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Endocrinology > The Adrenals and their Hormones (8) > Flashcards

The Adrenals and their Hormones (8) Flashcards

1
Q

What are the adrenal/suprarenal glands

A

Two glands superior of the kidneys embedded in the

perirenal fat

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2
Q

What are the adrenal glands surrounded by

A

a capsule

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3
Q

what do the adrenal glands consist of

A

the adrenal medulla- core of the gland and the adrenal cortex - outer layers surrounding the core

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4
Q

What are the 3 cortical zones

A

the adrenal cortex consists of 3 layers. Outer layer: Zona glomerulosa. Middle layer: Zona Fasciculata. Inner layer: Zona Reticularis

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5
Q

what supplies blood to the adrenal cortex

A

abdominal aorta and renal arteries

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6
Q

what are the two ways in which the blood passes to the cortical zones

A

Blood passes through the cells until it reaches the tributary of central vein in the centre of the
medulla. There are some arterioles which flow from the outer capsule to the adrenal medulla

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7
Q

what hormones does the adrenal medulla release

A

catecholamines

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8
Q

what hormones does the adrenal cortex release

A

corticosteroids

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9
Q

Structure of the zona fasciculata

A

recognisable form; lines of cells which run towards the zona reticularis

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10
Q

structure of the zona reticularis and zona glomerulosa

A

no distinguishable form of cells

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11
Q

What is the medulla made up of

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

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12
Q

what do chromaffin cells do (meddle with a cat)

A

synthesise and release catecholamines

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13
Q

what are catecholamines

A

polypeptide hormones synthesised from a tyrosine precursor

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14
Q

what catecholamines are produced

A

Adrenaline (80%). Noradrenaline (20%). Dopamine (very small amounts)

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15
Q

What are the different corticosteroids that are produced by the adrenal cortex

A

Mineralocorticoids- aldosterone. Glucocorticoids-cortisol. Sex Steroids - androgens and oestrogen

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16
Q

what does the zona glomerulosa synthesis and release

A

aldosterone

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17
Q

what does the zona fasciculata release

A

cortisol

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18
Q

what does the zona reticularis release

A

sex hormones

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19
Q

where are cortisol, androgens and oestrogen synthesised

A

in the zona fasciculata and zona reticularis

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20
Q

What are the adrenals responsible for the synthesis and release of?

A

Mineralocorticoids (C21). Glucocorticoids (C21) and androgens

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21
Q

What are the Gonads responsible for the synthesis and release of?

A

Progestogens (C21). Androgens (C19). Oestrogens (C18)

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22
Q

Explain the synthesis pathway of adrenal cortical hormones (add pic)

A

Cholesterol is precursor of all of the steroids and is a 21 carbon long molecule. An enzyme converts Cholesterol to Pregnenolone and initiates the process of steroid production. 17-α hydroxylase is an important enzyme as it allows glucocorticoids and androgens to be made from the precursors pregnenolone and progesterone. A dehydrogenase enzyme initiates the mineralocorticoid pathway from pregnenolone.

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23
Q

what is the precursor for the production of aldosterone

A

progesterone

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24
Q

what are the precursors of oestrogens

A

androgens

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25
Q

why arent corticosteroids stored

A

they are lipophilic and can pass easily through the membranes where they bind with intracellular or nuclear membrane receptor. Therefore they cannot be stored, as this will result in excessive binding with receptors and
hence over stimulation

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26
Q

what is androstenedione

A

a week androgen that can be converted to testosterone and dihydrotestosterone

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27
Q

androgens produced in the adrenal cortex are

A

weak but they are more powerful in the testes

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28
Q

How is Corticosteroid transported in the blood

A

The vast majority of corticosteroids are bound to plasma proteins to avoid being taken up by non target cells. Cortisol:75% bound to corticosteroid binding globulin (CBG or Transcortin), 15% bound to albumin, 10% free (unbound) biologically active. Aldosterone: 60% bound to corticosteroid binding globulin and 40% free (unbound)

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29
Q

What do plasma proteins do

A

The plasma proteins act as a store and transport mechanism – they transport the hormone where
the unbound-bound hormone equilibrium is unbalanced, i.e. where the hormone needs to be
released

