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Semester 2-MEH > Session 9-Adrenal Glands > Flashcards

Session 9-Adrenal Glands Flashcards

1
Q

What are the three layers of the adrenal cortex?

A

Zona glomerulosa
Zona fasiculata
Zona reticularis

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2
Q

Which hormones are produced in zona glomerulosa?

A

Mineralocorticoids eg aldosterone (salt)

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3
Q

Which hormones are produced in zona fasiculata?

A

Glucocorticoids eg cortisol (sugar)

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4
Q

Which hormones are produced in zona reticularis?

A

Glucocorticoids and small amounts of androgens (sex hormones)

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5
Q

How can the layers and hormones of the adrenal cortex be remembered?

A

GFR salt, sugar, sex

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6
Q

Which cells are present in the adrenal medulla?

A

Chromaffin cells

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7
Q

What is the precursor for steroid hormones?

A

Cholesterol

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8
Q

True or false: steroid hormones are lipid soluble

A

TRUE

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9
Q

Which family of intracellular receptors do steroid hormones bind to?

A

Nuclear receptor family

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10
Q

What happens when steroid hormones bind to intracellular receptors?

A

Modulates gene transcription

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11
Q

Name five types of steroid hormones

A 
Glucocorticoids
Mineralocorticoids 
Androgens
Oestrogens
Progestins
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12
Q

How do corticosteroids exert their actions?

A

By regulating gene transcription

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13
Q

Describe how corticosteroids regulate gene transcription

A

1) corticosteroids readily diffuse across plasma membrane
2) bind to glucocorticoid receptors
3) binding causes dissociation of chaperone proteins
4) receptor ligand complex translocates to nucleus
5) dimerisation with other receptors
6) receptors bind to glucocorticoid response element (GREs) or other transcription factors and regulate

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14
Q

What is the most abundant mineralocorticoid and where is it synthesised and released?

A

Aldosterone

Zona glomerulosa of adrenal cortex

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15
Q

What is the main carrier protein of aldosterone?

A

Serum albumin

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16
Q

How does the aldosterone receptor exert its actions?

A

Regulates gene transcription

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17
Q

True or false: aldosterone plays a central role in regulation of plasma Na+, K+ and arterial blood pressure

A

TRUE

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18
Q

What are the main actions of aldosterone in distal tubules and collecting ducts of nephron?

A

Promotes expression of Na+/K+ pump which promotes reabsorption of Na+ and excretion of K+ and this influences water retention, blood volume and blood pressure

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19
Q

What leads to more renin release from the kidney?

A

Decrease in renal perfusion
Drop in BP
Increased sympathetic tone from baroreceptor activation

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20
Q

Where is angiotensinogen released from?

A

Liver

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21
Q

Where is angiotensin I converted to angiotensin II and which enzyme catalyses this conversion?

A

Lung endothelial cells

Angiotensin converting enzyme (ACE)

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22
Q

What are the three effects of angiotensin II that lead to increased BP and blood volume?

A

1) vasoconstriction
2) stimulates aldosterone release -> increased expression of Na+/K+ pump -> increased reabsorption of Na+ and water back into blood
3) stimulates posterior pituitary to release ADH -> translocation of aquaporin channels -> reabsorption of water back into blood

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23
Q

What is hyperaldosteronism?

A

Too much aldosterone produced

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24
Q

What is primary aldosteronism and what can cause this?

A

Defect in adrenal cortex

Bilateral idiopathic adrenal hyperplasia and aldosterone secreting adrenal adenoma (Conn’s syndrome)

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25
Q

What is secondary hyperaldosteronism and what causes this?

A

Over activity of RAAS

Renin producing tumour, renal artery stenosis

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26
Q

How can you differentiate between primary and secondary hyperaldosteronism?

A

Primary has low renin levels so high aldosterone: renin ratio

Secondary has high renin levels so low aldosterone:renin ratio

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27
Q

What are the signs of hyperaldosteronism?

A 
High BP
Left ventricular hypertrophy 
Stroke
Hypernatraemia 
Hypokalaemia
28
Q

What is the treatment for hyperaldosteronism?

A

Aldosterone-producing adenomas removed by surgery

Spironolactone = mineralocorticoid receptor antagonist

29
Q

What is the most abundant corticosteroid and where is it synthesised and released?

A

Cortisol

Zona fasiculata in response to ACTH

30
Q

What is the negative feedback effect on the hypothalamus of cortisol?

A

Inhibits ACTH and CRH release

31
Q

What is the carrier protein for cortisol?

A

Transcortin

32
Q

What are the catabolic effects of cortisol?

A
  • Increased proteolysis in muscle
  • Increased gluconeogenesis in liver
  • Increased lipolysis in adipose tissue
33
Q

Why is cortisol a useful medication for allergic reactions?

