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Diabetes and Endocrinology > The Adrenal Gland and Clinical Aspects > Flashcards

The Adrenal Gland and Clinical Aspects Flashcards

1
Q

What are the endocrine components of the adrenal gland?

A

Adrenal medulla

Adrenal cortex

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2
Q

What are the features of the adrenal medulla?

A

Constitutes 25% of adrenal gland
Modified sympathetic ganglion derived from neural crest tissue
Secretes catecholamines, mainly epinephrine but also norepinephrine and dopamine

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3
Q

What are the features of the adrenal cortex?

A

Constitutes 75% of the adrenal gland
Secretes 3 classes of steroid hormones; mineralocorticoids (regulation of Na+ and K+), glucocorticoids (maintenance of plasma glucose), sex steroids

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4
Q

What classes of steroid hormones are secreted by the adrenal cortex?

A

Mineralocorticoids
Glucocorticoids
Sex steroids

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5
Q

What are the zones of the adrenal cortex and what hormones do they produce?

A

Zona glomerulosa -> aldosterone
Zona fasciculata -> glucocorticoids
Zona reticularis -> sex hormones

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6
Q

What hormones are produced in the zona glomerulosa?

A

Aldosterone

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7
Q

What hormones are produced in the zona fasciculata?

A

Glucocorticoids

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8
Q

What hormones are produced in the zona reticularis?

A

Sex hormones

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9
Q

What are all steroid hormones derived from?

A

Cholesterol

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10
Q

What results in different end products of steroid hormones?

A

All steroid hormones are derived from cholesterol but different enzymes are found in different adrenal zones, resulting in different end products e.g. enzymes needed to make aldosterone are found only in the zona glomerulosa

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11
Q

What are the main products of the adrenal cortex?

A

Cortisol and aldosterone

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12
Q

What is the prehormone of testosterone and oestrogen?

A

DHEA

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13
Q

What are defects in 21-hydroxylase a common cause of?

A

Congenital adrenal hyperplasia, resulting in a deficiency of aldosterone and cortisol, and associated physiological dysfunction of salt and glucose balance

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14
Q

Why are accumulating steroid precursors channelled into excessive adrenal androgen production in people with defects in 21-hydroxylase?

A

Because androgen biosynthesis is unaffected

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15
Q

How does a deficit in 21-hydroxylase result in adrenal hyperplasia?

A

Lack of 21-hydroxylase inhibits the synthesis of cortisol
This removes the negative feedback on ACTH and CRH release
Increased ACTH secretion is responsible for the enlargement of the adrenal glands
Negative feedback of ACTH or CRH synthesis remains
Results in adrenal hyperplasia

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16
Q

Where are the adrenal glands located?

A

Situated on the superior pole of the kidney in the retroperitoneal space

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17
Q

Where does the left adrenal vein drain?

A

Into left renal vein

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18
Q

Where does the right adrenal vein drain?

A

Directly into inferior vena cava

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19
Q

What does loss of cortisol cause?

A

Means that animal cannot deal with stress, particularly in terms of maintaining blood glucose levels

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20
Q

What is cortisol crucial for in regards to the brain?

A

Crucial in helpting to protect the brain from hypoglycaemia

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21
Q

What is the action of cortisol on glucagon? Why is this important?

A

Permissive action - this is vital as glucagon alone is inadequate in responding to a hypoglycaemic challenge

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22
Q

What does removal of the adrenal glands render animals incapable of?

A

Maintaining their ECF volume

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23
Q

What class of corticosteroid is aldosterone?

A

Mineralocorticoid

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24
Q

What is the role of aldosterone?

A

Acts on the distal tubule of the kidney to determine the levels of minerals reabsorbed/secreted
Increases reabsorption of Na+ ions and promotes the secretion of K+ ions

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25
Q

What does aldosterone increase reabsorption of?

A

Na+ ions

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26
Q

What does aldosterone promote the secretion of?

