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Metabolism, Endocrinology and Haematology > The Adrenal Glands > Flashcards

The Adrenal Glands Flashcards

1
Q

What are the three gross layers of the adrenal glands?

A

Capsule, Cortex, Medulla

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2
Q

Where are the adrenal glands found?

A

Above the kidneys

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3
Q

What three layers can the cortex be broken down into?

A

Zona glomerulosa, Zona fasiculata, and Zona reticularis

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4
Q

What is the adrenal medulla and what do they secrete?

A

Chromaffin cells which secrete 80% adrenaline and 20% noradrenaline

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5
Q

What does the Zona Glomerulosa secrete?

A

Secretes mineralocortcoids (eg. alsosterone (salt))

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6
Q

What does the Zona fasiculata secrete?

A

Secretes glucocorticoids (eg. cortisol (Sugar))

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7
Q

What does the Zona reticularis secrete?

A

Secretes glucocorticoids and small amounts of androgens

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8
Q

What kind of hormones are secreted from the adrenal cortex?

A

Steriod hormones derived from cholesterol

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9
Q

Where are steroid hormones synthesised?

A

In adrenal glands and gonads

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10
Q

How do steroid hormones exert change?

A

They are lipid soluble hormones that bind to intracellular receptors of the nuclear receptor family to modulate gene transcription

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11
Q

What are examples of steroid hormones found in the adrenal cortex?

A
  • Glucocorticoid
  • Mineralocorticoid
  • Androgens
  • Oestrogen
  • Progestins
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12
Q

What stage of steroid hormone synthesis would be responsible for congenital adrenal hyperplasia?

A

21-hydroxylase enzyme deficiency

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13
Q

How do corticosteroids regulate gene transcription?

A
  • They readily diffuse across membranes and bind to glucocorticoid receptors in the cytoplasm.
  • This causes dissociation of chaperone proteins
  • Receptor-ligand complex translocates to nucleus where dimerisation can occur
  • Receptors bind to glucocorticoid response elements (GREs) or other transcription factors
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14
Q

What is aldesterone?

A

Most abundant form of mineralocorticoid

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15
Q

Where is aldesterone made?

A

Synthesised and released by Zona glomerulosa of adrenal cortex

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16
Q

How does aldesterone work and what does it affect.

A
  • Binds to intracellular aldosterone receptors and exerts action by altering gene transcription
  • Plays role in regulation of plasma Na+, K+ and arterial blood pressure.
  • Central component of renin-angiotensin-aldosterone system (RAAS)
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17
Q

How does aldosterone regulate plasma Na+/K+ concentration and blood pressure?

A
  • Mainly works in distal tubules and collecting ducts of nephron
  • Promotes expression of Na+/K+ ATPase pumps to promote reabsorption of Na+ and excretion of K+
  • This increases water retention and therefore increases blood volume and pressure.
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18
Q

What is the input of the RAAS?

A
  • Hypotension
  • Hypovolaemia
  • This causes a decrease in renal perfusion, decrease in blood pressure ans increased sympathetic tone
  • Baroreceptor activation leads to more renin being released from the kidney
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19
Q

What effect does more renin release have on the RAAS?

A

Causes the cleaving of angiotensinogen (released by the liver) into Angiotensin I.

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20
Q

What does Angiotensin Cleaving Enzyme (ACE) do in RAAS?

A

Cleaves Angiotensin I into Angiotensin II in lung epithelial cells

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21
Q

What effect does Angiotensin II have on the body?

A

Causes:

  • Vasoconstriction in arterioles
  • Promotes synthesis of aldosterone on the adrenal cortex leading to the reabsorption of Na+ and water back into the blood
  • Stimulates posterior pituitary to secrete ADH to aid further water reabsorption with aquaporins.
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22
Q

What are the main outputs of the RAAS?

A

Increased blood volume and pressure.

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23
Q

How could ACE inhibitors be used clinically?

A

ACE inhibitors limit the production of Angiotensin II which means it can be used as a antihypertensive drug

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24
Q

What is Hyperaldosteronism?

