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Z MD1 Endocrine block > adrenals > Flashcards

adrenals Flashcards

1
Q

what is cholesterol made from if not eaten in the diet

A

Acetyl-CoA in the liver

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2
Q

what is the division of corticosteroids

A

glucocorticoids (cortisol) mineralocorticoids (aldosterone)

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3
Q

pathway for cholesterol metabolism

A

acetyl Coa –> acetoacetyl CoA –> HMG CoA –> mevalonic acid + CoA –> squalene –> cholesterol

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4
Q

what is the feedback system for cholesterol

A

too much cholesterol –> negatively feeds back on HMGCoA reductase (converts HMG CoA –> Mevalonic acid+CoA)

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5
Q

what is the role of aromatase

A

androgens –> oestrogens

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6
Q

how are steroids removed from the body

A

they are eliminated after oxidation by CYP3A4 in the ER of the liver –> bile acids

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7
Q

what is the direct and indirect pathways of the way steroids change gene expression

A

sex steroids –> goes straight into the nucleus where it binds a SRE glucocorticosteroids –> goes into the cytosol and binds its R (which removes the Rs inhibitor - heat shock protein) - then go enter the nucleus and bind to its HRE

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8
Q

which drug is an inhibitor of the androgen receptor

A

cyproterone acetate

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9
Q

what clinical conditions is cyproterone acetate used for

A
  • hirsutism in females - male-to-female gender change - prostate cancer - benign prostatic hyperplasia - priapism - chemical castration
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10
Q

what are the anterior pituitary hormones that stimulate sex steroid and corticosteroid production

A

FSH and LH –> sex steroids ACTH –> glucocorticosteroids

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11
Q

general function of mineralocorticoids

A

promote retention of sodium and water by the kidneys –> increased BP and BV

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12
Q

3 ways aldosterone is regulated

A
  • angiotensin II
  • ACTH
  • local potassium levels
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13
Q

functions of cortisol

A
  • stimulates protein breakdown (gluconeogenesis) - inhibits protein synthesis - increases blood glucose levels - inhibits the utilization of glucose by adipose tissue - facilitates lipid breakdown, and also fat deposition in certain areas - promotes weight gain by stimulating appetite
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14
Q

which hormone opposes cortisol

A

DHEA

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15
Q

how is cortisol moved through the blood

A

bound to transcortin

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16
Q

how do glucocorticoids suppress immune function

A

by suppressing cytokine synthesis (by elevating IKBa - inhibitor to NFKB)

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17
Q

how is dexamethasone

A

potent synthetic glucocorticoid

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18
Q

what are some of the uses of dexamethasone

A
  • anti-inflammatory - counteract range of side effects of oncology Tx - promote maturation of the foetal lungs - altitude sickness - adrenal insufficiency
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19
Q

why do you need to slowly reduce the use of corticosteroids

A

because taking the steroids the adrenals significantly reduce steroid production, and therefore when you remove them quickly it may take some weeks to recover from the induced adrenal insufficiency

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20
Q

what is the action of leuprorelin

A

analogue of GnRH = interrupts the normal pulsatile stimulation of the GnRH receptors to indirectly downregulate the secretion of LH and FSH

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21
Q

use of leuprorelin

A
  • chemical castration via inhibition of FSH and LH release - breast, ovarian and prostate cancer
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22
Q

where is testosterone produced in males

A

in Leydig cells

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23
Q

function of sertoli cells

A

spermatogenesis

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24
Q

what hormone/s do sertoli cells need to function

A

FSH and testosterone

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25
Q

what hormone/s do Leydig cells need to function

A

LH

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26
Q

what part of the adrenal gland produces testosterone in both males and females

A

zona reticularis

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27
Q

hormonal therapy for prostate cancer

A
  • androgen deprivation therapy - blocks the effect of testosterone - leuprorelin - agonist of Rs for release of LH and FSH
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28
Q

hormonal therapy for breast cancer

A
  • tamoxifen - oestrogen R antagonist - letrozole - aromatase inhibitor
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29
Q

what is the discrimination of the “neuro” and “endocrine” parts of the adrenal gland

A

adrenal medulla (modified sympathetic ganglion) - secretes catecholamines adrenal cortex (true endocrine gland) - secretes steroids

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30
Q

4 regions of the adrenals

A

adrenal medulla zona reticularis zona fasciculata zona glomerulosa

31
Q

what does the adrenal medulla secrete

A

catecholameines (neurohormone)

32
Q

what does the zona reticularis secrete

A

sex hormones

33
Q

what does the zona fasciculata secrete

A

glucocorticoids

34
Q

what does the zona glomerulosa secrete

A

aldosterone

35
Q

what is the order of the layers of the adrenal gland from outside to inside

A

capsule zona glomerulosa zona fasciculata zona reticularis adrenal medulla

36
Q

what stimulates the release of cortisol

A

HPAA

37
Q

what are some other functions of CRH other than stimulation of ACTH

A
  • effects on inflammation and immune responses - inhibition of appetite - signals the onset of labour - links to mood disorders
38
Q

what is POMC

A

pro-hormone for ACTH and beta-endorphin in the anterior pituitary

39
Q

how does POMC make alpha-MSH

A

outside the pituittry ACTH is converted to alpha-MSH

40
Q

functions of alpha-MSH

A

melanin synthesis immune response decreased food intake

41
Q

explain the diurnal rhythm of cortisol release

A
  • peaks in the morning - low in the night
42
Q

how does cortisol protect against hypoglycaemia

A

by stimulating catabolism of energy stores (permissive for glucagon and catecholamine actions)

