Zona Glomerulosa

Zona Fasiculata




Zona Reticularis
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Steroid Hormones
Glucocorticoids
CHO, lipid & fat metabolism
Increases blood glucose levels & gluconeogenesis
Increases protein breakdown
Inhibits protein synthesis

Mineralcorticoids
Elecrolyte & fluid balance
Increases sodium & water retention
Regulated by renin & andiotensin
Sex Steroids
Low synthesis in adrenals compared to gonads
Virilising hormones may be secreted
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Conditions Affecting Adrenal Cortex
Adrenocortical Hyperfunction
Cushings syndrome
Increased glucocorticoid levels
Hyperaldosterone
Excessive water retention Ht
Adrenogenital syndromes
Excess androgens (testosterone) in peripheral tissue
Dehydroepiandrosterone
Androstentendione

Adrenocortical Insufficiency
Acute Adrenocortical Insufficiency
Chronic Adrenocortical Insuffeciency (Addisons)

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Acute Adrenocortical Insufficiency
Aetiology & pathogenesis
Sepsis Waterhouse-Friderichsen syndrome
Neisseria meningitidis (classic)
Pseudonomas; pneumococci; H. influenzae (others)
Unclear pathogenesis endotoxin induced vascular injury
(massive haemorrhage) with associated DIC
Sudden withdrawal of long term corticosteroid
treatment
Inability of atrophic adrenals to produce glucocorticoids
Stress with underlying chronic adrenal insufficiency
Acute adrenal crises on limited physiological reserves




Massive adrenal
haemorrhage, resulting in
primary acute adrenal
insufficiency
Metastatic breast
carcinoma affecting the
adrenal gland and causing
primary chronic adrenal
insufficiency
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Chronic Adrenocortical Insufficiency
Addisons Disease
Aetiology & pathogenesis
Primary Addisons disease
Secondary causes
Tuberculosis caseous necrosis of adrenal cortex
Autoimmune adrenalitis
Ass with e.g. pernicious anaemia; thyroiditis; IDDM
AIDS
Metastatic disease
Systemic amyloidosis
Fungal infections
Haemochromatosis
Sarcoidosis




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Morphology
Primary autoimmune adrenitis
Irregularly shrunken glands
TB; fungi; sarcoidosis
Granulomas in adrenals
Metastatic Ca
Adrenals enlarged
achitecture obscured
Secondary hypoadrenalism
Adrenals small & flattened
Atrophy of corticol cells
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Clinical Features
Insidious onset
Progressive weakness & fragiability
Non-specific complaints (anorexia; N/V; WL)
Primary adrenal disease
Hyperpigmentation (increased ACTH)
Hyperkalaemia & hyponatraemia
Hypotension (volume depletion) & dehydration
Hypoglycaemia
Sexual dysfunction
Adrenal crises
Infections; trauma; sugery intractable vomiting; abdominl
pain; hypotension; vascular collaspe death
Diagnosis
Low plasma cortisol
Laboratory findings.
1. A low serum Na level and a high serum P level together
with a characteristic clinical picture suggest the possibility of Addisons
disease.
2. Adrenal insufficiency can be specifically diagnosed by:
low levels of plasma glucocorticoids and
mineralocorticoids, or urinary 17 hydroxycorticosteroid
(17 OHCS) or 17 ketogenic steroid (17 KGS);
demonstrating failure to increase plasma cortisol levels,
or urinary 17 OHCS or 17 KGS excretion, upon
administration of ACTH (in patients with primary adrenal
insufficiency, those with secondary adrenocortical insufficiency will have
a significant increase in plasma cortisol or 24 - h urinary corticosteroid
levels.)
3. To distinguish between primary and secondary adrenal insufficiency, me
have to find the level of plasma ACTH: primary shows increased, and
secondary shows decreased level.
Features of Addisons d.
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This is a caseating granuloma of tuberculosis in the adrenal gland.
Tuberculosis used to be the most common cause of chronic adrenal
insufficiency.
Now, idiopathic (presumably autoimmune) Addison's disease is much more
often the cause for chronic adrenal insufficiency.
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The pair of adrenals in the center are normal.
Those at the top come from a patient with adrenal atrophy (with either Addison's
disease or long-term corticosteroid therapy).
The adrenals at the bottom represent bilateral cortical hyperplasia.
This could be due to a pituitary adenoma secreting ACTH (Cushing's disease), or
Cushing's syndrome from ectopic ACTH production, or idiopathic adrenal hyperplasia.
Case Discussion

A 26-year old man is admitted to the
Intensive Care Unit
3 days vomiting hourly
Drowsy
BP 60/30
Deeply pigmented
Na+ 125 mmol/l (N 135-145)
K+ 5.4 mmol/l (N 3.5-5.0)
Questions
Diagnosis
Pathogenesis
What hormone is deficient
Diagnostic test
Treatment
Complications
Addisons disease
Pathogenesis
Destruction of adrenal glands
Autoimmune
Tuberculosis
Tumour/infiltration
Infective (meningococcus)
Hormone deficiency
Cortisol
Aldosterone
Diagnostic test
Synacthen test
Treatment
Cortisol replacement
Hydrocortisone/Cortisone
Aldosterone replacement
Fludrocortisone
Complications
Adrenal crisis intercurrent illness
Synacthen test
Pituitary
Cortisol
Adrenal
gland
Synacthen
(=synACTHen)
Baseline cortisol may be
normal in Addisons disease
Synacthen test: uses
synthetic ACTH analogue
Normal response: rise in
cortisol