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Endocrinology > 8- The Adrenals And Their Hormones > Flashcards

8- The Adrenals And Their Hormones Flashcards

1
Q

Describe the structure of the adrenal gland

A

Adrenal Medulla = the centre of the
adrenal gland
• The outer part of the adrenal gland is the Cortex
• The adrenal cortex consists of THREE zones:
Zona Glomerulosa
Zona Fasciculata
Zona Reticularis

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2
Q

Describe the adrenal medulla

A

Made up of chromaffin cells (essentially post-ganglionic nerve fibres in a specialised form)
This means that there is part of the sympathetic nervous system where the cells innervated by the pre-ganglionic fibres will release their substances, not as neurotransmitters, but as hormones into the general circulation
Summary: CATECHOLAMINES ARE ASSOCIATED WITH CHROMAFFIN
CELLS IN THE ADRENAL MEDULLA

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3
Q

What are the products of the medulla and cortex

A 
• MEDULLA - Catecholamines
Adrenaline - 80% Noradrenaline - 20%
Dopamine - very small amounts
• CORTEX - Corticosteroids
Mineralocorticoids
• Aldosterone Glucocorticoids
• Cortisol Sex Steroids
• Androgens
• Oestrogens
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4
Q

Corticotrophin (ACTH) stimulates the adrenal production of cortisol

A

True

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5
Q

Cortisol is an important stimulator of the normal inflammatory response

A

False

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6
Q

Aldosterone secretion is principally controlled by the pituitary gland
Aldosterone is a mineralocorticoid
Aldosterone stimulates renal sodium excretion
Renin directly stimulates aldosterone production in the adrenals
Angiotensin I is a potent vasoconstrictor molecule

A

Ftfff

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7
Q

The adrenal cortex is the site of synthesis of catecholamines [a]
The left adrenal vein drains directly into the inferior vena cava [b]
The left adrenal gland is very close to the spleen [c]
All corticosteroids are synthesized from the initial precursor cholesterol [d]
Aldosterone is synthesised in the zona glomerulosa cells [e]

A

Ffttt

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8
Q

Which hormones are produced in the adrenals and which in the gonads

A

• Gonads:
Progestogens (C21) Androgens (C19) Oestrogens (C18)
Adrenals: Mineralocorticoids (C21) Glucocorticoids (C21) (Androgens)

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9
Q

What can Androstenedione can be converted into

A

testosterone and dihydrotestosterone

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10
Q

How are corticosteroids transported in the blood

A

Once in the blood, the corticosteroids could vanish by being taken up by non- target cells
• To provide protection, the vast majority of corticosteroids are bound to plasma proteins
• Cortisol
75% - bound to corticosteroid binding globulin (CBG or Transcortin) 15% - bound to albumin
10% - free (unbound) - BIOACTIVE!
• Aldosterone
60% bound to corticosteroid binding globulin 40% free (unbound) - BIOACTIVE!

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11
Q

What causes cortisol and aldosterone levels to fluctuate

A

Cortisol levels change depending on the time of day
• In addition, cortisol is released in PULSES - so there will be pulsatile release on
top of the circadian rhythm
• Aldosterone is NOT controlled by the pituitary so the time of day is NOT
important - but your position is important because aldosterone is involved in
the control of fluid and balance

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12
Q

How much more cortisol do we have than aldosterone

A

X1000

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13
Q

Describe the action of aldosterone

A

Stimulates Na+ reabsorption in the distal convoluted tubule and cortical
collecting duct
This is particularly important in the kidneys but is also important in sweat
glands, gastric glands and colon)
• Stimulates K+ and H+ secretion in the distal convoluted tubule and cortical
collecting duct
So it will have an effect on pH regulation of the blood

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14
Q

Describe aldosterone mechanism of action

A

Being a steroid hormone, aldosterone passes through cell membranes and binds to intracellular receptors
• The hormone-receptor complex moves to the nucleus and attaches to the DNA and switches on particular genes - it acts as a transcription factor
• Many of the proteins produced will be enzymes or pumps
• The proteins may well stimulate pumps like the ATPase pump on the
basolateral membrane which pumps sodium into the blood
• Aldosterone stimulates the synthesis of ion channels - in particular, sodium ion channels in the apical membrane

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15
Q

Describe the juxta glomerullar apparatus

A

Important in the control of aldosterone
• Aldosterone stimulates reabsorption of sodium ions so the concentration of sodium ions in the blood increases
• The increase in plasma osmolality stimulates the release of VASOPRESSIN
• Vasopressin works on the kidney collecting duct to increase water
reabsorption so the consequence of aldosterone is an expansion of
extracellular fluid volume
• Long Term - if you have a maintained expansion of extracellular fluid volume this leads to hypertension
• The main mechanism for controlling aldosterone resides in the KIDNEYS
• In the nephron, the glomerulus receives blood from an afferent arteriole and the blood leaves via an efferent arteriole
• The cells lining the ascending limb of the loop of Henle actually touch the cells that line the afferent arteriole
• There are specialised cells that lined this part of the afferent arteriole called the JUXTA-GLOMERULAR CELLS (because they are next to the glomerulus)
• The area of cells lining the ascending limb of the loop of Henle which are adjacent to the juxta-glomerular cells is called the MACULA DENSA
• The cells of the Macula densa respond to changes in SODIUM ION
CONCENTRATION
• Juxta-glomerular cells - source of an ENZYME called RENIN (pronounced
‘reenin’) which is important in the production of aldosterone

