ADRENAL CORTEX AND GLUCOCORTICOIDS

Sunday, June 5, 2016
ADRENAL GLAND
(Glucocorticoids)
DR.NILESH KATE.
M.D.
ASSOCIATE PROFESSOR,
DEPARTMENT OF PHYSIOLOGY.

OBJECTIVES
 Physiological actions
 Pharmacological actions
 Effect of stress – General adaptation
syndrome
 Applied aspects –
 Cushing’s syndrome
 Addison's disease.

PHYSIOLOGICAL ACTIONS
 Metabolic effect.
 On carbohydrate metabolism.
 On fat metabolism
 On protein metabolism
 Electrolyte & water metabolism
 On various organ systems.
 Anti-inflammatory & anti-allergic
effect.

METABOLIC EFFECT.
 Carbohydrate metabolism.– anti-insulin
effect leads to hyperglycemia.
 Basically provide fuel molecules in
circulation.
 To maintain overnight metabolic stability.
 Increased gluconeogenesis
 Utilization of glucose in peripheral tissue.

ON FAT METABOLISM
 Lipolytic effect –
 Permissive role in lipolysis.
 Indirect stimulation of lipolysis.
 Fatty acid synthesis inhibition by liver.
 Lipogenic role.– redistribution of fats

ON PROTEIN METABOLISM
 Catabolic effect.
Alanine pyruvic acid glucose
formation
 Anti -Anabolic effect. (except liver)

Electrolyte & water metabolism
 Retention of sodium & water.
 Mineralocorticoids activity.
 Aldosterone secretion.
 Promotion of diuresis.(Inactivation of
ADH & Antagonizing action on DCT)
 Adrenal cortex insufficiency
 Water intoxication.

Permissive action
 Small amount of Glucocorticoids must
be present for
 Glucagon & catecholamine's – for
caloregenic action.
 Catecholamine's – for Lipolytic &
glycogenolytic action.
 For pressor response & bronchodilatation.

Effect on muscles.
 Contractility & work performance.
 Skeletal -- ach synthesis at N-M Junction
 Cardiac – Na-K ATPase & β adrenergic
receptors.
 Decreased in muscle mass & strength
(excess of cortisol).
 Weak & thin extremities.

Effect on bones.
 bone resorption.
 osteoclastic activity. & collagenase
activity.
 Inhibition of bone formation.
 Inhibiting osteoblastic activity.
 Apoptosis of osteoblast & osteocytes.
 Osteoporosis.

Effect on connective tissue.
 collagen synthesis.
 Thinning of skin.
 Thinning of capillaries.

Effect on vascular system.
 Sustain myocardial performance.
 Vaso-pressure effect. –
 enhancing catecholamine & angiotensin II
 Decrease vasodilator PG.

Effect on kidney.
 G.F.R.
 Calcium & phosphate
excretion.
 excretion of water load.

ON STRESS
 Stress is defined as an undue
response to strain which may be
physical, mental, internal or
external
 General Adaptation SyndromeGeneral Adaptation Syndrome

STRESSSTRESS
Physical
Emotions
Hypoglycaemia
Tissue actions
C.R.H.C.R.H. CIRCADIAN
RHYTHM
Negativefeedback
Glucocorticoids
(-)
(-)
(+)
A.C.T.H.A.C.T.H.
(+)
ÎÎ Heart rate
Î Force of contraction
Î Blood sugar
Î Permissive action

Central nervous sytem.
 GR- Receptors mainly in limbic system.
 In Addison’s disease.( decreased levels)
 Mood changes – irritability. Inability to
concentrate.
 Increased sensitivity to olfactory & gustatory
stimuli.
 In cortisol excess.
 Increased brain excitability
 Decreased threshold – convulsions.

G.I.T
 gastric acid
secretions.
 proliferation of
gastric mucosal
cells.
 Peptic ulceration.

BLOOD CELLS &
LYMPHATIC ORGANS.
 Polycythemia. –
stimulate
erythropoiesis.
 Thrombocytosis.
 Neutrophilia.

BLOOD CELLS &
LYMPHATIC ORGANS.
 Eosinopenia &
basopenia.
 Lymphopenia.

