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MEH > 12 The Adrenal Glands > Flashcards

12 The Adrenal Glands Flashcards

1
Q

What are the sections of the adrenal cortex?

A

Zona glomerulosa
Zona fasiculata
Zona reticularis

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2
Q

What is released from the Zona glomerulosa?

A

Mineralcorticoids
E.g. aldosterone

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3
Q

What does the Zona fasiculata release?

A

Glucocorticoids
E.g. CORTISOL, corticosterone, cortisone

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4
Q

What does the Zona reticularis release?

A

Glucocorticoids + Androgens-sex hormones

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5
Q

How are steroid hormones synthesised?

A

From cholesterol
In adrenal glands and gonads

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6
Q

Are steroid hormones lipid or water soluble?

A

Lipid soluble

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7
Q

Adrenal gland structure

A

Capsule
Cortex
Medulla

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8
Q

What cells produce adrenaline and nor adrenaline?

A

Chromaffin cells

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9
Q

What hormones are released in the medulla?

A

Adrenaline
Noradrenaline

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10
Q

How to remember what is secreted by the layers of the cortex?

A

The deeper you go the sweeter it gets
Salt sugar sex

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11
Q

What is the main glucocorticoid?

A

Cortisol

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12
Q

What is cholesterol a precursor of?

A

Steroid hormones

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13
Q

What do steroid hormones regulate?

A

Gene transcription

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14
Q

What is aldosterone and where is it released form?

A

Mineralcorticoid
Zona glomerulosa - outer layer of cortex

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15
Q

How is aldosterone transported?

A

Steroid hormone so by carrier proteins:
Serum albumin mainly
Transcortin

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16
Q

Aldosterone function

A
  • regulation of plasma Na+, K+
  • regulation of arterial BP
  • promotes expression of Na+/K+ pump - NA+ in, K+ out - influences water retention, blood volume and BP
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17
Q

What does RAAS stand for?

A

Renin-angiotensin-aldosterone system

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18
Q

How does aldosterone exert its actions?

A

Regulating gene transcription

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19
Q

What is a change is BP detected by?

A

Baroreceptors

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20
Q

Actions of angiotensin II

A
  • vasoconstriction
  • stimulation of adrenal cortex - aldosterone released causing increased expression of Na+/K+ so increased water reabsorption
  • stimulation of posterior pituitary - ADH released causing more aquaporins in nephron so increased water reabsorption
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21
Q

What is hyperaldosterionism?

A

Excessive aldosterone production

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22
Q

Signs of hyperaldosteronism

A

High BP
Stroke
Left ventricular hypertrophy
Hypernatraemia
Hypokalaemia

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23
Q

Treatment of hyperaldosteronism

A
  • Primary - aldosterone producing adenomas removed by surgery
  • Spironoalactone
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24
Q

What is primary hyperaldosteronism due to?

A
  • defect in adrenal cortex
  • most commonly: bilateral idiopathic adrenal hyperplasia
  • aldosterone secreting adrenal adenoma
  • low renin levels
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25
Q

What is secondary hyperaldosteronism due to?

A
  • due to over activity of RAAS
  • renal artery stenosis
  • high renin levels
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26
Q

What is cortisol and where is it released from?

A

Corticosteroid - glucocorticoid
Zona fasiculata

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27
Q

What hormone is cortisol released in response to?

A

ACTH
Adrenocorticrotopic hormone

28
Q

How is cortisol transported?

A

Carrier protein- transcortin

29
Q

How does cortisol exert its actions?

A

Regulating gene transcription

30
Q

Actions of cortisol

A
  • increased protein breakdown in muscles
  • increased lipolysis in fats
  • increased gluconeogensis in liver
  • resistance to stress
  • anti-inflammatory effects
  • depression of immune response
31
Q

Effects of glucocorticoids on metabolism

A
  • increased glucose production (in liver)
  • breakdown of protein (in muscle)
  • redistribution of fat
32
Q

Effects of cortisol in liver

A
  • increased gluconeogensis
  • increased glycogen storage due to increased glucose production
33
Q

Effects of cortisol of muscle
What does it inhibit?

A

Increased protein degradation
Inhibits insulin induced GLUT 4 translocation - prevents glucose uptake

34
Q

Where is the GLUT 4 transporter found?

