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LCRS - endo > Therapeutic use of adrenal steroids. > Flashcards

Therapeutic use of adrenal steroids. Flashcards

1
Q

What is the primary stimulator of cortisol and androgen/oestrogen release from the adrenals?

A

ACTH

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2
Q

What stimulates aldosterone release from the adrenals?

A

Angtiotensin II.

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3
Q

What parts of the adrenals are cortisol, sex steroids and aldosterone released from?

A

Cortisol - zona fasciculata.

Sex steroids - zona reticularis.

Aldosterone - zona glomerulosa

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4
Q

Draw a diagram to show feedback loop for cortisol, stimulation of cortisol secretion and stimulation of aldosterone secretion

A
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5
Q

What enzyme family is responsible for steroid hormone synthesis?

A

Cytochrome p450c family.

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6
Q

What are the primary actions of cortisol and aldosterone?

A

Aldosterone - salt balance - promote Na+ retention, K+ loss, water retention, indirect effect on BP.

Cortisol - memory, blood glucose control, inflammation mediator, metabolism regulator.

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7
Q

What are the two types of corticosteroid receptors, what binds to them?

A

Glucocorticoid Receptors (GR) - cortisol

Mineralocorticoid receptors (MR) - aldosterone.

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8
Q

Compare the distribution of GRs and MRs.

A

GR - wide distribution, MR - in kidneys.

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9
Q

Compare the selectivity of GRs and MRs.

A

GRs - selective for glucocorticoids, MRs - do not distinguish between aldosterone and cortisol.

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10
Q

Compare the affinity of MRs and GRs for cortisol.

A

MRs - high affinity, GRs - low affinity.

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11
Q

Considering cortisols high affinity for MRs, why doesn’t it have the same effects as aldosterone?

A

Enzyme 11 beta-hydroxysteroid dehydrogenase 2 (11 beta HSD).

Catalyses cortisol –> inactive cortisone.

11 beta HSD found in kidneys - protects MR receptor from cortisol at site of aldosterone action

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12
Q

Why is hypokalaemia a symptom of Cushing’s?

A

Cushing’s = high cortisol.

Excess cortisol leaves 11 beta HSD unable to inactivate all of it, so some persists and binds to MR receptor with aldosterone like effects.

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13
Q

What is hydrocortisone used for?

A

Glucocorticoid - cortisol receptor. High doses give aldosterone like effects.

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14
Q

What is prednisolone used for?

Glucocorticoid - cortisol replacement.

A

Asthma, rheumatoid arthritis and other inflammatory diseases.

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15
Q

What is dexamethasone used for?

A

Glucocorticoid - cortisol replacement.

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16
Q

How do hydrocortisone, prednisolone and dexmethasone differ?

A

Hydrocortisone - mineralocorticoid activity at high doses.

Prednisolone - weak mineralocorticoid activity.

Dexamethasone - no mineralocorticoid activity.

17
Q

What is fludrocortisone used for?

A

Aldosterone replacement.

18
Q

How might corticosteroids be administered?

A

Oral - hydrocortisone, prednisolone, dexamathasone, fludrocortisone.

Parenteral (iv or im) - hydrocortisone, dexamethasone.

19
Q

Compare the durations of hydrocortisone, prednisolone and dexamathasone in the blood.

A

–Hydrocortisone – duration ~ 8h

–Prednisolone – duration ~ 12h

–Dexamethasone – duration ~ 40h

20
Q

How are corticosteroid drugs distributed through the body?

A

In the blood bound to plasma proteins - cortisol binding globuline and albumin.

21
Q

Why might corticosteroid replacement therapy be used to treat a patient with Addison’s disease and how?

A

Addison’s disease - loss of functional adrenal gland –> cortisol, aldosterone deficiency.

Oral hydrocortisone and fludrocortisone.

22
Q

Why is a large dose of iv hydrocortisone given in acute conditions?

A

It overwhelms 11 beta HSD allowing MR binding and aldosterone like effects, helping Na reabsorption.

23
Q

How can corticosteroid replacement therapy be used to treat secondary adrenocortical failure (ACTH deficiency)?

A

Administration of oral hydrocortisone (aldosterone is normal).

RAAS system functional.

24
Q

How is an Addisonian crisis treated?

A

iv 0.9% sodium chloride to rehydrate patient

High dose hydrocortisone

–i.v. infusion or i.m. every 6h, mineralocorticoid effect at high dose (11bHSD overwhelmed)

l5% dextrose if hypoglycaemic

25
Q

Define congenital adrenal hyperplasia (CAH).

A

congenital lack of enzymes
needed for adrenal steroid synthesis

26
Q

what enzyme converts testosterone to oestrogen/17 beta oestrodial?

A

aromatase.

27
Q

In CAH, which enzyme is most commonly lacking?

A

21 hydroxylase - 95% of cases.

28
Q

How might CAH with 21 hydroxylase deficiency be diagnosed?

A

17 alpha-hydroxyprogesterone build up which can be measured.

29
Q

Why can hirsutism and virilisation result from 21 hydroxylase deficiency?

A

cortisol not being produced, so ACTH rises which stimulates adrenal androgen production.

30
Q

What are the objectives of corticosteroid replacement therapy in patients with CAH?

A

Replace cortisol,

suppress ACTH in order to suppress adrenal androgen secretion.

Replace aldosterone.

31
Q

How is CAH treated?

A

Dexamethasone 1/day in the evening (when cortisol should be low)

Or hydrocortisone 2-3/day, evening.

Aim to suppress androgen production.

Also fludrocortisone to replace aldosterone.

32
Q

How can effectiveness of CAH therapy be monitored and optimised?

A

Regularly measure 17 OH progesterone - adjust dose of glucocorticoid accordingly if not within desired range/patient isn’ happy.

33
Q

What difficulties can arise when administering large doses of glucocorticoid to suppress ACTH?

A

Androgen production decreases but excess cortisol can cause Cushing’s.

34
Q

Why else can glucocorticoid management be difficult in corticosteroid replacement therapy? How is this handled?

A

cortisol = stress hormones -

normally approx. 20mg/day

in stress approx. 200-300mg/day (e.g. illness).

Patient only receiving fixed dose of cortisol, so no additional response to stress.

In minor illness - give 2x normal dose.

35
Q

What is given to Addison’s patients during surgery?

A

I.m hydrocortisone before and at 6-8 hours intervals until recovery.

36
Q

What should patients with Addison’s wear and carry at all times?

A

Steroid alert card, MedicAlert bracelet.

37
Q
A

LCRS - endo (12 decks)

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