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Endocrine Systems and Cancer > 3) Adrenal Cortex > Flashcards

3) Adrenal Cortex Flashcards

1
Q
  1. Adrenal Gland Location
A

on top of the kidneys

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2
Q
  1. Arterial blood supply to adrenal glands
A

via abdominal aorta & renal arteries

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3
Q
  1. Drainage of venous blood from adrenal glands
A

drainage into vena cava (inferior) & renal arteries

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4
Q
  1. Adrenal gland composition
A

inner medulla

outer cortex surrounded by thin capsule

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5
Q
  1. Adrenal cortex zones and hormones they secrete
A

outer zone- zona glomerulosa- secreting mineralocorticoids like aldosterone

middle zone- zona fasciculata- secreting glucocoritcoids like cortisol and adrenal androgens

inner zone- zona reticularis- secreting adrenal androgens and cortisol

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6
Q
  1. Adrenal medulla hormones
A

catecholamines

e.g adrenaline, noradrenaline, dopamine

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7
Q
  1. Cortisol chemical type and production
A

Glucocorticoid

Produced in adrenal cortex

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8
Q
  1. Importance of Cortisol
A

metabolic balance maintenance

responding to stress

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9
Q
  1. Necessary concentrations of Cortisol for body cell functioning
A

physiological concentrations

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10
Q
  1. Cortisol basal secretory rate levels and changes
A

basal secretory rate is 10 to 30mg/day

10 fold increase during stress and highest levels during morning

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11
Q
  1. Glucorticoids Mechanism of Action
A

steroid Hormones bind to intracellular receptors

promote and inhibit synthesis of specific proteins depending on target cells

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12
Q
  1. Maintenance of metabolic rate by Cortisol during stress
A

acting as permissive hormone

allows other hormones to induce effects in controlled manner

cortisol increases transcription rate of lipocortin, which inhibits phospholipase A2

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13
Q
  1. Cortisol action at hypothalamus
A

binds to DNA

inhibits transcription of CRH (cortisol releasing hormone)

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14
Q
  1. Cortisol’s Cellular effects
A

stress Response- maintains vascular tone

immune Response- immunosuppressive and anti-inflammatory actions

protein Metabolism- increased mobilisation of amino acids in skeletal tissue and muscles

carbohydrate Metabolism- increased gluconeogenesis and hepatic enzymes that support gluconeogenesis

fat Metabolism- increased lipolysis in fat cells hence increased mobilisation of glycerol (and fatty acids for energy)

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15
Q
  1. Cortisol state in blood circulation and effect on metabolic clearance rate of glucocorticoids
A

bound to plasma proteins

decreases metabolic clearance rate of glucocorticoids

acts as buffer as not biologically active

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16
Q
  1. Cause of Cushing’s Syndrome
A

overproduction of glucocorticoids

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17
Q
  1. Physiological effects of glucorticoids seen in Cushing’s Syndrome
A

centripetal obesity- increased fat metabolism

severe skeletal muscle wasting and weakness- increased protein metabolism

round moon face- increased fat deposition

mild facial hirsutism in women only, oily skin and acne- excessive adrenal androgens

stretch marks- effects on connective tissues and increased fat metabolism

bruising and slow wound healing- collagen breakdown and suppressed immune system

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18
Q
  1. Internal effects of hypercortisolism of Cushing’s syndrome
A

high blood pressure- excess cortisol binds to mineralcorticoid receptor- resulting in salt and water retention

osteoporosis- increased calcium mobilisation from bone- inhibition of osteoclast function- enhanced osteoclast binding- decreased calcium absorption

diabetes- high blood sugar due to changed glucose metabolism

infections- suppression of immune system by decreasing peripheral lymphocytes

      - inhibiting neutrophil accumulation
      - suppressing histamine and prostaglandin synthesis
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19
Q
  1. Mechanism of action of hormones that control glucorticoid secretion
A

corticotrophin releasing hormone (CRH) secreted from hypothalamus  stimulates ACTH secretion from anterior pituitary

arginine vasopressin stimulates CRH and together stimulate larger rise in ACTH than CRH alone

adrenocorticotrophic hormone (ACTH) acts on adrenal cortex to stimulate release of glucocorticoids (mainly cortisol)

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20
Q
  1. Reduction of amino acid utilisation for protein formation by Cortisol
A

everywhere except the liver

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21
Q
  1. Adrenal androgens that ACTH stimulates secretion of
A

androstenedione

dehydroepiandrostenedione (DHEA)

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22
Q
  1. Hypertension due to Cortisol
A

cortisol binding to aldosterone receptor and activating it

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23
Q
  1. Enzyme responsible for converting Cortisol into Cortisone
A