A

Anti-inflammatory effects: inhibits macrophage activity and leads to mast cell degranulation

34
Q

What effects do glucocorticoids have in the liver?

A
  • Increased glycogen storage
  • increased gluconeogenesis by increased activity of enzymes and increased amounts of enzymes (indirectly increased glucose levels so increased insulin and increased glycogen stores)
35
Q

What effects do glucocorticoids have in adipose tissue?

A
  • Re-distribution of fat, especially in abdomen, face and back
  • Decreased glucose utilisation
  • decreased sensitivity to insulin
  • increased lipolysis
36
Q

What effects do glucocorticoids have on muscle?

A
  • cortisol inhibits insulin-induced GLUT4 translocation in muscle (prevents glucose uptake)
  • increased protein degradation
  • decreased protein synthesis
  • decreased glucose utilisation
  • decreased sensitivity to insulin
37
Q

What is Cushing’s syndrome?

A

Chronic excessive exposure to cortisol

38
Q

What is the external cause of Cushing’s syndrome?

A

Prescribed glucocorticoids

39
Q

What are the endogenous causes of Cushing’s syndrome?

A
  • benign pituitary adenoma secreting ACTH (Cushing’s disease)
  • excess cortisol produced by adrenal tumour (adrenal Cushing’s)
  • non pituitary-adrenal tumours producing ACTH eg small cell lung cancer (rare)
40
Q

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

A
  • moon shaped face
  • “buffalo hump”
  • abdominal obesity
  • purple striae due to excess proteolysis
  • acute weight gain
  • hyperglycaemia
  • hypertension
41
Q

Give two examples of steroid drugs

A

Prednisolone

Dexamethasone

42
Q

Which conditions are steroid drugs used to treat?

A

Inflammatory disorders:
Asthma
Inflammatory bowel disease
RA

43
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency

44
Q

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

A

Destructive atrophy from autoimmune response

45
Q

True or false: Addison’s disease affects more men than women

A

FALSE - other way round

46
Q

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

A
  • postural hypotension
  • lethargy
  • weight loss
  • anorexia
  • increased skin pigmentation
  • hypoglycaemia
47
Q

What is the precursor of ACTH?

A

POMC

48
Q

How does Addison’s disease lead to hyperpigmentation?

A

Decreased cortisol -> negative feedback on anterior pituitary decreased -> increased POMC -> increased melanocyte stimulating hormone (MSH) and ACTH -> hyperpigmentation

49
Q

What is Addisonian crisis?

A

Life threatening emergency due to adrenal insufficiency

50
Q

What is Addisonian crisis precipitated by?

A
  • severe stress
  • salt deprivation
  • infection
  • trauma
  • cold exposure
  • over exertion
  • abrupt steroid drug withdrawal
51
Q

What are the symptoms of Addisonian crisis?

A
  • nausea
  • vomiting
  • pyrexia
  • hypotension
  • vascular collapse
52
Q

What is the treatment of Addisonian crisis?

A

Fluid replacement

Cortisol

53
Q

What are the two main androgens and what are they partially regulated by?

A

DHEA
Androstenedione

ACTH and CRH

54
Q

What is DHEA converted to in males?

A

Testosterone in testes

55
Q

What do female adrenal androgens do?

A

Promote libido

Converted to oestrogens by other tissues and after menopause, this is the only source of oestrogens

56
Q

What do androgens promote in both sexes?

A

Axillary and pubic hair growth

57
Q

True or false: adrenal medulla is a modified sympathetic ganglion of autonomic nervous system

A

TRUE

58
Q

Complete the sentence:

Chromaffin cells in adrenal medulla lack _______ but act as postganglionic nerve fibres that release hormones into blood: __________ (80%) and ________________ (20%)

A

Axons
Adrenaline
Noradrenaline

59
Q

What are catecholamines derived from?

A

Tyrosine

60
Q

Why do some chromaffin cells secrete noradrenaline as opposed to adrenaline?

A

Lack N-methyl transferase enzyme

61
Q

Which receptor increases heart rate and heart contractility?

A

Beta 1

62
Q

Which receptor leads to bronchodilation?

A

Beta 2

63
Q

Which receptor leads to vasoconstriction?

A

Alpha 1

64
Q

Which receptor leads to vasodilation?

A

Beta 2

65
Q

What is phaeochromocytoma?

A

Chromaffin cell tumour

Tumour stains dark with chromium salts

Rare catecholamine-secreting tumour (mainly noradrenaline)

66
Q

What are the characteristics of phaeochromocytoma?

A
  • severe hypertension
  • headaches
  • palpitations
  • diaphoresis (excessive sweating)
  • anxiety
  • weight loss
  • elevated blood glucose

Semester 2-MEH (21 decks)

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