Adrenal Gland Flashcards

1
Q

Where is the adrenal gland located?

A
  • Above the kidneys
  • Left adrenal gland and right adrenal gland
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2
Q

What are important anatomical landmarks near the adrenal gland?

A
  • Inferior vena cava (huge veins comes in the legs, picks up renal veins) - behind it is adrenal gland
  • 57 arteries come out aorta and survive adrenal gland but only 1 central adrenal vein
  • Left adrenal vein drains into renal vein, Right adrenal vein drains into IVC. Both adrenals have many arteries but 1 vein
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3
Q

Describe the microanatomy of the adrenal glands

A
  • Adrenal cortex (secretes corticosteroids) : Zone glomerulosa, Zone fasciculata, Zone reticularis
  • Adrenal medulla (secretes catecholamines)
  • Catecholamines : adrenalin/epinephrine 80% , noradrenaline/norepinephrine 20%
  • Corticosteroids: mineralcorticoids (aldosterone), glucocorticoids (Cortisol), sex steroids (androgens, oestrogens)
  • Zone glomerulosa- aldosterone , Zone fasciculata & reticularis- cortisol (androgens, oestrogens)
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4
Q

What is a steroid? Draw the structure of cholesterol.

A
  • A molecule based on cholesterol
  • C17 important- often hydroxylated
  • C17 & C20 bonded directly - there is an enzyme that cleaves this
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5
Q

What is an enzyme? What is its purpose in making steroids?

A
  • Protein that catalyses a specific reaction
  • Various enzymes present in cells
  • Specific enzymes catalyse the synthesis of particular alterations to the molecule
    (diagram: left two columns occur in adrenal gland, 17, 21 etc (hydroxylase on that position)
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6
Q

What is aldesterones mechanism of action?

A
  • Major net effect is to conserve body sodium by stimulating its reabsorption
  • Aldesterone binds to receptor & turns on synthesis of pumps. Na+ pumped in from urine into blood. So blood pressure raised and increases water resorption because water moves by osmosis
  • Stimulates Na+ reabsorption in distal convoluted tubule and cortical collecting duct in kidney (sweat glands, gastric glands, colon)
  • Stimulates K+ & H+ secretion, also in distal convoluted tubule and cortical collecting duct
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7
Q

How is a fall in blood pressure detected?

A
  • Macula densa measures blood pressure constantly
  • If blood pressure falls, it releases renin

( decreased renal perfusion pressure - associated with decreased arterial BP)

(increased renal sympathetic activity- direct to JGA cells)

(decreased Na+ load to top of loop of henle - macula densa cells)

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8
Q

How is aldosterone regulated?

A
  • Renin comes out of kidney due to low blood pressure
  • Liver always making angiotensin (inactive)
  • Renin binds to it, chops up side chain, activates production of angiotensin I
  • Angiotensin I converted to Angiotensin II in lung - this constricts blood vessels (maintain blood pressure)
  • Angiotensin II binds to receptors in zona glomerulosa of adrenal cortex, switches on enzyme hydroxylases, increase synthesis of aldosterone
  • Aldosterone out of adrenal gland to kidney, causes retention sodium from urine
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9
Q

What is the regulator of aldosterone release?

A
  • Angiotensin II
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10
Q

What is the effect of angiotensin II on the adrenal gland?

A
  • Activation of following enzymes :

Side chain cleavage, 3 hydroxysteroid dehydrogenase, 21 hydroxylase, 11 hydroxylase, 18 hydroxylase

  • Occurs in zona glomerulosa
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11
Q

What is the structure of aldosterone

A
  • DOuble bonds with O (ketone) instead of -ol
  • oxidised
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12
Q

What are the physiological effects of cortisol?

A
  • It is the normal stress response
  • Metabolic effects: peripheral protein catabolism, hepatic gluconeogenesis, increased blood glucose concentration, fat metabolism (lipolysis in adipose tissue), enhanced effects of glucagon and catecholamines
  • Weak mineralcorticoid effects
  • Renal & cardiovascular effects: excretion of water load, increased vascular permeability

(not fight or flight - this occurs in medulla. pre-fight or flight response)

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13
Q

How is cortisol secretion regulated?

A

ACTH - adrenocorticotropic hormone

  • Stress enters cerebral cortex
  • Hypothalamus releases CRH (corticotrophin releasing hormone)
  • CRH stimulates synthesis and release of ACTH from corticotrophic cells in anterior pituitary gland
  • ACTH stimulates adrenal gland to produce cortisol at the zona fasciculata
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14
Q

Describe the negative feedback of cortisol?

A
  • Cortisol negatively feebacks at 2 levels : hypothalamus (using portal circulation) & pituitary directly
  • Lots of cortisol turns off production of ACTH
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15
Q

Draw the HPA axis (hypothalmo pituitary adrenal):

A
  • Draw negative sign
  • 3 dots signify different cells (corticotrophs gonadotrophs etc)
  • Write out full words
  • Remember two arrows
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16
Q

What are the effects of ACTH on the adrenals?

