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Endocrinology > Adrenal > Flashcards

Adrenal Flashcards

1
Q

From superficial to deep, what are the layers of the adrenal cortex and what do they produce?

A

Zona glomerulosa - produces mineralocorticiods (aldosterone)

Zona fasciculata - produces glucocorticoids (cortisol)

Zona reticularis - produces androgens

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2
Q

Describe the steps of the renin-angiotensin-aldosterone-system (RAAS)

A
  1. Low sodium sensed by macula densa cells of the juxtaglomerular apparatus in the kidneys stimulated renal production of renin
  2. Renin converts angiotenisogen (produced by the liver) to angiotensin I
  3. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II
  4. Angiotensin II vasoconstricts and releases aldosterone from the zona glomerulosa
  5. Aldosterone acts on the kidneys to increase sodium and water retention increasing blood pressure
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3
Q

What formation of glucocorticoids-glucocorticoid receptor activates transcription and which suppresses transcription?

A

Dimer activates transcription

Monomer suppresses transcription (by blocking NK kappa B)

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4
Q

How do glucocorticoids work?

A

Binding to intracellular receptors and altering DNA transcription

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5
Q

What cells are within the adrenal medulla and what do they do?

A

Chromaffin cells

Convert tyrosine to catecholamines

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6
Q

What is Addison’s disease?

A

Destruction of the adrenal cortex causing adrenal insufficiency (commonly autoimmune but can be infectious)

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7
Q

How does Addison’s disease present?

A

Non specific weight loss, fatigue

Dizziness

Skin pigmentation

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8
Q

What causes the skin pigmentation in Addison’s disease?

A

Excess ACTH acts on melanocytes

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9
Q

What do the stress hormones do to blood sugar levels?

A

Increase them

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10
Q

What blood results would you expect to see in Addison’s disease?

A

Hyponatraemia
Hyperkalaemia
(from loss of mineralocorticoid)

Hypoglycaemia
(from loss of cortisol)

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11
Q

How do you diagnose Addison’s disease?

A

Short Synatchen test

Measure cortisol before and after administering synthetic ACTH

If cortisol isn’t raised >550mmol/l, patient has Addison’s Disease

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12
Q

How is Addison’s disease treated?

A

Hydrocortisone replacement

Fludocortisone replacmeent

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13
Q

Patient presents with vomiting and abdominal pain. Blood results show hyponatreamia and hyperkalaemia.

What is the diagnosis?

A

Addisonian crisis

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14
Q

How is an Addisonian crisis managed?

A

Hydrocortisone IV
IV fluids
(IV glucose may also be needed)

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15
Q

What do patients with Addison’s disease do with their medications if they are ill?

A

Double doses

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16
Q

What should you consider if a child is diagnosed with a adrenocortical tumour?

A

Genetic condition (e.g.Li Fraumeni syndrome)

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17
Q

What features suggest a malignancy in an adrenocortical tumour?

A

Functional tumours
Large
Necrosis (present as fever)

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18
Q

What is a neuroblastoma?

A

Tumour of nervous tissue which often arises in adrenal medulla

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19
Q

Who tends to develop neuroblastomas?

A

Young children

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20
Q

What is a phaeochromocytoma?

A

Tumour of adrenal medulla chromaffin cells which secrete catecholamines causing symptoms

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21
Q

How do phaeochromocytoma present?

A

Episodes of

  • Headache
  • Hypertension
  • Sweating
  • Tachycardia
  • Anxiety
  • Tremor
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22
Q

How do you diagnose phaeochromocytoma?

A

Urine/plamsa catecholamine to confirm catecholamine excess

MRI abdomen to find source of excess

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23
Q

How do you treat phaeochromocytoma?

A

a-blocker (phenoxybenzamine) then ß-blocker

Then excision or chemotherapy if malignant

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24
Q

What is congenital adrenal hyperplasia (CAH)?

A

Group of conditions caused by deficiency of an enzyme involved in steroid synthesis resulting in steroid deficiencies

25
Q

What enzyme is most commonly deficient in congenital adrenal hyperplasia (CAH)

A

21a-hydroxylase

26
Q

What does a 21a-hydroxylase deficiency cause?

A

Loss of aldosterone and cortisol but excess androgen

27
Q

What are the two classifications of congenital adrenal hyperplasia (CAH) and how do they present?

A

Classical:
severe enzyme deficiency presenting in infancy with
- adrenal insufficiency
- genital ambiguity

Non-Classical:
milder enzyme deficinecy presenting with
- precocious puberty
- hirsutism
- acne
- oligomenorrhoea
- infertility
28
Q

How can congenital adrenal hyperplasia (CAH) be diagnosed?

A

Raised progesterone, 17-OH progesterone

Genetic mutation analysis

29
Q

What is Cushing’s syndrome?

A

Collection of symptoms caused by excess cortisol

30
Q

What is Cushing’s disease?

A

Excess cortisol caused by pituitary adenoma producing excess cortisol

31
Q

How does Cushing’s syndrome present?

