Adrenal Disorders Flashcards

1
Q

What does the adrenal cortex produce?

A

Corticosteroids

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2
Q

What three zones can the adrenal cortex be divided into.

A

-Glomerulosa
-Fasciculata
-Reticularis

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3
Q

Summarize aldosterone’s action.

A

Regulates blood pressure, sodium and lowers potassium.

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4
Q

What enzymes do Angiotensin II activate (through side chain cleavage)

A

-3 Hydroxysteroid dehydrogenase
-21 hydroxylase
-11 hydroxylase
-18 hydroxylase

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5
Q

What enzymes do ACTH activate (through side chain cleavage).

A

-3 Hydroxysteroid dehydrogenase
-17 hydroxylase
-21 hydroxylase
-11 hydroxylase

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6
Q

What kind of adrenal failure is Addison’s disease?

A

Primary.

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7
Q

How does Addison’s disease develop?

A

Autoimmune disease where the immune system decides to destroy the adrenal glands.

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8
Q

What is the most common cause of addisons disease? (World wide)

A

Tuberculosis of the adrenal glands.

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9
Q

Why do patients with Addison’s disease have low blood pressure.

A

No cortisol or aldosterone being produced

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10
Q

Why do patients with Addison’s have a good tan.

A

Adrenal gland hormones are low so the pituitary secretes lots of ACTH, ACTH is made from a large precursor protein called Pro opiomelanocortin (POMC). This needs to be cleaved into ACTH and Melanin.

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11
Q

List 4 consequences of adrenocortical failure.

A

-Fall in blood pressure
-Loss of salt in the urine
-Increased plasma potassium
-Fall in glucose due to
glucocorticoid deficiency

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12
Q

Why would adrenocortical failure lead to a fall in blood pressure.

A

Impaired cortisol/aldosterone production.

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13
Q

Why would adrenocortical failure lead to loss of sodium in urine and increased plasma pottasium.

A

Impaired aldosterone production, aldosterone is responsible for water and sodium reabsorption and potassium excretion in the kidneys.

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14
Q

Why would you have a fall in blood glucose in an adrenocortical failure.

A

Glucocorticoid insufficiency.

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15
Q

Describe the tests that can be done to diagnose Addison’s disease.

A

Measure 9am cortisol and tests for ACTH.

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16
Q

What will the test results for 9am cortisol & ACTH be for someone with Addison’s disease.

A

9am cortisol= Low
ACTH= High

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17
Q

Which 3 drugs are given for the treatment of adrenal failure?

A

-HYDROCORTISONE three time daily (10+5+2.5mg)
-PREDNISOLONE 3mg daily
-Fludrocortisone 50 to 100 mcg daily

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18
Q

What is the most common cause of congenital Adrenal Hyperplasia?

A

21-hydroxylase deficiency.

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19
Q

Which hormones will be deficient in someone with 21-hydroxylase deficiency?

A

Aldosterone and cortisol

20
Q

How long can you survive with complete 21 hydroxylase deficiency?

A

Less than 24 hours.

21
Q

Which hormones will be in excess in someone with complete 21 hydroxylase deficiency.

A

Sex steroids and testosterone

22
Q

What is hirsutism?

A

Excessive hair growth

23
Q

What is virilisation?

A

The development of adult male characteristics in young males or females.

24
Q

What is the main problems that can present in someone with partial 21 Hydroxylase deficiency?

A

Hirsutism and Virilisation

25
Q

What hormone does 11 deoxycorticosterone behave like.

A

Aldosterone

26
Q

What would cause 11 deoxycorticosterone to build up?

A

11 hydroxylase deficiency

27
Q

In excess what can 11 deoxycorticosterone cause

A

-Hypertension
-Hypokalaemia

28
Q

What is the difference between cushing’s disease and syndrome?

A
  • Cushing’s syndrome is excess cortisol in body
  • Cushing’s disease is a type of Cushing’s syndrome where there’s a pituitary tumour causing excess cortisol
29
Q

What are the causes of Cushing’s syndrome? (4)

A
  • Taking too many steroids
  • Adrenal adenoma secreting cortisol
  • Pituitary dependent Cushing’s disease (most common)
  • Ectopic ACTH from lung cancer (lung cancer cells that randomly excess ACTH)- ectopic means in the wrong place
30
Q

How does the dexamethasone test work?

A
  • It’s a very potent artificial steroid
  • we give 0.5mg every 6 hours for 48 hours
  • Normal patients’ pituitary will respond via negative feedback (thinks its cortisol) and decrease cortisol production to 0
  • Any cause of Cushing’s will fail to suppress the cortisol production
31
Q

What types of drugs do we use to deal with the high cortisol?

A
  • Enzyme inhibitors
  • Receptor blocking drugs
32
Q

What specific drugs are used to treat Cushing’s?

A

Inhibitors of steroid biosynthesis:
-Metyrapone
-Ketoconazole

33
Q

How does metyrapone work?

A

-Inhibition of 11 beta-hydroxylase
-Steroid synthesis in zona fasciculata (and reticularis) is arrested at the 11- deoxycortisol stage.

34
Q

Does 11-deoxycortisol have any negative feedback?

A

No

35
Q

What effects does aldosterone have?

A

It controls blood pressure by controlling sodium and lowering potassium

36
Q

What is Conn’s Syndrome?

A
  • Benign adrenal cortical tumour (zona glomerulosa)
  • Aldosterone in excess (aldosterone controls bp, Na and lowers K remember)
  • Hypertension and hypokalaemia
37
Q

What kind of drugs are used to treat Conn’s syndrome?

A

Mineralocorticoid receptor (MR) antagonists.

38
Q

What are MR antagonists?

A

Mineralocorticoid receptor (MR) antagonists are considered to be potassium-sparing diuretics that exert their effect by blocking MR in the kidney.

39
Q

What are two examples of MR antagonists?

A

-spironolactone
-eplerenone

40
Q

What is a phaeochromocytoma?

A

These are tumours of the adrenal medulla which secrete catecholamines (adrenaline and noradrenaline)

41
Q

What are the clinical features of phaeochromocytomas?

A

-Hypertension in young people
-Episodic severe hypertension

42
Q

What can the high adrenaline in Phaeo lead to?

A

Ventricular fibrillation + death

43
Q

How is phaeochromocytoma managed?
(1st to last step)

A

-Alpha blockade first
-Patients may need IV fluid as alpha blockade commences
-Beta blockade added to prevent tachycardia

44
Q

What do we need to take care with when preparing to operate on someone with phaeochromocytoma?

A

Patient needs careful preparation as anaesthetic can worsen a hypertensive crisis.

45
Q

What are two MR antagonists?

A

Spironolactone & epleronone