adrenal gland disorders

1. University of kashmir
Deptt.of clinical biochemistry
Addison’s disease
&
Cushing’s syndrome
Mujeebfazili
21
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2. Adisson’s disease & Cushing’s syndrome
Adrenal glands:
 Paired Suprarenal gland ,endocrine in nature situated at the top of the
kidneys .
 Each gland composed of two parts ,the adrenal cortex and adrenal medulla .
Both secreting different sets of hormones.
 Adrenal cortex produces various steroid hormones necessary for life ,and the
medulla produces catecholamine {nor epinephrine ,epinephrine ,dopamine}.
 Adrenal cortex is mesodermal in origin and adrenal medulla is ectodermal in
origin
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Hypoadrenalism Hyperadrenalism

3. Position and histology of Adrenal Glands
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 Zonaglomerulosa:
 Secretion of mineralocorticoids which
involves ALDASTERONE AND
DEOXYCORTICOSTERONE.
 Maintains the homeostasis of minerals
{electrolytes}especially Na+ and K+.and H20.
 Contains ALDASTERONE SYNTHASE.
 SECRETION CONTROLLED BY RASS
MECHANISM .
 Zonafasiculata:
 Secretion of glucocorticoids which includes
CORTISOL and CORTICOSTERONE
CORTISONE.
 Increases blood glucose concentration in a
manner opposite to that of insulin . Also
helps in protein and fat metabolism {fatty
acid mobilization }.
 Secretion controlled by ACTH.
 Zonareticularis:
 Produces ANDROGENS. Like
dehydroxyepiendrosterone.{DHEA}
 Secretion controlled by ACTH.

4.  Renin angiotensin aldosterone mechanism & ACTH
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5. PROPIOMELANOCORTIN: acts as a precursor of
ACTH and various other hormones
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NH2
COOH
31kDa ,285 amino acid residues.
1-39
{1-13} {18-39}

6. Acth action
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7. Biosyntheseis of steroidhormones :
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cholestrol
Pregnenolone
progestrone 17-hydroxyl-
progestrone
Dehydr-
epiandrosterone17-Hydroxy-
pregnenolone
11-deoxycortisol
corticosterone
Androstenedione
11-Deoxy-
corticosterone
ALDASTERON
E
CORTISOL
Cholestrole
desmolase
3β-
hydroxysteroid
DH
21β-
hydroxylase
11β-
hydroxylase
Aldasterone
synthase
17 -
hydroxylase
17,20 lyase
17,20 lyase17 -
hydroxylase
Testasterone

8. Glucocortioids
Mineralocorticoid
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9. Functions :
Glucocorticiods
 Stimulation of
gluconeogenesis.
 Decreases glucose utilization
by the cells.
 Plays a role in fat and protein
metabolism
 Mobilization of fatty acids and
amino acids.
 Anti inflammatory action.
Mineralocorticoids
 Increases renal tubular
reabsorption of Na &secretion
of K ions ,along with passive
water uptake.
 They stimulate sodium and
potassium transport in sweat
gland’s, salivary glands and
intestinal epithelial cells .
 Controlled both by RAAS and
ACTH.
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10. Addisonsdiseaseanditsetiology:
• It results from inability of adrenal cortices to produce sufficient
adrenocortical hormones {hypo secretion}.
• Addison’ disease is a rare endocrine, or hormonal disorder that affects
about 1 in 100,000 people.
• It occurs in all age groups and afflicts men and women equally. It was
first identified by Dr. Thomas Addison in 1849 in London.
Causes:
• Primary atrophy and injury of adrenal cortices .In 80%of cases atrophy is
caused due to formation of auto antibodies.
• Cancer of adrenal cortices.
• Tuberculous destruction of the adrenal glands.
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11. Effects :
Mineralocorticoid deficiency:
 Loss of Na+ , cl- and water
in urine in large volumes .
 Decreased extracellular
fluid volume.
 Hyperkalemia and mild
acidosis occurs .
 Plasma volume decreases.
 Cardiac output and blood
pressure decreases.
 Patient dies within 4 days
to 2 weeks .
Glucocorticoid deficiency :
 Loss of gluconeogenesis ,hence
impossible to maintain glucose level
between meals .
 Loss of mobilization of fats and
proteins .
 Melanin pigmentation of mucous
membranes, occasionally e.g. lips etc.
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12. General features and treatment :
 Fatigue and weakness
 Loss of appetite.
 Vomiting ,nausea ,diarrhea, abdominal pain.
 Dizziness.
 Loss of weight.
Tretment :
 Small quantities of mineralocorticoids and glucocorticoids
administration daily .
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13. Cushing’s syndrome and it’s etiology:
 Cushing’s syndrome was first described by Harvey Cushing in 1932 .CS
occurs due to hyper secretion of adrenal cortex.
 About two to three people per million are affected each year.
 It most commonly affects people who are 20 to 50 years of age. Women
are affected three times more often than men.
 etiology:
 Adenomas of adenohypophysis, hence increased secretion of ACTH.{Cushing
disease ,basophil carcinoma].
 Malfunctioning of hypothalamus leading to high levels of CRH.
 Adenomas of the adrenal cortex.
 Ectopic secretion of ACTH by a tumor elsewhere in the body.
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14. Symptoms :
• Apperence of moon face .
• Acne and hirusitism .
• Hypertension .
• Fat deposition in thoracic and upper abdominal regions leading
to BUFFALO TORSO. .
• Decreased collagen cause purplish striae on soft tissues of the
body.
• They are prone to infections due to compromised immune
system.
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15. BEFORE AFTER
ACNE AND
HIRUSTISM
BUFFALO TORSO
Purple striae

16. Physiological Effects and treatment :
 Increases blood glucose level ,even above 200mg/dl after meals
due to enhanced gluconeogenesis and reduced glucose
consumption.
 Decreased protein level in body tissues .
 Suppressed immune response
 Dimished proteins often causes osteoporosis.
Treatment :
 Removal of tumor by surgery or radiation therapy.
 Administration of drugs that blocks steroid hormone production
enzymes including metyrapone,ketoconazole and
amninoglutethimide .
 Inhibitors of ACTH secretion .
 Finally Adrenalectomy ,followed by adrenal steroids supplements
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17. Refrences :
1. Gyton and hall medical physiology .
2. Anatomy and physiology by j.b tortora.
3. https://pituitary.org/knowledge-base/disorders/adrenal-
insuffieciency-addison-s-disease.
4. http://joe.endocrinology-journals.org
5. http://www.nlm.nih.gov/medlineplus/cushingssyndrome.h
tml
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18. mujeeb fazili 3rd sem ku
Thank u