Steroids Flashcards
1
Q
Low potency Glucocorticoids
A
- Hydrocortisone
- DOA is 8-12 hours
- equal glucocorticoid & mineralocorticoid effect
- replacement for adrenal insufficiency
- closely mimic normal circadian rhythm
2
Q
Medium Potency Glucocorticoids
A
- Prednisone
- Prednisolone
- Methlyperednisolone
- Triamcinolone
- DOA 12-36 hours
- used in CA, inflammation, allergy, and autoimmune disorders
3
Q
High Potency Glucocorticoids
A
- Betamethasone
- Dexamethasone
- Budesonide
- DOA is 24-72 hours
- useful in skin disorders (psoriasis, dermatitis), neoplastic disorders, Crohn’s disease
4
Q
Mineralocorticoids Drugs
A
Fludrocortisone (Florinef)
5
Q
Glucorticoids Drugs
A
- cortisone and hydrocortisone
- Dexamethasone (Decadron)
- Betamethasone (Diprolene)
- Budesonide (Rhinocort)
- Triamcinolone
- Prednisone (Prednisone Intensol)
- Predisolone (Prelone)
- Methlypredisolone (Medrol)
- Desoximetasone (Topicort)
- Desonide (Tridesilon)
- Fluticasone (Flonase)
- Ciclesonide (Omnaris)
- Clobetasol (Clobevate)
6
Q
Adrenal Androgens Drugs
A
Dehydropiandrosterone (DHEA)
7
Q
Synthesis of Adrenal Steroids
A
- Adrenal Cortex has 3 layers that produce steroid hormones
- outer layer produce mineralocorticoids - aldosterone
- middle layer produce glucocorticoids -cortisol
- inner layer produce adrenal androgens - DHEA
8
Q
Mineralocorticoids synthesis and MOA
A
- Synthesis of Aldosterone: adrenal cortex is stimulated by angiotensim II to release aldosterone - effected by K+ levels and ACTH
- MOA: Aldosterone binds to mineralocorticoid receptor to affect gene transcription
- Fludrocortisone is replacement drug for pt with Addison’s disease - don’t replace aldosterone due to electrolyte disturbances
9
Q
Aldosterone acts on
A
- most important: stimulates the reabsorption of Na+ and associated passive reabsorption of water in tubule of kidney
- sweat and salivary glands
- mucosal cells in intestine
10
Q
High levels of Aldosterone causes
A
- fibrosis in heart and blood vessels
- vascular remodeling
- development of CHF
11
Q
Glucocorticoids MOA
A
- Steroid crosses cell membrane and binds to intracellular glucocorticoid receptor
- leads to change in gene transcription (reduction of synthesis of inflammatory cytokines, upregulation of synthesis of annexin A1)
- play important role in anti-inflammatory and immunomodulatory effects
- response can take hours to days
12
Q
Metabolic effects of Glucocorticoids
A
- cortisol is released by adrenal cortex in circadian diurnal pattern
- Release is greatly increased by stress
- also effects carbo, protein, and lipid metabolism, decrease bone formation, anti-inflammatory, immunosuppressive
13
Q
Carbohydrate and Protein Metabolism of Glucocorticoids
A
- Increase gluconeogenesis (glucose formation)
- Reduce glucose uptake and utilization by peripheral tissues
- Increase protein breakdown (catabolic effects)
- activate lipolysis (provides fatty acids for gluconeogenesis)
- Outcomes: decrease muscle mass, thinning of skin, hyperglycemia (worse for DM)
14
Q
Glucocorticoids impact on bone
A
-decrease calcium absorption
-increase calcium excretion
-antagonist to Vitamin D - no Ca+ absorption
-inhibit osteoblast activity
-osteroporosis
stunts growth
15
Q
Lipid Metabolism of Glucocorticoids
A
- long term elevation of glucocorticoids
- cause fat redistribution
- outcomes: increase fat in back of neck (buffalo hump), increase facial fat (moon face), loss of fat in extremities (thin legs), avascular necrosis of femur head (cause fx)
