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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
Q
  1. Adrenal Cortex secretion when stimulated by ACTH
A

cortisol

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26
Q
  1. ACTH secretion
A

by anterior pituitary gland in short bursts or pulses

controlled by a pulse generator in hypothalamus

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27
Q
  1. Other name for Arginine vasopressin (AVP)
A

vasopressin

argipressin

antidiuretic hormone (ADH)

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28
Q
  1. Problems in that pathway for secretion of Cortisol
A

hypothalamus- defects in CRH production

pituitary gland- defects in ACTH secretion or bioactivity

adrenal gland- defects in cortisol biosynthesis or secretion

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29
Q
  1. Frequency of pituitary hormones, the problems they can cause and their treatment
A

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)

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30
Q
  1. Problems arising from an overproduction in Cushing ’s syndrome
A

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)

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31
Q
  1. Hypocortisolism also known as
A

cortisol deficiency- Addison’s Disease

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32
Q
  1. Causes of Addison’s Disease
A

rare disease caused by the destruction of the adrenal glands

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33
Q
  1. Addison’s disease results in
A

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

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34
Q
  1. Role of melanocyte stimulating hormone (MSH)
A

stimulates melanocytes in the skin

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35
Q
  1. Secretion on MSH and ACTH
A

corticotrophs in the anterior pituitary

36
Q
  1. Action of melanocyte stimulating hormone (MSH)
A

acts on melanocytes in the epidermis of the skin

stimulates secretion of melanin

37
Q
  1. Melanin controls
A

controls pigmentation in the skin

38
Q
  1. Physiological changes occurring in hypocortisolism
A

reduced plasma cortisol stimulates over-secretion of both ACTH and MSH

increases melanin secretion and causes excessive skin pigmentation (negative feedback)

39
Q
  1. Control of cortisol secretion
A

by ACTH from anterior pituitary

indirectly by hypothalamic CRH as it stimulates ACTH

40
Q
  1. External regulation of the primary control of ACTH
A

circadian or diurnal rhythms of daylight and darkness

41
Q
  1. Fluctuation of cortisol and ACTH levels during the day
A

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
Q
  1. Cortisol counteracts over-response of insulin
A

by increasing carbohydrate metabolism

raising plasma glucose

43
Q
  1. Cortisol suppresses inflammation and immune responses
A

by stimulating the transcription of genes coding for anti-inflammatory proteins

44
Q
  1. Prolonged stress results in
A

continued cortisol secretion

results in muscle wastage, immune and inflammatory responses and hyperglycaemia

45
Q
  1. Drugs that have similar effects to that of prolonged stress
A

glucocorticoids

46
Q
  1. Cortisol has a negative feedback
A

glucocorticoids

47
Q
  1. High levels of cortisol supress
A

ACTH

CRH

AVP secretion

48
Q
  1. Normal plasma levels of ACTH
A

10 pmol/L

49
Q
  1. Challenge tests for negative feedback
A

use of synthetic drugs on the negative feedback control of the anterior pituitary

50
Q
  1. Dexamethasone affects cortisol levels
A

stimulates raised cortisol levels which suppress ACTH secretion by anterior pituitary

ACTH levels reduced to 2 pmol/L

51
Q
  1. Metyrapone affects cortisol and ACTH
A

stimulates raised cortisol levels which suppress ACTH secretion by anterior pituitary

ACTH levels reduced to 2 pmol/

52
Q
  1. Aldosterone biomolecule type
A

primary mineralocorticoid

53
Q
  1. Aldosterone mechanism of action
A

acts on kidney (distal tubule) promoting exchange of sodium and potassium ions (reabsorption of Na+ into the blood)

54
Q
  1. Primary physiological effects of mineralocorticoids
A

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
Q
  1. Reasons why loss of mineralocorticoid activity leads to the destruction of adrenal glands causing death within a few days
A

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
Q
  1. Stimulation of secretion of Aldosterone
A

