ADRENAL GLANDS

Adrenal glands are two conical pyramid shaped glands and are situated just above
each kidney. Each adrenal has an outer layer called as Adrenal cortex and a
central portion called as Adrenal medulla. Adrenal cortex is essential for life
where as Adrenal medulla helps to combat against emergency situations.

ADRENAL CORTEX

DIVIDED INTO THREE ZONES

Zona glomerulosa
It is the outermost zone in which cells are arranged with their long axis parallel
to the surface. It secretes mineralocorticoids.

Zona fasciculate
It is the intermediate zone in which cells are lying vertical to the surface. It
secretes glucorticoids.

Zona reticularis
It is the inner zone and cells are arranged irregularly with blood spaces in
between. It secretes sex steroids.

GLUCORTICOID REGULATORY MECHANISMS

1. CRH Corticotrophin Releasing Hormone from the hypothalamus

stimulates the secretion of ACTH Adrenocorticotrophic hormone from the
anterior pituitary
2. ACTH stimulates the secretion of glucorticoids

DIURNAL variation of ACTH secretion

Maximum between 6.00 am 9.00 am
Diurnal variation is Regulated by suprachiasmatic nuclei of hypothalamus

HYPOTHALAMUS →→→ANT PITUITARY →→→ ADRENAL

CORTEX→→→COTISOL
CRH ACTH
Free Glucorticoids inhibits ACTH secretion by inhibiting secretion of CRH and
ACTH

Mechanism - Glucorticoids stimulate DNA dependent mRNA synthesis

ACTIONS

Carbohydrate metabolism
DIABETOGENIC
z Leads to increase blood glucose
z Increase gluconeogenesis
z Prevents peripheral utilization of glucose

FAT METABOLISM

LIPOLYTIC ACTION
z Increase mobilization of fatty acids from adipose tissue to liver
z Increase lipase activity

Protein metabolism

CATABOLIC ACTION
Protein breakdown

ELECTROLYTE BALANCE

z Increases retention of sodium due to mild mineralocorticoid action.

z Increases secretion of aldosterone leading to increased water and sodium
reabsorption.
z Antagonises action of ADH on kidney.

PERMISSIVE ACTION

Glucorticoids are very essential for metabolic reactions to occur

Important for other hormones to exert their effect eg catecholamines to produce
pressor response

CNS

Glucocorticoids in excess decrease excitability of neurons causing convulsions

GIT

Increase gastric acid secretion therefore promoting peptic ulcer formation

BLOOD VESSELS
Glucorticoids are essential for normal vascular reactivity
Sensitizes the arterioles to vasoconstriction action of catecholamines

ANTIINFLAMATORY ACTION

Prevents tissue damage by stabilizing lysosomal membranes

Decrease hyperemia, exudation, migration and infiltration of leucocytes at the

site of injury
Decrease hypersensitivity response to antigen – antibody reaction

Decreases release of pyrogens from granulocytes. Lowers fever

BLOOD CELLS
Causes Neutrophilia
Basopenia
Eosinopenia
Lymphopenia
Polycythemia
Clotting time is reduced

APPLIED

CUSHING’S SYNDORME

EXCESS CIRCULATING LEVELS OF GLUCORTICOIDS

CAUSES
z ADRENAL TUMOURS SECRETING EXCESS GLUCORTICOIDS
z ADRENAL HYPERPLASIA
z EXCESS INTAKE OF GLUCORTICOIDS
CHARACTERISTIC FEATURES

1. PROTEIN CATABOLISM
Wasting of muscles
Growth retardation
Thinning of skin and subcutaneous tissues
Poor wound healing

2. CARBOHYDRATE METABLOISM

Diabetogenic
Cause hyperglycemia
Increased resistance to insulin

3. FAT METABOLSM

Redistribution of fat
Centripetal distribution OF FAT
Characterized by

z Thin extremities
z Fat deposition over abdomen
over face leads to MOON FACE
upper back causing BUFFALO HUMP

4. PROMOTES ATHEROSCLEROSIS BY INCREASING FFA ,LIPIDS

5. HYPERTENSION BY ITS MINERALOCORTICOID ACTION,
RETENTION OF SODIUM AND WATER
6. CNS : PSYCHOSIS ,EXCITABILITY, NERVOUSNESS
7. GIT : PEPTIC ULCER FORMATION
8. ANTIINFLAMATORY ACTION
9. OSTEOPOROSIS BY INCREASING BONE RESORPTION
10. BLOOD : Eosinopenia, neutrophilia, basopenia , polycythemia,
increased clotting time.
ADRENAL MEDULLA

Consist of two types of cells

I. Epinephrine secreting cells 80%
II. Nor epinephrine secreting cells 20%

z They stimulate the force of contraction of heart and increase heart rate.
z Adrenaline causes dilation of blood vessels in skeletal muscle and also
increases blood glucose level.