A

K+ ions

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27
Q

What is secretion of aldosterone primarily controlled by

A

The renin-angiotensin-aldosterone system (RAAS) - a complex reflex pathway originating in the kidney

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28
Q

What does increased aldosterone release stimulate?

A

Na+ (and H2O) retention and K+ depletion, resulting in increased blood volume and pressure

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29
Q

What does decreased aldosterone release result in?

A

Leads to Na+ (and H2O) loss and increased [K+]plasma, resulting in diminished blood volume and decreased blood pressure

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30
Q

What kind of tissue is the adrenal medulla?

A

Modified sympathetic ganglion - not true endocrine tissue

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31
Q

What is the role of the adrenal medulla?

A

Neuroendocrine role

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32
Q

Where do the post-ganglionic cells in the adrenal medulla release neurohormones?

A

Directly into the blood

33
Q

What kind of hormone is cortisol?

A

Glucocorticoid hormone

34
Q

What percentage of plasma cortisol is bound to a carrier protein?

A

95% - cortisol binding globulin

35
Q

What cells have cytoplasmic glucocorticoid receptors?

A

All nucleated cells

36
Q

Where does the hormone receptor complex migrate to?

A

Migrates to the nucleus, where it binds to DNA via a hormone-response element to alter gene expression, transcription and translation

37
Q

What is the pattern of cortisol release?

A

Plasma levels of cortisol show a characteristic pattern
There is a marked circadian rhythm, preceded by a similar pattern of release of ACTH
Cortisol burst persists longer than ACTH because the half life is much longer
Peak is around 6-9am
Nadir is around midnight
Other fluctuations during the day are due to effects of other stimuli which are related to stress

38
Q

What are the actions of cortisol on glucose metabolism?

A

Gluconeogensis - cortisol stimulates formation of gluconeogenic enzymes in the liver, enhancing gluconeogenesis and glucose production, aided by cortisol’s action on muscle

Proteolysis - cortisol stimulates the breakdown of muscle protein to provide gluconeogenic substrates for the liver

Lipolysis - cortisol stimulates lipolysis in adipose tissue which increases [FFA]plasma, creating an alternative fuel supply that allows blood glucose to be protected while also creating a substrate for gluconeogensis

Decreases insulin sensitivity of muscles and adipose tissue

39
Q

What are the non-glucocorticoid actions of cortisol?

A

Negative effect on calcium balance - decreased absorption from the gut, increased excretion at the kidney resulting in net Ca2+ loss, also increases bone resorption resulting in osteoporosis

Impairment of mood and cognition - depression and impaired cognitive function strongly associated with hypercortisolaemia

Permissive effects on norepinephrine - particularly in vascular smooth muscle
Cushing’s disease is strongly associated with hypertension and low levels of cortisol are associated with hypotension

Suppression of the immune system - cortisol reduces circulating lymphocyte count, reduces antibody formation and inhibits the inflammatory response

40
Q

What are the side effects of glucocorticoid therapy?

A

Increased severity and frequency of infection, loss of percutaneous fat stores giving appearance of thinning skin and making it more fragile

41
Q

What are the hypersecretion disorders of the adrenal cortex?

A

Cushing’s syndrome - cortisol and androgen hypersecretion, due to adenoma, carcinoma or bilateral hyperplasia

42
Q

What are the hypersecretion disorders of the adrenal medullae?

A

Phaeochromocytoma - catecholamines

43
Q

How can the catabolic role of cortisol lead to health problems?

A

Tissue breakdown - causes weakness of skin, muscle and bone
Sodium retention - hypertension and heart failure
Insulin antagonism - may cause DM

44
Q

What is the hypersecretion of cortisol in Cushing’s syndrome/disease most commonly due to?

A

A tumour in adrenal cortex or pituitary gland, or iatrogenic e.g. too much cortisol administered therapeutically

45
Q

What are the features of Cushing’s syndrome?