11-beta hydroxysteroid dehydrogenase

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24
Q
  1. Steroid hormones that ACTH has only minor role in the secretion of
A

mineralocorticoids, e.g. Aldosterone

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25
25. Adrenal Cortex secretion when stimulated by ACTH
cortisol
26
26. ACTH secretion
by anterior pituitary gland in short bursts or pulses controlled by a pulse generator in hypothalamus
27
27. Other name for Arginine vasopressin (AVP)
vasopressin argipressin antidiuretic hormone (ADH)
28
28. Problems in that pathway for secretion of Cortisol
hypothalamus- defects in CRH production pituitary gland- defects in ACTH secretion or bioactivity adrenal gland- defects in cortisol biosynthesis or secretion
29
29. Frequency of pituitary hormones, the problems they can cause and their treatment
present in 20% of people- most are small and benign can grow and cause problems due to secretion on pituitary hormones like ACTH treated with surgery, radiotherapy or drugs (e.g. prolactin or somatostatin analogues)
30
30. Problems arising from an overproduction in Cushing ’s syndrome
present in 20% of people- most are small and benign can grow and cause problems due to secretion of pituitary hormones like ACTH treated with surgery, radiotherapy or drugs (e.g. prolactin or somatostatin analogues)
31
31. Hypocortisolism also known as
cortisol deficiency- Addison’s Disease
32
32. Causes of Addison’s Disease
rare disease caused by the destruction of the adrenal glands
33
33. Addison’s disease results in
reduction in mobilisation of metabolic substrates- hypoglycaemia, weight loss increased susceptibility to stress pigmentation- due to increased ACTH stimulation of melanocyte stimulating hormone (MSH) due to negative feedback effects of reduced cortisol levels
34
34. Role of melanocyte stimulating hormone (MSH)
stimulates melanocytes in the skin
35
35. Secretion on MSH and ACTH
corticotrophs in the anterior pituitary
36
36. Action of melanocyte stimulating hormone (MSH)
acts on melanocytes in the epidermis of the skin stimulates secretion of melanin
37
37. Melanin controls
controls pigmentation in the skin
38
38. Physiological changes occurring in hypocortisolism
reduced plasma cortisol stimulates over-secretion of both ACTH and MSH increases melanin secretion and causes excessive skin pigmentation (negative feedback)
39
39. Control of cortisol secretion
by ACTH from anterior pituitary indirectly by hypothalamic CRH as it stimulates ACTH
40
40. External regulation of the primary control of ACTH
circadian or diurnal rhythms of daylight and darkness
41
41. Fluctuation of cortisol and ACTH levels during the day
both ACTH and cortisol show a circadian rhythm cortisol levels fall at night as a direct result of a fall in ACTH levels cortisol secretion peaks early in the morning cortisol levels fall at night as a result of a fall in ACTH levels cortisol secretion is low at night
42
42. Cortisol counteracts over-response of insulin
by increasing carbohydrate metabolism raising plasma glucose
43
43. Cortisol suppresses inflammation and immune responses
by stimulating the transcription of genes coding for anti-inflammatory proteins
44
44. Prolonged stress results in
continued cortisol secretion results in muscle wastage, immune and inflammatory responses and hyperglycaemia
45
45. Drugs that have similar effects to that of prolonged stress
glucocorticoids
46
46. Cortisol has a negative feedback
glucocorticoids
47
47. High levels of cortisol supress
ACTH CRH AVP secretion
48
48. Normal plasma levels of ACTH
10 pmol/L
49
49. Challenge tests for negative feedback
use of synthetic drugs on the negative feedback control of the anterior pituitary
50
50. Dexamethasone affects cortisol levels
stimulates raised cortisol levels which suppress ACTH secretion by anterior pituitary ACTH levels reduced to 2 pmol/L
51
51. Metyrapone affects cortisol and ACTH
stimulates raised cortisol levels which suppress ACTH secretion by anterior pituitary ACTH levels reduced to 2 pmol/
52
52. Aldosterone biomolecule type
primary mineralocorticoid
53
53. Aldosterone mechanism of action
acts on kidney (distal tubule) promoting exchange of sodium and potassium ions (reabsorption of Na+ into the blood)
54
54. Primary physiological effects of mineralocorticoids
increased reabsorption of sodium- Na+ ions loss in urine is decreased increased reabsorption of water- consequent expansion of the extracellular fluid volume (an osmotic effect that maintains normal blood pressure) increased renal excretion of potassium
55
55. Reasons why loss of mineralocorticoid activity leads to the destruction of adrenal glands causing death within a few days
increased reabsorption of sodium- Na+ ions loss in urine is decreased increased reabsorption of water- consequent expansion of the extracellular fluid volume (an osmotic effect that maintains normal blood pressure) increased renal excretion of potassium
56
56. Stimulation of secretion of Aldosterone
drop in the level of sodium ions in the blood rise in the blood levels of potassium ions angiotensin II (reduced blood flow to kidney  rennin- angiotensin I- angiotensin II) ACTH
57
57. Factors that suppress Aldosterone secretion