NOTE – Dopamine is also synthesised from the sympathetic ganglia.

RELEASE OF CATECHOLAMINES
Stimulation of pre-ganglionic splanchnic fibers
↓
release of Ach
↓
Stimulate medullary chromaffin cells
↓
Secretion of epinephrine and nor-epinephrine into the blood

ACTION OF CATECHOLAMINES
There exist two types of adrenergic receptors: α and β. They have different
sensitivities for different catecholamines and produce different response.
1. The α adrenergic receptors are sensitive to both epinephrine and
norepinephrine.
2. α receptors are of two types α1 and α2

LOCATION
α1 receptor - Post synaptic membrane
α2 receptor - Presynaptic nerve terminals of cholinergic and
adrenergic nerves

ACTION
α1 receptor - Excitatory
α2 receptor - Inhibitory
 3. β adrenergic receptors respond to epinephrine and very less to
norepinephrine.

ACTION
Excitatory action on myocardium.
Two types
β1 and β2, located mostly on the postsynaptic membrane.

LOCATION
β1 receptor - Cardiac muscle
β2 receptor - Skeletal muscular blood vessels. GIT and bronchioles

ACTION
β1 receptor - Tachycardia and increase myocardial contractility
β2 receptor - Relaxation of blood vessels

Epinephrine acts equally on both α and β receptors while norepinephrine

acts on α receptors.

HEART β1,β2 Tachycardia

SA node β1,β2 Increase in conduction
AV node velocity
β1,β2
Atria Increase in conduction
β1,β2 velocity and contractility
Ventricles Increase in contractility
and conduction velocity

Blood vessels α1α2 Constriction

Skeletal muscle and β2 Dilation
coronaries
Lungs β2 Bronchodilatation
Bronchial muscle α1 Decreased secretion
Glands β2 Increased secretion
GIT α1α2β2 Decreased motility
Stomach and intestine
Urinary bladder β2 Relaxation
Detrusor muscle α1 Contraction
Trigone and sphincter α1 Increases
Ureter
Skin α1 Pilorection
Pilomotor muscle α1 localised sweating
Sweat gland
Uterus α1 Constriction
β2 Relaxation
Eye α1 Constriction
β2 Relaxation for far vision
Liver α1β2 Glycogenolysis
Skeletal muscle β2 Increase contractility and
glycogenolysis

Pancreas α2 Inhibition of insulin and

glucagon secretion
β2 Stimulation of insulin
and glucagon secretion
Kidney β1 Renin secretion

APPLIED

Phaeochromocytoma: Tumour of chromaffin tissues. Secrete large amounts of

epinephrine and nor epinephrine.

FEATURES
1. Paroxysmal or sustained hypertension
2. Headache, sweating severe palpitation, substernal pain, anxiety
3. Increased body temperature, hyperglycemia
4. Increase in urinary excretion of catecholamines, VMA and metanephrines.
ALDOSTERONE

MECHANISM OF ACTION

Stimulate DNA dependent mRNA synthesis. Aldosterone binds to specific

cytoplasmic receptor and induces Aldosterone induced Protein synthesis (AIP)
which is responsible for Na+ transport. Net effect is increased transport of Na+
from tubular lumen into interstitium and ultimately into blood stream.

ACTIONS

1. Conservation of sodium and excretion of potassium

ALDOSTERONE cause- Retention of sodium from kidney.

Acts on PRINCIPAL CELLS of DCT and CT causing Na+ reabsorption in
exchange for K+ and H+ which are then excreted in urine.

Increases excretion of potassium from kidney.

1. Due to Na+ reabsorption, Aldosterone causes water retention leading to
increased GFR and RPF.

3. EFFECT ON ACID BASE BALANCE

Secretion of excess amount of Aldosterone causes hypokalemia which leads to

increase in intracellular H+.This leads to secretion of H+ over K+ in DCT and
results in Metabolic Alkalosis
Lack of secretion of Aldosterone leads to increase in intracellular K+ and
therefore metabolic acidosis.

