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After the MSA > Action of the adrenal Steroids and treatment of adrenal disorders > Flashcards

Action of the adrenal Steroids and treatment of adrenal disorders Flashcards

1
Q

What is the origin of the adrenal medulla?

A

Neural crest

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2
Q

What is secreted by the adrenal medulla?

A

Catecholamines

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3
Q

What is the origin of the adrenal cortex?

A

Mesoderm

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4
Q

What is secreted by the zona glomerulosa and what regulates?

A
  • Mineralocorticoids

* Regulated by ACTH, K+ and renin angiotensin II

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5
Q

What is secreted by zona fasciculate and what regulates

A
  • Mainly glucocorticoids (cortisol and corticosterone)

* Regulated by ACTH

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6
Q

What is secreted by the zona reticular and what regulates?

A
  • Mainly androgens

* Regulated by ACTH and unknown precursors

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7
Q

What is the main mineralocorticoid?

A

Aldosterone

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8
Q

What is the general role of mineralocorticoids?

A

Regulate salt/electrolyte and water balance

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9
Q

What are glucocorticoids used for therapeutically?

A
  • Replacement therapy
  • Anti-inflammatory
  • Immunosuppressive
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10
Q

Describe the regulation of adrenal corticosteroids

A
  • Adrenals are part of the HPA axis
  • CRF and ADH act on corticotrophins in the anterior pituitary inducing ACTH release
  • ACTH stimulates the synthesis and secretion of both glucocorticoids and mineralocorticoids from the adrenal cortex
  • The renin angiotensin system aids ACTH to promote mineralocorticoid secretion
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11
Q

Tetracosactide

A

Synthetic ACTH analogue (increases stimulation of the adrenal cortex)

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12
Q

Fludrocortisone

A

• Mimics mineralocorticoid effects

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13
Q

Prednisolone

A

• Mimics glucocorticoid effects

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14
Q

How can you test to see if there is a primary or a secondary adrenal insufficiency

A
  • Give tetracosactide (ACTH analogue)
  • If there is a problem with the pituitary or hypothalamus, the adrenal cortex should still work and hydrocortisone should be produced and detected
  • If no hydrocortisone can be detected primary
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15
Q

What is the rate limiting step in the biosynthesis of corticosteroid and mineralocorticoids and sex hormones

A
  • Conversion of cholesterol to pregnenolone

* Regulated by ACTH (and Angiotensin II)

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16
Q

Amioglutethimide

A
  • Inhibits the rate limiting step

* blocks the conversion of cholesterol to pregnenolone

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17
Q

Trilostane

A
  • Blocks 3 beta dyhd
  • Used to treat bushings and primary hyperaldosteronism
  • Prevents pregnenolone -> progesterone
  • Prevents 17a-OH-pregnenolone -> 17a-OH-progesterone
  • Prevents Dehydroepiandosterone -> androstenedione (sex hormone pathway)
18
Q

Metapyrone

A
  • Blocks 11B-OH: stops the beta hydroxylation of C11
  • Stops progesterone -> corticosterone
  • Stops 17a-OH-progesterone ->hydrocortisone
19
Q

Carbenoxolone

A
  • Inhibits the conversion of hydrocortisone to cortisone in the kidney
  • Blocks 11-B-dehd
20
Q

Describe the mechanism of action of glucocorticoids

A
  • Bind to intracellular receptors and migrate to the nucleus
  • Dimerize and regulate gene transcription
  • Rapid non-genomic effects of glucocorticoids and mediated through signalling systems in the cytosol
21
Q

What are common glucocorticoid drugs?

A
  • Hydrocortisone
  • Prednisolone
  • Dexamethasone
22
Q

What regulates the metabolic effects of glucocorticoids?

A

• Enzymes e.g. cAMP dependent protein kinase (PKA)

•

23
Q

What are the 4 ways glucorticoids can exert their effects?

A
  • Transactivaiton: glucocorticoid binds to G response element and upregulates transcription
  • Transrepression: transcription factors bind to negative G response element decreasing transcription
  • Fos/Jun: glucocorticoids reduce the binding of fos/jun transcription factors to AP-1 regulatory site
  • Nuclear factor: GR binds to transcription factor preventing transcription
24
Q

What are the 4 physiological roles of glucocorticoids?

A
  • Regulatory actions
  • Metabolic actions
  • Anti-inflammatory and immunosuppressive effects
  • Actions on mediators of inflammatory and immune responses
25
Q

What are the regulatory actions of glucocorticoids?