A

Too much aldosterone produced

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25
Q

What is primary hyperaldosteronism

A

A defect in adrenal cortex

- Low renin levels –> High aldosterone:renin ratio)

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26
Q

What is the most common form of hyperaldosteronism?

A
  • Bilateral ideopathic adrenal hyperplasia (adrenal glands get bigger)
  • Conn’s Syndrome ( aldosterone secreting adrenal adenoma)
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27
Q

What is secondary Hyperaldosteronism?

A

Due to over activity of the RAAS
Caused by:
- Renin producing tumor eg. jaxtamedullary tumour
- Renal artery stenosis

  • High renin levels –> low aldosterone:renin ratio
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28
Q

What is the best way to distinguish between primary and secondary Hyperaldosteronism

A

Best to distinguish between aldosterone:renin ratios

Primary: High aldosterone:Renin Ratio
Secondary: Low aldosterone:Renin Ratio

29
Q

What are the signs of Hyperaldosteronism?

A
  • High BP
  • Left ventricular hypertrophy
  • Stroke
  • Hypernatraemia
  • Hypokalaemia
30
Q

What are the treatments of Hyperaldosteronism?

A

Depends on the type:

  • Aldosterone-producing adenomas removed by surgery
  • Spironolactone (mineraloscorticoid receptor antagonist)
31
Q

What is cortisol

A

Most abundant corticosteroid and accounts for ~95% glucocorticoid activity

32
Q

What is aldosterone’s carrier protein?

A

Mostly serum albumin and to a lesser extent transcortin

33
Q

What is cortisol’s main carrier protein in plasma?

A

Transcortin

34
Q

Where is cortisol synthesised and released?

A

In the Zona fasiculata in response to ACTH

35
Q

What controls ACTH and CRH release?

A

Negative feedback mechanisms in the Hypothalamus-Pituitary Axis (in particular the hypothalamus)

36
Q

What actions does cortisol have on the body?

A
  • Increased proteolysis in muscle
  • Increased lipolysis in fat
  • Increased gluconeogenesis in liver
  • Provides resistance to stress by increasing supply of glucose and raising blood pressure by making vessels more sensitive to vasoconstrictors
  • Anti-inflammatory effects (by inhibiting macrophage activity and mast cell degranulation)
  • Depression of immune system
37
Q

How can cortisol be useful clinically?

A
  • Anti-inflammatory effects are useful for medications for allergic reactions
  • Depression of the immune system means that cortisol is often prescribed to organ transplant patients
38
Q

What are the net effects of glucocorticoid steroids on metabolism?

A
  • Increased glucose production
  • Breakdown of protein
  • Redistribution of fat
39
Q

What effect does glucocorticoid actions have on metabolism in muscle?

A
  • Increased protein degradation
  • Decreased Protein synthesis
  • Decreased glucose utilisation
  • Decreased sensitivity to insulin

Cortisol inhibits insulin-induced GLUT4 translocation in muscle (prevents glucose uptake –> “glucose sparing effect”)

40
Q

What effect does glucocorticoid actions have on metabolism of fat?

A
  • Decreased glucose utilisation
  • Decreased sensitivity to insulin
  • Increased lipolysis
41
Q

What effect does glucocorticoid actions have on metabolism in the liver?

A
  • Increased glycogen storage (as increased glucose= increased insulin= increased glycogenesis)
  • Increaded gluconeogenesis by increased activity of enzymes
  • Increased amounts of enzymes
42
Q

What is Cushing’s Syndrome?

A

Chronic excess exposure to cortisol

43
Q

What are the signs and symptoms of Cushing’s syndrome?

A
  • Plethoric moon-shaped face
  • “buffalo hump”
  • Abdominal obesity
  • Purple striae
  • Acute weight gain
  • Hyperglycaemia
  • Hypertension
44
Q

Where does the moon-face and buffalo hump come from?

A

Chronic high levels of cortisol results in redistribution of fat especially in abdomen, supraclavicular fat pads (“buffalo hump”) and on the face (“moon face”)

45
Q

What is the most common cause of Cushing’s syndrome?

A

External causes= Prescribed glucocorticoids

46
Q

What are the endogenous causes of Cushing’s syndrome?