A

Tumour in adrenal cortex - adenoma or carcinoma
Corticosteroid therapy
First degree hypercortisolism
ACTH independent

46
Q

What are the features of Cushing’s disease?

A

Tumour in pituitary gland
Ectopic ACTH secretion e.g. lung carcinoid
Second degree hypercortisolism
ACTH dependent

47
Q

What is more common, Cushing’s syndrome or Cushing’s disease?

A

Cushing’s disease most common - excess ACTH

Cushing’s disease 75% of cases, Cushing’s syndrome 20%

48
Q

What is Cushing’s disease characterised by?

A

Wasting of the extremities due to the catabolic action of cortisol, fat redistribution to face and trunk, central obesity

49
Q

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

A 
(from most occurrence to least occurrence) 
Central obesity 94% 
Hypertension 82% 
Glucose intolerance 80% 
Hirsutism 75% 
Amenorrhoea or impotency 75% 
Purple striae 65%
Plethoric facies 60%
Easy bruising 60%
Osteoporosis 60% 
Personality change 55%
Acne 50% 
Oedema 50%
Headache 40% 
Poor wound healing 40%
50
Q

What is the screening test for Cushing’s syndrome?

A

24 hour urinary free cortisol - normal 14-135nmol/24 hour

1mg overnight dexamethasone suppression test, taken at midnight, normal < 50nmol/l (1.8mg/dL)

51
Q

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

A 
Hypertension
Polyuria
Nocturia
Tiredness
Weakness
Hypokalaemia 
Raised plasma aldosterone 
Low plasma renin
52
Q

What are the features of pheochromocytoma?

A 
Rare neuroendocrine tumour 
Found in adrenal medulla 
Results in excess catecholamines
Diabetogenic due to adrenergic effect on glucose metabolism 
Responds well to surgery
53
Q

What is the result of the excess catecholamines caused by pheochromocytoma?

A

Increased heart rate, increased cardiac output, increased blood pressure

54
Q

What are the signs and symptoms of pheochromocytoma?

A

Hypertension - persistent in 70%

Paroxysmal attacks

  • headache
  • sweating
  • palpitations
  • tremor
  • pallor
  • anxiety/fear
55
Q

What percentage of pheochromocytomas are extra-adrenal?

A

10%

56
Q

What percentage of pheochromocytomas are malignant?

A

10%

57
Q

What percentage of pheochromocytomas are multiple?

A

10%

58
Q

What percentage of pheochromocytomas are of inherited origin?

A

30% - genes and familial syndromes

59
Q

What are the endocrine causes of hypertension?

A

Primary hyperaldosteronism

  • unilateral adenoma
  • bilateral hyperplasia

Rarer causes

  • pheochromocytoma
  • Cushing’s syndrome
  • acromegaly
  • hyperparathyroidism
  • congenital adrenal hyperplasia
60
Q

What is Addison’s disease?

A

Hyposecretion of all adrenal steroid hormones due to autoimmune destruction of the adrenal cortex

61
Q

What are the causes of Addison’s disease (primary adrenal insufficiency)?

A 
Autoimmune destruction 
Invasion
Infiltration
Infection
Infarction
Iatrogenic
62
Q

What is the most common cause of congenital adrenal hyperplasia?

A

21-hydroxylase deficiency

63
Q

What percentage of UK cases of adrenal failure are accounted for by autoimmune Addison’s disease?

A

> 85%

64
Q

What are the features of autoimmune Addison’s disease?

A

Positive autoantibodies to (21-hydroxylase) in 70% of cases
Lymphocytic infiltrate of adrenal cortex
Associated autoimmune diseases common
- thyroid disease 20%
- T1DM 15%
- premature ovarian failure 15%

65
Q

What are the common symptoms of primary adrenal failure?

