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brs (phase 1a) > (endo) adrenal gland > Flashcards

(endo) adrenal gland Flashcards

1
Q

where are the adrenal glands found?

A

superior to the kidneys

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2
Q

describe the arterial supply of the adrenal glands

A

each adrenal gland is supplied by three groups of arteries:

  • superior adrenal arteries
  • middle adrenal arteries
  • inferior adrenal arteries
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3
Q

describe the venous drainage of the adrenal glands

A

right adrenal gland = directly into the inferior vena cava

left adrenal gland = first, into the left renal vein and then into the inferior vena cava

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4
Q

how does the arterial supply of the adrenal glands compare to their venous drainage?

A

many arteries supply the adrenal glands but only one vein drains each one

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5
Q

how is the venous drainage of the right adrenal gland different to that of the left?

A 
right = directly into IVC
left = left renal vein into IVC
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6
Q

what are the two parts of the adrenal gland?

A 
adrenal cortex (outer)
adrenal medulla (middle)
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7
Q

what are the components of the adrenal cortex?

A

zona glomerulosa
zona fasciculata
zona reticularis

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8
Q

what is the function of the adrenal cortex?

A

secretes corticosteroids

mineralocorticoids, glucocorticoids, sex steroids

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9
Q

what is the function of the adrenal medulla?

A

secretes catecholamines

adrenaline, noradrenaline

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10
Q

name the corticosteroids secreted by each zone of the adrenal cortex

A

1) zona glomerulosa = mineralocorticoids (e.g. aldosterone)
2) zona fasciculata = glucocorticoids (e.g. cortisol)
3) zona reticularis = sex steroids (e.g. androgens, oestrogen)

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11
Q

name the catecholamines secreted by the adrenal medulla

A

adrenaline/epinephrine (80%)

noradrenaline/norepinephrine (20%)

[dopamine - noradrenaline precursor]

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12
Q

name the primary mineralocorticoid

A

aldosterone

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13
Q

name the primary glucocorticoid

A

cortisol

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14
Q

name the primary sex steroids

A

androgens, oestrogens, progestogens

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15
Q

what type of cells are found in the adrenal cortex?

A

epithelial cells and their associated capillary networks

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16
Q

what type of cells are found in the adrenal medulla?

A

neuroendocrine/chromaffin cells

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17
Q

what are chromaffin cells?

A

neuroendocrine cells found mostly in the medulla of the adrenal glands (i.e. phaeochromocytes)

= cells that receive neuronal input that then triggers the secretion hormones (e.g. adrenaline, noradrenaline) into the bloodstream

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18
Q

why is dopamine found in the adrenal medulla?

A

dopamine is the precursor molecule to noradrenaline, which is synthesised in the adrenal medulla

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19
Q

what is the primary molecule from which steroid hormones are synthesised?

A

cholesterol

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20
Q

describe how cholesterol is converted into progesterone

A

cholesterol TO pregnenolone = side-chain cleavage enzyme

pregnenolone TO progesterone = 3-beta hydroxy steroid dehydrogenase

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21
Q

which enzyme catalyses the conversion of cholesterol to pregnenolone?

A

side-chain cleavage enzyme

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22
Q

which enzyme catalyses the conversion of pregnenolone to progesterone?

A

3-beta hydroxy steroid dehydrogenase

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23
Q

which two corticosteroids are normally given rise to from progesterone?

A

1) aldosterone (mineralocorticoid)

2) cortisol (glucocorticoid)

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24
Q

describe how progesterone is converted into aldosterone

A

21 hydroxylase (progesterone to 11-deoxycorticosterone)

11 hydroxylase (11-deoxycorticosterone to corticosterone)

18 hydroxylase (corticosterone to aldosterone)

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25
Q

describe how progesterone is converted into cortisol

A

17 hydroxylase (progesterone to 17 hydroxy-progesterone)

21 hydroxylase (17 hydroxy-progesterone to 11 deoxycortisol)

11 hydroxylase (11 deoxycortisol to cortisol)

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26
Q

list the enzymes required to convert cholesterol into aldosterone

A

1) side-chain cleavage enzyme
2) 3-beta hydroxysteroid dehydrogenase

3) 21 hydroxylase
4) 11 hydroxylase
5) 18 hydroxylase

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27
Q

list the enzymes required to convert cholesterol into cortisol

A

1) side-chain cleavage enzyme
2) 3-beta hydroxysteroid dehydrogenase

3) 17 hydroxylase
4) 21 hydroxylase
5) 11 hydroxylase

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28
Q

what is the two main mechanisms of action of aldosterone?

