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Endocrinology > Adrenal Cortex > Flashcards

Adrenal Cortex Flashcards

1
Q

What is the endocrine fucntion of the adrenal cortex?

A

The adrenal cortex produces hormones that controls sex (androgens, estrogens), salt balance in the blood (aldosterone), and sugar balance (cortisol)

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2
Q

Where does the glucocorticoid production take place and what does it produce?

A

Aldosterone, which is produced in the zona glomerulosa, via a aldosterone synthase.

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3
Q

Function of aldosterone

A

maintain BP, promote renal sodium reabsorption and promote potassium excretion by acting via mineralocorticoid receptors

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4
Q

What can stimulate aldosterone production?

A

Low BP, ACTH effects, posture

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5
Q

What is the main glucocorticoid produced?

A

Cortisol in the zonae fasiculata and reticularis

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6
Q

How is cortisol secreted?

A

Interplay with hypothalamus and pituitary, using CRH and ACTH respectively. Occurs in response to stress

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7
Q

How is cortisol production regulated?

A

Negative feedback loop: Cortisol on hypothalamus and pituitary gland

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8
Q

What are glucocorticoids actions?

A

Bone

  • inhibit bone formation
  • increase resorption
  • induce negative calcium balance

Skin
- inhibit fibroblast activity causing bruising and poor wound healing

Glucose

  • increase blood glucose by decreasing tissue glucose uptake
  • increase hepatic gluconeogenesis
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9
Q

Cortisol action on water balance

A

Are inhibited by 11beta hydroxysteroid dehydrogenase. Important because cortisol and aldosterone are structurally similar, meaning both activate mineralocorticoid receptors. The protecting enzyme converts cortisol to cortisone - so circadian rhythm of cortisol cant affect water balance/status.

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10
Q

What androgens are produced in the adrenal cortex?

A

Precursors of testosterone and oestrogen.

- androstenedione, DHEA, DHEA-S

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11
Q

What is the difference between primary and secondary/tertiary adrenal insufficiency?

A

Primary is caused due to a problem in the adrenal, whilst secondary/tertiary is problems in the pituitary or hypothalamus.

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12
Q

What is primary AI caused by?

A

Decreased cortisol production due to:

  • autoimmune disease (70%),
  • infection (AIDS)
  • congenital (enzyme deficiency )
  • drugs (ketoconazole)
  • haemorrhage (heparin treatment),
  • metastatic tumour,
  • amyloid,
  • haemochromatosis or sarcoidosis.
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13
Q

What is secondary AI caused by?

A

Decreased ACTH production.

  • Pituitary tumours
  • autoimmune disease.
  • pituitary tumors or infection.
  • bleeding in the pituitary.
  • genetic diseases that affect the way the pituitary gland develops or functions.
  • surgical removal of the pituitary to treat other conditions.
  • traumatic brain injury link.
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14
Q

What are symptoms of adrenal insufficiency?

A

fatigue, weight loss, postural dizziness, anorexia, abdominal discomfort

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15
Q

What are the biochemical features of AI?

A

Hyponatraemia, hyperkalaemia, hypo/hyperglycaemia (uncommon)

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16
Q

What is adrenal crisis?

A

Acute adrenal crisis is a medical emergency caused by a lack of cortisol. Can occur in patients with AI

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17
Q

Symptoms and biochemical features of adrenal crisis?

A

severe weakness (hyponatraemia), syncope (hyperkalaemia), abdominal pain (hypoglycaemia), nausea, vomiting, back pain (hypercalcaemia) and confusion.

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18
Q

Explain the hyperpigmentation in primary AI?

A

Hyperpigmentation occurs as a byproduct of ACTH overmaturation. POMC is the ACTH precursor, which contains a Melanocyte stimulating hormone.
- The MSH increases melanocytes present result in hyperpigmentation

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19
Q

Biochemical features of primary AI?

