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Adrenal Gland

Located on top of kidneys

Appears to be fatty on the surface due to the fact that it produces only
lipophilic hormones

Location and Blood Supply

Supplied by three paired suprarenal arteries
o Left/right superior suprarenal artery (from inferior phrenic artery)
o Left/right middle suprarenal artery (from abdominal aorta)
o Left/right inferior suprarenal artery (from renal artery)
Drained by suprarenal vein which enters renal vein then inferior
vena cava
Anatomy of the Adrenal (superficial to deep)
Outer capsule = high collagen content for protection
Adrenal cortex
o Zona glomerulosa produces mineralocorticoids (salt)
Releases aldosterone, which is a mineralocorticoid
hormone
Increases renal retention of sodium by excreting potassium
Water osmotically follows ions thus adjusts blood pressure
Controlled by renin-angiotensin-aldosterone (RAA) pathway
o Zona fasciculata produces glucocorticoids (sugar)
Primary hormone product is cortisol
Promotes protein and fat breakdown
Gluconeogenesis = promotes glucose formation from the
substrates of protein and fat breakdown
Anti-inflammatory and immunosuppressant, thus cortisol
can be used to treat autoimmune disease
Resistance to stressors
o Zona reticularis produces androgens (sex)
Primary androgen secreted is DHEA
In post-pubertal males, most androgen secretion is
from the testes in the form of testosterone
In females, adrenal androgens undergo peripheral
conversion to estrogen by enzymes in adipocytes
After menopause, DHEA conversion allows a supply
of some estrogen (albeit a lot less than before)
Adrenal medulla = releases E and NE into bloodstream
Regulation of Aldosterone Secretion

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1. Stimulus = decreased blood volume from dehydration, Na+ deficiency,
hemorrhage
o Blood volume drop results in decreased BP
2. Juxtaglomerular cells of kidney detect BP of blood entering kidney
o Releases renin in response to decreased BP
3. Angiotensinogen from liver is activated by renin to from angiotensin I
4. Angiotensin I is acted on by angiotensin converting enzyme (ACE) from
lungs to bioactive angiotensin II, which:
o Directly increases vasoconstriction of arterioles to increase BP
o Activates zona glomerulosa to release aldosterone, which
increase blood volume, which also increase BP
5. Increase in BP provides negative feedback to juxtaglomerular cells
**Aldosterone is released not only as a result of angiotensin II, but high
potassium levels causes aldosterone release directly
In this case, cells of adrenal cortex = detector + control center
HPA Axis Regulation of Cortisol
1. Physiological and psychological stressors promote release of CRH by
hypothalamus
2. CRH promotes ACTH from anterior pituitary
3. ACTH stimulates zona fasciculata to produce cortisol
4. Cortisol exerts negative feedback on the hypothalamus and anterior
pituitary
5. Release of ACTH also causes release of DHEA from the zona reticularis
However, DHEA does not contribute to the negative feedback of ACTH
and CRH, only cortisol does
Adrenal Medulla
most inner portion of adrenal gland
Modified sympathetic ganglion of autonomic nervous system
o Expresses nicotinic ACh receptors
Nerve impulses to sympathetic centers in spinal cord activates
splanchnic nerve which then innervates medulla
Secretes 80% epinephrine and 20% norepinephrine
Stress Response
1. Alarm phase (sympathetic activation, fight/flight response)
o Epinephrine is released from adrenal medulla
o Cortisol is released from adrenal cortex
2. Adaptation occurs when stressor did not go away
o Cortisol levels are elevated
o Helps adaptation, coping or resistance to stressor
o Cortisol suppresses non-essential functions such as
inflammation, immune function parasympathetic functions,
SLUDD, reproduction, growth, healing)

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3. Exhaustion inability to cope with the stressor
o Prolonged sympathetic state leads to illness or death
o Adaptation phase can only be maintained for so long
Stressors
Emotional, hot or cold environment, toxins, infection, hemorrhage
Eustress helps preparation for certain challenges
Distress bad stress

Diseases of the Adrenal Gland

Commonly due to excessive or insufficient levels of cortisol
Less commonly due to disorders of aldosterone secretion and
medullary hypersecretion
Cushings Syndrome
Due to prolonged elevation of cortisol (hypercortisolism)
Endogenous source = ACTH secreting tumor on AP, functional adrenal
adenoma secreting cortisol
Exogenous source = glucocorticoid application
Symptoms
o Atrophy of skeletal muscle (since proteins are broken down for
gluconeogenesis)

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o Redistribution of body fat from appendages to face and back
(moon face, buffalo hump)
o Weight gain due to increased appetite
o Hyperlipidemia and hyperglycemia
o Skin striae
o Hypertension, hyperglycemia, which can lead to diabetes
o Osteoporosis, as growth is inhibited
o Susceptibility to infection and poor wound healing
Addisons Disease
Decreased glucocorticoid and aldosterone production
Autoimmune destruction of adrenal cortex or ACTH-R
Primary adrenal insufficiency due to atrophy of gland
Secondary adrenal insufficiency due to lack of CRH or ACTH
Withdraw symptom from exogenous cortisol (need to slowly take away
cortisol dose to wake up the endogenous cortisol synthesis pathway)
Symptoms of cortisol loss
o Hypoglycemia
o Weakness due to lack of glucose
o Weight loss
Symptoms of aldosterone loss
o Hyponatremia (decreased serum Na)
o Dehydration
o Hypotension
o Hyperkalemia (increased K), leading to cardiac arrhythmia by
bringing resting membrane potential closer to action potential
threshold
Congenital Adrenal Hyperplasia
Rare autosomal recessive disorder
21 hydroxylase enzyme deficiency leads to inability to produce cortisol
or aldosterone
Causes increase in CRH and ACTH
o Leading to excessive androgen production without negative
feedback
Leads to increased production of androgens and steroid metabolites
Presentation in males:
o Premature development of male secondary sexual characteristics
o Severe illness within days of birth due to hyponatremia and
hyperkalemia
o Treated with dexamethasone (exogenous cortisol) and salt
replacement therapy
Presentation in females:

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o Female virilisation: hirsutism, clitoral enlargement, deepened
voice, amenorrhea, breast atrophy, acne, increased libido