A

1) stimulates sodium reabsorption from the DCT and the collecting duct (= increasing water reabsorption and raising blood volume)
2) stimulates K+ and H+ ion secretion into the tubular filtrate from the bloodstream

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29
Q

where does aldosterone act?

A

1) kidney = distal convoluted tubule & cortical collecting duct
2) sweat glands
3) gastric glands & colon

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30
Q

how does aldosterone increase blood volume?

A

increased sodium reabsorption from the tubular filtrate into the bloodstream via apical ENaCs & basolateral Na+-K+ ATPases

increased sodium reabsorption stimulates more water reabsorption into the bloodstream in order to regulate the osmotic gradient, increasing blood volume

31
Q

which molecule regulates aldosterone secretion?

A

renin

32
Q

how does the renin-angiotensin system regulate aldosterone secretion?

A

liver releases angiotensinogen

angiotensinogen is converted into angiotensin I via renin

angiotensin I is converted into angiotensin II via ACE (angiotensin-converting enzyme) released in the lungs

angiotensin II acts on the zona glomerulosa of the adrenal gland to increase aldosterone synthesis

33
Q

from where is renin released?

A

juxtaglomerular apparatus

34
Q

when is renin released?

A

when the arterial blood pressure falls, the decrease is detected by baroreceptors that subsequently increase renin secretion from the juxtaglomerular apparatus into the bloodstream

35
Q

list the three factors that stimulate renin release

A

1) fall in afferent arteriole blood pressure and therefore the renal perfusion pressure, detected by baroreceptors
2) decrease in Na+ load to the top of the loop of Henle detected by the macula densa cells
3) increased sympathetic nervous system activity, detected by the beta-1 adrenergic receptors

36
Q

which receptors detect a fall in afferent arteriole blood pressure?

A

baroreceptors

37
Q

which cells detect a fall in Na+ load at the top of the loop of Henle?

A

macula densa cells

38
Q

which receptors detect increased renal sympathetic activity?

A

beta-1 adrenergic receptors

39
Q

besides increased aldosterone biosynthesis, what is the main function of angiotensin II?

A

vasoconstriction

40
Q

which enzymes are activated by angiotensin II and why?

A 
side-chain cleavage enzyme
3 hydroxysteroid dehydrogenase
21 hydroxylase
11 hydroxylase
18 hydroxylase

= aldosterone biosynthesis

41
Q

what is the main function of cortisol?

A

normal stress response
= 1) metabolic effects
= 2) weak mineralocorticoid effects
= 3) renal and cardiovascular effects

42
Q

what are the metabolic effects of cortisol?

A
  • peripheral protein catabolism
  • hepatic gluconeogenesis
  • fat metabolism (lipolysis in adipose tissue)

= increased blood glucose concentration
(enhanced effects of glucagon and catecholamines)

43
Q

what are the weak mineralocorticoid effects of cortisol?

A

the mineralocorticoid receptor binds both aldosterone and cortisol with equal affinity

(IN EXCESS) when cortisol binds to the MR in the kidney, it (like aldosterone) stimulates sodium reabsorption and regulates blood pressure

44
Q

what are the renal and cardiovascular effects of cortisol?

A

renal = excretion of water load

cardiovascular = increased vascular permeability

45
Q

how does cortisol cause an increase in the excretion of water in the kidneys?

A

at NORMAL levels, cortisol negatively feeds back to reduce CRH & ADH secretion

so with less ADH, there is less water reabsorption and more water excretion into the tubular fluid

(NB - in EXCESS, cortisol acts on the MR to stimulate sodium and therefore water retention)

46
Q

explain the negative feedback system involving cortisol

A

increased cortisol will cause reduced ACTH (pituitary gland) and reduced CRH (hypothalamus)

47
Q

which enzymes are activated by ACTH and why?

A 
side-chain cleavage enzyme
3 hydroxysteroid dehydrogenase
17 hydroxylase
21 hydroxylase
11 hydroxylase

= cortisol biosynthesis

48
Q

compare aldosterone regulation to cortisol regulation

A

aldosterone regulation = renin-angiotensin system (RAAS)

cortisol regulation = negative feedback system with the anterior pituitary gland (ACTH, CRH)

49
Q

differentiate between cortisol and prednisolone

A

prednisolone has one more double bond than cortisol giving it

1) a longer half-life
2) increased potency
3) increased binding affinity

50
Q

what is Addison’s disease?

A

primary adrenal failure

i.e. direct damage to the adrenal glands impairing aldosterone and cortisol biosynthesis

51
Q

define primary adrenal failure

A

when there is direct damage to the adrenal glands impairing aldosterone and cortisol biosynthesis

52
Q

what are the two possible causes of Addison’s disease?

