MEH 17 - The Adrenal Glands Flashcards

1
Q

What hormones are released from chromaffin cells of the adrenal medulla?
What are the 3 sections of the the adrenal cortex and what hormones do they release?

A

Medulla = Adrenaline (80%) + Noradrenaline (20%)
Cortex:
(outside in)
1) Zona glomerulosa - mineralocorticoids e.g.: aldosterone
2) Zona fasciculata - glucocorticoids e.g.: cortisol
3) Zona reticularis - glucocorticoids + angrodens e.g.: DHEA

Good Pneumonic = GFR - Salt, Sugar, Sex :)

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2
Q

What type of hormones are all the adrenal hormones?

Therefore, how do they exert their actions?

A
  • Steroid hormone, all synthesised from cholesterol in adrenal glands or gonads
  • Bind to nuclear receptors to modulate gene transcription as they are lipid soluble.
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3
Q

How do corticosteroids regulate gene transcription?

A

1) Binding to intracellular receptor causing dissociation of chaperone protein (e.g.: heat shock 90)
2) Receptor/ligand complex migrates to nucleus
3) Receptors bind to glucocorticoid response elements (GRE’s) or other transcription factors

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4
Q

What is the central role of aldosterone?

A
  • Promotes expression of Na/K pump. in distal tubules + collecting ducts, influencing water retention and therefore BP (promotes reabsorption of Na+/excretion of K+)
  • Drop in BP = activation of RAAS = increased BP
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5
Q

What is primary + secondary hyperaldosteronism?
How do you distinguish between the two?
What are the signs + treatment?

A

1) Primary = defect in adrenal cortex, e.g.: aldosterone secreting adrenal adenoma (Conn’s syndrome).
2) Secondary = overactivity of RAAS, e.g.: renin producing tumour or renal artery stenosis.

  • Primary has low renin levels, secondary has high.
  • High BP, LV hypertrophy, hypernatraemia, hypokalaemia.
  • Remove tumour by surgery, give spironolactone (aldosterone antagonist) for secondary.
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6
Q

What are the primary actions of cortisol?

A
  • Increased protein breakdown in muscle
  • Increased lipolysis in fat
  • Increased gluconeogenesis in liver
  • Resistance to stress (increased glucose, raising BP)
  • Anti-inflammatory effects
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7
Q

What is Cushing’s syndrome?
What are the common causes?
What are the signs + symptoms?

A
  • Chronic excessive exposure to cortisol
  • Most commonly caused by prescribed glucocorticoids, much less likely to be a pituitary adenoma secreting ACTH or cortisol producing adrenal tumour
  • Moon shaped face, buffalo hump (on neck), abdominal obesity, purple striae, acute weight gain, hyperglycaemia + hypertension.
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8
Q

What are steroid drugs often used to treat?

A
  • Inflammatory disorders due to anti-inflammatory effects
  • E.g.: asthma, RA, inflammatory bowel disease etc
  • E.g.: prednisolone + dexamethasone
  • Side effects = higher levels of cortisol
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9
Q

What is Addison’s disease?
Who does it affect?
What are the signs + symptoms?

A
  • Chronic adrenal insufficiency, due to destructive atrophy from autoimmune response.
  • Affects more women than men
  • Postural hypotension, lethargy, weight loss, anorexia, increased skin pigmentation + hypoglycaemia.
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10
Q

Why can Addison’s disease cause hyperpigmentation?

A
  • Both ACTH + MSH are synthesised from pro-opiomelanocortin (POMC)
  • Less cortisol means less negative feedback on ant pituitary
  • More MSH leading to melanin synthesis and hyperpigmentation
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11
Q

What is Addison’s crisis + what causes it?

What are the symptoms?

A
  • Life threatening emergency due to adrenal insufficiency - caused by severe stress, salt deprivation, infection, trauma, over exertion etc.
  • Nausea, vomiting, pyrexia, hypotension + vascular collapse
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12
Q

What is the primary role of male and female androgens?

A
  • In males = DHEA converted to testosterone in testes
  • In females = androgens promote libido and converted to oestrogen’s by other tissues
  • Promote axillary and pubic hair growth in both sexes
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13
Q

What are the affects of AD + NA in the heart, lungs + blood vessels?

A
  • Increased HR + contractility in heart (as B1 receptors, which are GaS)
  • Bronchodilation in lungs (as B2 receptors are GaS)
  • Vasoconstriction of blood vessels in skin and gut (as a1 are GaQ)
  • Vasodilation of skeletal muscle vessels (as B2 receptors are GaS)
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14
Q

What is a phaechromocytoma?

What symptoms does it lead to?

A
  • Phae (dark), chromo (colour), cyte (cell) oma (tumour stain dark).
  • Basically a chromaffin cell tumour - secreting catecholamines
  • Severe hypertension (deadly), headaches, palpitations, diaphoresis + anxiety.
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