atrial natriuretic hormone high sodium concentration potassium deficiency
58
58. Cause of primary Aldosterone excess
benign tumours of adrenal gland that secrete excess amounts of aldosterone
59
59. Result of primary Aldosterone excess
high blood pressure (hypertension) due to reabsorption of sodium and water increased potassium excretion (hypokalaemia) causing weakness, paralysis, metabolic alkalosis and polyuria
60
60. Cause of secondary Aldosterone excess
high levels of rennin-angiotensin due to reduced blood voume in some chronic heart diseases or liver cirrhosis which stimulates excess adrenal synthesis of Aldosterone
61
61. Result of secondary Aldosterone excess
hypokalaemia- but normal blood pressure
62
62. Biomolecule that adrenocortical hormones are synthesised from
cholesterol
63
63. Availability of cholesterol
synthesised within adrenal gland from acetyl CoA taken up from the blood by specific plasma membrane receptors that bind low-density lipoproteins (LDL) then transferred into cell body by endocytosis, where cholesterol is split from the lipoprotein, esterified and stored in cytoplasmic vacuoles
64
64. Rate limiting step in the biosynthesis of steroids
transfer of cholesterol from the outer to the inner mitochondrial membrane
65
65. Protein that mediates transfer of cholesterol from outer to inner membrane
steroidogenic acute regulatory protein (StAR)
66
66. Synthesis of StAR
de novo synthesis, under stimulation by ACTH from anterior pituitary
67
67. Enzyme conversion of cholesterol into pregenolone
cytochrome P450 side chain cleavage enzyme (CYP11A)
68
68. Pregenolone synthesis once made available
rapidly removed from the mitochondria sequentially modified by dehydrogenases and hydroxylating enzymes within endoplasmic reticulum and mitochondria go on to form 3 major types of adrenal hormones
69
69. Number of pathways for the synthesis of the major groups of hormones
3 major pathways
70
70. Aldosterone formation pathway
Cholesterol- Pregenolone- Progesterone  Aldosterone
71
71. Cortisol formation pathway
17-OH pregenolone- 17-OH progesterone- Cortisol
72
72. Pathway which forms Testosterone and Oestradiol
DHEA- Androstenedione- Testosternone- Oestradiol
73
73. Absence of conversion of Androstenedione into Testosterone
Doesn’t occur in the adrenal glands
74
74. Role of enzyme 17α-hydroxylase
diverts synthesis away from Aldosterone towards cortisol or adrenal androgens production
75
75. Deficiency in the enzyme 21 α-hydroxylase results in
inhibits production of Aldosterone & Cortisol synthesis of adrenal androgens DHEA and androstenedione is massively increased
76
76. Congenital Adrenal Hyperplasia (CAH)
reduction in cortisol secretion removes negative feedback of the hormone on the anterior pituitary gland ACTH secretion increases, providing increased stimulation to the adrenal cortex as adrenal cortex cannot synthesise cortisol or aldosterone it responds to the high levels of ACTH by increasing cell division (hyperplasia) which leads to enlargement of the gland
77
77. Masculinisation a typical sign of Congenital Adrenal Hyperplasia (CAH)
adrenal cortex cant synthesise cortisol or aldosterone it produces high levels of adrenal androgens extremely high levels of androgens cause masculinisation of females and excessive masculinisation of young males
78
78. Role of enzyme 17 α-hydroxylase
diverts synthesis away from aldosterone pathway to cortisol and adrenal androgen synthesis results in no cortisol and no adrenal androgens ACTH levels rise leading to CAH, but without masculinisation
79
79. Role of enzyme 11 β-hydroxylase
acts further down the synthetic pathways of both aldosterone and cortisol results in no cortisol and no aldosterone ACTH levels rise and DHEA levels also rise leading to CAH with masculinisation
80
80. Specialisation of the Adrenal Medulla to carry out its function
acts further down the synthetic pathways of both aldosterone and cortisol results in no cortisol and no aldosterone ACTH levels rise and DHEA levels also rise leading to CAH with masculinisation
81
81. Hormones the Adrenal Medulla secretes
adrenaline noradrenaline
82
82. Role of Adrenaline
prepares the body for physical and mental exertion exerts effects on tissues that are not directly innervated
83
83. Difference between Adrenaline and Noradrenaline
noradrenaline exerts same effects as Adrenaline, but mainly via CNS rather than endocrine system
84
84. Effects Noradrenaline produces by acting on the α-receptors
vasoconstriction iris dilation intestinal relaxation intestinal sphincter contraction piloerection bladder sphincter contraction
85
85. Effects Noradrenaline produces by acting on the β-receptors
vasodilatation cardioacceleration intestinal relaxation increased myocardial strength intestinal relaxation bronchodilatation calorigenesis glycogenolysis lipolysis bladder Wall Relaxation
86
86. Regulation of the synthesis of Catecholamines
changes in the levels of the rate limiting enzyme tyrosine hydroxylase
87
87. Induction of the synthesis of PNMT (phenyl ethanolamine N-methyltransferase) thats responsible for converting noradrenaline to adrenaline
cortisol

Endocrine Systems and Cancer (4 decks)

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