In mammals, the adrenal glands (also known as suprarenal glands) are endocrine glands that sit at the top of the kidneys. They are chiefly responsible for releasing hormones in response to stress through the synthesis of corticosteroids such as cortisol and catecholamines such as adrenaline (epinephrine) and noradrenaline. They also produce androgens in their innermost cortical layer. The adrenal glands affect kidney function through the secretion of aldosterone, and recent data (1998) suggest that adrenocortical cells under pathological as well as under physiological conditions show neuroendocrine properties; within normal adrenal glands, this neuroendocrine differentiation seems to be restricted to cells of the zona glomerulosa and might be important for an autocrine regulation of adrenocortical function.
A small gland that makes steroid hormones, adrenaline, and noradrenalineRuvarasheMutadza1
A small gland that makes steroid hormones, adrenaline, and noradrenaline. These hormones help control heart rate, blood pressure, and other important body functions. There are two adrenal glands, one on top of each kidney. Also called suprarenal gland.
In mammals, the adrenal glands (also known as suprarenal glands) are endocrine glands that sit at the top of the kidneys. They are chiefly responsible for releasing hormones in response to stress through the synthesis of corticosteroids such as cortisol and catecholamines such as adrenaline (epinephrine) and noradrenaline. They also produce androgens in their innermost cortical layer. The adrenal glands affect kidney function through the secretion of aldosterone, and recent data (1998) suggest that adrenocortical cells under pathological as well as under physiological conditions show neuroendocrine properties; within normal adrenal glands, this neuroendocrine differentiation seems to be restricted to cells of the zona glomerulosa and might be important for an autocrine regulation of adrenocortical function.
A small gland that makes steroid hormones, adrenaline, and noradrenalineRuvarasheMutadza1
A small gland that makes steroid hormones, adrenaline, and noradrenaline. These hormones help control heart rate, blood pressure, and other important body functions. There are two adrenal glands, one on top of each kidney. Also called suprarenal gland.
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Adrenal Function Tests-3.pptxwhfbdqbfwwfjgwngnegenhndngssfb
1. ADRENAL FUNCTION TESTS
Adrenal glands
Two small organs located above the
kidneys.
Have two functionally distinct parts
◦ Outer cortex(with three zones)
◦ Inner medulla – Catecholamines
2. HORMONES
Adrenal cortex zone Adrenocorticosteroid
hormone
Zona Glomerulosa Mineralocorticoids
Zona Fasciculata Glucocorticoids
Zona reticularis Androgens
3. Cyclopentanoperhydrophenanthrene
nucleus as their basic structure
All steroid hormones are derived from
cholesterol(major source -
circulation)
Most reactions catalyzed by enzymes
of Cyt P450 family.
Liver is the major site for steroid
catabolism
4. Glucocorticoids
21C steroids
Secreted in response to ACTH (secreted by
pituitory), which is in turn controlled by CRH.
Cortisol (also known as hydrocortisone) is
the predominant glucocorticoid
Mainly involved in the regulation of
carbohydrate, lipid and protein metabolism.
Powerful anti-inflammatory hormone.
Cortisol exerts negative feedback on CRH
and
ACTH secretion
Diurnal variation – highest in early morning,
lowest near midnight.
5. Mineralocorticoids
21 C steroid
Aldosterone is the most potent
naturally occurring mineralocorticoid.
Have effects on water and electrolyte
balance.(sodium conservation,
potassium and H ion excretion )
Regulated by renin –angiotensin
system
6. Sex steroid hormones
Secreted by zona reticularis.
Dehydroepiandrosterone,
dehydroepiandrosterone
sulfate(DHEA-S), Androstenedione-
Peripheral conversion to
testosterone.
Estrogen production negligible in
adrenal cortex.
Regulation not well understood yet
7. ADRENAL HYPERFUNCTION ADRENAL
HYPOFUNCTION
Cushing’s syndrome: Primary defect
in adrenal gland (Adrenal adenoma,
adrenal carcinoma etc)
Addison’s disease(primary
adrenal insufficiency)
Cushing’s disease/
Hyperpituitarism:Excess ACTH from
pituitary –pituitary adenoma
Secondary adrenal
insufficiency:hypothalamic/
pituitary disorder -
impaired secretion of
CRH/ACTH
Androgen-secreting tumors of
Ovaries, Testes, Ectopic ACTH by
other tumors
Administration of ACTH
Primary hyperaldosteronism/Conn’s
syndrome
8. Adrenal function tests
Help in diagnosis and monitoring of
adrenal hypo/hyperfunction disorders.
DHEA may be measured to determine
cause of hirsuitism, amenorrhoea,
infertility or precocious puberty in
females.
