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(LUSUMA) Metabolism, Endocrinology & Haematology > S9) The Adrenal Glands & Disorders > Flashcards

S9) The Adrenal Glands & Disorders Flashcards

1
Q

Describe the macroscopic and microscopic structure of the adrenal glands

A
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2
Q

What are the three areas in the adrenal cortex?

A
  • Zona glomerulosa
  • Zona fasiculata
  • Zona reticularis
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3
Q

Identify and describe the hormones in the different regions of the adrenal cortex

A
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4
Q

Steroid hormones are lipid soluble.

Describe their formation and function

A
  • Formation: synthesised from cholesterol in adrenal glands and gonads
  • Function: bind to receptors of the nuclear receptor family to modulate gene transcription
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5
Q

Provide five examples of steroid hormones

A
  • Glucocorticoids
  • Mineralocorticoids
  • Androgens
  • Oestrogens
  • Progestins
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6
Q

Corticosteroids exert their actions by regulating gene transcription.

In six steps, outline this process

A

⇒ Corticosteroids readily diffuse across plasma membrane

⇒ Bind to glucocorticoid receptors

⇒ Binding dissociates chaperone proteins

⇒ Receptor-ligand complex translocates to nucleus

⇒ Dimerisation with other receptors can occur

⇒ Receptors bind to GREs / other transcription factors

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7
Q

Aldosterone is the most abundant mineralocorticoid.

Describe its function and transport

A
  • Transport: carrier protein (mainly serum albumin or transcortin)
  • Function: central role in regulation of plasma Na+, K+ and arterial blood pressure
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8
Q

Aldosterone is a central component of renin-angiotensin-aldosterone system.

In light of this, explain its specific actions

A
  • Promotes expression of Na+/K+ pump increasing reabsorption in distal tubules and collecting ducts of nephron
  • This influences water retention, blood volume & therefore blood pressure
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9
Q

Outline all the cellular and hormonal mechanisms involved in RAAS

A
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10
Q

What is hyperaldosteronism?

A

Hyperaldosteronism is a physiological state/condition wherein there is an excessive production of aldosterone

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11
Q

Distinguish between the two forms of hyperaldosteronism

A
  • Primary – defect in adrenal cortex (high aldosterone:renin ratio)
  • Secondary – over-activation of RAAS (low aldosterone:renin ratio)
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12
Q

Identify two causes of primary hyperaldosteronism

A
  • Bilateral idiopathic adrenal hyperplasia (most common)
  • Aldosterone-secreting adrenal adenoma (Conn’s syndrome)
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13
Q

Identify two causes of secondary hyperaldosteronism

A
  • Renin producing tumour e.g. juxtaglomerular tumour (rare)
  • Renal artery stenosis
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14
Q

Identify 5 clinical signs of hyperaldosteronism

A
  • High blood pressure
  • Left ventricular hypertrophy
  • Stroke
  • Hypernatraemia
  • Hypokalaemia
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15
Q

The treatment for hyperaldosteronism depends on its form.

Describe the possible options

A
  • Aldosterone-producing adenomas removed by surgery
  • Spironolactone (mineralocorticoid receptor antagonist)
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16
Q

Cortisol is the most abundant corticosteroid & accounts for ~95% of glucocorticoid activity.

Describe its formation and transport

A
  • Formation: synthesised and released by zona fasiculata in response to ACTH
  • Transport: carrier protein in plasma (transcortin)
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17
Q

Cortisol is the most abundant corticosteroid & accounts for ~95% of glucocorticoid activity.

Describe its function and regulation

A
  • Function: cortisol receptor exerts its actions by regulating gene transcription
  • Regulation: negative feedback to hypothalamus inhibits CRH & ACTH release
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18
Q

Cortisol can act in 6 different ways.

Identify these

A
  • Increased proteolysis in muscle
  • Increased lipolysis in fat
  • Increased gluconeogenesis in liver
  • Resistance to stress
  • Anti-inflammatory effects
  • Depression of immune response
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19
Q

Cortisol is useful medication for allergic reactions

Describe its anti-inflammatory effects

A
  • Inhibits macrophage activity
  • Mast cell degranulation
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20
Q

Explain the resistance of cortisol to stress

A
  • Increased supply of glucose
  • Raise BP by making vessels more sensitive to vasoconstrictors
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21
Q

Identify one use of cortisol due to its ability to depress the immune response

A

Cortisol is prescribed to organ transplant patients

22
Q

Outline the HPA axis

A
23
Q

Explain how the glucocorticoid actions on metabolism lead to the following:

  • Increased glucose production
  • Breakdown of protein
  • Redistribution of fat
A
24
Q

What is Cushing’s syndrome?