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
Q
  1. Factors that suppress Aldosterone secretion
A

atrial natriuretic hormone

high sodium concentration

potassium deficiency

58
Q
  1. Cause of primary Aldosterone excess
A

benign tumours of adrenal gland that secrete excess amounts of aldosterone

59
Q
  1. Result of primary Aldosterone excess
A

high blood pressure (hypertension) due to reabsorption of sodium and water

increased potassium excretion (hypokalaemia) causing weakness, paralysis, metabolic alkalosis and polyuria

60
Q
  1. Cause of secondary Aldosterone excess
A

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
Q
  1. Result of secondary Aldosterone excess
A

hypokalaemia- but normal blood pressure

62
Q
  1. Biomolecule that adrenocortical hormones are synthesised from
A

cholesterol

63
Q
  1. Availability of cholesterol
A

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
Q
  1. Rate limiting step in the biosynthesis of steroids
A

transfer of cholesterol from the outer to the inner mitochondrial membrane

65
Q
  1. Protein that mediates transfer of cholesterol from outer to inner membrane
A

steroidogenic acute regulatory protein (StAR)

66
Q
  1. Synthesis of StAR
A

de novo synthesis, under stimulation by ACTH from anterior pituitary

67
Q
  1. Enzyme conversion of cholesterol into pregenolone
A

cytochrome P450 side chain cleavage enzyme (CYP11A)

68
Q
  1. Pregenolone synthesis once made available
A

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
Q
  1. Number of pathways for the synthesis of the major groups of hormones
A

3 major pathways

70
Q
  1. Aldosterone formation pathway
A

Cholesterol- Pregenolone- Progesterone  Aldosterone

71
Q
  1. Cortisol formation pathway
A

17-OH pregenolone- 17-OH progesterone- Cortisol

72
Q
  1. Pathway which forms Testosterone and Oestradiol
A

DHEA- Androstenedione- Testosternone- Oestradiol

73
Q
  1. Absence of conversion of Androstenedione into Testosterone
A

Doesn’t occur in the adrenal glands

74
Q
  1. Role of enzyme 17α-hydroxylase
A

diverts synthesis away from Aldosterone towards cortisol or adrenal androgens production

75
Q
  1. Deficiency in the enzyme 21 α-hydroxylase results in
A

inhibits production of Aldosterone & Cortisol

synthesis of adrenal androgens DHEA and androstenedione is massively increased

76
Q
  1. Congenital Adrenal Hyperplasia (CAH)
A

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
Q
  1. Masculinisation a typical sign of Congenital Adrenal Hyperplasia (CAH)
A

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
Q
  1. Role of enzyme 17 α-hydroxylase
A

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
Q
  1. Role of enzyme 11 β-hydroxylase
A

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
Q
  1. Specialisation of the Adrenal Medulla to carry out its function
A

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
Q
  1. Hormones the Adrenal Medulla secretes
A

adrenaline

noradrenaline

82
Q
  1. Role of Adrenaline
A

prepares the body for physical and mental exertion

exerts effects on tissues that are not directly innervated

83
Q
  1. Difference between Adrenaline and Noradrenaline
A

noradrenaline exerts same effects as Adrenaline, but mainly via CNS rather than endocrine system

84
Q
  1. Effects Noradrenaline produces by acting on the α-receptors
A

vasoconstriction

iris dilation

intestinal relaxation

intestinal sphincter contraction

piloerection

bladder sphincter contraction

85
Q
  1. Effects Noradrenaline produces by acting on the β-receptors
A

vasodilatation

cardioacceleration

intestinal relaxation

increased myocardial strength

intestinal relaxation

bronchodilatation

calorigenesis

glycogenolysis

lipolysis

bladder Wall Relaxation

86
Q
  1. Regulation of the synthesis of Catecholamines
A

changes in the levels of the rate limiting enzyme tyrosine hydroxylase

87
Q
  1. Induction of the synthesis of PNMT (phenyl ethanolamine N-methyltransferase) thats responsible for converting noradrenaline to adrenaline
A

cortisol

Endocrine Systems and Cancer (4 decks)

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