A 
Hyponatraemia
Hyperkalaemia 
Acidosis
Mildly elevated urea
Low/normal cortisol
Hypoglycaemia
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20
Q

What can cause adrenal crisis and what are some clinical features?

A

Precipitated by major stress

  • Shock
  • hypotension
  • abdomen pain
  • unexplained feve
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21
Q

How is the adrenal crisis treated?

A

The main treatment is rehydration and replacement

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22
Q

How is adrenal insufficiency investigated?

A

Using a short synacthen test

  • Administer IV tetracostratin (250ug) and take cortisol+ ACTH at 30 and 60 min
  • Abnormal response <500nmol/L
  • Flat response in primary AI
  • Impaired response for secondary
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23
Q

How can you elucidate the cause of adrenal insufficiency (primary or secondary)?

A

If there is an impaired cortisol response to the short synacthen test then ACTH >300ng/L is primary adrenal failure or <10ng/L is secondary adrenal failure (pituitary test follows).

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24
Q

What further investigations can be done in primary adrenal insufficiency?

A

Elucidating the cause by measurign 17-OH progesteron (CAH, idiopathic PAI), 21-OH antibody (congenital and autoimmune)

Examine how the rest of the adrenal hormones are affected, e.g. renin/aldosterone and androgens

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25
Q

How do you treat adrenal insufficiency?

A

Replace glucocorticoids and mineralocorticoids

- hydrocortisone and fludrocortisone - monitor efficacy using cortisol and renin curves

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26
Q

What is hypoaldosteronims?

A

Hypoaldosteronism is an endocrinological disorder characterized by decreased levels of the hormone aldosterone

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27
Q

What causes hypoaldosteronism?

A
  • Impaired renin production (hyporeninaemic hypoaldosteronism, diabetic neuropathy)
  • Inherited defects in aldosterone biosynthesis
  • Acquired forms (heparin therapy).
  • Pseudohypoaldosteronism: inherited resistance to actions of aldosterone
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28
Q

What are some metabolic changes to hypoaldosteronism?

A
  • hyponatraemia
  • hyperkalaemia,
  • acidosis,
  • mildly elevated urea
  • hypotension.
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29
Q

What biochemical test can be used to diagnose hypoaldosteronims

A
  • U&E panel: hyponatraemia, hyperkalaemia, urea
  • Acidosis: blood gas analyse/anion gap
  • Most accurate is renin/aldosterone measurement
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30
Q

Describe patterns in diagnosing hypoaldosteronism

A

Primary HA
- renin high, aldosterone low

Secondary HA
- low renin, low aldosterone

31
Q

What is cushing syndrome?

A

Syndrome characterised by elevated glucocorticoids - glucose

32
Q

What are some causes

A

80% ACTH dependent - secondary

  • pituitary adenoma
  • ectopic ACTH

20% adrenal origin

  • adrenal adenoma
  • adrenal carcinoma, nodular hyperplasia
33
Q

Clinical features of cushings syndrome

A

weight gain, central obesity, proximal wasting, muscle weakness/malaise, buffalo hump, moon face, acne, osteoporosis, hirsutism, purple striae, skin thinning, bruising, depression, decreased libido, psychosis, oligo-, amenorrhoea, hypertension, susceptibility to infections

34
Q

What are some non-cushings hypercortisolism?

A

non-cushings conditions causing elevated cortisol.

Seen in obesity, alcohol, depression, PCOS, serious illness/cancer.

35
Q

What test is used to diagnose cushings?

A

DST test
- overnight, give 1mg DST at midnight and measure cortiol at 9am

48hr

  • 2mg DST given when there is a physiological cause for high cortisol (non-cushing)
  • 0.5mg DST given at 0900, 1500, 2100, 0300 and cortisol measured at 09 on second day
36
Q

When is DST test inappropriate?

A

For cyclical cuhsings

37
Q

How can you elucidate cause of cushings?

