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Endocrinology > 6. Hyperadrenal disorders > Flashcards

6. Hyperadrenal disorders Flashcards

1
Q

What is the cause of Cushing’s disease?

A
  • Pituitary tumour making ACTH
  • ACTH makes adrenal gland grow
  • Too much cortisol
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2
Q

What happens to protein and fat in Cushing’s syndrome?

A
  • Cortisol switches protein synthesis off and fat synthesis on
  • Lose protein and gain fat
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3
Q

What are the clinical features of Cushing’s syndrome?

A
  • Too much cortisol
  • Centripetal obesity
  • Moon face
  • Buffalo hump (interscapular fat pad)
  • Proximal myopathy
  • Hypertension and hypokalaemia
  • Red striae, thin skin and easy bruising
  • Osteoporosis, diabetes
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4
Q

Why is bruising common in Cushing’s syndrome?

A
  • Normally, lots of protein in tissues under skin, used to heal
  • Protein synthesis turned off - start to leak and get bruises
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5
Q

Why is hypertension and hypokalaemia common in Cushing’s?

A
  • Cortisol starts to bind to receptors in the kidney
  • Retention of sodium
  • Excretion of potassium
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6
Q

What are the causes of Cushing’s syndrome?

A
  • Taking too many steroids orally (first question to ask patient)
  • Pituitary dependent Cushing’s disease
  • Ectopic ACTH from lung cancer
  • Adrenal adenoma making cortisol
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7
Q

How can you determine the cause of Cushing’s syndrome?

A

• CUSHINGS - LOW DOSE dexamethasone suppression test (gold standard)

  • give patient extra steroid
  • normally ACTH and cortisol should go to zero

• 24 hour urine collection for urinary free cortisol
- patients often forget to sample urine, not ideal

• Blood diurnal cortisol levels

  • normally high in the morning and low when sleeping
  • loss of rhythm, high levels at night - suspicious
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8
Q

How is the low dose dexamethasone suppression test carried out and how do people with Cushing’s react?

A
  • Blood test before
  • Give dexamethasone for 48 hours
  • Cushing’s - keep making cortisol, no reaction to dexamethasone
  • Does not tell you the cause
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9
Q

Why would people with Cushing’s die more quickly in the past?

A
  • Infection
  • Can’t synthesise proteins and heal
  • Immunosuppressed
  • Sepsis
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10
Q

How can Cushing’s be treated?

A

Inhibitors of steroid biosynthesis, e.g.
• metyrapone
• ketoconazole

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11
Q

What is Conn’s and how can it be treated?

A

• Too much aldosterone
• MR (mineralocorticoid receptor) antagonist
- spironolactone
- epleronone

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12
Q

What type of hormones are produced in the adrenal medulla?

A

Catecholamines

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13
Q

What is phaeochromocytoma?

A
  • Tumour of adrenal medulla

* Excess catecholamines

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14
Q

How do you block the effects of excess catecholamines?

A

• First give alpha blocker
- urgent issue is really high BP caused by catecholamines binding to alpha receptors in vasculature => vasoconstriction

• When BP decreases, give beta blocker

  • catecholamines stimulate beta receptors to cause vasodilation
  • BB prevents too much vasodilation
  • alpha blocker given first as you could have unopposed alpha mediated vasoconstriction causing a hypertensive crisis and possible stroke
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15
Q

Where is aldosterone, cortisol and 17b-oestradiol produced?

A
  • Aldosterone - zona glomerulosa
  • Cortisol - zona fasciculata
  • 17b-oestradiol - zona reticularis
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16
Q

How does metyrapone work?

A
  • Medication that inhibits 11b-hydroxylase
  • Slows down cortisol synthesis pathway
  • Reduces production of cortisol and corticosterone
  • Treatment for Cushing’s
  • ACTH levels rise because of this - no negative feedback from 11-deoxycorticosterone
17
Q

When is metyrapone used?

A

• Control prior to surgery

  • improves symptoms
  • promotes better post-op recovery
  • done as patients are predisposed to infection, very thin skin, weak blood vessels

• Control of Cushing’s symptoms after radiotherapy
- given for control until beneficial effects of radiotherapy come about

18
Q

What is the normal dose of oral metyrapone the same as?

A
  • Dose according to cortisol production

* Aim for mean serum cholesterol of 150-300 nmol/L

19
Q

What are the negative (biochemical) aspects of metyrapone?

