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Pharm > Lecture 27: Adrenocorticosteroids > Flashcards

Lecture 27: Adrenocorticosteroids Flashcards

1
Q

What are the two main parts of the Adrenal Gland?

A

The medulla and the cortex

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2
Q

What are the three parts of the cortex?

A
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
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3
Q

Which hormone does the adrenal medulla secrete?

A

Adrenaline

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4
Q

What kind of hormone is adrenaline?

A

A catecholamine

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5
Q

What kind of hormones does the cortex produce?

A

Steroid hormones

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6
Q

What is the order of the layers of the cortex from outside to inside?

A
  • Glomerulosa
  • Fasciculata
  • Reticularis
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7
Q

What does the Zona Glomerulosa secrete?

A

Aldosterone

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8
Q

What is Aldosterone important for?

A

Blood pressure regulation through its control on salt balance

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9
Q

What does the Fasciculata secrete?

A

Cortisol

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10
Q

What does Cortisol have an effect on?

A

Metabolism and immune response

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11
Q

What does the Zona Reticularis produce?

A

DHEA which is a precursor for testosterone and estrogen

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12
Q

What is the precursor for all adrenal steroid hormones?

A

Cholesterol

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13
Q

What does the HPA axis control?

A

Cortisol release from the zona fasciculata

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14
Q

What does the HPA axis involve?

A

The hypothalamus, anterior pituitary, and the adrenal cortex

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15
Q

What does ACTH do?

A

It is released from anterior pituitary and directly activates cells in the zona fasciculata to secrete cortisol

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16
Q

What does CRH do?

A

It is released from the hypothalamus and activates the anterior pituitary to releases ACTH

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17
Q

When does ACTH stimulate steroid production?

A
  • After meals

* Circadian rhythm (just before waking up)

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18
Q

Why can steroid hormones pass lipid membranes?

A

Because they are lipid soluble

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19
Q

Why don’t steroid hormone get packaged into vesicles?

A

Because they will pass through membranes so they have to be synthesized on demand

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20
Q

What does Cortisol exert negative feedback on?

A

The CRH (hypothalamus) and the ACTH (pituitary)

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21
Q

How does Cortisol affect stress signals?

A

It suppresses stress signals like cytokines involved in the stress response

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22
Q

What does Cortisol act on?

A

Glucocorticoid target tissues

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23
Q

What is Renin released by?

A

The juxtaglomerular apparatus (kidney)

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24
Q

What does Renin do?

A

It converts Angiotensinogen and Angiotensin I

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25
Q

What converts Angiotensinogen to Angiotensin I?

A

Renin

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26
Q

What does ACE do?

A

Converts AT1 to AT2

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27
Q

What converts AT1 to AT2?

A

ACE

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28
Q

What does AT2 do?

A

Triggers aldosterone release

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29
Q

What triggers aldosterone release?

A

AT2

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30
Q

What does Aldosterone do?

A

Targets the kidneys and promotes Na+/water reabsorption, K+ excretion (Mineralocorticoid Response)

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31
Q

What is the Mineralcorticoid response?

A

When hormones that act on the kidneys causes Na+/water reabsorption, and K+ excretion

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32
Q

What is the mechanism of steroid hormones?

A

They diffuse across the membrane and interacts with receptor in the cytoplasm. This causes it to dissociate from the heat shock protein (HSP) and move into the nucleus. The dimerized receptors interact with DNA and influence transcription of target genes at the GRE

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33
Q

How long does it take for steroid hormones?

A

They take hours to turn on and hours to turn off

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34
Q

What are the two targets of GR binding?

A

Lipocortin and COX-2

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35
Q

What are the two receptors for Corticosteroids?

A
  • Glucocorticoid receptor

* Mineralocorticoid receptor

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36
Q

What does the Glucocorticoid receptor stimulate?

A

The GC response

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37
Q

What does the Mineralocorticoid receptor stimulate?

A

The MC response

38
Q

What are all the hormones that target the GC and MC receptor derived from?

A

Cholesterol

39
Q

What are the two endogenous steroid hormones?

A

Cortisol and Aldosterone

40
Q

What are the synthetic hormones that target the steroid hormone receptors?

A
  • Dexamethasone
  • Prednisone
  • Fludrocortisone
41
Q

Which receptor does Dexamethasone have a high affinity for?

A

The GC receptor

42
Q

Which receptor does Fludrocortisone have a high affinity for?

A

The MC receptor

43
Q

Which receptor does Prednisone have a high affinity for?

A

The GC receptor but it has less affinity than Dexamethasone so it has some affinity for the MC receptor

44
Q

What receptor does Cortisol have a high affinity for?

A

Both GC and MC

45
Q

What receptor does Aldosterone have a high affinity for?

A

MC but it also has affinity for GC just less than MC

46
Q

What are some glucocorticoid target issues?

A
  • Adipose
  • Muscle
  • Liver
47
Q

What is the inactive form of cortisol?

A

Cortisone

48
Q

What enzyme affects the equilibrium between cortisone and cortisol?

A

11β-hydroxysteroid dehydrogenase type 1

49
Q

What does 11β-hydroxysteroid dehydrogenase type 1 do?

A

Activates Cortisol by converting cortisone to cortisol

50
Q

Where is 11β-hydroxysteroid dehydrogenase type 1 found?

A

In the liver, adipose and muscle. Places where Cortisol has effects

51
Q

How does 11β-hydroxysteroid dehydrogenase type 1 affect specificity of Cortisol?

A

It allows it to be more specifically targeted in tissues that express the enzyme

52
Q

What are the characteristics of Prednisone?