A

Potassium levels
- In patient with high ACTH 10% pituitary dependent and 100% ectopic have K<3.2 mmol/L (with alkalosis).

CRH test
- 95% pituitary dependent and <1% ectopic have exaggerated cortisol response in CRH test

DST (high dose)
-90% pituitary dependent and 10%ectopic will suppress cortisol >50% basal.

Imaging to see presence of tumours can be done

38
Q

How does petrosal sinus sampling work?

A

Acts to measure ACTH from veins that drain pituitary gland

  • Measured before and after IV CRH.
  • The ratio of central to peripheral allow for diagnosis
39
Q

How does the ratio of central to peripheral allow for diagnosis?

A

central: peripheral ratio >2 suggests cushings disease (A ratio of >3 is more sensitive (90-95%)).

40
Q

How is cushings syndrome treated?

A

Most common is to remove the tumour via a trans-sphenodial surgery.

  • non operable patients will receive radiotherapy
  • Limited medical treatment, but can be used whilst waiting for surgery/radiotherapy, e.g. metyrapone, ketoconazole, mitotane.
  • adrenalectomy if its an adrenal cause
41
Q

When can Nelsons syndrome occur?

A

Patients that had bilateral adrenalectomy as treatment for cushing disease.

  • manifest as hyperpigmentation,
  • ACTH increase
  • Enlarged pituitary tumours

Incidence- 50% within 10 years

42
Q

What is hyperaldosteronims?

A

Hyperaldosteronism is a medical condition wherein too much aldosterone is produced by the adrenal glands, which is non-suppressible with sodium loading

43
Q

Causes of hyperaldosteronism

A
  • idiopathic adrenal hyperplasia
  • Conns syndrome: aldosterone-producing adrenal hyperplasia
  • Adrenocorticoid carcinoma
44
Q

Who are susceptible to developing hyperaldosteronism?

A
  • hypertensives
  • with hypokalaemia
  • with adrenal incidentaloma
45
Q

How do you screen for hyperaldosteronism?

A

Screening of PA can be done using the aldosterone renin ratio

46
Q

Describe patient preperations ahead of renin aldosterone measurement

A
  • Unrestricted dietary salt intake day before
  • Out of bed for at least 2h
  • Discontinue meds: antihypertensives
47
Q

Why is direct plasma renin activity more accurate than direct renin concentration?

A

PRA is more effective measurement as DRC will be interfered by oestrogens

48
Q

Patients on either spironolactone, eplerenone, amiloride and triamterene need to what before renin:aldosterone measurement?

A

need to be discontinued 4 weeks prior to the measurement of PRR to limit interference

49
Q

Why cant AAR samples not be placed on ice?

A

because as the pro-renin becomes renin causing a skewed analysis

50
Q

TRUE OR FALSE.

Hypokalaemia can make interpretation hard as it decreases aldosterone and increases renin.

A

True

51
Q

What is a definite indication of primary hyperaldosteronism?

A

ARR>2000

52
Q

What follow up tests are useful for primary hyperaldosteronism?

A 
Saline infusion test
Oral sodium loading
Captopril challenge test
CT 
Adrenal vein sampling
53
Q

How is primary hyperaldosteronims treated?

A
  • Unilateral adrenalectomy where possible

- medical intervention include minaralocorticoid receptor antagonist, e.g.spironolactone, amiloride, eplerenone.

54
Q

What is secondary hyperaldosteronism?

A

due to overactivity of the renin–angiotensin–aldosterone system (RAAS)

55
Q

What causes secondary hyperaldosteronims?

A

Caused by nephrosis, cirrhosis, cardiac failure or associated with oedema and reduced oncotic pressure
- renin producing tumours as well

Overall- false sense of hypovolaemia and activates aldosterone secretion

56
Q

What are the results for DRC and PRA in 2nd hyperaldosteronism?

A

High as the renin causes the hyperaldosteronims

57
Q

What are familial hyperaldosteronism?