A
  • Activation of the following enzymes :

Side chain cleavage, 3 hydroxysteroid dehydrogenase, 21 hydroxylase, 11 hydroxylase, 17 hydroxylase

  • Occurs in zona fasciculata
17
Q

Describe what the diurnal rhythm of cortisol is:

A
  • Take blood tests of patients regulary from 10pm - 8 am while they sleep and not down cortisol levels (uses cannula)
  • Midnight cortisol is low (provided you sleep properly)
  • 5.00 am level rises
  • Peaks at around 8.30 am
  • Some people have blips at breakfqs lunch dinner
  • Important to know differences can occur depending on time - might not be bad
18
Q

Describe what you would see in cortisol levels in one individual:

A
  • Cortisol levels bit pulsatile
  • Instead of smooth curve, more pulses (ultradian rhythm)
19
Q

ACTH vs cortisol pulses:

A
  • Shows how ACTH pulses hour or half an hour later than cortisol
20
Q

What is Addisons disease? What can cause it?

A
  • Thomas Addison
  • Primary adrenal failure - adrenal gland destroyed
  • Tuberculosis of adrenal glands ( Tb bacterium grows in lungs because you inhale it, get pneumonia, if you survive it would destroy adrenal gland)
  • Autoimmune disease where immune system destroys adrenal cortex
  • Pituitary starts secreting a lot of ACTH and hence MSH
21
Q

Symptoms of Addisons disease:

A
  • Skin hyperpigmented
  • Low blood pressure, weakness, weight loss
  • Gastrointestinal - nausea, diarrhea, vommiting, constipation, abdominal pain
  • Skin vitiligo
  • ADRENAL CRISIS: fever, syncope, convulsions, hypoglycemia, hyponatremia, severe vomiting, diarrhea
22
Q

Why do patients with Addisons disease have a good tan?

A
  • POMC is a large precursor protein that is cleaved to form a number of smaller peptides, including ACTH, MSH, endorphins
  • POMC (Pro-opio-melanocortin)
  • People who have pathiologically high levels of ACTH may be tanned
  • ACTH is co-secreted with Melanin stimulating hormone (MSH) - makes you more pigmented
23
Q

What can you give as urgent treatment for Addisonian crisis?

A
  • Rehydrate with normal saline
  • Give dextrose (glucose) to prevent hypoglycaemia which could be due to the glucocorticoid deficiency
  • Give hydrocortisone or another glucocorticoid
24
Q

What is Cushing’s syndrome? What causes it?

A
  • Too much cortisol ; metabolism changes & put on weight
  • Tumour in adrenal gland or pituitary causes Cushings
  • Tumour of zona fasciculata ; one cell becomes tumour grows and grows & makes cortisol out of control
  • Tiny pituiatry tumour that makes excess of ACTH which drives adrenal gland to produce excess cortisol
  • Both Cushing’s syndrome
25
Q

What are the features of Cushing’s syndrome?

A
  • Red cheeks, moon face, mental changes (depression)
  • Fat pads, easy bruising, thin skin, stretch marks, pendulous abdomen, poor wound healing
  • Impaired glucose tolerance, high blood pressure, proximal myopathy, thin arms and legs
  • Too much corticosteroid you retain sodium,become oedematus, blood pressure goes up,
  • Lose protein, cortisol makes you retain sodium and lose protein (inhibits protein synthesis) wounds dont heal well, bruise a lot
26
Q

What are 4 possible causes of Cushing’s syndrome?

A
  • Taking steroids by mouth (common):

(Big dose of cortisol can suppress immune system - good for other autoimmune diseases, good for asthma)

  • Pituitary dependent Cushing’s disease (pituitary adenoma)
  • Ectopic ACTH (lung cancer) - cancers can express random genes, expresses ACTH, ectopic (wrong place)
  • Adrenal adenoma or carcinoma
27
Q
A
28
Q

What are the clinical signs of Cushing’s disease?

A
  • Thin skin, moon face, striae
  • Proximal myopathy
  • Centripetal obesity (lemon on sticks)
  • Diabetes, hypertension and osteoporosis
  • Immunosuppression (reactivation of TB)
  • These are also side effects of glucorticoids and signs you see in Cushing’s syndrome
29
Q

What does the adrenal medulla produce?

A
  • It makes the catecholamines :

adrenaline (epinephrine 80%) , noradrenaline (norepinephrine 20%)

30
Q
A
31
Q

How is adrnealine produced?

A
  • Comes from dopamine (not a steroid as not made from cholesterol)
  • Amino acid tyrosine oxidised to dopa oxidised to dopamine
  • Dopamine is one of amines that controls blood pressure
  • In adrenal medulla, dopamine modified by oxidisng to norepinephrine and then adding methyl group to make epinephrine (adrenaline)
  • Catecholamines stored in cytoplasmic granules & released in response to ACh from preganglionic sympathetic neurones
32
Q

What is the role of catecholamines?

A
  • Noradrenaline and adrenaline bind to alpha beta receptord and cause rapid activation of vasoconstriction
  • Fight or flight response e.g, tachycardia, sweating, increased blood glucose, alertness, vasoconstriction
  • Na & Adr circulate bound to albumin
  • Degraded by two hepatic enzymes: monoamine oxidase & catechol-O-methyl transferase