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LCRS Year 2 - Endocrinology > Therapeutic Use of Adrenal Steroids > Flashcards

Therapeutic Use of Adrenal Steroids Flashcards

1
Q

What is the process of adrenal steroid production?

A
  • Circadian stimulus + stress stimulates hypothalamus to produce CRH
  • CRH stimulates the anterior pituitary gland to produce ACTH
  • ACTH stimulates the adrenal gland to produce cortisol/other steroids
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2
Q

What are the 3 types of adrenal steroid produced and which adrenal gland regions are they produced in?

A
  • Cortisol (zona fasciculata)
  • Androgens, Oestrogens (zona reticularis)
  • Aldosterone/mineralocorticoids (zona glomerulosa)
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3
Q

What effect does cortisol have on the hypothalamus and anterior pituitary?

A

Negative feedback effect

- Inhibits CRH release (hypoth.) and ACTH release (ant. pit.)

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4
Q

What stimulates aldosterone release?

A
  • Angiotensinogen release released in the liver stimulates renin release in the kidneys. Angiotensin I release is stimulated and is converted to Angiotensin II by ACE. Angiotensin II has a positive effect on aldosterone release
  • Hyperkalaemia (ald. excretes K+)
  • Hyponatraemia (ald. retains Na+)
  • Reduced renal blood flow
  • B1-adrenoceptor stimulation
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5
Q

What are the principal physiological actions of the adrenal steroid steroids?

A

Cortisol - essential for life
Aldosterone - promotes Na+ retension and K+ excretion
Androgens/oestrogens - secondary sexual characteristics (less relevant here since the main producers of these are the gonads not the adrenals)

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6
Q

What are the two types of receptors for corticosteroids and what family of receptors are they members of?

A
  • Glucocorticoid receptors (GR)
  • Mineralocorticoid receptors (MR)

Part of the nuclear receptor super-family

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7
Q

What is the degree of distribution of GRs, what type of molecule are they selective for, and what is their affinity for cortisol?

A
  • Wide distribution
  • Selective for glucocorticoids
  • Low affinity for cortisol
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8
Q

What is the degree of distribution of MRs, what type of molecule are they selective for, and what is their affinity for cortisol?

A
  • Discrete distribution (kidney)
  • Do NOT distinguish between aldosterone and cortisol (non-selective for the two)
  • High affinity for cortisol
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9
Q

Which types, MR or GR, can cortisol and aldosterone bind to?

A

Cortisol - GR + MR

Aldosterone - MR only

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10
Q

What usually happens to prevent cortisol interfering too much with aldosterone binding to MRs and what happens when the body makes too much cortisol?

A

Cortisol inactivated by 11beta-hydroxysteroid dehydrogenase 2 (11betaHSD) so can’t bind to aldosterone receptors (MRs)

  • With excess cortisol, these enzymes are overwhelmed and cortisol binds to MRs
  • This is why you can regularly see hypokalaemia in Cushing’s syndrome due to overstimulation of MRs by the excess cortisol (excretion of K+, Na+ reabsorption)
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11
Q

What is the receptor selectivity of Hydrocortisone?

A

Glucocorticoid with mineralocorticoid activity at high doses(same overwhelming of 11betaHSD)

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12
Q

What is the receptor selectivity of Prednisolone?

A

Glucocorticoid with weak mineralocorticoid activity

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13
Q

What is the receptor selectivity of Dexamethasone?

A

Synthetic glucocorticoid with no mineralocorticoid activity

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14
Q

What is the receptor activity of Fludrocortisone?

A

Aldosterone analogue

- Used in long-term replacement therapy in cases of Addison’s disease

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15
Q

What is the administration route of corticosteroid drugs in long-term cases and which corticosteroid drugs are given this way?

A

Oral

  • Hydrocortisone
  • Prednisolone
  • Dexamethasone
  • Fludrocortisone
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16
Q

What is the administration route of corticosteroid drugs in acute cases (Addisonian Crisis) and which corticosteroid drugs are given this way?

A

Parenteral (IV or intramuscular)

  • Hydrocortisone
  • Dexamethasone
17
Q

Corticosteroid drugs distribute themselves in the body by what process in the circulation?

