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Y2 LCRS1 Endocrinology > Hyperadrenal Disorders > Flashcards

Hyperadrenal Disorders Flashcards

1
Q

Describe the effects of excess cortisol on protein and fat synthesis.

A

Decrease protein synthesis

Increase fat synthesis

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2
Q

Explain why people with Cushing’s disease get stretch marks.

A

They are putting on a lot of fat quickly, which stretches the skin. Because protein synthesis is switched off, you can’t make the protein required for skin growth so the skin tears.

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3
Q

Describe the clinical features of Cushing’s syndrome.

A
  • Too much cortisol
  • Moon face
  • Interscapular fat pad (buffalo hump)
  • Proximal myopathy
  • Easy bruising, striae, thin skin
  • Osteoporosis , diabetes
  • Centripetal adiposity (lemon on sticks)
  • Hypertension and hypokalaemia
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4
Q

Why does Cushing’s syndrome cause hypertension and hypokalaemia?

A

At high concentrations, cortisol can have mineralocorticoid effects –> increased sodium absorption and potassium excretion

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5
Q

State four causes of Cushing’s syndrome.

A
  • Pituitary adenoma
  • Ectopic ACTH e.g. from lung cancer
  • Oral glucocorticoid drugs
  • Adrenal adenoma secreting cortisol
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6
Q

What are the three main tests used to diagnose Cushing’s syndrome?

A
  • 24-hour urine free cortisol
  • Blood diurnal cortisol levels (or midnight serum cortisol when it should be lowest; highest at 9am)
  • Low dose dexamethasone suppression test
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7
Q

Describe the results you’d expect from a normal subject and a patient with Cushing’s syndrome in the 24-hour urine free cortisol and blood diurnal cortisol tests.

A

You would expect lower cortisol at night in a normal subject and high cortisol in the morning.

In someone with Cushing’s syndrome they would have high cortisol all the time.

NOTE: a problem with this test is that the cortisol levels are affected by stress.

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8
Q

What is dexamethasone? How much is given in the low dose dexamthasone suppression test?

A

0.5 mg 6 hourly for 48 hrs

Dexamethasone = artificial steroid

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9
Q

Explain the scientific basis of the low dose dexamethasone suppression test.

A
  • Dexamethasone is a glucocorticoid so by giving this extra glucocorticoid, it should suppress ACTH and reduce cortisol production.
  • So in a normal subject undertaking the dexamethasone suppression test, you would expect zero cortisol.
  • In a Cushing’s patient, cortisol will remain high despite the presence of dexamethasone.
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10
Q

State some surgical treatments for Cushing’s syndrome.

A

Treatment is dependent on cause:

  • Transsphenoidal Hypophysectomy (for Cushing’s disease)
  • Bilateral adrenalectomy
  • Unilateral adrenalectomy for adrenal mass
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11
Q

State two drugs that are used to treat Cushing’s syndrome before surgery.

A

Metyrapone

Ketoconazole

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12
Q

Draw the adrenal steroid synthesis pathway.

A

-

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13
Q

Which enzyme is inhibited by metyrapone?

A

11-Beta-hydroxylase

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14
Q

What effect does metyrapone have?

A
  1. cortisol synthesis blocked
  2. ACTH secretion increased
  3. plasma deoxycortisol increased
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15
Q

What is the mechanism of action of metyrapone?

A
  • Inhibition of 11beta-hydroxylase
  • Steroid sythesis in zona fasciculata (and reticularis) is arrested at the 11-deoxycortisol stage
  • 11-deoxycortisol has no negative feedback on hypothalamus and pituitary
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16
Q

State two uses of metyrapone.

A
  1. Preparation of a Cushing’s patient for surgery (improves their healing abilities and makes them better surgical candidates)
  2. Treatment of Cushing’s syndrome symptoms following radiotherapy (radiotherapy has a delayed effect)
17
Q

State two negative aspects of metyrapone.

A

Metyrapone –> accumulation of 11-deoxycorticosterone (because it doesn’t have any negative feedback effects on the ACTH axis). Since 11-deoxycorticosterone has mineralocorticoid effects so causes SALT RETENTION and HYPERTENSION.

Metyrapone inhibits two limbs of the steroid synthesis pathway so it funnels the precursors towards the sex steroid synthesis pathway. –> increased adrenal androgens, which has effects such as hirsuitism.

18
Q

State some unwanted effects of metyrapone.

A
  • Hypertension on long-term administration
  • Hirsutism
19
Q

What is ketoconazole and why is it no longer used?

A

Ketoconazole is an anti-fungal, which had an effect on the steroidsynthesis pathway.

