Iatrogenic complications of Steroid therapy Flashcards

1
Q

What is the significance of HSD2’s position next to the mineralocorticoid receptor?

A

Cortisol will be converted to cortisone before activating the receptor

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2
Q

What is the pattern of cortisol secretion during the day?

A

3 peaks, one around each meal time

  • Morning
  • Noon
  • Evening

It’s at its lowest in the early hours of the morning

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3
Q

How do glucocorticoids contribute to osteoporosis?

A

Activate osteoclasts

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3
Q

Why isn’t the growth suppression effects of glucocorticoids too much to worry about?

A

Better the disease they’re preventing would do worse

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4
Q

What increases the half life of cortisol?

A

Continual conversion into cortisone and back

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5
Q

Where is cortisol converted to cortisone?

A

The kidney

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5
Q

Do exogenous glucocorticoids cause peptic ulcers?

A

Maybe - usually given with NSAID though

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7
Q

Where is cortisone converted to cortisol?

A

In the liver

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9
Q

Which enzyme catalyses cortisol to cortisone?

A

11beta-HSD2

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10
Q

How does cortisol deficiency present?

A

weakness,

fatigue,

anorexia,

nausea,

vomiting,

hypotension

hypoglycaemia

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10
Q

What is the dosing frequency for cortisol?

A

2-3 times a day

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11
Q

Which enzyme catalyses cortisone to cortisol?

A

11beta-HSD1

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12
Q

What are some strategies to avoid adrenal suppression with glucocorticoid treatment?

A

Allow for ACTH secretion if possible

  • dose at normal physiology peaks
  • Alternate day dosing etc

Avoid systemic absorption

Third gen glucocorticoids

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13
Q

What is the major complication of cortisol therapy?

A

Adrenal suppression due to increase negative feedback on ACTH production

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15
Q

What do you do to cortisol treatment during infection?

A

Increase the dose

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16
Q

How are systemic effects prevent in 3rd gen glucocorticoids?

A

Lipophilic - stays in tissue

Pro-drug - activated in lungs

Low oral bioavailability

Highly protein bound in plasma