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Endocrinology Y2 > Therapeutic use of Adrenal Steroids > Flashcards

Therapeutic use of Adrenal Steroids Flashcards

1
Q

What is produced in the zone glomerulosa

A

Aldosterone

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2
Q

What is produced in the zone fasciculata

A

cortisol

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3
Q

What is produced in the zone reticularis

A

Androgens/oestrogens

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4
Q

Androgens/oestrogens are produced in which layer of the adrenals?

A

Reticularis

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5
Q

cortisol is produced in which layer of the adrenals?

A

Fasciculata

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6
Q

Aldosterone is produced in which layer of the adrenals?

A

Glomerulosa

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7
Q

Order of adrenal layers out to in?

A

GFR (medulla)

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8
Q

what stimulates aldosterone secretion

A

ATII

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9
Q

What stimulates cortisol secretion

A

ACTH

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10
Q

What does cortisol inhibit and where

A

ACTH and the Aden-hypophysis and CRH at the hypothalamus

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11
Q

what stimulates ACTH release

A

CRH

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12
Q

Principle effects of aldosterone?

A

Promotes Na+ retention and K+ loss via the kidneys

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13
Q

What receptors does cortisol act on

A

Glucocorticoid

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14
Q

What receptors does aldosterone act on

A

mineralocorticoid

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15
Q

distribution of glucocorticoid receptors

A

Widely in body

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16
Q

affinity of glucocorticoid receptors for cortisol?

A
  • Selective for glucocorticoids

- Low affinity for cortisol

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17
Q

distribution of mineralocorticoid receptors

A
  • Discrete distribution (found only in the kidney)
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18
Q

Selectivity of mineralocorticoid receptors?

A
  • Do not have selectivity i.e. bind both aldosterone and cortisol
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19
Q

What do mineralocorticoid receptors bind

A

Cortisol and aldosterone

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20
Q

Affinity of mineralocorticoid receptors for cortisol?

A

High affinity for cortisol

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21
Q

What protects mineralocorticoid receptors from cortisol? what does it covert it to?

A

11beta-hydorsteroid dehydrogenase

converts to cortisone

22
Q

In Cushings, how does hypernatraemia and hypokalaemia occur

A

In Cushing’s, there’s too much cortisol for the 11beta-hydorsteroid dehydrogenase to deal with, so cortisol does bind to the MRs, leading to sodium retention and hypokalaemia

23
Q

RECEPTOR SELECTIVITY of

Hydrocortisone?

A

Glucocorticoid with mineralocorticoid activity at high doses

24
Q

RECEPTOR SELECTIVITY of

Prednisolone?

A

Glucocorticoid with weak mineralocorticoid activity

25
Q

RECEPTOR SELECTIVITY of

Dexamethasone?

A

Synthetic glucocorticoid with no mineralocorticoid activity

26
Q

RECEPTOR SELECTIVITY of

Fludrocortisone?

A

Aldosterone analogue

27
Q

Example of an Aldosterone analogue

A

Fludrocortisone

28
Q

Example of a Synthetic glucocorticoid with no mineralocorticoid activity

A

Dexamethasone

29
Q

Example of a Glucocorticoid with weak mineralocorticoid activity

A

Prednisolone

30
Q

Example of a Glucocorticoid with mineralocorticoid activity at high doses

A

Hydrocortisone

31
Q

RoA of corticosteroids?

A

oral and parenteral

32
Q

4 examples of corticosteroids?

A

Hydrocortisone, prednisolone, dexamethasone and fludrocortisone

33
Q

Longest acting corticosteroid?

A

Dexamethasone

34
Q

What disease is primary adrenocortical failure known as

A

ADDISON’S DISEASE

35
Q

What is Secondary adrenocortical failure

A

ACTH deficiency

36
Q

What is acute adrenocortical failure

A

ADDISONIAN CRISIS

37
Q

What is congenital adrenal hyperplasia

A

CONGENITAL LACK OF ENZYMES NEEDED FOR ADRENAL STEROID SYNTHESIS

38
Q

What is lacking in primary adrenocortical failure

A

lack cortisol and aldosterone

39
Q

What is lacking in secondary adrenocortical failure

A

ACTH deficiency so Patients lack cortisol but aldosterone is normal

40
Q

What is lacking in Congenital adrenal hyperplasia

A

CONGENITAL LACK OF ENZYMES NEEDED FOR ADRENAL STEROID SYNTHESIS and so lacking cortisol and aldosterone and sex steroids

41
Q

Treatment for Primary adrenocortical failure

A

: hydrocortisone (larger dose in morning, as this mimics normal physiology) and fludrocortisone (both orally)

42
Q

Treatment for secondary adrenocortical failure

A

hydrocortisone

43
Q

Treatment for acute adrenocortical failure

A

i.v. 0.9% sodium chloride (to rehydrate patient), high dose hydrocortisone (i.v. infusion or i.m.- every 6 hours Mineralocorticoid effect at high dose (11b-HSD overwhelmed)), 5% dextrose if hypoglycaemic

44
Q

If someone is on glucocorticoid medication, what times do you need to increase their dose during life

A

During the morning should take higher dose
in minor illness
and surgery

45
Q

What is Iatrogenic Adrenocortical Failure

A

in patients on long‐term, high dose corticosteroid treatment
If they are on glucocorticoids for a long time, this can suppress adrenal function because they don’t have to produce cortisol themselves anymore -­‐ they have a suppressed HPA axis
These patients also need to increase their dose when they experience a stress

46
Q

What patients experience Iatrogenic Adrenocortical Failure

A

in patients on long‐term, high dose corticosteroid treatment

47
Q

What does ACTH stimulate

A

Cortisol AND sex steroids

48
Q

What three things trigger aldosterone

A

Hyperkalaemia ‐ because aldosterone increases urinary potassium
excretion
Hyponatraemia
Drop in Renal Blood Flow - juxtaglomerular apparatus detects a drop in renal blood flow and releases renin

49
Q

What is synthetic cortisol known as

A

Hydrocortisone

50
Q

What protein binds glucocorticoids in blood

A

Corticosteroid binding globulin and albumin

51
Q

Difference in hormones of primary vs secondary adrenocortical failure

A

Aldosterone is normal in secondary as it is only ACTH that is deficient

52
Q

First step in an addisonian crisis?

A

You need to replace the lost salt, restore circulating volume and improve
the blood pressure before proceeding

Endocrinology Y2 (18 decks)

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