The document discusses the anatomy, histology, and functions of the adrenal glands. It describes the adrenal cortex and medulla. The adrenal cortex secretes corticosteroids like cortisol and aldosterone which regulate metabolism, immune function, and electrolyte balance. The adrenal medulla secretes catecholamines like epinephrine. Tests are discussed to evaluate hypercortisolism, hypoadrenalism, hyperaldosteronism, and pheochromocytoma.

1. W.O. Balogun
Endocrinology Unit
Dept. Of Medicine, UCH

2. About anatomy
 Paired glands located supra renal
 Divided anatomically and functionally into 2 parts:
adrenal cortex and adrenal medulla
 Adrenal cortex:
 -zona glomerulosa
 zona fascilculata, and
 zona reticularis

3. Histological divisions

4. Anatomical location

5. Adrenal medulla
 Derived from embryonic neural crest ectoderm (same
tissue that produces the sympathetic ganglia).
 Synthesizes and secretes:
 Catecholamines (mainly Epinephrine but some NE).

6. Adrenal cortex
 Secretes corticosteroids
 Controlled by ACTH
 Zona glomerulosa: Mineralocorticoids
 Zona fasciculata: Glucocorticoids
 Zona Reticularis: Sex steroids

8. Mechanism of action of steroid
hormones
1) The steroid h. enters the cytoplasm of the cell
where it binds with a specific receptor ( protein
in nature).
2) The combined hormone receptor diffuse into
the nucleus.
3) Then it activates the transcription process of
specific genes to form a messenger RNA.
4) The messenger RNA diffuse to ‘ cytoplasm to
promote synthesis of specific protein &
enzymes within ribosomes’.

9. Actions of Glucocorticoids
 Intermediary metabolism
Acts in a concerted way to maintain or increase blood
glucose level
 Liver: Increase expression of gluconeogenic enzymes
 Adipocytes: mobilises FFA for gluconeogenesis
 Degrade muscle proteins for gluconeogenesis
 Causes low serum Ca by ↑ calcium
absorption/reabsorption from GI and kidneys; also ↑ bone
resorbption
 Inhibits pancreatic insulin secretion
 Blunts gonadotrophs sensitivity to GnRH

10. Actions of Glucocorticoid (2)
 Depresses immune system:
 Causes thymus atrophy
 Decreases IL-1 production
 Inhibits monocytes proliferation; decreases lymphocytes and
eosinophils concentration, increases neutrophils but
suppreses their activities
 Inhibits inflammation

11. Actions of glucocorticoid (3)
 Antiproliferative actions on fibroblasts and keratinocytes
 Stimulation of surfactant production in the lungs
 CVS: Increased cardiac contractility; increase vascular
reactivity to vasoconstrictors and decreased endothelia
permeability
 Kidneys: Causes increased GFR to excrete excess water load

12. Actions of glucocorticoid (4)
 Psychologic /CNS:
 Maintains emotional balance
 Suppression of REM sleep
 Acts on hippocampus to facilitate memory,
concentration and intellectual performance
 Eye: causes increased ocular prssure

13. Actions (5)
 Effects during stress:
 Increases lipolytic actions directly and via
cathecolamines, providing FFA for stress
 Counterregulates hypoglycaemia by increasing
gluconeogesis

15. MINERALOCORTICOIDS
ALDOSTERONE
 ELECTROLYTE BALANCE
 BLOOD PRESSURE
 RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

16. Actions and control of aldosterone

17. Functions of adrenal medulla
 The cathecolamines:
 Increase respiratory rate.
 Increase HR and cardiac output.
 Vasoconstrict blood vessels, thus increasing venous return.
 Stimulate glycogenolysis.
 Stimulate lipolysis.