ESCAPE PHENOMENON
Excessive secretion of Aldosterone causes hypernatremia leading to increase
ECFV. Then Na+ excretion is increased due to increased secretion of ANP.

REGULATION

RENIN ANGIOTENSIN SYSTEM

RENIN is released in circulation by decreased effective circulating blood

volume
Due to
z Hypovolemia
z Hyponatremia
z Hypotension
z Increased sympathetic activity.
z Standing position
z Secondary hyperaldosteronism in cases of CHF, cirrhosis and nephrosis
JGA ----Æ Renin

Angiotensinogen --------Æ Angiotensin I --------Æ

angiotensin –II -------Æangiotensin III -----------Æ adrenal cortex -------Æ
Aldosterone secretion -------------Æ retention of Na+ ------Æ Inreased ECFV ---
----Æ increased RPF--------INHIBITION TO JGA

CONN’S SYNDROME (primary hyperaldosteronism )

Excessive secretion of Aldosterone from adrenal cortex is characterized by

I. Increased plasma Aldosterone levels.
II. Rise in plasma sodium level
III. Decrease in plasma potassium level that causes
Muscular weakness, tetany
Metabolic alkalosis
Prolonged hypokalemia can cause kidney damage
IV. Hypertension due to sodium retention
V. Renin is decreased

Secondary hyperaldosteronism
Extra adrenal factors.
CHF cirrhosis and nephrosis
Renin is increased

ADDISON’S DISEASE (Primary Adrenocortical insufficiency)

Reduced secretion of Aldosterone and glucorticoids due to destruction of adrenal

cortex .

CAUSES
Autoimmune disorder
Tuberculosis
Malignancy

Clinical features

1. Hypotension
2. Loss of weight, anorexia, diarrhea, dehydration
3. Muscular weakness, lethargic
 4. Increased ACTH leading to pigmentation of skin , mucous membrane,
gums , darkening of areolas
5. water intoxication

MULTIPLE CHOICE QUESTIONS:

ALDOSTERONE:

1. All are action of aldosterone except:

a) Retention of sodium.
b) Excretion of potassium.
c) Increased water retention.
d) Retention of chlorides.

2. Regulation of aldosterone is due to :

a) Renin Angiotensin system.
b) Thyroid hormones.
c) Glucorticoids.
d) Growth hormones.

3. Renin is released in circulation by all except:

a) hypovolemia
b) hyponatremia.
c) Hypertension.
d) On standing.

4. One of the following is not true:

d) Angiotensinogen is not converted to angiotensin I.
e) Angiotensin II gets converted to angiotensin I.
f) Aldosterone cause retention of sodium.
g) Angiotensin II gets converted to Angiotensin III.

5. All are true of primary hyper aldosteronism except:

a) Increase in plasma potassium levels.

b) Increase in plasma sodium levels.
c) Hypertension.
d) There are aldosterone levels.
 6. In Addison's disease , one of the following is true:
g) loss of weight.
h) Constipation.
i) Hypotension.
j) Increased secretion of aldosterone.

ADRENAL GLANDS

1. In the adrenal medulla,

a) 80% cells are epinephrine secreting.
b) 80% cells are norepinephrine secreting type.
c) 20 % cells are epinephrine secreting.
d) 80% cells are both epinephrine and nor epinephrine secreting.

2. Mineralocorticoid is secreted by
a) zona glomerulosa.
b) Zona fasciculata.
c) Zona reticulata.
d) All of the above.

3. One of the following is true:

a) stimulation of beta receptors causes all except

b) Tachycardia.
c) Increase in conduction velocity at AV Node.
d) Increase renin secretion in kidney.

1. action of glucocorticoids are

a) Increase blood glucose levels.

b) Lipolytic action.
c) Cause protein breakdown.
d) All of the above.

1. One of the following is aggravated by glucocorticoids except

peptic ulcer.
2. Diabetes mellitus.
3. Hypertension.
4. Hypothyroidism.
 1. Cause of cushing's syndrome are all except
adrenal tumour.
2. Adrenel hyperplaia.
3. Excess intake of glucocorticoids.
4. Adrenal atrophy.

7. Patient with cushing syndrome present with all features except

a) Poor wound healing.

b) Hypertension.
c) Moon face.
d) Decreased blood glucose.