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30
Q

The circulating concentraion of corticosteroids

A

Cortisol is controlled by the hypothalamo-pituitary axis, and is released in pulses , which vary depending on time of day. This is known as circadian rhythm: At 8am its 140 – 690 nmol/ and at its 4pm 80 – 330 nmol/l. Aldosterones are released in pulses, and depend on body positioning: Upright 140 – 560 pmol/l. Nanomoles are 1000x greater than picomoles

31
Q

Why is body position important for aldosterone amount

A

aldosterone is involved in the control of fluid and balance

32
Q

What is the action of aldosterone

A

It 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. It also 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

33
Q

What is the only way we have of regulating potassium in the blood

A

Aldosterone stimulating K+ secretion

34
Q

what is hyperaldesteronism responsible for

A

high blood pressure

35
Q

what is the mechanism of action of aldosterone

A

Aldosterone diffuses into the distal convoluted tubule from the blood. It then binds to an intracellular receptor within the cell; mineralocorticoid receptor (MR).
Being a steroid hormone, aldosterone passes through cell membranes and binds to intracellular receptors. The hormone-receptor complex is transported to the nucleus and binds to specific DNA. This activates transcription, translation and synthesis of specific proteins. The proteins then act as: ion channels – in the apical membrane, allowing Na+ to be reabsorbed into the distal convoluted tubule form the tubular fluid, and ion pumps – on the basolateral membrane, pumping Na+ into the blood from the distal convoluted tubule, completing the reabsorption.

36
Q

what is the main mineralcorticoid in humans

A

aldosterone

37
Q

What do the cells lining the ascending limb of the loop of Henle touch

A

the cells that line the afferent arteriole

38
Q

what happens to plasma osmolality in the presence of aldosterone

A

Plasma smolality increases. Aldosterone stimulates reabsorption of sodium ions so the concentration of sodium ions in the blood increases

39
Q

What does the increase in plasma osmolality stimulate

A

the release of vasopressin

40
Q

What does vasopressin do in the kidney collecting duct

A

it increases water reabsorption so the consequence of aldosterone is an expansion of extracellular fluid volume.

41
Q

What are the juxta-glomerular cells

A

Specialised cells that line the renal afferent arteriole and contain many secretory granules. The secretory granules contain an enzyme called renin which is important in the production of aldosterone

42
Q

Where does the main mechanism for controlling aldosterone reside

A

in the kidney nephrons

43
Q

give an overview of blood supply in the nephron

A

the glomerulus receives blood from an afferent arteriole and the blood leaves via an efferent arteriole

44
Q

what is the juxtaglomerular apparatus

A

The juxtaglomerular apparatus describes the combination of the juxtaglomerular and macula densa cells.

45
Q

What are the macula densa cells

A

They are the cells that line the ascending limb of the loop of Henle which are adjacent to the juxta-glomerular cells. They respond to changes in sodium ion concentration, so they are effectively specialised Na+ sensors.

46
Q

What is the afferent arteriole adjacent to

A

the point where the ascending loop of Henle meets the distal convoluted tubule. This is also in close proximity to the glomerulus.

47
Q

What happens in conditions involving excessive aldosterone ?

A

Aldosterone increases plasma osmolality which stimulates vasporessin release. This causes an expansion of extracellular fluid. If you have a maintained expansion of extracellular fluid volume this leads to hypertension

48
Q

What causes renin release from the juxtaglomerula cells in the distal convoluted tubule (3) ?

A

Decreased renal perfusion pressure (normally associated with decreased arteriole blood pressure).
Increased renal sympathetic activity (direct to juxta-glomerular cells). Decreased Na+ load to top of the loop of Henle.

49
Q

How does increased renal sympathetic activity cause renin release?

A

The JGA (juxta-glomerular apparatus) has sympathetic innervation. The sympathetic system is activated when the blood pressure falls. This leads to renin release

50
Q

How does decreased Na+ loads to top of loop of Henle cause renin release?

A

Decreased sodium concentration at the top of the loop of Henle. This leads to activation of JGA as it is recognised by the Na+ sensing macula densa cells, which leads to increased renin release.