  • It is no longer used because of its hepatotoxicity.

Off label use for Cushing’s - treatment and control of symptoms prior to surgery. Orally active.

20
Q

What are the effects of ketoconazole on steroid production?

A

Ketoconazole inhibits cytochrome P450 short chain cleavage enzyme.

This enzyme converts cholesterol –> pregnenolone

This means that it inhibits the production of glucocorticoids, mineralocorticoids and sex steroids. - off-label use in Cushing’s

21
Q

State some unwanted actions of ketoconazole.

A

LIVER DAMAGE (could be fatal) - monitor liver function weekly, clinically and biochemically

22
Q

What is Conn’s syndrome?

A

Aldosterone secreting adenoma of the adrenal gland (zona glomerulosa)

23
Q

What are the two main features of Conn’s syndrome?

A

Hypertension

Hypokalaemia

24
Q

What is primary hyperaldosteronism?

A

Hyperaldosteronism caused by an adrenal adenoma.

25
Q

What can you test to exclude secondary hyperaldosteronism?

A

Check for suppression of the renin-angiotensin system

Measure aldosterone and if that’s high, measure the renin and that should be low because if would be suppressed by the high blood pressure.

26
Q

What is the usual treatment plan for someone with Conn’s syndrome?

A

NB: Conn’s syndrome = primary hyperaldosteronism

  • Medical management (spironolactone) - aldosterone receptor antagonist
  • Surgery to remove the adenoma

If the adrenal hyperplasia is bilateral then you can stay on the spironolactone.

27
Q

What is spironolactone and how does it work?

A

Spironolactone is an aldosterone receptor antagonist/MR competitive antagonist

It reduces the effects of aldosterone so it decreases sodium reabsorption and decreases potassium excretion in the kidneys (potassium sparing diuretic).

28
Q

What is the active metabolite of spironolactone that acts as a mineralocorticoid receptor antagonist?

A

Canrenone - this is a competitive antagonist of the mineralocorticoid receptor.

29
Q

What treatment would you give for someone with bilateral adrenal hyperplasia?

A

Long-term spironolactone

You don’t want to remove both adrenals because then they wouldn’t produce any cortisol or aldosterone so you give them long-term spironolactone to reduce the effects of excess aldosterone.

30
Q

Describe the pharmacokinetics of spironolactone.

A

Orally active

Highly protein-bound and metabolised in the liver

31
Q

State some unwanted effects of spironolactone.

A

Spironolactone is very non-specific so it has several side effects

  • Progesterone receptor agonist –> menstrual irregularities
  • Androgen receptor antagonist –> gynaecomastia
    *
32
Q

Name another mineralocorticoid receptor antagonist that has fewer side effects than spironolactone. Explain why this is so.

A

Eplerenone

Fewer side effects:

  • Similar affinity to the MR compared to spironolactone
  • BUT less binding to androgen and progesterone receptors compared to spironolactone, so better tolerated
33
Q

What is phaeochromocytoma?

A

Tumour of the adrenal medulla that is producing excessive amounts of catecholamines

(adrenaline and noradrenaline)

34
Q

What are the features of phaeochromocytoma?

A
  • Hypertension in the young
  • Episodic severe hypertension (after abdominal palpation)
  • They will get sudden bursts of panic attacks, anxiety, palpitations and a rapid rise in blood pressure.
35
Q

Why must you be careful when pressing on the abdomen of a person with phaeochromocyroma?

A

Pressing on the phaeochromocytoma can cause release of adrenaline when examinig the abdomen

36
Q

State some fatal consequences of phaeochromocytoma.

A
  • Severe hypertension can cause myocardial infarction or stroke
  • High adrenaline can cause ventricular fibrillation + death
  • Thus this is a medical emergency
37
Q

Describe the steps that must be taken when preparing a phaeochromocytoma patient for surgery.

A

Anaesthetic could precipitate a hypertensive crisis.

  • You give the patient an alpha-blocker to prevent the vasoconstriction caused by adrenaline binding to alpha-receptors.
  • Alpha-blockers cause a drop in blood pressure so they are usually given with a bit of fluid.
  • Then you give beta-blockers to prevent tachycardia.
  • Once all the receptors are blocked, it means that a massive release in adrenaline will not be able to have its effects.
38
Q

What percentage of phaeochromocytoma is intra-adrenal? Malignant? Bilateral?

A
  • 90% intra-adrenal (so 10% extra-adrenal; sympathetic chain)
  • 10% malignant
  • 10% bilateral

It is a very rare condition.

Y2 LCRS1 Endocrinology (18 decks)

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