A

• Accumulation of 11-deoxycorticosterone and 11-deoxycortisol
• 11-deoxycorticosterone has mineralocorticoid properties (works like aldosterone)
- sodium retention
- potassium excretion
- hypertension
• When the drug blocks 2 limbs of the pathway, all the precursors funnel towards sex steroid synthesis
- increase in adrenal androgens
- hirsuitism and acne

20
Q

What are the negative side effects of metyrapone?

A
  • Nausea, vomiting, dizziness
  • Sedation
  • Hypoadrenalism - leads to impaired performance of skilled tasks
  • Hypertension on long-term administration
  • Hirsuitism
21
Q

What is ketoconazole used for?

A
  • Mainly used as anti-fungal agent - withdrawn due to hepatotoxicity
  • Inhibits cortisol production at higher concentrations - unlicensed use for operation preparation
  • Short-term use
22
Q

How does ketoconazole work?

A
  • Inhibits Cytochrome P450 SCC enzymes (cholesterol => pregnenolone)
  • Blocked production of glucocorticoids, mineralocorticoids and sex steroids
23
Q

What are the negative side effects of ketoconazole?

A
  • Nausea, vomiting, abdominal pain
  • Alopecia
  • Gynaecomastia, oligospermia, impotence, decreased libido
  • Ventricular tachycardias
  • Liver damage - patients monitored ever week as it can be fatal
24
Q

How can Cushing’s syndrome be treated (invasively)?

A
  • Pituitary surgery (transsphenoidal hypophysectomy)
  • Bilateral adrenalectomy - remove both adrenal glands, provide hormone replacement
  • Unilateral adrenalectomy for adrenal mass

(round of medical treatment until patient is safe for one of the above operations, depending on cause)

25
Q

What is the cause of Conn’s syndrome and what are the features?

A
  • Benign adrenocortical tumour
  • Excess aldosterone - retain sodium, lose potassium
  • Hypertension and hypokalaemia
26
Q

What 2 (3) things should you look out for when diagnosing Conn’s syndrome?

A

1) Primary hyperaldosteronism
• Tumour just making aldosterone
• Patient has high BP and blood test shows low potassium
2) Renin-angiotensin system should be suppressed
• If aldosterone is high, measure renin - suppressed by very high BP

• High BP, low potassium, low renin => Conn’s syndrome

27
Q

How can Conn’s syndrome be treated?

A

1) Mineralocorticoid receptor antagonists - spironolactone, epleronone
- prevents the produced aldosterone from working at the MR
2) Remove the tumour

Stay on (long-term) spironolactone if bilateral adrenal hyperplasia, as surgery will remove production of any cortisol or aldosterone

28
Q

Why is spironolactone used before surgery?

A
  • Bad to give general anaesthetic to someone with high BP

* Reduces BP for surgery preparation

29
Q

Describe the mechanism of action of spironolactone

A
  • Converted to several active metabolites including Canrenone (competitive antagonist of MR)
  • Blocks sodium channels too
  • Prevents Na+ reabsorption and K+ excretion in kidney tubules - potassium sparing diuretic
30
Q

What is Eplerenone and how does it compare to Spironolactone?

A
  • MR antagonist
  • Newer
  • As effective
  • Fewer side effects
  • More specific - interferes less with progesterone and androgen receptors
  • More expensive
31
Q

What happens in Phaeochromocytoma?

A
  • Tumours of the adrenal medulla
  • Produces more adrenaline
  • Rapid effect
  • With sudden releases of adrenaline from tumour => massive rise in blood pressure (can cause a sudden stroke)
  • Sudden onset panic, anxiety, tachycardia and severe hypertension (can last about 10 minutes)
  • Fatal if going into ventricular fibrillation
32
Q

What can cause a sudden release in phaeochromocytoma?

A
  • After abdominal palpation

* Trauma

33
Q

How is a phaeochromocytoma patient prepared before surgery and why?

A

• Preparation as:
- anaesthetic can cause tumour to suddenly release adrenaline
- hypertensive crisis
• First give drug to block adrenaline receptor - alpha blocker
- IV fluid as blockade commences due to drop in BP
• Then give beta blocker
- prevents tachycardia
• Therefore, if adrenaline is released, receptors are blocked so there is no effect

34
Q

Where are the majority of phaeochromocytomas found and how curable by operation are they?

A
  • inside the adrenal - 90%

* curable by operation - 90%

35
Q

How common is phaeochromocytoma?

A

Extremely rare

Endocrinology (17 decks)

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