ADRENAL FUNCTION
Embryology and Anatomy

2 Embryologically distinct but conjoined glands

Outer: Adrenal Cortex

Inner: Adrenal Medulla
G-Zone
- Refers to the zona glomerulosa (Outermost layer which is 10%)
- Synthesizes mineralocorticoids (Aldosterone)
- Functions:

Sodium Homeostasis

Potassium Homeostasis

Acid-Base Balance

Cell:

Distinct in a way that they have small cytoplasmic:
Nuclear Ratio.

With dense chromatin with intermediate lipid inclusions
F-Zone
- Zone Fasciculata (75%)
- Synthesizes glucocorticoids (cortisol)
- Function: Glucose homeostasis
- Cells has a high cytoplasmic to nuclear ratio
- It Generates DHEA (Dehydroxyepiandrosterone) which plays a
role in zona reticularis
R-Zone
- Zona Reticularis
- Innermost layer (10%)
- Sulfates DHEA to DHEAS
- Cells: Sharply demarcated with lipid-deficient cords of irregular,
dense cells with lipofuscin deposits.
DHEA
- Serves a raw material
Cortex
- Cortisol, Sex Hormones
Medulla
- Epinephrine and norepinephrine
CORTISOL
- Principal glucocorticoid.
- 90% is inactive (requires hypoglycemia).
- Increases blood glucose level.
- The only adrenal hormone that inhibits the secretion of ACTH.
- With anti-inflammatory and immunosuppressive actions.
- Secretion is diurnal (6am-8am).
- Sample that can be used in analysis: Serum, plasma, saliva, and
urine.
Urinary Metabolites:

17-Hydroxycorticosteroid
- Measure by Porter-Siber Method
- Reagent: Phyenyl hydrazine in

17-Ketogenic Steroids
All hormones produced by the adrenal cortex are steroids
(hormones that are synthesized by cholesterol making them
appear with fatty characteristics).
Clinical Disorders
Hypercortisolism “Cushings Syndrome”
- Excessive production of ACTH or Cortisol
- Overuse of corticosteroids.
Signs:

Weight gain but with thin extremities.

Hyperglycemia

Thinning of the skin

Lymphocytopenia
Diagnosis:

Appearance of the Clinical Symptoms

Laboratory Findings:

Cortisol excess

Loss of Diurnal Rhythm

Suppression Resistance

Urine Free Cortisol (and/or metabolites)

Screening Test:

24hr urinary free cortisol test

Overnight dexametha
HYPOCORTISOLISM

Primary Hypocortisolism (Primary Adrenal Insufficiency)
- Also called Addison’s disease
- It is caused by 90% destruction of the adrenal cortex
- Screening test: ACTH Stimulation Test
- Associated with Koilonychia or spooning of the nails with bronze
pigmentation.

Secondary Hypocortisolism (SAI)
- It is due to hypothalamic-pituitary insufficiency
- Screening test: ACTH Stimulation Test
CORTEX STEROIDOGENESIS
- Controlled by 3 factors:

Substrate Availability

Enzyme activities

Inhibitory Feedback loops
- All adrenal steroids are derived by sequential enzymatic
conversion of a common substrate, CHOLESTEROL (made by
“pregnenolone” which is the precursor or generally bad
cholesterol).
- Adrenal Parenchymal cells: Functions in “Storage”.
Disorders
Congenital Adrenal Hyperplasia (CAH)
- Inherited family of enzyme disorders causing decreased cortisol
production.
- 5 enzymes:

P450 (StAR deficiency) – most fatal (Deficiency in
aldosterone and DHEA)
- Symptoms:

Shock (hypovolemic/hypoglycemic)

Salt-washing

Anomalous sexual development (Boy but with female
characteristics).

Hirsutism

Infertility
Impotence – Sexual drive issues
Infertility – Sex cell issues
Enzyme Deficiency
21-Hydroxylase Deficiency