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Year2 Endo > Adrenal gland > Flashcards

Adrenal gland Flashcards

1
Q

how many carbons are in cholesterol and describe the structure

A

26

see google docs

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2
Q

What does the adrenal cortex secrete

A

Corticosteriods

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3
Q

Name 3 types of corticosteroids

A 
Mineralocorticoids ( aldosterone) 
Glucocorticoids ( cortisol) 
Sex steroids( androgens, oestrogens)
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4
Q

what is a steroid

A

Hormone that is made from cholestrol

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5
Q

What is the precursor material for steroid hormones

A

Cholesterol

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6
Q

what is the effect of angiotensin II on the adrenals

A 
Activation of : 
1) 3 Hydroxysteroid dehydrogenase 
2) 21hydroxylase
3) 11 hydroxylase 
4) 18 hydroxylase 
by side chain cleavage
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7
Q

what is the precursor molecules for aldosterone

A

cholesterol

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8
Q

What does aldosterone do

A

Control blood pressure , sodium and lowers potassium

retains water and sodium in kidney and increase K excretion

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9
Q

what is the effect of ACTH on the adrenals

A

Activation of following enzymes by side chain cleavage:

1) 3 hydroxysteroid dehydrogenase
2) 21 hydroxylase
3) 11 hydroxylase
4) 17 hydroxylase

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10
Q

How does cholesterol turn to aldosterone

A

Cholesterol –> progesterone –> 21 hydroxylase ( enzyme) –> 11-deoxycorticosterone
–> 11 hydroxylase ( enzyme) –> corticosterone –> 18hyroxylase ( enzyme) –> aldosterone

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11
Q

How does cholesterol turn into cortisol

A 
1)
Cholestenone
2) Progesterone
( 17 hydroxylase) 
3)  17-OH progesterone
21 hydroxylase
4) 11-deoxycortisol 
11 hydroxylase
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12
Q

How does cholesterol turn into sex steroids

A

1) cholesterol
2) progesterone
17 hydroxylase
3) Sex steroids
4) Androgens
5) Oestrogens

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13
Q

How does cortisol fluctuate throughout the day

A

Diurnal rhythm

Highest after waking and lowest at night

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14
Q

What is 1ary adrenal failure and what is the common cause?

A

disease that destroys the adrenal cortex

causes:
1) autoimmune ( common in uk) ( antibodies attack adrenal cortex)
2) TB of adrenal glands ( worldwide)
3) Congenital adrenal hyperplasia

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15
Q

Symptoms of adrenocortical failure ( ie Addison’s)

A

Fall in blood pressure
Loss of salt in the urine
Increased plasma potassium
( first 3 due to lack of cortisol)
Fall in glucose due to glucocorticoid deficiency
High ACTH resulting in pigmentation
High ACTH due to loss of negative feedback by cortisol on the pituitary.
POMC → ACTH + MSH (leading to hyperpigmentation).
Also breaks down into endorphins, enkephalins and other peptides.
Vitiligo
Muscular weakness
Eventual death due to severe hypotension : Addisonian crisis

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16
Q

Why do you get hyperpigmentation / tanned in Addison’s disease

A

Loss of negative feedback of cortisol to pituitary –> lead to high levels of ACTH

to make ATCH
POMC –> ACTH + MSH ( MSH leads to hyperpigmentation)

Note : could also be due to autoimmune vitiligo ( which may coexist)

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17
Q

Why do pateints with Addison’s have low bp?

A

No cortisol / aldosterone so bp low

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18
Q

Causes of adrenocortical failure

A

Adrenal glands destroyed

or enzymes in steroid synthetic pathway not working ( common)

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19
Q

What tests do you do for Addions

A

1) 9 am cortisol ( low in Addison’s)
2) look out for ACTH ( high in Addison’s)
3) Short synACTHen test where you give 250ug of synACTHen IM ( intramuscular) to measure cortisol response if after a while cortisol levels don’t increase = Addison’s

20
Q

What does a typical Addison’s pateints results

A

A typical Addison’s patient:
cortisol at 9am of 100 (normal range = 270-900)
cortisol of 150 after administration of synacthen measured at 9:30am (normal range = >600)

21
Q

What are treatment of Adrenal failure

A

1) Fludrocortisone ( 50 - 100mg daily)
2) 1-2 dehydro - hydrocortisone aka prednisolone ( 4-4mg once daily)
3) Oral hydrocortisone ( 3x daily would prefer prednisolone instead)

22
Q

Why use fludrocortisone not aldosterone

A

Fludrocortisone is aldosterone with a H replaced by a F.