A

Binding to plasma proteins

  • Cortisol binding globulin (CBG)
  • Albumin

Only the free hormone which is active

18
Q

What are the durations of action of hydrocortisone, prednisolone, and dexamethasone?

A

Hydrocortisone - 8hrs
Prednisolone - 12hrs
Dexamethasone - 40hrs

Don’t need to remember specific hours just that they’re all different and it makes them useful in different clinical scenarios

19
Q

What is Addison’s disease and which hormones need replacing?

A

Primary adrenocortical failure

- Lack cortisol and aldosterone

20
Q

What drugs can be given to replace cortisol and aldosterone in cases of Addison’s disease?

A
  • Hydrocortisone to replace cortisol

- Fludrocortisone to replace aldosterone

21
Q

What is involved in secondary adrenocortical failure, what hormones are missing and what is different to Addison’s disease?

A

Secondary adrenocortical failure is failure of pituitary to produce ACTH

  • only cortisol needing replaced
  • different to Addison’s due to aldosterone being completely normal so only cortisol replacement required
22
Q

What drugs are given to replace the hormones missing in secondary adrenocortical failure?

A

Hydrocortisone - replacement for cortisol

No need for aldosterone replacement

23
Q

What is acute adrenocortical failure also known as?

A

Addisonian crisis

24
Q

How do you go about treating acute adrenocortical failure (Addisonian crisis)?

A
  • IV 0.9% NaCl to rehydrate patient (MOST IMPORTANT)
  • High dose hydrocortisone (IV/IM infusion every 6h), gives mineralocorticoid effect at high dose (11betaHSD overwhelmed)
  • 5% dextrose if hypoglycaemic
25
Q

What is congenital adrenal hyperplasia (CAH)?

A

Congenital lack of enzymes needed for adrenal steroid synthesis

26
Q

Which enzyme is deficient in the majority of CAH cases? (95%)

A

21-hydroxylase

27
Q

What happens to the other adrenal hormones in 21 hydroxylase deficiency?

A
  • Sex steroids go up due to accumulation of 17a-hydroxyprogesterone
  • ACTH rises with no negative feedback to stop it, high ACTH then drives further adrenal androgen production as well as the hyperplasia of the adrenal gland (growth)
28
Q

What are the 3 issues needing solved in congenital adrenal hyperplasia?

A
  • Not enough cortisol
  • Not enough aldosterone
  • Too much sex steroid
29
Q

What are the objectives of therapy in cases of CAH?

A
  • Replace cortisol (hydrocortisone)
  • Suppress ACTH and, thus, adrenal androgen production (sex steroid)
  • Replace aldosterone in salt-wasting forms
30
Q

What is the normal corticosteroid replacement therapy course?

A

Glucocorticoid dose (dexamethasone 1/day pm) OR (hydrocortisone 2-3/day pm high dose)

  • Try to reduce ACTH
  • Fludrocortisone
31
Q

How is corticosteroid replacement therapy monitored/optimised?

A

Measuring:

  • 17-OH progesterone (pre-cursor steroid that would usually accumulate, levels should fall after therapy)
  • Clinical assessment of patient
  • Patients can become Cushingoid - Glucocorticoid dose too high
  • Patients can become hirsute (hirsutism) - Glucocorticoid dose too low and ACTH has risen resulting in rise of testosterone production
32
Q

What are the normal and under-stress cortisol production rates?

A

Normal - 20mg/day

Under-stress - 200-300

33
Q

What is important to do if your Addison’s patient is vulnerable to stress/illness?

A

Increase glucocorticoid dosage
- if they get the flu etc then they have to mimic the normal rise of cortisol so when they get stressed/get ill then double their dose until they get better as that’s what the body would be doing normally in that situation

34
Q

When should glucocorticoid dosage be increased and to what degree?

A
  • In minor illness (2x normal dose)
  • Surgery - hydrocortisone IM with pre-med and at 6-8 hour intervals to ensure proper recovery. Can be oral admin once eating and drinking again
35
Q

What must you tell patients with adrenocortical failure and why is this?

A

Should carry a steroid alert card and wear a MedicAlert bracelet/necklace
- alerts paramedics etc to the fact that they MUST give this patient a large dose of hydrocortisone as they’re at risk of Addisonian crisis if they collapse because they can’t respond to stress properly

LCRS Year 2 - Endocrinology (21 decks)

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