51
Q

What is the Renin-Angiotensin-Aldosterone System

A

liver produces angiotensinogen (a large protein). Renin breaks down angiotensinogen to angiotensin I. Then, ACE (angiotensin converting enzyme) converts angiotensin I to angiotension II. Angiotensin II stimulates the zona glomerulosa to produce aldosterone.

52
Q

How does Renin stimulate the production and release of aldosterone

A

via the Renin-Angiotensin-Aldosterone System

53
Q

what are the effects of angiotensin II

A

vasoconstriction and stimulates the zona glomerulus of the adrenal cortez to synthesise and release aldosterone.

54
Q

what other factors affect aldosterone production

A

Corticotrophin (released from the anterior pituitary gland) enhances the renin-angiotensin system. Increased K+ and decreased Na+ also stimulates aldosterone release.

55
Q

How does angiotensin regulate ions

A

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

56
Q

What does aldosterone production lead to

A

increased Na+ reabsorption in the distal convoluted tubule, therefore increasing water reabsorption which increases the volume of the (blood) – increasing BP.

57
Q

What can chronic extracellular fluid increase lead to

A

hypertension which can be treated with ACE inhibitors which are the main antihypertensives used.

58
Q

What are the metabolic effects of cortisol

A

Stimulates peripheral protein catabolism. Hepatic gluconeogenesis. Increased blood glucose. Fat metabolism (Lypolysis in adipose tissue). Enhances effects of glucagon and catecholamines.

59
Q

What is the main glucocorticoid in humans

A

Cortisol is a glucocorticoid synthesised in the cortex of the adrenal glands.

60
Q

Why are the arms and legs really thin in Cushing’s syndrome

A

Cortisol stimulates peripheral protein catabolism so excessive production of cortisol causes a lot of muscle loss

61
Q

What are the renal and cardiovascular effects of cortisol

A

Excretion of water load. Increased vascular permeability

62
Q

what are the other effects of cortisol

A

Mineralcorticoid effects and some effects on bone an CNS growth

63
Q

What are the effects of large (pharmacological) amounts of cortisol

A

anti-inflammatory action, immunosuppressive action and anti-allergic action

64
Q

What do the effects of large amounts of cortisol result from?

A

decreased production of molecules such as prostaglandins, leukotrienes and histamines. they may also affect movement and function of leukocytes and the production of interleukins.

65
Q

What is the mineralocorticoid receptor?

A

It is what aldosterone binds to. Aldosterone acts almost entirely on the mineralocorticoid receptor (MR). Cortisol binds to the Glucocorticoid Receptors and the Mineralocorticoid Receptors equally.

66
Q

what enzyme in the kidney converts bioactive cortisol to cortisone (inactive)

A

11b-hydroxysteroid dehydrogenase 2

67
Q

Why isnt cortisol constantly binding with mineralocorticoid receptor despite having a concentration in the blood 1000x that of aldosterone?

A

the receptor is located with an enzyme which removes cortisol from the environment by converting it to cortisone

68
Q

What is the mechanism of action of cortisol

A

Cortisol binds to intracellular receptor, and the complex is transported to the nucleus where it binds to
DNA stimulating protein synthesis. Annexin 1 and annexin 1 receptor are synthesised. Annexin 1 leaves the cell and has an autocrine effect, preventing prostaglanding synthesis by blocking arachidonic acid production

69
Q

what does cortisol play an important role in

A

in the endocrine response to stress

70
Q

How is cortisol controlled (hypothalamo-pituitary-adrenal axis)

A

Corticotrophin- releasing hormone (CRH), and Vasopressin are control hormones released by the
hypothalamus, which control the release of corticotrophin. Corticotrophin (ACTH) is released from the adenohypophysis and has a short auto-negative feedback loop to the hypothalamus (inhibiting CRH and vasopressin release). Cortisol has negative feedback effects direct to the pituitary (inhibiting cortiocotrophin release) and indirectly to the hypothalamus (inhibiting CRH and vasopressinrelease).

71
Q

What stimulates cortisol release

A

Stressors via brain nerve pathway and circadium rhythm (biological clock) stimulate the release of
CRH and vasopressin from the hypothalamus, therefore increasing cortisol (and small amounts of
androgen) release.

72
Q

What is the circadian rhythm for cortisol

A

it originates from the biological clock and 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.

73
Q

What is Dehydroepiandrosterone (DHEA) ?

A

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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