A

A group of inherited conditions in which the adrenal glands, which are small glands located on top of each kidney, produce too much of the hormone aldosterone

58
Q

What 3 types of familial hyperaldosteronism are there?

A

Type I - glucocorticoid remediable aldosteronism
Type II - 7p22 mutation
Type III - germline mutations in the K channel subunit KCNJ5

59
Q

Familial hyperaldosteronims type I?

A
  • inherited autosomal dominant disorder
  • chimeric gene causes’
  • This chimeric gene result in the expression of an aldosterone synthase gene in zonae fasiculata and glomerulus
  • Expression controlled by ACTH

Treatment is using DST/prednisone

60
Q

What is syndrome of apparent mineralocorticoid excess?

A

Congenital deficiency of 11-beta-HSD 2 enzyme causing cortisol to act on the mineralocorticoid receptor. Causes water imbalances.
- Symptoms: hypertension, suppressed renin/aldosterone, hypokalaemic alkalosis, increase cortisol:cortisone ration

61
Q

What is syndrome of apparent mineralocorticoid excess caused by ?

A

Excess intake of glycyrrhetinic acid (liquorice, cough medicine, chewing tobacco)

62
Q

Treatment of syndrome of apparent mineralocorticoid excess

A

carbonic anhydrase inhibitor known as acetazolamide.

63
Q

What are congenital adrenal hyperplasias?

A

Group of autosomal recessive disorders where an enzyme deficiency leads to decreased cortisol

  • Often associated with the overproduction of steroids.
  • Severity is dependent on what enzyme is affected
64
Q

Describe what happens in 21 hydroxylase deficiency?

A

This condition is associated with no cortisol and no aldosterone production. This results in high 17 hydroxyprogesterone and excess androgen production.

65
Q

Symptoms of 21 hydroxylase deficiency?

A

Ambiguous genitalia in female neonates – clitoromegaly (looks like penis) or fusion of labia (scrotum)

66
Q

Biochemical features of 21 hydroxylase deficiency?

A

Hypoglycaemia, dehydration, vomiting and pigmentation

- Can cause salt-crisis causing collapse during stress or illness

67
Q

What are the milder forms of 21 hydroxylase deficiency associated with?

A

Cause rapid growth (still short stature) and precocious puberty (due to increased androgens)

Non-classical form has onset in adulthood, which presents in female as hirsuitism, virilism, amenorrhoea (diagnose with SST and 17-OH P)

68
Q

11 hydroxylase deficiency

A

deficiency in the enzyme catalysing the last step in cortisol production and penultimate in aldosterone
- The aldosterone and cortisol production is blocked. It results in 11 deoxycortisol and 11 deoxycorticosterone

69
Q

Biochemical features of 11 Hydroxylase

A

Low potassium, high BP, can cause virilisation in women

Mild forms: 17OHP moderately raised, but 11deoxycortisol is high

70
Q

17 hydroxylase deficiency

A

block aldosterone intermediates becoming cortisol intermediates.
- Aldosterone is produced, but not cortisol or androgens

71
Q

17 hydroxylase deficiency features

A

Males are born feminised, whilst females will have a delayed puberty.
- Hypotension

72
Q

Cholesterol side chain cleavage

A

Complete adrenal steroid deficiency. Same for cortisol and aldosterone

73
Q

How is congenital adrenal hyperplasia treated?

A

Hormones not produced need to be replaced.

  • hydrocortisone (increase dose at times of stress/illness), fludrocortisone, testosterone/oestrogen
  • If previous child has 21hydroxylase then prenatal diagnosis using free neonatal DNA can be used to diagnose - Treat with steroid cover during pregnancy
74
Q

Investigating congenital adrenal hyperplasia

A

The first line tests include U&E, 9am cortisol, BP and physical examination. 2nd line tests include SST with 17OHP, renin & aldosterone, 11DOC, karyotyping, androgen profile, urine steroid profile.

Endocrinology (12 decks)

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