The Adrenal Gland Flashcards

1
Q

Adrenal medulla synthesises________________.

A

Catecholamines

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2
Q

Name the three zones of the adrenal cortex and what each zone synthesises

A

Zona golmerulosa - synthesises mineralcorticoids
Zona fasciculata - synthesises glucocorticoids
Zona reticularis - adrenal androgens

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3
Q

ACTH

A

Adrenocorticotrophic hormone
Stimulates production of cortisol (a glucocorticoid)
Cortisol exhibits negative feedback on ACTH release

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4
Q

CRH

A

Corticotrophin releasing hormone

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5
Q

Cortisol effects (4)

A

Increase hepatic gluconeogenesis and muscle glycogen storage
Increasing breakdown of plasma and muscle protein to amino acids
Increasing release of glycerol & free fatty acids from adipose tissue
Anti-inflammatory effects

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6
Q

___________is the precursor for adrenal steroid hormone synthesis.

A

Cholesterol

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7
Q

Cortisol measurement

A

95% bound to transcortin
Level of free cortisol is very small
Measured by immunoassay

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8
Q

Diurnal rhythm

A

Levels are high in the morning and low at night

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9
Q

Main function of ______________ is to promote sodium reabsorption and potassium excretion in the kidney.

A

Aldosterone

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10
Q

Aldosterone synthesis also sensitive to changes in circulating ___________ levels.

A

Potassium

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11
Q

Steps in steroid metabolism in aldosterone

A

Cholesterol
Pregnenolone
Progesterone
11-deoxycorticosterone
Corticosterone
18-hydroxycorticosterone
Aldosterone

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12
Q

Steroid metabolism of cortisol

A

Pregnenolone -> 17a-hydroxypregnenolone or progesterone ->17a-hydroxyprogesterone
11-Deoxycortisol
Cortisol

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13
Q

Steroid metabolism of androgens (dehydroepiandrosterone (DHEA) and androstenedione)

A

17a-hydroxypregnenolone or 17a-hydroxyprogesterone

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14
Q

The role of the adrenal gland in the renin-angiotensin system

A

Angiotensin II stimulates aldosterone (mineralcorticoid) release from adrenal cortex

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15
Q

Where is angiotensinogen produced?

A

Liver

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16
Q

Where is renin released?

A

Kidneys

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17
Q

Where is ACE produced?

A

Lungs

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18
Q

Posture affects ______________.

A

Plasma aldosterone

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19
Q

Addison’s disease

A

Hypofunction of the adrenal cortex
Acute adrenal insufficiency => life-threatening emergency

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20
Q

Clinical features of Addison’s disease

A

Lethargy
Weakness
Anorexia
Weight loss

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21
Q

Features of acute adrenal crisis

A

Severe hypovolaemia
Shock
Hypoglycaemia

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22
Q

Treatments of addisons disease

A

Life-long glucocorticoid & mineralcorticoid replacement therapy

23
Q

Causes of addisons disease (primary adrenal hypofunction)

A

Autoimmune destruction of the adrenal gland
Tb
Adrenal haemorrhage

24
Q

Causes of secondary adrenal hypofunction

A

Sudden withdrawal of glucocorticoid drugs
Secondary to hypopituitarism as a result of ACTH stimulation

25
Q

4x Hyp- of adrenal hypofucntion

A

Hyponatraemia
Hyperkalaemia
Hyperuremia
Hypoglycaemia

26
Q

What is the test for cortisol?

A

9am plasma cortisol
SynACTHen
Tests the capacity of the adrenal cortex to respond to ACTH

27
Q

2 conditions associated with hyperfunction of the adrenal cortex

A

Cushings’s syndrome
- overproduction of cortisol, although increased mineralcorticoid and androgen levels may also be seen
Conn’s syndrome
- excess production of aldosterone

28
Q

Causes of cushing’s disease

A

Prolonged exposure to excess cortisol
Can lead to hypertension and hypokalaemic
Increased androgen => hirsutism

29
Q

Iatrogenic cushings features

A

Increased cortisol but not increased mineralcorticoid activity as cortisol administered was synthetic

30
Q

Causes of Cushings (4)

