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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
What does aldosterone increase reabsorption of?
Na+ ions
26
What does aldosterone promote the secretion of?
K+ ions
27
What is secretion of aldosterone primarily controlled by
The renin-angiotensin-aldosterone system (RAAS) - a complex reflex pathway originating in the kidney
28
What does increased aldosterone release stimulate?
Na+ (and H2O) retention and K+ depletion, resulting in increased blood volume and pressure
29
What does decreased aldosterone release result in?
Leads to Na+ (and H2O) loss and increased [K+]plasma, resulting in diminished blood volume and decreased blood pressure
30
What kind of tissue is the adrenal medulla?
Modified sympathetic ganglion - not true endocrine tissue
31
What is the role of the adrenal medulla?
Neuroendocrine role
32
Where do the post-ganglionic cells in the adrenal medulla release neurohormones?
Directly into the blood
33
What kind of hormone is cortisol?
Glucocorticoid hormone
34
What percentage of plasma cortisol is bound to a carrier protein?
95% - cortisol binding globulin
35
What cells have cytoplasmic glucocorticoid receptors?
All nucleated cells
36
Where does the hormone receptor complex migrate to?
Migrates to the nucleus, where it binds to DNA via a hormone-response element to alter gene expression, transcription and translation
37
What is the pattern of cortisol release?
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
What are the actions of cortisol on glucose metabolism?
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
What are the non-glucocorticoid actions of cortisol?
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
What are the side effects of glucocorticoid therapy?
Increased severity and frequency of infection, loss of percutaneous fat stores giving appearance of thinning skin and making it more fragile
41
What are the hypersecretion disorders of the adrenal cortex?
Cushing's syndrome - cortisol and androgen hypersecretion, due to adenoma, carcinoma or bilateral hyperplasia
42
What are the hypersecretion disorders of the adrenal medullae?
Phaeochromocytoma - catecholamines
43
How can the catabolic role of cortisol lead to health problems?
Tissue breakdown - causes weakness of skin, muscle and bone Sodium retention - hypertension and heart failure Insulin antagonism - may cause DM
44
What is the hypersecretion of cortisol in Cushing's syndrome/disease most commonly due to?
A tumour in adrenal cortex or pituitary gland, or iatrogenic e.g. too much cortisol administered therapeutically
45
What are the features of Cushing's syndrome?
Tumour in adrenal cortex - adenoma or carcinoma Corticosteroid therapy First degree hypercortisolism ACTH independent
46
What are the features of Cushing's disease?
Tumour in pituitary gland Ectopic ACTH secretion e.g. lung carcinoid Second degree hypercortisolism ACTH dependent
47
What is more common, Cushing's syndrome or Cushing's disease?
Cushing's disease most common - excess ACTH Cushing's disease 75% of cases, Cushing's syndrome 20%
48
What is Cushing's disease characterised by?
Wasting of the extremities due to the catabolic action of cortisol, fat redistribution to face and trunk, central obesity
49
What are the signs and symptoms of Cushing's disease/syndrome?
``` (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
What is the screening test for Cushing's syndrome?
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
What are the symptoms and signs of Conn's syndrome?
``` Hypertension Polyuria Nocturia Tiredness Weakness Hypokalaemia Raised plasma aldosterone Low plasma renin ```
52
What are the features of pheochromocytoma?
``` Rare neuroendocrine tumour Found in adrenal medulla Results in excess catecholamines Diabetogenic due to adrenergic effect on glucose metabolism Responds well to surgery ```
53
What is the result of the excess catecholamines caused by pheochromocytoma?
Increased heart rate, increased cardiac output, increased blood pressure
54
What are the signs and symptoms of pheochromocytoma?
Hypertension - persistent in 70% Paroxysmal attacks - headache - sweating - palpitations - tremor - pallor - anxiety/fear
55
What percentage of pheochromocytomas are extra-adrenal?
10%
56
What percentage of pheochromocytomas are malignant?
10%
57
What percentage of pheochromocytomas are multiple?
10%
58
What percentage of pheochromocytomas are of inherited origin?
30% - genes and familial syndromes
59
What are the endocrine causes of hypertension?
Primary hyperaldosteronism - unilateral adenoma - bilateral hyperplasia Rarer causes - pheochromocytoma - Cushing's syndrome - acromegaly - hyperparathyroidism - congenital adrenal hyperplasia
60
What is Addison's disease?
Hyposecretion of all adrenal steroid hormones due to autoimmune destruction of the adrenal cortex
61
What are the causes of Addison's disease (primary adrenal insufficiency)?
``` Autoimmune destruction Invasion Infiltration Infection Infarction Iatrogenic ```
62
What is the most common cause of congenital adrenal hyperplasia?
21-hydroxylase deficiency
63
What percentage of UK cases of adrenal failure are accounted for by autoimmune Addison's disease?
> 85%
64
What are the features of autoimmune Addison's disease?
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
What are the common symptoms of primary adrenal failure?
``` 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
What are the potential clues for diagnosis of adrenal failure?
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
How do. you diagnose adrenal insufficiency?
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
What is CRH and ACTH release promoted by?
Stress
69
What is CRH and ACTH release aggravated by?
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
What is the action of cortisol on gluconeogenesis?
Cortisol stimulates formation of gluconeogenic enzymes in the liver, enhancing gluconeogenesis and glucose production, aided by cortisol's action on muscle
71
What are the usual daily doses of glucocorticoid replacement therapy?
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
What is the typical method of mineralocorticoid replacement?
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
Why is care required when withdrawing chronic glucocorticoid treatment?
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
What patients require special care when undergoing steroid treatment?
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
What action should be taken in regards to steroid treatment when excess stress is being experienced by the patient?
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
What are the important self-care rules for patients on steroids?
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
What percentage of cases of congenital adrenal hyperplasia are due to 21-hydroxylase deficiency?
> 90%
78
What are the effects of congenital adrenal hyperplasia?
Severe cases - neonatal salt-losing crisis - ambiguous genitalia (females) Incomplete defects - pseudo-precocious puberty (males) - hirsutism (females)
79
What is the common approach to diagnosing/treating adrenal disorders?
``` 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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