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Diabetes & Endocrinology > The Adrenal Gland Clinical Case & Discussion > Flashcards

The Adrenal Gland Clinical Case & Discussion Flashcards

1
Q

Describe the four layers of the adrenal gland

A 
Capsule
Zona glomerulosa
Zona fasiculata
Zona reticularis 
Adrenal medulla
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2
Q

Where is aldosterone synthesised?

A

In the zona glomerulosa of the adrenal cortex

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3
Q

Where is cortisol synthesised?

A

In the bona fasiculata of the adrenal cortex

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4
Q

Where are the sex steroids produced (adrenal)?

A

In the bona reticularis

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5
Q

What is synthesised in the adrenal medulla?

A

Norepinephrine, epinephrine

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6
Q

Describe the hypathalamo hypopituitary adrenal axis

A

Involves CRH synthesis in the hypothalamus and then synthesis of ACTH in the pituitary which then synthesises hormone production in the adrenal gland. As levels of cortisol increase, there is a negative feedback control on the system and the hypothalamic and subsequent secretions are reduced

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7
Q

What is the most common cause of primary adrenal insufficiency causing hyposecretion?

A

Addison’s Disease

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8
Q

What proportion of UK adrenal failure cases are caused by Addison’s disease?

A

> 85%

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9
Q

What is the basic autoimmune pathology of Addison’s?

A

In 70% of cases there is a production of positive adrenal autoantibodies to 21-OHase
There is then subsequent infiltration of the adrenal cortex and associated autoimmune conditions are common

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10
Q

Generally, does type 1 or type 2 diabetes present more acutely?

A

Type 1 - the gland has a reserve function which allows its actions be well preserves until a tipping point is reached and symptoms rapidly manifest

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11
Q

What is the location of the defect in the vast majority of Addison’s cases?

A

The adrenal glands

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12
Q

What are some symptoms commonly associated with primary adrenal failure?

A

Weakness, fatigue, anorexia, weight loss, skin pigmentation, vitiligo, hypotension, unexplained vomiting or diarrhoea

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13
Q

Why can hyper pigmentation be seen in Addison’s disease?

A

The hypothalamus detects the reduced cortisol in the plasma and stimulates further ACTH release from the pituitary, which in excess causes the stimulation melanocytes which cause the pigment change

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14
Q

What tests should be done for Addison’s?

A

Random cortisol - Nb that the tester must be aware of when the test was done in order to determine whether the results correlate with normal fluctuating daytime levels

Synacthen test and basal ACTH

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15
Q

Describe the basic investigative pathway where adrenal insufficiency is suspected

A

Rapid ACTH stimulation test/snynacthen test done on suspicion, if confirmed, a plasma ACTH level is measured and if suppressed the diagnosis points towards secondary adrenocortical insufficiency
If the plasma ACTH is shown to be elevated it is suggestive of primary adrenocortical insufficiency

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16
Q

What is the main drug used for glucocorticoid replacement?

A

Hydrocortisone (cortisol)

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17
Q

What is the main drug used for mineralocorticoid replacement?

A

Fludrocortisone - binds to mineralocorticoid receptors (aldosterone)

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18
Q

What is important to note regarding patients on long term steroids and their adrenal function?

A

They may be hypoadrenal even if the steroid treatment is for another condition. They will recover from this

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19
Q

What are the three self-care rules for patients on steroids?

A
  1. never miss steroid doses to maintain control
  2. double the medication dose in the event of illness
  3. If severe vomiting or diarrhoea, take emergency injection and call for help
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20
Q

What hormones are affected in Cushing’s syndrome?

A

Cortisol and androgens (sex hormones)

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21
Q

What is the effect of cortisol in with regard to sodium?

A

It causes sodium retention and may lead the HTN and HF

22
Q

Why is cortisol diabetogenic and potentially damaging, (although essential)?

A

It is catabolic and will preserve BG at all costs, in order to protect the brain from hypoglycaemia. In doing so it may cause tissue breakdown and weakness of the skin, muscle and bone as well as HTN and HF due to sodium retention and is potentially causative of DM as it opposes the actions of isulin

23
Q

What are some of the clinical signs of Cushing’s syndrome?

A 
'Moon face'
Muscle atrophy replaced with fat
Pendulous breasts and abdomen
Thin hands and feet
Bruising
Think skin ulcers
Peripheral oedema
'Buffalo hump'
Cardiac failure
DM
24
Q

What proportion of Cushing’s cases are ACTH-dependent?

A

80%

25
Q

What are the two possible causes for ACTH-dependent Cushing’s syndrome?

A

75% cases: pituitary tumour

5% cases: ectopic ACTH secretion e.g. lung carcinoid

26
Q

What are the causes of ACTH-independent Cushing’s syndrome?