A

Pituitary adenoma - ACTH-producing tumour
Ectopic ACTH secretion by various tumours
Adrenal adenoma or carcinoma producing cortisol
Iatrogenic

31
Q

3 tests used in the initial screening for Cushing’s

A

24hr urinary free cortisol
Overnight dexamethasone suppression
48hr low-dose dexamethasone suppression test

32
Q

Explain the urinary free cortisol test

A

Increased UFC => cushings/pseudo-cushings/obesity

33
Q

Explain overnight and 48hr low-dose dexamethasone suppression tests

A

Test for cushing’s
Dexamethasone is a synthetic glucocorticoid which binds cortisol receptors in pituitary => suppression of ACTH release => suppression of cortisol secretion by the adrenals in normal individuals
Fewer false positives are seen with 48hr low-dose

34
Q

3 tests in finding the cause of hypercortisolism

A

High dose dexamethasone suppression test
Plasma ACTH measurement
Corticotrophin-releasing hormone (CRH) test

35
Q

Explain the high dose dexamethasone suppression test

A

Dexamethasone administered
Plasma cortisol measured at 9am over three days
Failure of suppression suggests an adrenal tumour or ectopic ACTH source

36
Q

ACTH is ___ when adrenal tumour is the cause of
Cushings

A

Low

37
Q

Explain the CRH test

A

Distinguishes between Cushing’s disease and ectopic ACTH secretion
ACTH and cortisol measured at intervals over 2 hours
Rise of both cortisol and ACTH suggests pituitary source
No response in ectopic ACTH secretion

38
Q

10% patients with Cushings disease do NOT respond to _____ but they usually show suppression to HDDST

A

CRH

39
Q

10% of ectopic ACTH syndrome may respond to CRH but these patients fail to suppress with ______________.

A

Dexamethasone.

40
Q

Causes of Conn’s syndrome

A

Adrenal adenoma
Bilateral hyperplasia of Zona glomerulosa
Adrenal carcinoma - rare
Glucocorticoid-suppressive hyperaldosteronism (autosomal dominant)

41
Q

Clinical features of Conn’s syndrome

A

Hypertension (sodium retention)
Muscle weakness (hypokalaemia)
Tetany (hypokalaemia)
Many patients are asymptomatic

42
Q

What enzyme is involved in the in the conversion of cortisol to cortisone?

A

11beta-Hydroxysteroid dehydrogenase

43
Q

What inhibits 11beta-hydroxysteroid dehydrogenase? (2)

A

Liquorice & carbenoloxone

44
Q

Secondary hyperaldosteronism

A

(hyper-reninaemic hyperaldosteronism)
More commonly seen than primary hyperaldosteronism

Common causes include:
Heart failure
Liver cirrhosis
Nephrotic syndrome

45
Q

Laboratory findings in Conn’s syndrome

A

Hypokalaemia
Plasma sodium slightly above ref range

46
Q

Features of congenital adrenal hyperplasia

A

CAH is a group of inherited autosomal recessive metabolic disorders of adrenal steroid hormone synthesis
Depending on which enzyme in the pathway is deficient
95% due to 21-hydroxylase deficiency
Lack of cortisol and negative feedback; ACTH levels are high & drive androgens biosynthesis
High levels of 17 hydroxyprogesterone are secreted used in diagnosis

47
Q

Classical CAH

A

Lack of cortisol and aldosterone => adrenal crisis => dehydration => shock => death
Excess adrenal androgen production => ambiguous genitalia or precocious puberty

48
Q

Non-classical CAH

A

Milder, non-life threatening
Partial enzyme deficiency
Premature development of pubic hair

49
Q

Diagnosis of CAH (4)

A

Hormone measurement
Clinical evaluation
History and physical examination
Newborn screening USA

50
Q

Treatment of CAH

A

Glucocorticoid (dexamethasone)
Fludrocortisone (classical CAH deficiency)

51
Q

Phaeochromocytoma

A

Tumour secreting catecholamines (usually non-adrenaline)
10% malignant
Hypertension, headache, pallor

52
Q

Diagnosis of phaeochromocytoma

A

Measurement of metanephrines

53
Q

Symptoms of Cushing’s Syndrome

A

Muscle weakness
Poor wound healing
Easy bruising
Moon face
Acne
Hypertension
Skin thinning