A

(breakdown)
Thin skin
Proximal myopathy
Osteoporosis

(altered lipid metabolism)
Central obesity
Moon face
Buffoon hump

(androgen excess)
Acne
Hirsutism
Amenorrhoea

32
Q

What are 4 causes of Cushing’s syndrome?

A

Functional pituitary adenoma producing excess ACTH

Adrenal hyperplasia producing excess cortisol

Ectopic tissue producing excess ACTH

Excess exogenous steroids

33
Q

What is the commonest cause of Cushing’s syndrome?

A

Excess exogenous steroids

34
Q

What are the first line tests in the diagnosis of Cushing’s syndrome and how are they performed?

A

Overnight dexamethasone suppression test

  • give 1mg PO dexamethasone at midnight and measure cortisol at 8am
  • suppresses to <50nmol/l
  • no suppression in Cushing’s

24h urinary cortsiol

  • normal <280nmol/l
  • raised in Cushing’s
35
Q

What is the definitive diagnostic test for Cushing’s syndrome and when is it used?

A

Low dose dexamethasone suppression test

  • give 0.5mg dexamethasone BD for 2 days and measure cortisol after last dose
  • suppresses to <50nmol/l
  • no suppression in Cushing’s
36
Q

What test can distinguish pituitary Cushing’s disease from other causes of Cushing’s syndrome?

A

High dose dexamethasone test (2mg dexamethasone 6 hourly for 2 days)

  • if this suppresses cortisol levels, suggests pituitary cause
  • no suppression, ectopic/adrenal cause
37
Q

What test can distinguish adrenal Cushing’s syndrome from other causes?

A

Measuring serum ACTH

ACTH is very low in adrenal Cushing’s

38
Q

What results would you expect to see in high dose dexamethasone suppression test and by measuring serum ACTH in:

  1. Pituitary Cushing’s
  2. Adrenal Cushing’s
  3. Ectopic Cushing’s?
A
  1. Dexa - suppresion of cortisol ; ACTH - raised
  2. Dexa - no suppression ; ACTH - low
  3. Dexa - no suppression ; ACTH- raised
39
Q

How is Cushing disease treated?

A
  1. Hypophysectomy (first line)
  2. Radiotherapy
  3. Bilateral adrenalectomy
40
Q

How is adrenal Cushing’s treated?

A

Adrenalectomy

41
Q

How is ectopic Cushing’s treated?

A

Remove ectopic tissue

42
Q

Name 3 drugs which can be used to treat Cushing’s syndrome.

A

Metyrapone
Ketoconazole
Pasirotide

43
Q

What is a common source of ectopic ACTH?

A

Small cell lung cancer

44
Q

What produces aldosterone?

A

Zona glomerulosa of adrenal cortex

45
Q

What produces cortisol?

A

Zona fasciculata of adrenal cortex

46
Q

What produces androgens?

A

Zona reticularis of adrenal gland

47
Q

What stimulates aldosterone release?

A

Low sodium (indirectly via RAAS)

High potassium (directly)

48
Q

What does aldosterone do?

A

Acts on MR receptor on distal convulated tubule and collecting tubule to increase sodium reabsorption and potassium excretion

(keeps sodium, removes potassium)

49
Q

What is primary aldosteronism?

A

Autonomous production of aldosterone causing hypertension, hypokalaemia and metabolic alkalosis

50
Q

What is the biochemical presentation of hyperaldosteronism?

A

Hypernatreamia
Hypokalameia
Alkalosis

51
Q

What is the clinical presentation of hyperaldosteronism?

A

Hypertension (sodium retention)

Weakness, cramps (hypokalaemia)

Confusion, vomiting, tetany (alkalosis)

52
Q

Name 2 causes of primary aldosteronism.

A

Bilateral adrenal hyperplasia

Adrenal adenoma (Conn’s syndrome)

53
Q

Name a gene mutation which may predispose to primary hyperaldosteronism.

A

KCNJ5

54
Q

How do you diagnose primary hyperaldosteronism?

A
  1. Confirm aldosterone excess with
    - raised aldosterone-renin-ratio
    - saline suppression test (2l of saline don’t suppress aldosterone by 50%)
  2. Confirm type with
    - PET-CT overlay
    - Adrenal vein sampling
55
Q

How do you treat bilateral adrenal hyperplasia?

A

Spironolactone (MR antagonist)

56
Q

How do you treat Conn’s syndrome?

A

Unilateral adrenalectomy

57
Q

What is secondary adrenal insufficiency?

A

Adrenal failure from lack of ATCH stimulation due to pituitary tumour or exogenous steroids

58
Q

How does secondary adrenal insufficiency present clinically?

A

Non specific weight loss, fatigue

Dizziness

Without skin pigmentation (lack of ACTH is the problem)

59
Q

How is secondary adrenal insufficiency treated?

A

Hydrocortisone (replacement for cortisol)

no mineralocorticoid replacement needed

Endocrinology (10 decks)

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