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ADRENAL GLAND

ADRENAL CORTEX
ADRENAL MEDULLA

Goals for learning


Functional anatomy of adrenal gland
Hormones and their synthesis
Functions of the hormones
Cellular mechanism
Regulation of their secretion
Effect of their altered secretion

Adrenal gland
Adrenal

cortex
Zona glomerulosa-Mineralocorticoid
Aldosterone, Deoxycorticosterone
Zona fasciculata-Glucocorticoids

Cortisol, Corticosterone, Cortisone


Zona reticularis-Adrenal androgens
Androsterone, DHEA sulphate
Adrenal Medulla
Epinephrine
Nor epinephrine
Dopamine

Cholesterol
Pregnenolone

17 OH Pregnenalone

DHEA

Progesterone

17 OH Pregnenalone

Andro
stenedione

11 Deoxy
Corticosterone
Corticosterone

11 Deoxycortisol
Testosterone
Cortisol

Estradiol

Glucocorticoids
Cortisol
Corticosterone
Cortisone
Predinisolone

(synthetic)
Dexamethasone (synthetic)
Concentration

of cortisol is 13.5
microgram/100 ml,
Secretion 15-20mg/day
Transport
Cortisol binding globulin(CBG)/ transcortin

GLUCOCORTICOIDS
CORTISOL
This

is a C21 steroid produced mainly from zona


fasciculata.
It combines with cortisol binding globulin.
96 % of the cortisol is transported in bound form.
Only 4 % is transported in free form.
It stays in circulation for 1 to 2 hours.
It is degraded in the liver and conjugated to form
glucuronides. It is excreted in urine.

MECHANISM OF ACTION
These

hormones enter the cell and combine with


receptors in the cytoplasm. Hormone receptor
complex induces portion of DNA to form m
RNA.
The m RNA causes protein formation. These
proteins are responsible for actions of
glucocorticoids.
Onset of action is 45-60 min

Functions
Metabolism

CHO, Proteins, Lipids, Mineral and Water


Permissive Action
Effect on ACTH secretion
Vascular permeability
On Nervous System
On Blood cells and Lymphatic organs
Resistance to Stress
Anti inflammatory and Antiallergic Effects

On carbohydrate metabolism
It

stimulates gluconeogenesis by the liver by


increasing glucose-6-phosphatase.
It decreases rate of glucose utilization by the
peripheral tissues by inhibiting phosphorylation
(anti-insulin action)
Increases glycogen synthesis in liver by increasing
activity of glycogen synthase.

On protein metabolism
It

causes protein breakdown in skeletal


muscles.
Cortisol enhances amino acid uptake by the
liver cells & enhances transamination - (AA
synthesis), deamination (glucose
formation)
Hence proteins like plasma proteins
produced by liver are increased

On fat metabolism
It

causes fatty acid mobilization from


adipose tissue increasing free fatty acids in
plasma.
It stimulates absorption of lipids from the
intestine.
It causes redistribution of fats in the body.

Water and Mineral metabolism


Mild

mineralocorticoid activity retains Na


& excretes K
Increases angiotensinogen synthesis in liver
leading to Na retention via aldosterone
Provides adequate GFR via anti-ADH
activity

Permissive action
On

glucagon & catecholamines to exert


calorigenic action
On catecholamines to exert lipolytic effect
& glycogenolytic effect.
On catecholamines to exert pressor
response & bronchodilation.

In stress
Offers

resistance to Stress
Stress causes increase in ACTH secretion
followed by secretion of cortisol
Stress causes General Adaptation Syndrome in
2 phases:
1 Stage of Alarm
2 Stage of Resistance: in which cortisol
interacts with catecholamines activation of
sympatho-adrenal medullary system.

Effect on blood cells


Eosinopenia
Lymphopenia
Basopenia

Neutrophilia
Polycythemia
Platelet count

It

On Bone

causes demineralization of bone


Retards development of cartilage
Thinning of epiphyseal plate
Breaks down bone matrix
Decreases calcium deposition
Increases calcium excretion
Decreases calcium absorption from GIT
Results in osteoporosis and tetany

Anti inflammatory & Antiallergic


Effect
Pharmacological

doses
Inhibits Phospholipase A2
Reduces the release of arachidonic acid &
consequently reduces the formation of leukotriens,
thromboxanes, prostaglandins and prostacyclins.
It reduces leucocyte margination, chemotaxis,
phagocytosis of bacteria.
It prevents development of fibroblasts & delays
wound healing

REGULATION
Cortisol

secretion is controlled by ACTH.


ACTH is secreted in irregular bursts
throughout the day. Plasma cortisol rises and
falls in response to these bursts. Plasma
cortisol is high in mornings (20mg/dl ) and
very low (5mg/dl) in evenings.

Trauma
Afferents
from NTS

Emotions
Circadian rhythm
CRH
cortisol

ACTH

Adrenal cortex

CUSHINGS SYNDROME
Excess

secretion of glucocorticoids.

Causes

Adrenocortical tumours

Anterior pituitary tumours

Ectopic ACTH producing tumour

Prolonged glucocorticoid therapy.


Cushings syndrome caused due to tumours of

anterior pituitary is called Cushings disease.

Signs & symptoms


Fat

collects in the abdominal


wall, face and upper back
producing buffalo hump and
moon face.
Skin and subcutaneous tissues
are thin.
Muscles are poorly
developed.
Wounds heal poorly, minor
injuries cause bruises
Osteoporosis occur.
There is insulin resistant
diabetes mellitus due to
gluconeogenesis .

There

Signs & symptoms

is salt and water


retention, K+ depletion and
weakness due to
mineralocorticoid activity of
cortisol .
Protein depletion occurs due
to its excessive catabolism.
Hypertension develops due
to increased
deoxycorticosterone
production.
Reddish purple striae appear
in the skin due to rupture of
subdermal tissues

Treatment
Removal

of tumour in adrenal or pituitary

gland.
If removal of pituitary tumour is not
possible, then removal of both adrenals with
supplementation of steroids.

Summary
Hormones

of Adrenal Cortex
Glucocorticoids-Mechanism, Functions
Cushings Syndrome

Study questions
Name

the layers of adrenal cortex and list the


hormones secreted by them
Describe the functions of glucocorticoids
What is permissive action of a hormone. Give
suitable example?
Discuss the anti-inflammatory functions of
glucocorticoids
Explain the cause and clinical features of
cushings syndrome