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ESA2 - Metabolism, Endocrinology and Haematology > The Adrenal Glands > Flashcards

The Adrenal Glands Flashcards

1
Q

True or False:

The adrenal glands are outside of the renal fascia

A

False

Encapsulated within renal fascia

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2
Q

How many layers does the adrenal cortex have?

A

3

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3
Q

What are the layers of the adrenal cortex?

A

Zona glomerulosa, zona fasiculata, zona reticularis

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4
Q

What is produced in the zona glomerulosa of the adrenal cortex?

A

Mineralocorticoids (eg aldosterone)

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5
Q

What is produced in the zona fasiculata of the adrenal cortex?

A

Glucocorticoids (eg cortisol)

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6
Q

What is produced in the zona reticularis of the adrenal cortex?

A

Glucocorticoids + small amounts of androgens

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7
Q

What is produced in the adrenal medulla?

A

Adrenalne and noradrenaline

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8
Q

What are chromaffin cells?

A

They are neuroendocrine cells found mostly in the medulla of the adrenal glands

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9
Q

What are corticosteroids?

A

Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex

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10
Q

What is an example of a mineralocorticoid?

A

Aldosterone

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11
Q

What is an example of a glucocorticoid?

A

Cortisol

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12
Q

What are steroid hormones synthesised from?

A

Cholesterol

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13
Q

What is the adrenal cortex derived from in embryonic development?

A

Mesoderm

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14
Q

What is the adrenal medulla derived from in embryonic development?

A

Neural crest cells

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15
Q

How do corticosteroids exert their actions?

A

By regulating gene transcription

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16
Q

Outline how corticosteroids regulate gene transcription

A

1) Diffuse across plasma membrane
2) Bind to glucocorticoid receptors
3) Chaperone proteins on receptors dissociate
4) Receptor-ligand complex translocates to nucleus
5) Dimerisation with other receptors can occur
6) Receptors bind to glucocorticoid response elements (GREs) or other transcription factors

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17
Q

What is a hormone response element?

A

A hormone response element (HRE) is a short sequence of DNA within the promoter of a gene that is able to bind a specific hormone receptor complex and therefore regulate transcription

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18
Q

Where is aldosterone synthesised and released by?

A

Zona glomerulosa of adrenal cortex

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19
Q

What carrier proteins bind to aldosterone?

A

Serum albumin and transcortin

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20
Q

What is the role of aldosterone?

A

RAAS
In distal tubules and collecting ducts - promotes expression of Na+/K+ pump to promote reabsorption of Na+ and excretion of K+, influencing water retention, blood volume and thus blood pressure

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21
Q

Outline the RAAS

A

1) Renin released from kidney cleaves angiotensinogen (released from liver) into angiotensin I
2) ACE in lungs cleaves angiotensin I into angiotensin II
3) Angiotensin II stimulates aldosterone release from adrenal cortex, vasoconstriction of arterioles and ADH release from the posterior pituitary
4) ADH release -> translocation of aquaporin channels in nephron aids reabsorption of water back into blood
4) Aldosterone increases expression of Na+/K+ pump in collecting ducts - increased reabsorption of Na+

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22
Q

How is the RAAS initiated?

A

Input eg hypotension, hypovolaemia

Decrease in renal perfusion, drop in blood pressure, increased sympathetic tone from baroreceptor activation leads to more renin release from kidney

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23
Q

What is primary hyperaldosteronism due to?

A

Defect in adrenal cortex

eg bilateral idiopathic adrenal hyperplasia, conn’s syndrome, aldosterone secreting adenoma

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24
Q

Describe the renin and aldosterone levels in primary hyperaldosteronism

A

Low renin - high aldosterone

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25
Q

What is secondary hyperaldosteronism due to?

A

Over activity of the RAAS

eg renin producing tumour, renal artery stenosis

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26
Q

Describe the renin and aldosterone ratio in secondary hyperaldosteronism

A

High renin levels

Low aldosterone:renin ratio

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27
Q

What are some signs of hyperaldosteronism?

A

High BP, LV hypertrophy, stroke, hypernatraemia, hypokalaemia

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28
Q

How can hyperaldosteronism be treated?

A

Surgery, spironolactone (mineralocorticoid receptor antagonist)

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29
Q

What is cortisol synthesised and released by?

A

Zona fasiculata

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30
Q

What is cortisol synthesised and released in response to?

A

CRH (corticotropin-releasing hormone) released from hypothalamus -> ACTH (Adrenocorticotropic hormone) released from anterior pituitary -> cortisol released from adrenal cortex

31
Q

What is cortisol’s carrier protein in plasma?

A

Transcortin

32
Q

What are the catabolic effects of cortisol?

A

Increased protein breakdown in muscle
Increased gluconeogenesis in liver
Increased lipolysis in fat

33
Q

Aside from catabolic effects, what are the other actions of cortisol?

A

Resistance to stress, anti-inflammatory effects (inhibits macrophage activity+mast cell degranulation), depression of immune response

34
Q

Why is cortisol perscribed to organ transplant patients?

A

It depresses the immune respnse

35
Q

Outline the HPA axis

A

Stressor (eg pain, fever, hypoglycaemia, low BP):

1) Hypothalamus releases CRH to anterior pituitary
2) Anterior pituitary releases ACTH to adrenal cortex
3) Adrenal cortex releases cortisol to target tissues

36
Q

What are the net effects of glucocorticoid actions on metabolism?

