ENDO - Physiology of The Adrenal Gland Flashcards

1
Q

Describe the layers of the adrenal glands.

A
  • Cortex consisting of the zona glomerulosa, zona fasciculata and zona reticularis
  • Adrenal medulla
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2
Q

Describe the different hormones produced by different parts of the adrenal glands.

A
  • Glomerulosa produces aldosterone (a mineralocorticoid)
  • Fasciculata produces cortisol and corticosterone (a glucocorticoid)
  • Reticularis produces sex hormones (mainly testosterone and its precursors)
  • Medulla produces the fight or flight hormones adrenaline and noradrenaline
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3
Q

Describe the anatomy of the adrenal glands. PART 1

A
  • Only the adrenal medulla receives secretomotor innervation from the sympathetic nervous system
  • Sympathetic innervation of the adrenal medulla arises from the splanchnic nerve. The splanchnic nerve originates from between T3-L3, but those fibres innervating the adrenal gland arise from T8-T11
  • Some of these preganglionic fibres synapse in the coeliac ganglion, which gives rise to post-ganglionic fibres which innervate blood vessels
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4
Q

Describe the anatomy of the adrenal glands. PART 2

A
  • Other preganglionic fibres directly innervate medullary chromaffin cells via a cholinergic synapse to stimulate adrenaline and noradrenaline secretion.
  • Each chromaffin cell is innervated by a preganglionic, cholinergic sympathetic fibre.
  • Acetylcholine binds to nicotinic receptors on the chromaffin cell, which depolarises the membrane leading to calcium influx (through opening of a voltage-gated calcium channel), and subsequent exocytosis of noradrenaline and adrenaline filled vescicles
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5
Q

Describe some of the general effects of adrenaline and noradrenaline.

A
  • Tachycardia
  • FFA mobilisation
  • Pupil and bronchial dilation
  • Reduced GI motility
  • Glycogenolysis - rise in plasma glucose
  • Piloerection and cutaneous vasoconstriction
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6
Q

Describe the responses of the sympathetic nervous system.

A
  • Stress-activated
  • Response is fast (milliseconds) and targeted (each organ can be directly stimulated by discrete neuronal fibres).
  • Sustaining such neural activation for long is energy demanding due to the amount of ATP required for action potential generation
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7
Q

Describe the responses of the adrenal glands.

A
  • Much slower to respond (minutes)
  • Effects are not targeted to specific organs, because adrenaline is released into the blood stream.
  • Activation of a single nerve fibre can cause the release of adrenaline - much less energy demanding to produce an effect and because adrenaline can be released continuously if needed for very little energy, effects are sustained over longer periods of time
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8
Q

Pheochromocytomas are chromaffin cell tumours that secrete excess adrenaline and noradrenaline. With this in mind, suggest some presenting complaints of someone with this.

A
  • Heat intolerance
  • Sporadic tachycardia
  • Hypertension
  • Pallor
  • Hyperglycaemia
  • Pani attacks
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9
Q

Describe what the zona glomerulosa and the JGA produce.

A
  • Zona glomerulosa produces aldosterone exclusively
  • JGA - collection of cells surrounding afferent arteriole and DCT - produce renin (in low sodium and blood volume)
  • Both contribute to RAAS
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10
Q

Describe the mechanism of action of aldosterone. PART 1

A
  • Works on the collecting ducts and DCT to increase sodium reabsorption
  • Binds to the mineralocorticoid receptor in the cell nucleus
  • Increased expression of ENaC in the apical membrane.
  • Influx of sodium channels down their concentration gradient, out of the filtered fluid and into the cell.
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11
Q

Describe the mechanism of action of aldosterone. PART 2

A
  • Assuming the presence of aquaporins (which are inserted into the membrane by vasopressin in response to low blood volume), the electrochemical gradient produced by the influx of sodium also leads to the influx (and thus reabsorption) of water.
  • This is how aldosterone helps to maintain blood volume and pressure
  • Mineralocorticoid receptor also increases expression of the Na-K-ATPase, which swaps two potassium ions for three sodium ions, thus reabsorbing sodium back into the blood stream
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12
Q

If not well controlled what can aldosterone receptor antagonists do?