18. SEX HOMONES
 ANDROGENS (TESTOSTERONE)
 ESTROGENS
LESS THAN GONADS

19. Function tests

20. Disorders of function
 Excess: Hypercotisolism; hyperaldosteronism;
 Deficiency: Hypoadrenalism

21. Regulation of
adrenal gland
secretion ACTH
Cortisol
Cortisol

22. REGULATION OF CORTISOL SECRETION
HYPOTHALAMUS
CRH
ANTERIOR PITUITARY
ACTH
ADRENAL CORTEX
TARGET ORGANS
CORTISOL
STRESS
DIURNAL
RHYTHM
+ +
-
-
INCREASED
BLOOD GLUCOSE
BLOOD AA
BLOOD FATTY ACIDS

23. Concept of circadian rhythm
Group of hormones with pulsatile patterns of secretion
and well-defined amplitude, frequency and rhytmicity
within the circadian

24. Pattern of cortisole and ACTH level during
the day

25. Tests of Hypercortisolism
Plasma cortisol assays: limited usefulness. Episodic
secretions, affected by stress, ↑oestrogen, depression,
starvation, alcoholism, CKD
Urinary free cortisol:
Urine collected for 24 hrs to measure unbound cortisol-
fraction excreted unchanged. Provides an integrated
measure of serum cortisol. Very useful to confirm
Cushing syndrome
17-hydroxycorticosteroids measurement
Late night salivary cortisol

26. Tests of hypercorticolism (2)
Dexamethasone suppresion tests: dexamethasone, a potent
steroid is used
Principle: suppress HPA axis; normally, ACTH decreases,
causing low plasma or urinary corticosteroids. Fail to suppress in
cushing
 Low-Dose (overnight): given oral 1 mg. 80-99% with C.S.
showed abnormal response. False positive in hospitalised,
alcohol, depression, anxiety, uraemia, high oestrogen states
High-Dose:- can be overnight (8mg) or for 2 days (2mg 6-
hourly). The supraphysiologic dose given to distinguish
Cushing disease from ectopic ACTH or adrenal tumours;
cortisol suppresses to about 50%. Fairly useful

27. Test of Pituitary-adrenal reserve
Principle: stress or challenge HPA to provoke rise in
cortisol
ACTH: to stimulate release of cortisol
Metyrapone: inhibits cortisol release , causing ↑ACTH
CRH: direct stimulation of pituitary corticotrophs
Insulin –induced hypoglycaemia testing

28. Androgens: Tests
 Direct measurement better than dynamic testing
 Measure assays of hormones directly, e.g DHEA,
DHEA sulphate, androstenedione, testrosrone

29. Tests for Hypoadrenalism
ACTH stimulation test/Synacthen test
250µg of tetracosactrin administered; plasma
cortisol>550nm/l after 30 min normally
Subnormal responses in hypoadrenalism
Plasma ACTH level. Helps distinguish primary from
secondary hypoadrenalism
Insulin-induced hypoglycaemia stress test

30. Others:
Electrolytes
Low Na and high potassium in hypoadrenalism
Hypokalemia in Heprcorticolism
FBC: anaemia; leukocytosis
Radiodiagnosis for localisation
Inferior petrosal sinus sampling of ACTH to
distinguish Cushing disease from ectopic

31. Hyperaldosteronism
Serum K: Hypokalemia
Confirmation is by demonstrating subnormal supine and
erect plasma renin activity and elevated plasma
aldosterone
NB: Patient not on diuretic therapy for ≥3 weeks
 Aldosterone: Renin >30 in Primary aldosteronism
24-hour urinary aldosterone (especially when plasma
aldosterone not elevated but suppressed renin)
Saline infusion test: aldosterone fails to suppress with
expansion of ECF
Oral salt loading test for 3 days: aldosterone fails to
suppress

32. Adrenal medulla function tests
In phaeochromocytoma:
Screening by 24 hr urine metabolites e.g VMA or
metanephrines of cathecolamines. Useful.
NB: VMA less subject to drug interference but less
sensitive to metanephrines
Plasma or urinary free cathecolamines. More
specialised

33. THANK YOU