9. Adrenal function tests
Plasma Cortisol level
Plasma ACTH level
ACTH stimulation test/ CoSyntropin
test
Corticotropin-releasing hormone(CRH)
stimulation test
Dexamethasone Suppression Test
17-Hydrocortisol level
Urinary free Cortisol
Estimation of aldosterone in blood
11. Plasma Cortisol level
Diurnal rhythm
◦ Secretion maximum in morning
◦ Minimum at midnight
Normal range
◦ 5-25 microgm/dl in morning(8 am)
◦ 2-5 microgm/dl in night(10 pm)
Determined by immunoassay
(ELISA/CLIA/RIA)
Loss of diurnal rhythm may be an early
indication of lesion at any point in
hypothalamic –pituitary- adrenal axis
12. Plasma ACTH
ACTH CORTISOL PROBABLE
DISORDER
Low High Primary
hyperadrenalism
Low Low Secondary
adrenal
insufficiency
High Low Primary
adrenocortical
insufficiency
High High Pituitory
adenoma
(Cushings
13. Synacthen test/ACTH stimulation
tests
Used to assess adrenal reserve
capacity
Used to demonstrate the failure of
adrenal gland to produce cortisol in
response to ACTH
Stimulation of adrenal cortex by
synthetic
ACTH(eg:synacthen/cosyntropin)inject
14. Normal response shows a rise in
serum cortisol > 18microg/dl within
60mts of i.v administration of
synacthen
A person with primary adrenal failure
doesnot respond.( rise <18microg/dl)
Confirms the diagnosis of Addison’s
disease
15. CRH Stimulation tests
Definitive to differentiate pituitary
causes from other causes
Rise in ACTH secretion and cortisol
levels following injection
If there is no ACTH response after
CRH stimulation tests, the disease is
of pituitary origin
16. Dexamethasone Suppression Tests
Used in diagnosis of Cushing’s syndrome.
Low dose Dexamethasone Suppression Tests
Dexamethasone is a potent suppressor of
pituitary ACTH secretion and thereby cortisol
level,causing 50% fall in serum cortisol with a
dose as low as 1mg
Patient takes dexamethasone tab at night and
plasma cortisol is determined at 8 am the
following morning
Morning cortisol <5microgm/dl rules out
adrenal tumors.
17. High dose dexamethasone
suppression test
Done to confirm Cushings disease
Administer 2mg dexamethasone every
6 hrs for 2 days & cortisol measured
next day morning.
This dose suppresses plasma cortisol
in Cushings disease.(drop atleast
50%)
If plasma cortisol level is not
suppressed, adrenal tumors producing
high levels of cortisol or ectopic ACTH
producing tumors are usually the
18. Urinary excretion of steroids
Urinary steroids are 17 ketosteroids
and 17 hydroxy steroids
17 ketosteroids are derived from both
adrenal steroids and androgen from
gonads, major contribution by cortisol
and cortisone
17 hydroxy steroids are derived mainly
from adrenal steroids
Diagnostic value to assess functional
status of adrenal cortex, particularly in
females
19. Estimation of aldesterone in
blood
Increased levels are seen in primary
hyperaldosteronism /Conn’s syndrome
and bilateral adrenal hyperplasia
Decreased aldosterone levels are
seen in Addison’s disease
20. Estimation of plasma renin
activity
Helps to differentiate between primary
and secondary hyperaldosteronism
Enzyme activity is high in secondary,
low in primary hyperaldosteronism
21. Urinary free Cortisol
In plasma 70% cortisol is bound to
cortisol binding globulin/transcortin
20% cortisol is bound to albumin
Rest is free,which is the biologically
active form
A definite fraction of unbound/free
cortisol is exreted in urine unchanged
24 hr urine sample is collected
Estimation of urinary free cortisol is a
sensitive index of adrenal activity:
Hyper/Hypofunction.
22. Lab findings in Adrenal
hyperfunction
Cause Plasma
cortisol
Urinary
cortisol
Plasma
ACTH
Dexamethasone
suppression
Adrenal
adenoma
Increased Increased decreased No suppression
Adrenal
carcinoma
Increased Increased decreased No suppression
Pituitory
adenoma
Increased Increased Increased Suppression with
high dose
Ectopic ACTH Increased Increased Increased No suppression
23.
24. Lab findings in Adrenal
hypofunction
Cause for
adrenal
insufficienc
y
Plasma
cortisol
Urinary
cortisol
Plasma
ACTH
ACTH
stimulation
CRH
stimulation
Primary low low High No effect No effect
Secondary low low Low Normal/
exaggerate
d
No effect
25.
26. Lab findings in Conn’s
syndrome
Plasma Aldosterone levels are high
Plasma renin activity is decreased due
to feedback
Serum electrolytes-hypernatemia,
hypokalemia
pH is elevated(hypokalemic alkalosis)
Osmolality is elevated
31. Assignment Questions( 5*4 =
20 marks)
1. List the adrenal function test with
significance of each.
2. List the lab findings in adrenal
hyperfunction.
3. List the lab findings in adrenal
hypofunction.
4. In tabular form, give the pattern of
hormone levels in various endocrine
abnormalities in males and females.