A

Striated muscle and adipose

35
Q

Effects of cortisol on adipose

A

Increased lypolysis
Decreased glucose utilisation

36
Q

Most common cause of Cushing’s syndrome

A

Excessive use of prescribed glucocorticoids

37
Q

External cause of Cushing’s syndrome

A

Excessive use of prescribed glucocorticoids

38
Q

Endogenous causes of Cushing’s syndrome

A

Rare
- benign pituitary adenoma secreting ACTH (Cushing’s disease)
- excess cortisol produced by adrenal tumour (adrenal Cushing’s)
- non pituitary-adrenal tumours producing ACTH

39
Q

What causes Cushing’s disease?

A

Benign pituitary adenoma secreting ACTH

40
Q

How should steroid drugs be stopped?

A

Dosage reduced gradually, not stopped suddenly

41
Q

What are steroid drugs used to treat?

A

Inflammatory disorders

42
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency

43
Q

Most common cause of Addison’s disease?

A

Destructive atrophy (wasting away) from auto immune response

44
Q

Signs and symptoms of Addison’s disease

A
  • postural hypotension
  • lethargy
  • weight loss
  • anorexia
  • increased skin pigmentation
  • hypoglycaemia
45
Q

How does Addison’s disease cause hyperpigmentation

A
  • Insufficient adrenal function
  • Decreased cortisol
  • Negative feedback on ant. Pit reduced
  • More POMC needed to synthesis ACTH
  • More MSH produced&raquo_space; hyperpigmentation
  • ACTH at high level can stimulate receptors of MSH receptors
46
Q

MSH meaning

A

Melanocyte stimulating horome

47
Q

ACTH meaning

A

Adrenocorticotopic hormone

48
Q

Where are androgens released from?

A

Zona reticularis

49
Q

What is the only source of oestrogen for women after menopause?

A

Adrenal androgens converted in oestrogen

50
Q

What do chromaffin cels act as?

A

Postganglionic nerve fibres

51
Q

What do chromaffin cells lack?

A

Axons

52
Q

Where are adrenaline and noradrenaline released from?

A

Chromaffin cells in adrenal medulla

53
Q

Hormonal action of adrenaline on the heart, lungs + blood vessels including the receptors involved

A

Heart - increased HR and contractibility (B1)
Lungs - bronchodilation (B2)
Blood vessels - vasoconstriction in high level (a1) + vasodilation in circulating level (B2)

54
Q

How to remember which receptors are in heart and lungs

A

1 heart 2 lungs
Heart B1
Lungs B2

55
Q

What is phaeochromocytoma?

A

Chromaffin cell tumour
Phaeo- dark
Chromo - colour
Cyte - cell
Oma - tumour

56
Q

Characteristics of phaeochromocytoma

A
  • severe hypertension
  • headaches
  • palpitations
  • excessive sweating
  • weight loss
57
Q

what is Addisonian crisis?

A

Life threatening emergency due to adrenal insufficiency

58
Q

Symptoms of Addisonian crisis

A

Vomiting
Pyrexia - fever
Hypotension
Vascular collapse

59
Q

Treatment of Addisonian crisis

A

Fluid replacement
Cortisol

60
Q

What is Addisonian crisis caused by?

A

Severe stress
Salt deprivation
Infection
Cold exposure
Trauma
Over exertio
Abrupt steroid drug withdrawal

61
Q

What is an aldosterone secreting adrenal adenoma also called?

A

Conn’s syndrome

62
Q

Why do patients with Cushing’s syndrome have purple striae

A

Central obesity from fat redistribution due to cortisol stress the the skin
Weak + thin skin increases proteolysis > purple striae

63
Q

How is noradrenaline converted to adrenaline

A

Enzyme N-methyl transferase

64
Q

What is the best way to distinguish between primary and secondary hyperaldosteronism?

A

primary - low renin levels
secondary - high renin levels

65
Q

What is POMC a precursor of?

A

a-MSH
ACTH
B-endorphins

66
Q

Outline QISS receptors

A
  • Q : a1: stimulates DAG + IP3
  • I : a2: inhibits adenylyl cyclase > reduces cAMP + PKA
  • S : B1: activates adenylyl cyclase > increases cAMP > activates PKA
  • S : B2: activates adenylyl cyclase > increases cAMP > activates PKA

MEH (23 decks)

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