface –
upper part-peritoneum of omental bursa
lower part-tail of pancreas,lienal artery
Posterior surface –
lateral area-left kidney
medial area-left crus of diaphragm
Hilum – lower end of anterior surface
 ANATOMY cont.
The surfaces of the suprarenal glands are surrounded
by areolar tissue containing much fat & closely
invested by a thin fibrous capsule, which is difficult to
remove on account of the numerous fibrous processes
& vessels entering the organ through the furrows on its
anterior surface and base
 HISTOLOGY
EXTERNAL CORTEX
INTERNAL MEDULLA
 CORTEX – 3parts
(outside inwards)
Zona Glomerulosa
Zona Fasciculata
Zona Reticularis

 MEDULLA
 HISTOLOGY (cont.)
CORTEX :
1. zona glomerulosa situated just beneath the capsule,
rounded cells - very granular & stain deeply
2. zona fasciculata composed of columns of cells
arranged in a radial manner – intracellular finer
granules & lipoid materials
3. zona reticularis composed of irregularly arranged
cylindrical masses of cells – intracellular pigment
granules which makes this zone darker than the rest of
the cortex
 HISTOLOGY (cont.)
MEDULLA :
Extremely vascular ,large irregular
polyhedral chromaphil cells – finely
granular cytoplasm
Large anastomosing venous sinusoids
bathing the medullary cells directly in
blood at some places where the
endothelium is deficient.
Loose network of supporting non-striped muscle fibers –
richly supplied with non-medullated nerve fibers & occasional
sympathetic ganglia
VASCULATURE, LYMPHATICS & NERVES
ARTERIAL :
1. superior adrenal – branch of inferior phrenic
2. middle adrenal – branch of aorta
3. inferior adrenal – branch of renal artery
VASCULATURE, LYMPHATICS & NERVES
(cont.)
VENOUS : arise from medullary venous plexus
solitary drainage
emerge from the hilum
1. right adrenal (0.5cm)– directly to inferior vena cava
2. left adrenal (2.0cm) – to left renal vein

In 20% of cases right adrenal vein drains to accessory

right hepatic vein or at the confluence of a vein
VASCULATURE, LYMPHATICS & NERVES
(cont.)
LYMPHATICS :
to the lumbar glands

NERVES :
from celiac & renal plexus
enters through the lower & medial part of
the capsule 
ends in the medulla
 PHYSIOLOGY
ADRENAL MEDULLA :
Secretes epinephrine(E), nor-epinephrine(NE)
In humans,80% of output is epinephrine
Effects are same as direct symphathetic nervous stimulation
Synthesis of catacholamines begins with tyrosine, which is
taken up by the chromaffin cells in the medulla & converted
to NE/E .
NE/E are stored in electron-dense granules along with ATP &
neuropeptides.
Release is stimulated by ACh from pregangloinic sympathetic
fibers innervating the medulla and Stress factors
 PHYSIOLOGY(cont.)
EFFECTS :
1. increase rate & force of contraction of the heart
2. constriction of the blood vessels
3. dilation of bronchioles
4. stimulation of lipolysis in fat cells
5. increased metabolic rate
6. dilation of the pupils
7. inhibition of certain non-essential processes
eg. gi secretion and motor activities
 PHYSIOLOGY(cont.)

ADRENAL CORTEX :
Adrenal steroid
biosynthesis pathway-
1. aldosterone
2. cortisol
3. androgens
 GLUCOCORTICOIDS
CORTISOL : major glucocorticoid
Control of cortisol secretion
 GLUCOCORTICOIDS(cont.)
CORTISOL :
Mechanism of action –
1. cortisol binds to cytoplasmic receptor
2. hormone-receptor complex is transferred to the
nucleus
3. complex binds to nuclear DNA response element

Cortisol circulates in blood bound to transcortin, only

10% of the hormone is in free form.
 GLUCOCORTICOIDS(cont.)
METABOLIC EFFECTS OF CORTISOL :
1. stimulation of gluconeogenesis, particularly in liver
2. mobilization of amino acids from extrahepatic
tissues
3. inhibition of glucose uptake in muscles and adipose
tissue
4. stimulation of fat breakdown in adipose tissue
GLUCOCORTICOIDS(contd.)
IMMUNOSURPPRESSIVE ACTIONS:
Reduce lymphocyte & eosinophil counts
Increase neutrophil count
Suppress histamine release
Promote lymphocyte apoptosis
Reduce prostaglandin synthesis
 MINERALOCORTICOIDS
ALDOSTERONE : major mineralocorticoid
Control of aldosterone secretion –
1. K+ concentration in extracellular fluid
(even small increase in K+ strongly stimulates)
2. angiostensin II level in blood
(the Renin-Angiotensin-Aldosterone-Axis)
3. others -
ACTH (short-term stimulation)
Na+ deficiency stimulates
Atrial natriuretic peptide(ANP), high Na+ and low
K+ concentration supress aldosterone secretion
 MINERALOCORTICOIDS(cont.)
ALDOSTERONE :
Mechanism of action –
1. renal resorption sodium & water
2. renal excretion of potassium
 MINERALOCORTICOIDS(cont.)
REMOVAL OF THE ADRENALS LEADS TO DEATH
Effects of lack of ALDOSTERONE activity –
‘salt and water wasting & K+/H+ retention’
-hyponatremia
-hypovolemia
-hyperkalemia
-acidosis
-decreased cardiac outputshock/death
 DISEASE STATES
ADDISON’S DISEASE :
Adrenal insufficiency
Characterised by hypoadrenocorticism ie. both
mineralocorticoid(aldosterone) and
glucocorticoid(cortisol) deficiency
Lethal unless hormone
replacement(mineralocorticoid) treatment is
instituted
Death due to shock & electrolyte inbalances
 DISEASE STATES (cont.)
CONN’S DISEASE :
Primary hypersecretion of aldosterone
High BP is usually the only finding due to salt & water
retention
Associated hypokalemia can present with muscle
fatigue
Treatment includes spironolactone or surgical
removal of the adrenal adenoma
 DISEASE STATES (cont.)
CUSHING’S DISEASE :
Causes – exogenous steroid
administration(commonest)
Maybe due to ACTH secreting pituitary
adenoma(cushing’s syndrome) or ectopic ACTH/CRH
secretion from nonendocrine tumours(small cell lung
carcinoma,thymic and pancreatic carcinoma) or
adrenal neoplasia.
Characterised by hyperadrenocorticism ie. increased
levels of both glucocorticoids & mineralocorticoids
 DISEASE STATES (cont.)
CUSHING’S DISEASE (cont.) :
Typically presents with moon facies, interscapular
buffalo hump, truncal obesity but thin extremities,
hypertension, muscle fatigue, osteoporosis, glucose
intolerance etc
Management depends on the etiology : surgical for
neoplastic causes followed by post-operative radiation
therapy.Ketoconazole decreases adrenal
steroidogenesis.
 DISEASE STATES (cont.)
PHEOCHROMOCYTOMA :
Adrenal medullary tumour – arising from the chromaffin cells of
the sympathetic nervous system.
Extra-adrenal pheochromocytomas arise from the celiac, superior
mesenteric & inferior mesenteric ganglia
Epinephrine/Nor-epinephrine secretion causes episodic
tachycardia, hypertension, sweating & flushing
Dopamine secretion occurs in the familial syndromes(5% cases
autosomal dominant either alone or in association with MEN type
Iia/b) & are not associated with hypertension
Treatment with alpha-adrenergic blockers
(phentolamine/phenoxybenzamine) and surgical resection
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