A

1) autoimmune damage to the adrenal cortex (commonest cause in the UK)
2) tuberculosis of the adrenal gland (commonest worldwide cause)

53
Q

why do patients with Addison’s disease appear tanned?

A

due to impaired levels of cortisol + via the negative feedback system, there is increased ACTH secretion via the APG

increased ACTH requires more POMC to be cleaved: a byproduct of which is aMSH, which stimulates skin pigmentation (i.e. tan)

54
Q

what are the characteristic symptoms of Addison’s disease?

A

increased pigmentation (visible tan/bronzing)

autoimmune vitiligo can co-exist

low blood pressure (due to lack of aldosterone & cortisol)

55
Q

what is a ‘salt-losing Addisonian crisis’?

A

in Addison’s disease, impaired biosynthesis of aldosterone + cortisol = deficiency

reduced sodium reabsorption and therefore more salt (& therefore water) loss in the urine

= low blood pressure
= eventual death

56
Q

how can Addison’s disease present both with hyperpigmentation and vitiligo?

A

hyperpigmentation = increased ACTH requiring more POMC cleavage, producing increased levels of aMSH

vitiligo = can sometimes have autoimmune damage to melanocytes, leading to reduced melanin production so white patches of skin

57
Q

what are the common symptoms of Addison’s disease?

A

skin = hyperpigmentation, vitiligo

gastrointestinal = nausea, vomiting, diarrhoea, constipation, abdominal pain

general = low BP, weight loss, weakness

58
Q

what are the common symptoms of Addisonian crisis?

A

hyponatraemia, hypoglycaemia, syncope

severe diarrhoea & vomiting

fever

convulsions

59
Q

describe how an Addisonian crisis is treated

A

1) rehydrate with normal saline
2) give dextrose to prevent hypoglycaemia that may have been caused by glucocorticoid deficiency
3) give hydrocortisone or another glucocorticoid

60
Q

why is rehydration with normal saline required to treat an Addisonian crisis?

A 
Addisonian crisis 
= mineralocorticoid/aldosterone deficiency
= reduced salt reabsorption
= reduced water reabsoprtion
= low blood pressure

!! saline required to correct blood volume deficit and hypotension !!

61
Q

why is dextrose required to treat an Addisonian crisis?

A

to prevent/treat hypoglycaemia that may have been caused by glucocorticoid deficiency

(NB - the glucocorticoid, cortisol, has metabolic effects)

62
Q

what is Cushing’s syndrome?

A

a condition caused when you have too much cortisol (or another glucocorticoid)

63
Q

what are the main symptoms of Cushing’s syndrome?

A 
red cheeks
moon face
fat pad (buffalo hump)
easy bruising
thin skin
red/purple striae
centripetal obesity
proximal myopathy (muscle wasting)
poor wound healing (skin ulcers)
  • impaired glucose tolerance (diabetes)
  • depression
  • high blood pressure/hypertension
  • osteoporosis
64
Q

list four possible causes of Cushing’s syndrome

A

1) taking steroids by mouth
2) pituitary-dependent Cushing’s disease (pituitary adenoma)
3) ectopic ACTH (lung cancer)
4) adrenal adenoma or carcinoma

65
Q

what are female and male-specific signs of Cushing’s disease?

A

females = amenorrhoea, hirsutism

males = erectile dysfunction

66
Q

from where is the medulla derived from?

A

ectodermal neural crest cells

67
Q

what is the main precursor for adrenaline and noradrenaline synthesis?

A

tyrosine

then converted into dopamine then converted into norepinephrine and then into epinephrine

68
Q

where are catecholamines stored?

A

within the neuroendocrine/chromaffin cells of the adrenal medulla

69
Q

what stimulates catecholamine release from the adrenal medulla?

A

released from their cytoplasmic granules in response to the acetylcholine from preganglionic sympathetic neurones

70
Q

what is the function of catecholamines?

A

‘fight or flight’ response

i.e. tachycardia, sweating, alertness, increased blood glucose, vasoconstriction

71
Q

how do noradrenaline and adrenaline circulate in the bloodstream?

A

bound to albumin

72
Q

which two hepatic enzymes are responsible for catecholamine degradation?

A

1) monoamine oxidase

2) catechol-O-methyl transferase

73
Q

how is catecholamine release from the adrenal medulla regulated?

A

adrenal medulla is under autonomic control

i.e. preganglionic sympathetic neurones that release ACh

brs (phase 1a) (7 decks)

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