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BRS YEAR 2 > Endo - Adrenal Disorders 1 > Flashcards

Endo - Adrenal Disorders 1 Flashcards

1
Q

What are steroids derived from?

A

Cholesterol

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2
Q

What does the adrenal cortex produce?

A

Corticosteroids

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3
Q

What does the zone glomerulosa produce?

A

Mineralocorticoids

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4
Q

What does the zona fasciculata produce?

A

Glucocorticoids

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5
Q

What does the zona reticularis produce?

A

Sex steroids

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6
Q

What does angiotensin 2 activate?

A 
Side chain cleavage
3-Hydroxysteroid dehydrogenase
21 hydroxylase
11 hydroxylase
18 hydroxylase
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7
Q

What does angiotensin 2 cause?

A

Aldosterone production

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8
Q

How does aldosterone act?

A

Increases Na reabsorption and K excretion therefore controls blood pressure

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9
Q

What does ACTH activate?

A 
Side chain cleavage
3 hydroxysteroid dehydrogenase
17 hydroxylase
21 hydroxylase
11 hydroxylase
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10
Q

What does ACTH cause?

A

Cortisol production

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11
Q

Describe the pattern of cortisol secretion?

A

Diurnal - peaks at around 8:30 in the morning and is lowest around midnight/1am

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12
Q

Describe the pathway from cholesterol to aldosterone

A 
Cholsterol
Progesterone
11-deoxycorticosterone
corticosterone
aldosterone
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13
Q

Describe the pathway of cholesterol to cortisol

A 
Cholesterol 
Progesterone
17- hydoxyprogesterone
11-deoxycortisol
cortisol
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14
Q

Describe the pathway of cholesterol to oestrogen

A 
Cholesterol
Progesterone
17-hydroxyprogesterone
Sex steroids
Androgens
Oestrogen
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15
Q

What is Addison’s disease?

A

Primary adrenal failure

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16
Q

What is the commonest cause of Addison’s in the UK?

A

Autoimmune

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17
Q

What is the commonest cause of Addison’s worldwide?

A

TB bacteria destroying the adrenal gland

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18
Q

Why does Addison’s cause tanning?

A

We get an increase in ACTH due to negative feedback which is a product of POMC breakdown, along with MSH to increase pigmentation

19
Q

What does POMC break down into?

A

MSH, ACTH, endorphins, enkephalins, other peptides

20
Q

Where is POMC synthesised?

A

In the pituitary

21
Q

What are the signs of Addison’s?

A 
Skin pigmentation
Autoimmune vitiligo 
Darkening of hair
Loss of weight 
Muscular weakness
Hypotension
22
Q

What are the 3 main causes of adrenocortical failure?

A

TB Addisons
Autoimmune Addisons
Congenital adrenal hyperplasia

23
Q

What are the consequences of adrenocortical failure?

A 
Hypotnesion
Loss of salt in urine (hyponatremia)
Hyperkalemia
Hypoglycaemia (glucocorticoid deficiency)
Tanning
Eventual death due to severe hypotension
24
Q

What is the normal range for cortisol?

A

270-290nM

25
Q

How do we test for Addison’s

A

Low 9am cortisol
High ACTH
No response after injecting 250µg synACTHen

26
Q

Why do we not give aldosterone for treatment of adrenal failure?

A

Half life too short for daily administration

27
Q

What do we use to treat adrenal failure?

A

Fludrocortisone 50-100mcg/daily

28
Q

Why do we use fludrocortisone?

A

Fluorine doesn’t occur naturally in steroids therefore slows down metabolism and has much longer lasting effects (18h)

29
Q

Why do we not give oral hydrocortisone?

A

It ca be given but has too short a half life to be given once daily and can be harmful if given in too high a frequency therefore we opt for alternatives in replacing cortisol

30
Q

What is another name for 1,2-dehydrocortisone?

A

Prednisolone

31
Q

What dose of prednisolone can we give?

A

1mg, 2,5mg, 5mg once daily

32
Q

Why is prednisolone absorption slowed?

A

Not enteric coated

33
Q

Instead of prednisolone, what can we give alongside fludrocortisone?

A

We can give hydrocortisone 3 times daily (10, 5, 2.5 mg) to replicate the diurnal pattern of cortisol

34
Q

What is congenital adrenal hyperplasia?

A

Missing enzyme

35
Q

What is the most common enzyme missing?

A

21-hydroxylase

36
Q

What do we have in complete 21-h deficiency?

A

Cortisol and aldosterone deficient

Excess sex steroids (mainly testosterone)

37
Q

What is the survival rate for complete 21-h deficiency

A

Less than 24 hours unless given IV saline - as a neonate you are no longer dependent on placenta therefore have an Addisonian salt losing crisis

38
Q

What may we see in girls with complete 21-h deficiency?

A

Ambiguous genitalia (virilisation), prompting us to give hydrocortisone - we don’t notice in boys

39
Q

What do we have in partial 21-h deficiency?

A

Still deficient in cortisol and aldosterone but there is enough to get by
Still excess sex steroids and testosterone

40
Q

What is the presentation like in partial 21-h deficiency?

A

Presentation is much later, with hirsutism in girls and precocious puberty in boys

41
Q

What do we see in 11-h deficiency?

A

We should lose aldosterone and cortisol but 11-deoxycorticosteorne behaves just like aldosterone:
No cortisol or aldosterone
Excess 11-deoxycorticosterone, sex steroids and testosterone

42
Q

What is the presentation of 11-h deficiency?

A

Virilisation, hypertension and hypokalaemia

43
Q

What do we see in 17-h deficiency?

A

Deificient in cortisol and sex steroids

Excess 11-deoxycorticosterone and aldosterone

44
Q

What is the presentation of 17-h deficiency?

A 
Hypertension
Hypokalemia 
Sex steroid deficiency 
No puberty (you look like a child)
Glucocorticoid deficiency (low glucose)

BRS YEAR 2 (37 decks)

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