A

Corticosteroid therapy induced Cushing’s

Adrenal tumour

27
Q

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

A

Over production of ACTH in the pituitary - tumour

28
Q

What are the very first tests to do for suspected hypercortisolism?

A

Overnight dexamethasone test

24 hour urine free cortisol test

29
Q

What are the two tests done to confirm suspected hypercortisolism?

A

24 hour urine free cortisol

Low dose dexamethasone test

30
Q

What test can be done to determine between ACTH-dependent and ACTH-independent hypercorticolism once confirmed?

A

Paired morning-midnight ACTH cortisol test

31
Q

What test can be done to determine whether ACTH dependent hypercortisolism is caused by a pituitary pathology?

A

High dose dexamethasone test

32
Q

What tests can be done to localise a hypercorticolising pathology?

A

MRI Sella turcica
CT adrenals
BIPSS
CT chest

33
Q

What are the two screening tests for Cushings syndrome?

A

24 hour urinary free cortisol

1mg dexamethasone supression test

34
Q

Explain the physiology and interpretation of low and high dose dexamethasone testing

A

Dexamethasone is an exogenous steroid that provides negative feedback to the pituitary gland to suppress the secretion of adrenocorticotropic hormone (ACTH). Specifically, dexamethasone binds to glucocorticoid receptors in the anterior pituitary gland, which lie outside the blood brain barrier, resulting in regulatory modulation

Interpretation
Low-dose and high-dose variations of the test exist. The test is given at low (usually 1–2 mg) and high (8 mg) doses of dexamethasone and the levels of cortisol are measured to obtain the results

A low dose of dexamethasone suppresses cortisol in individuals with no pathology in endogenous cortisol production. A high dose of dexamethasone exerts negative feedback on pituitary ACTH-producing cells, but not on ectopic ACTH-producing cells or adrenal adenoma.

35
Q

In Cushing’s caused by adrenal carcinoma, what would you expect cortisol levels to be elevated or depressed? What about ACTH levels?

A

Cortisol levels would be increased as it is a hypersecreting condition. The ACTH levels would be low, as although there is no pituitary pathology the negative feedback from the high levels of cortisol will suppress the CRH hypothalamic secretion and therefore the pituitary ACTH secretion

36
Q

Is congenital adrenal hyperplasia a hypersecreting or hyposecreting disorder?

A

Hyposecreting

37
Q

What hormone is affected in Conn’s syndrome? Is this a hypo or hypersecreting condition?

A

Aldosterone

Hypersecreting

38
Q

What are the two most common causes of Conn’s syndrome (hyperaldosteronism)
Are these primary or secondary causes?

A

Adrenal adenoma
Bilateral adrenal hyperplasia

Primary causes

39
Q

What is the effect of an aldosterone producing tumour in the adrenal gland(s)?

A

The increase in aldosterone results in increased urine K+, increased Na+ and H20 retention => increased blood volume and BP

40
Q

What screening tests can be done for aldosterone -producing adrenal adenomas?

A

Plasma Renin Activity (PRA)
Plasma Aldosterone concentration (PA(C))

A plasma aldosterone : plasma renin activity ratio test

41
Q

What does a PA:PRA ratio of >20 indicate?

A

Primary hyperaldosteronism

42
Q

What does a PA:PRA ratio of 20?

A

Secondary hyperaldosternoism or essential hypertension

Less reliable

43
Q

What does a high PRA with high PAC indicate?

A

Secondary hyperaldosteronism - requires investigation

44
Q

What does a low pRA with high PAC indicate?

A

Primary hyperaldosteronism - requires investigation

45
Q

When hypertension and hypokalaemia are seen in a patient what condition should be suspected?

A

Conn’s syndrome

46
Q

What hyper secretive disorder affects the adrenal medulla?

A

Phaeochromocytoma

47
Q

What type of hormones are affected in phaeochromocytoma?

A

Catecholamines

48
Q

What is the most common symptom of pheochromocytoma? What other set of symptoms may present?

A 
Hypertension (70% of cases)
Paroxysmal attacks
-headache
-sweating
-palpitations
49
Q

What are the two major causes of hypertension (endocrine)? Why?

A

Unilateral adrenal adenoma

Bilateral hyperplasia

50
Q

What is a key difference between congenital adrenal hyperplasia and bilateral hyperplasia?

A

Congenital adrenal hyperplasia is hyposecreting

Bilateral hyperplasia is hypersecreting

51
Q

What genetic defect is the cause of over 90% of congenital adrenal hyperplasia cases?

A

21-hydroxylase deficiency

Diabetes & Endocrinology (18 decks)

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