A 
Weakness, fatigue, anorexia, weight loss (100%) 
Skin pigmentation or vitiligo (92%)
Hypotension (88%)
Unexplained vomiting or diarrhoea (56%)
Salt craving (19%) 
Postural symptoms (12%)
66
Q

What are the potential clues for diagnosis of adrenal failure?

A

Disproportion between severity of illness and circulatory collapse/hypotension/dehydration
Unexplained hypoglycaemia
Other endocrine features - hypothyroidism, body hair loss, amenorrhoea
Previous depression or weight loss

67
Q

How do. you diagnose adrenal insufficiency?

A

Non-specific symptoms, need to consider diagnosis
Routine bloods - U&Es, FBC, glucose
Random cortisol
Synacthen test and basal ACTH
(if suspicion is high, treat with steroids and do synacthen test later)

68
Q

What is CRH and ACTH release promoted by?

A

Stress

69
Q

What is CRH and ACTH release aggravated by?

A

Alcohol
Caffeine
Lack of sleep

All of these disinhibit the hypothalamo-pituitary axis
Alcohol in particular depresses the neurones involved in negative feedback, further enhancing stress effect and increasing levels of CRH and ACTH

70
Q

What is the action of cortisol on gluconeogenesis?

A

Cortisol stimulates formation of gluconeogenic enzymes in the liver, enhancing gluconeogenesis and glucose production, aided by cortisol’s action on muscle

71
Q

What are the usual daily doses of glucocorticoid replacement therapy?

A

Hydrocortisone 20-30mg
Prednisolone 7.5mg
Dexamethasone 0.75mg

Given in divided doses to mimic normal diurnal variation e.g. hydrocortisone 20mg at 8AM and 10mg at 6PM

72
Q

What is the typical method of mineralocorticoid replacement?

A

Replacement using synthetic steroid, fludrocortisone
Binds to mineralocorticoid (aldosterone) receptors
50-300 micrograms daily

Adjust dose according to clinical status e.g. postural BP, oedema, U&Es, plasma renin evil

73
Q

Why is care required when withdrawing chronic glucocorticoid treatment?

A

Due to enhanced negative feedback effects of exogenous cortisol
Additional therapeutic cortisol enhances the negative feedback on the hypothalamus and pituitary, reducing release of CRH and ACTH
Loss of trophic action of ACTH on the adrenal gland causes atrophy of the gland
Risk of adrenal insufficiency if withdrawal is too fast

74
Q

What patients require special care when undergoing steroid treatment?

A

Hypo-adrenal patients on replacement steroids
Patients on steroid doses sufficient to suppress the pituitary adrenal axis
Patients who have received such treatment during the previous 18/12

75
Q

What action should be taken in regards to steroid treatment when excess stress is being experienced by the patient?

A

Minor short-lived illness/stress - double glucocorticoid dose
Major illness or operation - 100mg hydrocortisone IV stat, especially if nil-by-mouth or GI upset
50-100mg hydrocortisone IV 8 hourly
As stress abates, reduce hydrocortisone by 50% per day until patient is back on their usual replacement dose

76
Q

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

A

Never miss a steroid dose
Double the hydrocortisone dose in the event of intercurrent illness e.g. flu, UTI
If severe vomiting or diarrhoea, call for help, likely to need IM hydrocortisone

77
Q

What percentage of cases of congenital adrenal hyperplasia are due to 21-hydroxylase deficiency?

A

> 90%

78
Q

What are the effects of congenital adrenal hyperplasia?

A

Severe cases

  • neonatal salt-losing crisis
  • ambiguous genitalia (females)

Incomplete defects

  • pseudo-precocious puberty (males)
  • hirsutism (females)
79
Q

What is the common approach to diagnosing/treating adrenal disorders?

A 
Clinical suspicion 
Testing to assess functional status 
Determine aetiology 
If tumour - can it be removed, is chemo/radiotherapy required 
Follow course of disease 
Correct endocrine deficiency 
Aetiology specific treatment

Diabetes and Endocrinology (24 decks)

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