A
  • Negative feedback: acts on hypothalamus and pituitary (CRF and ACTH) leading to reduced glucocorticoid release
  • Cardiovascular: reduced vasodilation and fluid exudation
  • Musculoskeletal: decreasing osteoblast and increasing osteoclast activity to give a tendency for osteoporosis
26
Q

What are the metabolic actions of glucocorticoids?

A
  • Decreased uptake and utilisation of glucose accompanied by increased gluconeogenis to cause hyperglycaemia and increased glycogen storage
  • Increases catabolism and decreases anabolism, leading to muscle wasting
  • Lipids: permissive effect on lipolytic hormones and a redistribution of fat as observed in cushings syndrome
27
Q

What are the anti-inflammatory and immunosuppressive effects of glucocorticoids?

A
  • Anti inflammation: decreased influx and activity or leukocytes
  • Chronic inflammation: decreased activity of mononuclear cells, decreased angiogenesis and fibrosis
  • Lymphoid tissue: decreased clonal expansion of T and B cells and decreased activation of cytokine secreting T cells
  • Switch from Th-1 to Th-2 responses (dampening down cell mediated and acquired response)
28
Q

What are the actions of glucocorticoids on mediators of inflammatory and immune responses

A
  • Decreased production and action of cytokines including interleukins, TNF-a, cell adhesion factors and induced nitric oxide
  • Reduced generation of eicosanoids due to decreased COX-2 expression
  • Reduced generation of IgG and complement components in the blood
  • Increased release of anti-inflammatory factors
  • Overall reduction in the activity of the innate and acquired immune system
29
Q

What is the main clinical use of mineralocorticoids?

A

Replacement therapy in Addisons

30
Q

Describe the mechanism of action of fludrocortisone

A
  • Increases Na+ reabsorption in the distal tubules
  • Increases K+ and H+ efflux
  • Acts on the intracellular receptors that modulate DNA transcription
31
Q

Spironolactone

A
  • Competitive antagonist
  • Potassium sparing diuretic
  • Used to treat hyperaldosteronsim, resistant hypertension, heart failure and oedema
32
Q

Why is aldosterone not appropriate as a therapeutic agent?

A

The liver converts >75% of oral aldosterone to an inactive metabolite

33
Q

What are the causes of Addison’s disease?

A
  • 7/10 due to autoimmune disease e.g. adrenalitis
  • TB
  • Metastatic cancers
  • Atrophy due to prolonged steroid therapy
  • haemochromatosis
  • Amyloidosis
34
Q

What are the symptoms of Addisons disease?

A
  • Anorexia
  • Nausea and vomiting
  • WEakness
  • Hypotension
  • Skin pigmentation
  • Low sodium/ high potassium
  • Chronic dehydration
  • Sexual dysfunciton
35
Q

Describe the treatment of Addisons disease

A
  • Corticosteroid replacement therapy for life
  • hydrocortisone main
  • Prednisolone or dexamethasone
  • If greater mineralocorticoid effects are needed, aldosterone is replaced with fludrocortisone
36
Q

What is the main cause of hyperaldosteronism?

A

• Adrenal adenoma - Conn’s syndrome

37
Q

How is Conn’s syndrome/adrenal adenoma treated?

A
  • Surgical adrenalectomy

* Before surgery: use of a aldosterone antagonist e.g. spironolactone

38
Q

Congenital adrenal hyperplasia

A

• C-21 hydroxyls enzyme is missing
- non hydroxylated versions of cortisol, corticosterone and aldosterone are made
- these lack normal activity and don’t negatively feedback on the HPA
• Treat with cortisol to replace the missing cortisol and cause negative feedback
• Replace the mineralocorticoid

39
Q

What are the side effects of glucocorticoids?

A
  • Suppression of response to infection and injury
  • Opportunistic infections can be problematic
  • Oral fungal and yeast infections can occur
  • Impaired would healing
  • Osteoporosis
  • Hazard of fractures
  • Hyperglycaemia
  • Muscle wasting and weakness
  • Inhibition of growth in children
  • CNS effects
  • Glaucoma
40
Q

What is Cushing’s syndrome characterised by?

A
  • Moon face and red cheeks
  • Buffalo hump
  • Thinning of skin
  • Increased abdominal fat
  • Easily bruising
  • Poor wound healing
  • Mood swings

After the MSA (22 decks)

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