25.7 Biochem: Iatrogenic complications of steroid therapy Flashcards Preview

Week 25: Endocrine > 25.7 Biochem: Iatrogenic complications of steroid therapy > Flashcards

Flashcards in 25.7 Biochem: Iatrogenic complications of steroid therapy Deck (20)
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1
Q

When do cortisol levels peak in normal diurnal variation?

A

8.30am or so

2
Q

Why do we see pigmentation/bronze glow in Addison’s disease?

A

Melanocortin secreted

3
Q

What are the signs/symptoms of Addison’s disease?

A

Fatigue, anorexia, nausea, vomiting, low blood pressure, hypoglycaemia

4
Q

What do we use to treat Addison’s patients?

A

Cortisol (20mg) or cortisone (25mg)

5
Q

What do we need to give Addison’s patients if there are signs of Aldosterone deficiency?

A

Fludrocortisone

6
Q

What are some side effects of glucocorticoid treatment? (2x supressions)

A

Immunosupression, adrenal supression

7
Q

What can occur if we overtreat aka have too much cortisol?

A

Weight gain, muscle/bone loss, salt retention

8
Q

How does too much cortisol get dealt with by the kidney and the liver?

A

Cortisol gets converted in kidney to cortisone (with 11-B HSD 1) which is inactive

The liver then converts cortisone back to cortisol

9
Q

Which has a longer half life, cortisone or cortisol?

A

Cortisol because it gets converted and reconverted

10
Q

Why can we use fludrocortisone to supplement lack of aldosterone?

A

Because its mineralocorticoid activity is 300x that of cortisione

11
Q

What does a ‘dissociated steroid’ refer to?

A

Better at either trans activation or trans repression

12
Q

What is a long term complication of steroid therapy? What can we do to minimise this?

A

Atrophy of adrenals

Allow for ACTH secretion (use short half life drugs, alternate day dosing and minimise systemic absorption)

13
Q

What is Ciclesonide?

Why is it better than previous drugs?

What is its bio availability like?

A

A 3rd generation pro-drug

Enzymes for degradation found in lungs (not mouth or larynx so no fungal infections)

Also has low oral bioavailability because is lipophilic and protein bound

14
Q

What is the role of glucocorticoids in development of peptic ulcers?

A

Debatable (chronic inflammatory disease may cause someone to prescribe an NASAID and a glucocorticoid resulting in a synergistic effect)

15
Q

What is some evidence that contradicts the connection between cortisol and peptic ulcers?

A

In rats cortisol is protective against stress ulcers

16
Q

What is the relationship between glucocorticoids and osteoporosis?

A

Yes glucocorticoids cause osteoporosis in high doses

17
Q

How can dexamethisone cause osteoporosis?

A

Increase RANKL, decrease OPG (enhances reabsorption, decreases bone mass)

18
Q

What can inhaled corticosteroids do in premenopausal women?

A

12 puffs a day for 20 years, doubles the risk of hip fracture

19
Q

What can happen in children given asthma medication?

A

Budesonide can cause a loss of 1.1cm in stature

but shoudn’t be a contraindication

20
Q

RANKL and OPG, how do they alter osteoclast signalling?

A

RANKL: promotes bone reabsorption
OPG: inhibits bone reabsorption

(bone reabsorption is bad)