A

Increased glucose production, breakdown of protein, redistribution of fat

37
Q

Why does cortisol release lead to increased glycogen storage?

A

Increases glucose -> increased insulin so liver glycogen stores increase

38
Q

What are the effects of cortisol on muscle?

A

Increased protein degradation
Decreased protein synthesis
Decreased glucose utilisation
Decreased sensitivity to insulin

(Cortisol inhibits insulin-induced GLUT4 translocation in muscle so has glucose sparing effect)

39
Q

What are the effects of cortisol on fat?

A

Redistribution of fat especially in abdomen, supraclavicular fat pads, dorso-verical fat pad and face

(Buffalo hump and moon face)

Decreases glucose utilisation
Decreases sensitivity to insulin
Increases lipolysis

40
Q

What is Cushing’s syndrome?

A

Chronic excessive exposure to cortisol

41
Q

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

A

Prescribed glucocorticoids

42
Q

What are some endogenous causes of Cushing’s syndrome?

A

1) Pituitary adenoma secreting ACTH (Cushing’s DISEASE)
2) Excess cortisol produced by adrenal tumour (Adrenal Cushing’s)
3) Non pituitary-adrenal tumours producing ACTH+/CRH eg small cell lung cancer

43
Q

What is Cushing’s disease?

A

An excess of cortisol in the blood level CAUSED BY a pituitary tumour secreting adrenocorticotropic hormone

44
Q

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

A 
Moon-shaped face
Buffalo hump
Abdominal obesity
Purple striae (proteolysis - skin weaker)
Acute weight gain
Hyperglycaemia
Hypertension
45
Q

What are some examples of steroid drugs?

A

Prednisolone, dexamethasone

46
Q

What are steroid drugs often used to treat?

A

Inflammatory diseases, allergies, organ transplant, auto-immune conditions

47
Q

What is an important point about stopping steroid medication?

A

Steroid dosage should be reduced gradually and not stopped suddenly

48
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency

49
Q

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

A

Destructive atrophy from autoimmune response

50
Q

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

A

Postural hypotension, lethargy, weight loss, anorexia, increased skin pigmentation, hypoglycaemia

51
Q

Why does Addison’s disease lead to increased skin pigmentation?

A

Decreased cortisol -> negative feedback on anterior pituitary reduced -> more POMC required to synthesise ACTH -> more a-MSH produced -> melanin synthesis

52
Q

What are the symptoms of an Addisonian crisis?

A

Nausea, vomiting, pyrexia, hypotension, vascular collapse

53
Q

What is an addisonian crisis?

A

A life threatening emergency due to adrenal insufficiency

54
Q

What is an addisonian crisis often precipitated by?

A

Stress, salt depravation, infection, trauma, cold exposure, over exertion, abrupt steroid drug withdrawal

55
Q

How is an addisonian crisis treated?

A

Fluid replacement, cortisol

56
Q

What are some examples of androgens excreted by the zona reticularis?

A

DHEA and androstenedione

57
Q

True or False:

The adrenal medulla is a modified sympathetic ganglion of the autonomic nervous system

A

True

58
Q

How is noradrenaline converted to adrenaline?

A

N-methyl transferase

59
Q

Why do 20% of chromaffin cells secrete noradrenaline as opposed to adrenaline (like the other 80%)?

A

20% lack the N-methyl transferase enzyme to convert NA into adrenaline

60
Q

What type of receptors are adrenergic receptors?

A

GPCRs

61
Q

What adrenergic receptors in the heart increase HR and contractility?

A

B1

62
Q

What adrenergic receptors in the lungs cause bronchodilation?

A

B2

63
Q

What adrenergic receptors in the blood vessels cause vasoconstriction?

A

a1

64
Q

What adrenergic receptors in the blood vessels cause vasodilation?

A

B2

65
Q

What adrenergic receptors in the kidney causes increased renin secretion?

A

B1, B2

66
Q

What adrenergic receptors in the muscle cause increased glycolysis and glygogenolysis?

A

a1, B2

67
Q

What adrenergic receptors in the pancreas increase glucagon secretion?

A

a2

68
Q

What adrenergic receptors in the pancrease decrease insulin secretion?

A

a2, B2

69
Q

What adrenergic receptors in adipose tissue increases liplysis?

A

B2

70
Q

How does adrenaline increase HR?

A

1) B1 adrenergic receptor - G-alpha S subunit
2) GDP for GTP exchange, dissociation of alpha subunit
3) Stimulates adenylyl cyclase - cAMP
4) cAMP can directly activate HCN chanels - funny current
5) cAMP activates PKA - phosphorylation of HCN channels, phosphorylation of L-type Ca2+ channels - potentiates opening, creasing the slope of the upstroke of the AP

71
Q

What is pheochromocytoma?

A

Chromaffin cell tumour

Catecholamine-secreting (mainly NA) tumour that may precipitate life-threatening hypertension

72
Q

What are some characteristics of pheochromocytoma?

A

Severe hypertension, headaches, palpitations, diaphoresis, anxiety, weight loss, hyperglycaemia

73
Q

What are catecholamines derived from?

A

Tyrosine

ESA2 - Metabolism, Endocrinology and Haematology (19 decks)

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