A
  • Not effective topically
  • Widely used (oral intake, injection)
  • Must be metabolized to prednisolone to become effective
53
Q

What are the characteristics Prednisolone?

A
  • Strong topical effect

* Active form of prednisone

54
Q

What converts Prednisone to the active form?

A

11β-hydroxysteroid dehydrogenase type 1

55
Q

Why does cortisol activate the MR receptor but not cause an MR response?

A

Because tissues that are sensitive to aldosterone express an enzyme called 11β-hydroxysteroid dehydrogenase type 2 that inactivates cortisol

56
Q

What does 11β-hydroxysteroid dehydrogenase type 2 do?

A

Inactivates cortisol in tissues that contain the MR receptor

57
Q

What would happens if people were deficient in 11β-hydroxysteroid dehydrogenase type 2?

A

Cells with the MR receptor would be susceptible to the effects of cortisol

58
Q

How does licorice affect 11β-hydroxysteroid dehydrogenase type 2?

A

It inhibits 11β-hydroxysteroid dehydrogenase type 2 causing the glucocorticoid to have an inappropriate affect in aldosterone target tissues causing BP to go up

59
Q

What is apparent mineralocorticoid excess?

A

A genetic disease where there are mutations in 11β-hydroxysteroid dehydrogenase type 2 which breaks down cortisol in aldosterone responsive tissue

60
Q

How do glucocorticoids/circulating cortisol affect glucose?

A

They increase circulating glucose

61
Q

How do glucocorticoids/circulating cortisol affect fat/lipid balance?

A

They promote fat deposition in the trunk but fat breakdown in the limbs

62
Q

How do glucocorticoids increase circulating glucose?

A

Cause glucose synthesis in the liver and inhibit insulin

63
Q

How do glucocorticoids affect muscle and bones?

A

It leads to loss of muscle and bone mass in limbs

64
Q

What is the most common effects of glucocorticoids?

A

They suppress inflammation and the immune response

65
Q

What does Phospholipase do?

A

Cleaves phospholipids into arachidonic acid

66
Q

What is Arachidonic acid?

A

The precursor to inflammatory mediators

67
Q

What does Cyclo-oxygenase 2 (COX2) do?

A

Generates signalling molecules called prostanoids in inflammation

68
Q

What are the inflammatory targets of Glucocorticoids?

A

Glucocorticoids inhibit phospholipase A2 and inhibits Cyclo-oxygenase 2 (COX2)

69
Q

What are the key glucocorticoid-mediated mechanisms in inflammation?

A
  • Inhibit arachidonic acid synthesis

* Inhibit prostanoid synthesis

70
Q

What is COX2 and what does it do?

A

An inflammatory mediator early in the process of inflammation and converts arachidonic acid to various prostanoids

71
Q

How does Glucocorticoid regulation of COX-2 have it effects?

A

Because it is lipophilic it affects the transcription of the COX-2 gene leading to long-term suppression of COX-2 expression

72
Q

What protein is increased in expression by glucocorticoids?

A

Lipocortins/Annexins

73
Q

What are Lipocortins/Annexins?

A

A large family of proteins characterized by annexin repeats

74
Q

How do Lipocortins/Annexins play a part in anti-inflammatory role?

A
  1. Direct effects on Leukocytes, inhibits their tissue infiltration
  2. Suppression of phospholipase A2 activity which prevents generation of AA
75
Q

What is Lipocortin expression induced by?

A

GC receptor activation

76
Q

What is Addison’s disease?

A

Chronic adrenocortical insufficiency where there is low production of glucocorticoids and often mineralocorticoids

77
Q

What is Addison’s treated with?

A

GC/MC supplementation

78
Q

What are the symptoms of Addison’s disease?

A

Fatigue, salt balance, sugar balance problems, skin discorloration

79
Q

What is Cushing’s syndrome?

A

Adrenal overactivity leading to excessive cortisol caused by tumors or drug induced

80
Q

What are the symptoms of Cushing’s symptoms?

A
  • Round face, fat deposition in the trunk

* Muscle loss, osteoporosis - protein and bone catabolism

81
Q

What do all the therapeutic uses of Glucocorticoids revolve around?

A

Their anti-inflammatory and immunosuppressive actions

82
Q

What does negative feedback from glucocorticoid administration do?

A

Supresses CRH and ACTH production

83
Q

What are the symptoms similar to if an individual stops taking glucocorticoids abruptly?

A

Addisonian crisis: Hypoglycemia, hyponatremia, hyperkalemia and low BP

84
Q

What happens if someone stops taking glucocorticoids abruptly?

A

Because the glucocorticoids suppress CRH and ACTH production the body won’t produce its own cortisol

85
Q

What is required when stopping long term course glucocorticoids?

A

Tapering

86
Q

What is the metabolic side effects when taking too much glucocorticoids?

A

Hyperglycemia

87
Q

What is the immunosuppressive effect when taking too much glucocorticoids?

A

Latent infection can emerge because they suppress the immune system

88
Q

What disease do the effects of taking too much glucocorticoids resemble?

A

Cushing syndrome

89
Q

What is the Catabolic effect when taking too much glucocorticoids?

A

Osteoporosis and muscle wasting

90
Q

What is the anti-inflammatory effect when taking too much glucocorticoids?

A

Slow wound healing and ulceration

91
Q

How can non-specific mineralocorticoid effects arise when taking too much glucocorticoids?

A

Enzymes in the kidneys that deactivate GCs can become saturated, causing them to have effects on MR receptors

92
Q

Can too much glucocorticoid cause psychosis?

A

Yes

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