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16
Q

What are the 3 causes of renin release

A

Decreased renal perfusion pressure (normally associated with decreased
arteriole blood pressure)
• Increased renal sympathetic activity (direct to juxta-glomerular cells)
The JGA (juxta-glomerular apparatus) has sympathetic innervation The sympathetic system is activated when the blood pressure falls This leads to renin release
Decreased Na+ load to top of the loop of Henle
Decreased sodium concentration at the top of the loop of Henle This leads to activation of JGA and the release of renin

17
Q

How does renin stimulate aldosterone release

A

LIVER produces ANGIOTENSINOGEN (a large protein)
• Renin (released by juxta-glomerular cells) breaks down angiotensinogen to
ANGIOTENSIN I
• Then, ACE (angiotensin converting enzyme) converts angiotensin I to
ANGIOTENSIN II
• ANGIOTENSIN II stimulates the zona glomerulosa to produce aldosterone
• Angiotensin II also has OTHER EFFECTS:
VASOCONSTRICTOR
• Other factors affecting aldosterone production:
Corticotrophin has a permissive effect - it will enhance the renin- angiotensin system
Angiotensin regulates ions
If the blood plasma sodium ion concentration falls, it has a direct effect in stimulating aldosterone production - so there is more sodium reabsorption and sodium concentration returns to normal
Aldosterone is also the main mechanism for regulating POTASSIUM in our bodies - an increase in potassium concentration stimulates aldosterone production leading to increased secretion of potassium

18
Q

Describe the metabolic effects of cortisol

A

Stimulates peripheral protein catabolism
• Cushing’s syndrome (excessive production of cortisol) - arms and
legs are really thin because they’ve lost a lot of muscle Hepatic gluconeogenesis
Fat metabolism
Enhances effects of glucagon and catecholamines
Stimulates glycogenolysis
Makes tissues less responsive to insulin
OVERALL EFFECT IS TO INCREASE BLOOD GLUCOSE CONCENTRATION
• There are some mineralocorticoid effects
• There are some renal and cardiovascular effects
• There are some other effects (e.g. on bone, CNS, growth)

19
Q

What are the effects of large amounts of cortisol

A

ANTI-INFLAMMATORY ACTION
• IMMUNOSUPPRESSIVE ACTION
• ANTI-ALLERGIC ACTION
These are all associated with decreased production of molecules such as prostaglandins, leukotrienes, histamine etc. as well as on the movement and function of leukocytes and the production of interleukins.

20
Q

Describe corticosteroid receptors

A

Mineralocorticoid Receptor is what aldosterone binds to (they are called mineralocorticoids because they have an effect on salt and water balance
• Aldosterone acts almost entirely on the mineralocorticoid receptor (MR)
• Cortisol binds to the Glucocorticoid Receptors and the Mineralocorticoid
Receptors equally
• The concentration of cortisol in the blood is about 1000 times greater than that
of aldosterone but cortisol isn’t constantly binding with MR because:
The kidneys have an enzyme which converts bioactive CORTISOL to CORTISONE (inactive)
Enzyme: 11β-hydroxysteroid dehydrogenase 2
This enzyme constantly removes the cortisol so it doesn’t interfere with the mineralocorticoid receptors

21
Q

Decreased cortisol mechanism of action

A

Cortisol binds to its intracellular receptor and has a GENOMIC EFFECT
• Example of how cortisol might work:
One of the proteins produced by the cell in annexin 1
Annexin 1 leaves the cell and has an autocrine effect - it binds to its own annexin 1 receptor
This binding has an effect on a phospholipase enzyme which works on the phospholipids in the membrane to produce arachidonic acid (precursor for prostaglandins)
Cortisol blocks the production of arachidonic acid thereby decreasing prostaglandin synthesis

22
Q

Describe control of cortisol

A

Corticotrophs are controlled by hypothalamic hormones
• Cortisol has negative feedback effects direct to the pituitary and indirectly to
the hypothalamus
• ACTH has an auto-negative feedback loop to the hypothalamus
• There is a circadian rhythm for cortisol which originates from the biological
clock which resides in the suprachiasmatic nucleus
• Because of the variation in cortisol levels with time, blood sampling should be
arranged so that it is taken at times when cortisol levels are expected to be at its highest or lowest

23
Q

What is DHEA-Dehydroepiandrosterone

A

This is a very weak androgen
• Precursor for androgens and oestrogens
• Converted to active hormones within target cells (which have appropriate
enzymes)
• Peak serum levels at 20-30 years, then decreasing steadily with increasing age
• Particularly important in post-menopausal women as a precursor for
oestrogen (and androgen) synthesis by target tissue in the absence of ovarian steroids

Endocrinology (12 decks)

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