therapeutic steroid use Flashcards
What is the function of 11 beta HSD
inactivates 11-hydroxy steroids in the kidney, thus protecting the nonselective mineralocorticoid receptor (MR) from occupation by glucocorticoids.
what are the therapeutic effects of glucocorticoids
- anti-inflammatory
- anti-allergy
- immunosupression
- replacement (if not producting steroids by self)
- shock (in massive one off doses)
- CNS swelling
- metabolic (ketosis)
- reproductive
- anti-neoplastic
what is the half life of cortisol
60 minutes
how can we increase potency of a steroid (pharmacologically)
- C1-2 double bonds
- methylation
- fluorination
why cant we give prednisone to certain species
in order to have desired effect it must be converted by 11 beta HSD to prednisolone. horses and cats cannot do this as well as other species
pharmacologically, how can you increase the half life of a steroid
- esterification
- prolongation of half life depends on the solubility of esther
what are the adverse effects of glucocorticoids in animals
- Pu/PD
- hunger
- liver enzyme induction
- infections
- sespsis
- failed wound healing
- GI hemorrhage
- iatrogenic hyperadrenocorticism
- diabetes mellitus
- if withdrawn suddenly, temporarily cant make ACTH and cant cope with stress
what happens with long term glucocorticoid therapy
adrenocortical atrophy
what is iatrogenic hyperadrenocoricism and justify why this is a confusing name
when there is adrencortical atrophy due to exogenous glucocorticoids it is called iatrogenic hyperadrenocorticism because the clinical presentation will be due to chronic glucocorticoid excess
but PHYSIOLOGICALLY from and endogenous production point of view there is HYPOADRENOCORTICISM and if we stop exogenous steroid suddenly we can get glucocorticoid withdrawal syndrome
what happens to glucocorticoids and mineralcorticoids when we take steroid therapy away
- glucocorticoids fail
- mineralcorticoids do nothing
what are clincial signs of corticosteroid withdrawal syndrome
- depression
- anorexia
- vomiting
- vague illness
- abdominal discomfort
- similar to primary hypoadrenocorticism but will have normal Na/K
- if in a stressful situation: collapse, vascular collapse, GI hemorrhage, shock +/- death
how do you mitigate the risk of GWS
- minimum doses for clinical effect
- least potent steroid for needs
- short acting so can control
- intermittent dosing (alternate days)
- tapered therapy
depo injections taper themselves
what is the challenge with immunoassays and prednisolone use
prednisolone and cortisol are structurally similar enough that the machine will pick up prednisolone in the serum and mistake it for cortisol, thus giving falsely high cortsiol levels
dexamethason will not because it is different enough
how can we tell if the signs of HAC are due to an exogenous steroid
- ACTH stim is only useful test for detecting iatrogenic hyperadrenocorticism