A
  • Cushing’s Syndrome is a clinical condition arising due to chronic excessive exposure to cortisol
  • It leads to the re-distribution of fat especially in abdomen, supraclavicular fat pads, dorso-cervical fat pad, (buffalo hump), & on face (moon face)
25
Q

Describe the aetiology of Cushing’s syndrome in terms of its endogenous and exogenous causes

A
26
Q

Identify some signs and symptoms of Cushing’s syndrome

A
  • Plethoric moon-shaped face
  • Buffalo hump
  • Abdominal obesity
  • Purple striae
  • Acute weight gain
  • Hyperglycaemia
  • Hypertension
27
Q

Identify two examples of steroid drugs

A
  • Prednisolone
  • Dexamethasone
28
Q

Steroid drugs have anti-inflammatory & immunomodulatory effects, thus are used to treat inflammatory disorders.

Provide some examples of these conditions

A
  • Asthma
  • Inflammatory bowel disease
  • Rheumatoid arthritis
  • Other auto-immune conditions
29
Q

Describe the possible side effects due to steroid drugs

A

Side-effects are the same as the effects of higher levels of cortisol, plus can also have mineralocorticoid effects

30
Q

How might one stop steroid drug usage?

A

Steroid dosage should be reduced gradually and not stopped suddenly

31
Q

What is Addison’s disease?

A
  • Addison’s disease is a clinical condition due to chronic adrenal insufficiency, commonly due to the destructive atrophy from autoimmune response
  • Affects more women than men and the exact reason for autoimmunity is unknown
32
Q

Identify some rare causes of Addison’s disease

A
  • Fungal infection
  • Adrenal cancer
  • Adrenal haemorrhage e.g. following trauma
33
Q

Identify some signs and symptoms of Addison’s disease

A
  • Postural hypotension
  • Lethargy
  • Weight loss
  • Anorexia
  • Increased skin pigmentation
  • Hypoglycaemia
34
Q

What is the reason for the hyperpigmentation presenting in Addison’s disease?

A
  • Increased melanin synthesis due to increased MSH & increased POMC
  • ACTH can also directly activate melanocortin receptors on melanocytes
35
Q

What is Addisonian Crisis?

A
  • Addisonian Crisis is a life threatening emergency due to adrenal insufficiency
  • It is often precipitated by severe stress, salt depravation, infection, trauma or abrupt steroid drug withdrawal
36
Q

How does Addisonian Crisis present?

A
  • Nausea
  • Vomiting
  • Pyrexia
  • Hypotension
  • Vascular collapse
37
Q

What is the treatment for Addisonian Crisis?

A
  • Fluid replacement
  • Cortisol
38
Q

Identify the two types of androgens

A
  • Dehydroepiandrosterone (DHEA)
  • Androstenedione
39
Q

Describe the role of androgens in males and females respectively

A
  • Male – DHEA converted to testosterone in testes (insignificant after puberty)
  • Female – adrenal androgens promote libido and are converted to oestrogens by other tissues (only source of oestrogens after menopause)
40
Q

Describe the role of androgens in both sexes

A

Promote axillary and pubic hair growth

41
Q

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

Describe the role of is chromaffin cells

A

Chromaffin cells in adrenal medulla lack axons but act as postganglionic nerve fibres that release hormones into blood – adrenaline (~80%), noradrenaline (~20%)

42
Q

Explain why adrenaline is the dominant hormone produced by the adrenal medulla

A
43
Q

Outline, in detail, the biological signalling pathway induced at adrenergic receptors

A
44
Q

Outline the various hormonal actions of adrenaline

A
45
Q

Outline the cellular mechanism by which adrenaline increases heart rate

A
46
Q

What is a phaeochromocytoma?

A
  • A phaeochromocytoma is a chromaffin cell tumour which secretes catecholamines (mainly adrenaline)
  • It may precipitate life-threatening hypertension
47
Q

How do phaeochromocytomas present?

A
  • Severe hypertension
  • Headaches
  • Palpitations
  • Diaphoresis (excessive sweating)
  • Weight loss
  • Elevated blood glucose
48
Q

Compare and contrast adrenal hormones in terms of the following:

  • Synthesis
  • Precursor
  • Mode
  • Storage
  • Solubility
  • Receptors
  • Typical effect on enzymes
  • Speed of response
  • Effect of bilateral adrenalectomy
A
49
Q

What are the clinical tests of adrenocortical function used in the differential diagnosis of adrenocortical disease?

A
  • Plasma cortisol levels
  • ACTH level
  • 24hr urinary excretion of cortisol and its breakdown products (17-hydroxysteroids)
  • Dynamic function tests e.g. dexamethasone suppression tests and ACTH stimulation tests
50
Q

Describe the action of dexamethasone

A

Dexamethasone is a potent synthetic steroid that, when given orally would normally suppress (by feedback inhibition) the secretion of ACTH and thus cortisol

51
Q

Describe the role of dynamic function tests in diagnosing adrenocortical diseases

A
  • Dexamethasone suppression of plasma cortisol by >50% is characteristic of Cushing’s disease
  • A normal response to, Synacthen, a synthetic analogue of ACTH which normally increases plasma cortisol by >200 nmol/L, indicates Addison’s disease

(LUSUMA) Metabolism, Endocrinology & Haematology (20 decks)

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