ANATOMY (GROSS & HISTOLOGY)

PHYSIOLOGY
ADRENAL DISORDER
CAUSES
EXAMINATION
INVESTIGATION

Mineralocorticoid
Glucocorticoid
Androgens

Medulla
Catecholamines

Cortex

ZONA
GLOMERULOSA
(G)

ZONA
FASCICULATA
(F)

ZONA
RETICULARIS
(R)

HORMONE
SECRETED

Mineralocorticoids

Glucocorticoids

Adrenal androgens

REGULATION /
CONTROL

Renin-angiotensinaldosterone system

Hypothalamicpituitary axis

Hypothalamicpituitary axis

ACTH
DEPENDENT

Only for the first step

in steroid biosynthesis

+
Na

reabsorption

+
K

secretion

H+
secretion

Stimulation of
gluconeogenesis

( gluconeo, proteolysis, lipolysis & glu

utilisation, insulin sensitivity)

Antiinflammatory effects

(induces the synthesis of lipocortin which inhibit

phospholipase A2, inhibit the release of
histamine & serotonin from mast cells

Suppression of immune
response

(inhibit production of IL-2 & proliferation of T

lymphocytes)

Maintenance of vascular
responsiveness to
catecholamines

(up-regulating 1-adrenergic receptor in

arterioles)

Inhibition of bone formation

Increase in GFR

Effect on limbic system

( osteoblast collagen production, intestinal

Ca2+ absorption)
(vasoD of aferent arterioles)

( REM, slow-wave sleep, awake time)

ADRENAL
MEDULLA

ADRENAL CORTEX
HYPER

CUSHINGS
SYNDROME

HYPO
PRIMARY
HYPERALDOSTERONISM

ADDISONS
DISEASE

PHEOCHROMOCYTOMA

Primary

Destruction of
adrenal gland

Secondary

Pituitary
dysfunction

Adrenal
insufficiency

AUTOIMMUNE (80%)

TB

Metastatic tumour
(lung, breast, renal) &
lymphoma

Adrenal haemorrhage
(WaterhouseFriedrichsen
syndrome)

Opportunistic
infection of HIV (CMV,
fungal infection)

Amyloidosis

Congenital (late-onset
CAH)

Destruction of adrenal
gland

Mineralocorticoid &
glucocorticoid deficiency

Mineralocorticoid deficiency

Glucocorticoid deficiency

in urinary excretion of Na, in urinary

excretion of K

Disturbances in carbohydrate, fat and

protein metabolism, decrease liver glycogen

Inability to concentrate urine, with

electrolyte imbalance

Hypoglycaemia and anorexia

severe dehydration

plasma hypertonicity, acidosis, hypotension

circulatory collapse

Often diagnosed late

Weakness, fatigue
Loss of appetite, loss of weight, anorexia
Dizziness, syncope
GI symptom: Nausea, vomiting, abdominal pain, diarrhoea,
constipation
Skin pigmentation (ask if has been sitting in the sun)
Mood: Depression, psychosis, low self-esteem
Myalgia, arthralgia
Addisonian crisis: oliguria, weak, confused, comatose,
hypoglycaemic symptoms (cold peripheries, excessive sweating,
hunger, syncope)
* Think of Addisons in all those with unexplained abdominal symptoms

 Examine for hyperpigmentation:

Hand: palmar creases

Mouth and lips
Areas usually covered by clothing: nipple
Areas irritated by belts, straps, collars or rings

Look for vitiligo

Look for sparse axillary hair and pubic hair
Examine the abdomen for adrenal scar
Examine blood pressure for postural hypotension
DXT: hypoglycaemia
Signs of critical deterioration (Addisonian crisis):
Shock (low BP, tachycardia)
hypothermia

BUSE
Low Na
High K
Low HCO3
Azotemia

FBC

RBS / DXT

Elevated
hematocrit
Low WBC
count
Relative
lymphocytosis
Increased
eosinophils

Hypoglycemia
(< 3 mmol/L)

AXR
CXR

Calcifications in the
adrenal areas - PTB

Small heart

 A single depressed plasma cortisol level in a

Primary
(2
patient Plasma
who is severely stressed or in shock is
ACTH
highly suggestive
ofnegative
adrenal insufficiency
level
Plasma cortisol
feedback)
Short ACTH stimulation
test (Synacthen
level at 30 test):
90
IV
Tetracosactide
250 g
Plasma
ACTH
Preinjection
level
plasma cortisol

level (N= 138

690 nmol/L)

minutes post
injection ( 500
nmol/L
Failure to
respond
adrenal
insufficiency (?
Primary /
secondary)

Secondary

Negative
Synacthen
test

ADDISONS

DISEASE
High
plasma
ACTH level

 Tumour of chromaffin cells

80% of pheochromocytomas are found in the
adrenal medulla, usually benign
Extra-medulla tumors 1-3% in chest and
neck (usually malignant)
20% multiple, 10% malignant
Part of familial syndromes MEN Type II
(Sipples syndrome), neurofibromatois and
von Hipple-Lindau disease

 Hypertension, may be paroxysmal or persistent. Due

to secretion of one or more of catecholamine
hormones or precursors: norepinephrine,
epinephrine, dopamine or dopa.
Tachycardia, sweating, postural hypotension,
tachypnea, flushing, cold and clammy skin, severe
headache, angina, palpitation, dyspnoea
Paroxysmal attacks may be provoked by exercise,
anaesthesia, palpation of tumor, postural changes,
urination, beta-blockers

 Screening
- Two 24 h urines for catecholamines is the best screening
investigation
- 24 h urine for VMA (15% false negative) and metanephrine
(10% false negative) - needs vanilla-tree diet before collection
If the diagnosis is established, or strongly suspected
MIBG scan - meta-iodo-benzylguanidine labeled with 131I
- Increased uptake by pheochromocytoma
CT scan of adrenals - patient should be alpha- and betablocked to avoid hypertensive episode after contrast
administration