A
  • Opposite effects of hyperaldosteronaemia
  • If not well controlled, including hyponatraemia, hyperkalaemia and hypervolaemia
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13
Q

In abnormal aldosterone production cases, what can cause alkalosis?

A
  • In the cells of the collecting duct and convulted tuble, potassium-hydrogen exchange channels prevent the body from losing too much potassium by shuttling some potassium back out of the cell and into the extracellular fluid in exchange for hydrogen ions.
  • In cases where aldosterone production is too high, and thus the expression of the Na-K-ATPase is high, the exchange of hydrogen ions will increase, leading to alkalosis
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14
Q

Describe Conn syndrome.

A

Adrenal aldosteronoma
- High secretion of aldosterone
- Manifests as hypertension and hypokalaemia

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15
Q

How can renovascular hypertension affect aldosterone production?

A
  • Narrowing of arteries supplying kidneys
  • Increase in renin production
  • Increase in aldosterone production
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16
Q

Describe cortisol production

A
  • Hypothalamus produces CRH.
  • Anterior pituitary gland releases ACTH in response to CRH.
  • ACTH stimulates the adrenal glands to produce and release cortisol into the blood
17
Q

Describe the patterns surrounding cortisol release.

A
  • Circadian fluctuation in release, with a peak in the morning and a dip in the evening
  • Released in response to physiological and psychological stress - particularly high during major surgery
18
Q

Describe the physiological effects of cortisol.

A
  • Causes mobilisation of amino acids and fatty acids from muscle and adipose respectively, leading to increases in circulating plasma levels.
  • Increases the expression of the enzymes necessary for gluconeogenesis in the liver, leading to increased circulating glucose levels.
  • Increase in hunger and food intake
19
Q

How does cortisol affect the immune system?

A

Significant anti-inflammatory properties.
- Basis for the use of corticosteroid injections to treat inflammatory diseases, such as joint pain

20
Q

Describe the effects of cortisol at the kidneys.

A
  • Cortisol also has minor mineralocorticoid activity and has equal affinity for the mineralocorticoid receptor with aldosterone.
  • Cortisols affects on sodium balance are minimised by the presence of an enzyme called 11B-HSD in cells, which converts cortisol to the inactive cortisone.
  • Interestingly, liquorice can cause hypertension and hypokalaemia due to its antagonistic effects on 11B-HSD activity
21
Q

Describe the presenting complaints consistent with Cushing’s.

A
  • Red cheeks
  • Buffalo hump (fat pads)
  • Easy bruising due to anti-inflammatory effects
  • Abdominal markings
  • Weight gain due to raised appetite
22
Q

Compare and contrast Cushing’s Syndrome and Cushing’s Disease.

A
  • Cushing’s Syndrome - Too much cortisol production by adrenal gland
  • Cushing’s Disease - Too much ACTH production by pituitary gland
23
Q

Why does Cushing’s Syndrome lead to elevated cortisol and decreased ACTH?

A

Because cortisol acts in a negative feedback fashion to downregulate ACTH secretion

24
Q

Describe sex steroid hormone production. PART 1

A
  • Zona reticularis produces a small amount of sex steroid hormones.
  • Under control from ACTH and possibly other stimulatory factors as well, including cortical androgen stimulating hormone
  • Adrenal releases two pre-androgen hormones, called DHEAS and androstenedione.
  • Travel in the blood stream to extraadrenal tissues (such as adipose) where they are converted to testosterone
25
Q

Describe sex steroid hormone production. PART 2

A
  • Adrenal also produces a very small amount of oestrogen
  • Physiological effects of adrenal androgens is not fully understood, but is thought to be important in pubic hair growth and in male external sex characteristics in child development