Normal half life of aldosterone is too short for safe once daily administration. As fluorine does not exist in natural steroid its presence reduces metabolism. It binds both to Mineralocorticoid receptor and Glucocorticoid receptors and has a half life of 3.5 h and effects can be seen for 18h

23
Q

Why cant use used oral hydrocortisone as a treatment of adrenal failure

A

too short half life for once daily administration .

If taken more more than OD it creates peaks and troughs which are v harmful

24
Q

why use prednisolone instead of oral hydrocortisone

A

Prednisolone has longer half life + is more potent (higher binding affinity)

25
Q

What doses of prednisolone are available

A

1mg ]2.5 mg

5mg

26
Q

What does it mean if prednisolone is not enteric coated

A

it slows absorption of the drug

27
Q

What 3 enzymes can be effected and which one is the commonest cause of congenital adrenal hyperplasia

A

21 hydroxylase deficiency

others are
11 hydroxylase deficiency
17 hydroxylase deficiency

28
Q

What are the 2 types of congenital adrenal hyperplasia

A

complete ( gene for emzyme missing) or partial ( mutation in enzyme)

29
Q

What hormones will be missing in congenital adrenal hyperplasia : 21 deficiency ( both partial and full)

A

Aldosterone and cortisol

without these you will survive less than 24h

30
Q

What hormones will be in excess in congenital adrenal hyperplasia : 21 deficiency ( both partial and full)

A

sex steroids and testosterone

31
Q

When does congenital adrenal hyperplasia present

A

As a neonate ( typically with a salt losing Addisonian crisis)
girls may have ambiguous genitalized (virilised by adrenal testo)

(before birth in utero foetus gets steroids across placenta )

32
Q

How do foetus get steroids while in utero

A

across the placenta

33
Q

Why does complete congital hyperplasia affect girls?

A

girls may have ambiguous genitalized (virilised by adrenal testo)

Boys will not be noticed as not normal

34
Q

what age does congenital adrenal hyperplasia : 21 deficiency present ( both partial and full)

A

Any age as they survive

35
Q

what is the difference between partial 21 hydroxylase deficiency and full deficiency

A

in partial 21 hydroxylase there will be a bit of aldosterone and cortisol to get by with

36
Q

What are symptoms of partial 21 hydroxylase deficiency

A

Main problem in later life is hirsutism and virilisation in girls and precocious puberty in boys due to adrenal testosterone

37
Q

What hormones will be missing in congenital adrenal hyperplasia : 11 deficiency ( both partial and full)

A

cortisol and aldosterone

38
Q

What hormones will be in excess in congenital adrenal hyperplasia : 11 deficiency ( both partial and full)

A

Sex steroids and testosterone and 11- deoxycorticosterone ( as prog turned to 11 deoxycorticosterone due to presence of 21 hydroxylase but 11CC can’t get converted further to aldosterone and cortisol)

39
Q

What are some symptoms of 11 hydroxylase deficiency

A

Virilisation, hypertension and low K

40
Q

What does 11 deoxycorticosterone do

A

Behaves live aldosterone

in excess can cause hypertension and hypokalaemia

41
Q

What hormones will be missing in congenital adrenal hyperplasia : 17 deficiency ( both partial and full)

A

Cortisol and sex steroids

42
Q

What hormones will be in excess in congenital adrenal hyperplasia : 17 deficiency ( both partial and full)

A

11-deoxycorticosterone and aldosterone ( mineralocorticoids)

43
Q

What are some symptoms of 17 hydroxylase deficiency

A

Hypertension, low K, sex steroid deficiency and glucocorticoid deficiency (low glucose).

44
Q

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Year2 Endo (13 decks)

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