A
  • Cushing’s Disease: Benign pituitary adenoma secreting ACTH
  • Adrenal Cushing’s: Excess cortisol produced by adrenal tumour
  • Ectopic Tumours: Non-pituitary-adrenal tumours producing ACTH (&/or CRH) eg. small cell lung cancer
47
Q

What are examples of steroid drugs and what are they used to treat?

A

eg. Prednisolone and Dexamethasone

Used to treat:

  • Asthma
  • Inflammatory bowel disease
  • Rheumatoid arthritis
  • Other auto-immune conditions
  • Supress immune system after organ transplants
48
Q

What effects do steroid drugs have?

A

Anti-inflammatory and immunomodulatory effects

49
Q

What side effects do steroid drugs have?

A

The same effects as higher levels of cortisol, plus can have a mineralocorticoid effects

50
Q

What is Addison’s Disease?

A

Chronic Adrenal insufficiency

51
Q

What is the most common cause of Addison’s Disease?

A

Destructive atrophy from autoimmune response

52
Q

What are the signs and symptoms of Addison’s Disease?

A
  • Postural hypotension
  • Lethargy
  • Weight Loss
  • Anorexia
  • Increased skin pigmentation
  • Hypoglycaemia
53
Q

Why does hyperpigmentation occur in Addison’s?

A

Decreased cortisol –> Negative feedback on anterior pituitary reduced –> more POMC required to synthesise ACTH –> More ACTH and MSH

  • Increased MSH as consequence of increased POMC leads to hyperpigmentation by stimulating melanocytes
  • ACTH also activates melanocortin receptors on melanocytes so will contribute to hyperpigmentation
54
Q

What is an Addisonian Crisis?

A

Life threatening emergency due to adrenal insufficiency

55
Q

What leads to an Addisonian Crisis?

A
  • Severe stress
  • Salt deprivation
  • Infection
  • Trauma
  • Cold exposure
  • Over exertion
  • Abrupt steroid drug withdrawal
56
Q

What are symptoms of Addisonian Crisis?

A
  • Nausea
  • Vomiting
  • Pyrexia
  • Hypotension
  • Vascular Collapse
57
Q

What is the treatment for an Addisonian Crisis?

A
  • Rapid fluid replacement

- Intravenous Cortisol

58
Q

Where are androgens synthesised?

A

Zona reticularis secretes weak androgens Dehydroepiandrosterone (DHEA) and androstenedione

59
Q

What regulates androgen secretion?

A

Partially regulated by ACTH and CRH

60
Q

What does DHEA do in males?

A

DHEA is converted to testosterone in testes.
Before puberty this the main source of testosterone, but after puberty the testes play a greater role so DHEA is irrelevant

61
Q

What do androgens do in females?

A

Adrenal androgens promote libidoand are converted oestrogens by other tissues.
After menopause this is the only source of oestrogens

62
Q

What do androgens do in both sexes?

A

Promote axillary and pubic hair growth

63
Q

What is adrenal medulla?

A

Modified sympathetic ganglions of the autonomic nervous system

64
Q

What do chromaffin cells in the medulla do?

A

They lack axons but act postganglionic nerve fibres that release hormones into the blood.
Releases 80% adrenaline and 20% noradrenaline

65
Q

Why do chromaffin cells release a mixture of noradrenaline and adrenaline?

A

~20% of chromaffin cells lack N-methyl transferase enzyme that converts noradrenaline into adrenaline and so releases some noradrenaline

66
Q

How does adrenaline and noradrenaline exert its actions?

A

By binding to GCPRs

67
Q

What is a phaeochromocytoma?

A

Chromaffin cell tumour

  • A rare, catecholamine-secreting tumour (mainly noradrenaline)
  • May precipitate into life-threatening hypertension
68
Q

What are the characteristics of phaeochromocytoma?

A
  • Severe hypertension
  • Headaches
  • Palpitations
  • Diaphoresis (excessive sweating)
  • Anxiety
  • Weight loss
  • Elevated blood glucose
69
Q

What are catecholamines derived from?

A

Tyrosine

Metabolism, Endocrinology and Haematology (1 decks)

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