Adrenal glands

• There are two adrenal glands lying on the superior pole of kidneys.
• Each gland consists of two components
1. Outer adrenal cortex
2. Inner adrenal medulla
• The adrenal cortex produces steroid hormones.
• Structurally, it is divided into 3 functional zones (inner ward)
1. Zona glomerulosa (mineralocorticoids, like
aldosterone)
2. Zona fasciculata (glucocorticoids, cortisol)
3. Zona reticularis (adrenal androgens)
Adrenal medulla produces two hormones (catecholamines)
1. Adrenaline/epinephrine
2. Noradrenalin/norepinephrin
 Action of catecholamines
1. On Cardiovascular system
Heart (β1): ↑Inotropic activity (contractility)
↑Chronotropic activity (heart rate)
Blood vessels: AD/NA + α1-AR = Vasoconstriction
AD/NA + β2-AR = Vasodilation
2. On Respiratory system:
AD/NA + β2-AR = Bronchoconstriction
3. On GIT: Inhibits motility
Constricts sphincters
4. On CNS (α2): ↑Mental alertness
Leads to nervousness in excess
• On Metabolism:
CHO (β2): ↑Glycogenolysis
↑Gluconeogenesis ↑BGC
Fat (β2): ↑ Lipolysis, stimulate hormone sensitive lipase
↑ Utilization of fat
Proteins: ↑ Protein catabolism
6. ↑MR
 Physiologic effects of cortisol
1. Metabolic Effects
On CHO metabolism
• ↑Gluconeogenesis ↑BGC
• ↓Glucose utilization = Hyperglycemia
On Protein metabolism Fat metabolism
• ↓Protein synthesis ↑Lipolysis
• ↓Amino acid uptake ↑Mobilization of fat and
• ↑Protein catabolism redeposition on unusaul areas
On electrolytes Na+ reabsorption
It has aldosterone K+ excretion
like action Ca2+ excretion
2. Anti-inflammatory action: It suppresses inflammatory reactions
• Stabilizes lysosomal membrane
• Inhibits formation of inflammatory mediators
• Decreases capillary permeability
 Function of cortisol (cont´d)
3. Immunosuppressant action
• Inhibits activation and proliferation of both T-lymphocytes
and B-lymphocytes
• Leads to a general depression of lymphoid tissue
4. Plays a permissive action with catecholamines. Cortisol
enhances synthesis and release of catecholamines
5. Anti allergic action
6. Growth inhibitory effect
-↓GH secretion
Cortisol -Activates osteoclasts
-Inhibits osteoblasts
-Inhibits protein synthesis
7. Cortisol ↑HCl secretion, contributes to PUD
8. Cortisol stimulates surfactant production in lungs
 Regulation of cortisol secretion
Cerebral cortex
Limbic system
Emotion Stress
Circadian + + Fear
rhythm +
Pain
OC Anaesthesia
_ MB Surgery
CRH + Hemorrhage

Corticotrops + Pyrogens
Hypoglycemia
_ Histamine
ACh, 5-HT

ACTH
+
Adrenal cortex
Zona fasciculata

↑↑ Cortisol: Free
Bound
 Aldosterone
Function
• ↑Na+ reabsorption Renal tubuled
• ↑K+ and H+ secretion Sweat and salivary ducts
• ↑Aldosterone = ↑Na+ = ↑Osmolality = ↑ADH
Regulation of aldosterone secretion
• Four important factors controlling aldosterone secretion
1. Hyponatrimia (↓Na+) 3. ACTH from adenohypophysis
2. Hyperkalemia (↑K+) 4. Angiotensin II

↑Aldosterone
 Cushing’s syndrome
It is excessive secretion of the corticol
Causes
Primary hypersecretion from adrenal cortex due to:
a. Bilateral hypertrophy and hyperplasia
b. Carcinoma of the adrenal cortex
Secondary to hyperactivity of pituitary ACTH due to:
a. Hypertrophy and hyperplasia of corticotrops
b. Carcinoma of corticotrops, Cushing’s disease
Ectopic secretion of ACTH (lung carcinoma)
 Clinical features of Cushing’s disease
 Central obesity: moon face, buffalo hump, trunkal
obesity (enlarged abdomen)
 Thin skin, abdominal striae
 Thin limb, flat buttock: muscle wasting
 Hypertension and hypokalemia
 Hyperglycemia: steroid (adrenal) diabetes mellitus
 Stunted growth, osteoporosis
 Poor (delayed) wound healing, susceptible to infection
 Back pain, depression, psychosis
 Menstrual irregularity, hirsuitism, acne, loss of libido
 Hyperaldosteronism
 Excessive secretion of aldosterone
 Two types
A. Primary aldosteronism (Conn’s syndrome)
-Adrenocortical in origin
-Unilateral or bilateral adenoma
B. Secondary aldosteronism
-↑↑Aldosterone = ↑↑Ang-II
Clinical features
 Hypertension
 Hypokalemia
 Adrenocortical insufficiency
 It is the deficiency of cortisol and aldosterone
 Two types
I. Primary adrenocortical insufficiency: it is due to disease of
the adrenal gland itself = Addison’s disease
Causes -Autoimmune problem to the gland
-infection to the gland
-Damage to the gland
-Surgical removal of the gland
II. Secondary adrenocortical insufficiency: adenohypophysial
disorder (↓↓ACTH)
Clinical features
 Hyperpigmentation - Hyperkalemia
 Hypoglycemia - Hypotension
 Hyponatrimia
 Adrenal androgens
 Produced in small amount from ZF and ZR
 The adrenal androgens are: Dehydroepiandrosterone (DHEA)
and androstendione
 Both of them are converted into testosterone in the circulation
 No significant estrogens are secreted in the adrenal cortex, but
androgens can be converted into estrogens in the adipose tissue
Androgens Testosterone
aromatase Estrogens
 Progesterone is formed in the adrenal cortex as an intermediate
compound, but it is not normally released into the blood.
Function of adrenal androgen
 Initiate the development of 2o-sexual characteristics such as
enlargement of genital organs, growth of hairs in the axillary
and pubital areas