43
Q

what is the effect on cortisol on calcium balance

A

decreased absorption increased excretion (bone breakdwon)

44
Q

what does hyperaldosteronism cause

A

hypernatremia hypokalaemia hypertension

45
Q

What is Cushing’s syndrome

A

a pituitary tumour that autonomously secretes ACTH -> excess cortisol

46
Q

what does excess cortisol cause

A
  • glucose excess (hyperglycaemia) - protein shortage - abnormal fat distribution with weight gain - wasting of muscle, skin and bone - hypertension - inhibition of linear growth
47
Q

symptoms of Cushing’s syndrome

A
  • excess gluconeogensis –> hyperglycaemia - muscle protein breakdown - lipolysis –> wasting - fat deposits in trunk and face - increased appetite - mood face - striae on abdomen - osteoporosis
48
Q

what is Addison’s disease

A

primary adrenal insufficiency = hyposecretion of cortisol

49
Q

what causes Addison’s disease

A

autoimmune destruction of adrenal cortex

50
Q

what are the symptoms of Addison’s disease

A
  • cardiac arrhythmias (due to K+ retention) - hypotension (due to Na+ depletion) - hypoglycaemia and decreased stress response (due to decreased cortisol) - GI symptoms - darkening of the skin - muscle weakness - increased susceptibility to infection
51
Q

what are the cells called that produce catecholamines

A

chromaffin cells (in the adrenal medulla)

52
Q

what are the catecholamines in the body

A

adrenaline noradrenaline dopamine

53
Q

actions of catecholamines

A
  • fight or flight response (increased HR, contractility, TPR and BP) - metabolic effects (increased glucose and FFA, increased BMR) - central effects (increased arousal and alertness) - stress responses
54
Q

what is the response of the body to acute and chronic stress

A
  • increased ADH (retain water) - increased adrenaline –> vasoconstriction –> increased renin –> increased aldosterone - increased adrenaline –> increased glucagon and decreased insulin - increased CRH –> increased cortisol
55
Q

explain cortisone acetate

A

very weak metabolite of glucocorticoid

56
Q

explain the 3 “pathways” from cholesterol

A
  • mineralocorticoid pathway to aldosterone - glucocorticoid pathway to cortisol - sex hormone pathway to oestrogen and testosterone
57
Q

2 broad types of hypercortisolism

A

ACTH dependent (eg pituitary adenoma) ACTH independent (adrenal problem)

58
Q

what is the difference between cushings disease and cushings syndrome

A

cushings disease - pituitary adenoma cushings syndrome - ACTH independent

59
Q

other than addison’s disease, what other things can cause adrenocorticol insufficiency

A
  • enzyme defect in cortisol biosynthesis - metabolic defect - infectious disease (adrenal destruction by TB)
60
Q

what are the serum levels of Na and K in someone with Addison’s disease

A

low serum sodium and high serum potassium

61
Q

where is Addisonian pigmentation generally seen on the body

A

knuckles of hands knees gums and oral mucosa

62
Q

commonest cause of adrenal adrogen excess

A

21-hydroxylase deficiency (congeital adrenal hyperplasia)

63
Q

what causes the hyperplasia of the adrenals in CAH

A

the prenatal ACTH stimulation

64
Q

3 presentations of CAH in females

A
  • infant with ambiguous genitalia - premature pubic hair and enlarged clitoris - adolescent hirsutism and acne
65
Q

2 presentations of CAH in males

A
  • adrenal crisis in a baby aged 2-3 weeks - premature sexual development at 2-3 years
66
Q

clinical uses of cortisol

A
  • replacement if inadequate production (eg. pituitary disease or Addison’s disease) - treat inflammatory conditions
67
Q

clinical presentation of someone with excess aldosterone

A

hypertension (Na retention) weakness (hypokalaemia)

68
Q

clinical presentation of someone with deficiency in aldosterone

A

dehydration postural hypotension cardiac arrhythmias (hyperkalaemia)

69
Q

if you were to remove the adrenal glands… what kills you

A

the loss of mineralocorticoid activity

70
Q

what is the syndrome called due to adrenocortical tumour causing mineralocorticoid excess

A

Conn’s syndrome

71
Q

what is a pheochromocytoma

A

tumour of the adrenal medulla

72
Q

clinical presentation of pheochromocytoma

A

episodic bursts of palpitations, enormous hypertension, pallor, and feeling of impending doom

73
Q

hormones secreted by the adrenal medulla

A

adrenaline and noradrenaline

Z MD1 Endocrine block (4 decks)

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