 Anti-inflammatory effect.
 local reactions
 tissue damage.
 fibroblastic activity.
 endogenous
pyrogens.
 Antiallergic & anti-immunity effect.
PHARMACOLOGICAL ACTIONS

Other actions
 Maturation of CNS, Retina & skin.
 Maturation of lungs.
 Phosphatidyl acid phosphatase.
 Choline phosphotransferase.
 Surfactant.
 Maturation of GIT.

APPLIED ASPECTS.
 Secretions -- Cushing’s syndrome.
(hypercortisol state.)
 Secretions – Addison’s disease.
( hypocortisol state.)

Cushing’s syndrome.
 Group of
clinical
conditions –
due to
prolonged
excessive levels
of
Glucocorticoids
.

ACTH dependent
 Cushing's disease
 Ectopic ACTH syndrome
 Ectopic corticotropin- releasing
hormone syndrome
ACTH independent
 Iatrogenic
 Adrenal adenoma
 Micronodular hyperplasia
 Macronodular hyperplasia
24
Causes -- Classification

Characteristic features. ( Harvey
Cushing)
 carbohydrate metabolism.carbohydrate metabolism.
steroid (adrenal) diabetes.steroid (adrenal) diabetes.
Hyperlipidemia & ketosis.Hyperlipidemia & ketosis.
HyperglycemiaHyperglycemia
Glycosuria .Glycosuria .

FAT METABOLISM.
 Centripetal
distribution of fat
 Thin extremities.
 This case described
by Cushing in 1912.

Fat metabolism.(cont….)
 Deposition of fat. (lemon on toothpick)
Pendular abdomen.
Reddish purple striaeFace (moon like)

Abdominal striae.
Pendular
abdomen
Rupture of thin
skin due to
stretching.

Buffalo hump (upper back)

Fish mouth
Before treatment After treatment. Hirsutism

Protein metabolism.
 Negative nitrogen balance
 Steroid myopathy.
 Skin- thin & paper like
 Poor wound healing
 Hair – thin & rough, loss of scalp hair.
 Thin extremities – muscle wasting.

Other symptoms
Water & electrolyte metabolism
oedema & hypertension.
Bone – osteoporosis
Blood – Polycythemia
Thrombocytosis
Eosinopenia
Basopenia
Lymphopenia.
CNS – Psychosis,
restlessness excitability.
Sexual changes -- Amenorrhea

TESTS FOR CUSHING’S
SYNDROME
 Plasma cortisol levels
 Dexamethasone suppression test.
 Insulin induced hypoglycemia.
 24 hr urinary free cortisol.
 To distinguish between ACTH
DEPENDENT & ACTH INDEPENDENT.
 Metyrapone test.- levels of 11-deoxycortisol
after 24 hr administration of metyrapone.

Addison’s disease
 Adrenal insufficiency is known as
Addison’s disease.
 Causes
a) Auto--immune disease.
b) Destruction of adrenal gland due to cancer
or Tuberculosis.
c) Bilateral adrenalectomy.
d) Malignant tumors.

ADDISON’S DISEASES
(THOMAS ADDISON - 1855)
 1 Muscular weakness
 2. Hypoglycemia
 3. Hypotension
 4. Anaemia
 5. Hypo volemia and Haemo concentration
 6. Resistance to stress and infection is less
 7. Disturbed electrolyte balance
 8. Persons suffer from anorexia, nausea, vomiting and
weight loss.
 9. Addisonian crisis.

Pigmentation of skin.
Increased ACTH
secretion for long time
β- MSH activity.
Generalised
pigmentation of skin
(melanin deposition)

Pigmentation of skin.
Pigmentation of palm & face,
cheek, tongue, gums & ear.

Addisonian Crisis”
Stress precipitates a collapse.
Causes.—
After adrenalectomy.
After abrupt withdrawal of therapeutically
administered Glucocorticoids.
Treatment
Mineralocorticoids & Glucocorticoids
administration daily

OBJECTIVES
 Physiological actions
 Pharmacological actions
 Effect of stress – General adaptation
syndrome.
 Applied aspects –
 Cushing’s syndrome.
 Addison's disease.

ADRENAL CORTEX AND GLUCOCORTICOIDS

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