The main difference between inhaled steroids and systemic steroids is that:
Inhaled steroids do not have the side effects of systemic steroids because they are metabolized by the lung and have a high first pass effect to avoid systemic effects.
Glucocorticoids (cortisol) are produced in
endogenous glucose-regulating steroids
Take home message about glucocorticoids:
Steroids stop production of arachidonic acid thus preventing inflammation. This is the mechanism by which glucocorticoids inhibit inflammation.
Response time to steroids
Takes from 14 hours to days because gene expression is involved.
Short acting glucocorticoids:
"1.Hydrocortisone 1/1 2. Cortisone 0.8/0.8"
Intermediate acting glucocorticoids:
"1.Prednisone 4/0.3, 2. Prednisolone 5/0.8, 3. Methyl-Prednisolone 5/0.5, 4. Triamcinolone 5/0 "
Long acting glucocorticoids
"1. Beta-Methasone 36/0 2. Dexa-Methasone 30/0 3. Para-Methasone 10/0"
High levels of glucocorticoids in blood.
Core fat deposit, thin arms, moon-face
Why use steroids - 3
stronger than NSAIDS for inflam; for low endogenous steroids; suppress immune response
3 types steroids
Salt (mineral); Sugar (glucocorticoids); Sex (androgens & estrogens)
5 effects of steroids
incr blood glucose; suppress protein synth; change fat metabolism (make core fat); incr RBC & decr WBC; Na & water retention
7 steroid anti-inflammatory effects
decr capillary permeability; decr WBC adhesion to endothelium; decr mediators (prostaglandins & leucotrienes); decr WBC production; stabilize WBC lysosomal mems; decr macrophage activity; antagonize histamine & kinin activity
2 general steroid effects
decr collagen & fibroblasts; decr immune response
list 6 diseases helped by steroids
allergies; asthma; arthritis; lupus; inflamm bowel disease; skin inflamm disease; transplants; newborns
7 major adverse effects of steroids
infection (suppress immune & inflam);
incr BP and loss of K+ (retention Na+ & water); changes in blood glucose (hyperglycemia);
decr muscle mass (changes prot metabolism);
fat redistribution (Cushing's appearance);
osteoporosis/ bone loss (1/4 long-term patients);
Cushingoid characteristics (long term steroids) x 5
hyperglycemia; altered fluid & electrolyte; osteoporosis; weakness; fat: moon face, core fat, thin arms
Why quitting steroids quickly is bad x4
adrenal suppression (endogenous steroids limited by presence (negative feedback w/ hypothalamus & ant pit)); leads to hypotension, hypoglycemia, my- & arthalgia, weakness
problem w/ stress & long-term steroids
adrenal suppression; endogenous steroids not available for stress response
2 low-risk uses for steroids
low endogenous glucocorticoids (adrenal insufficiency); short term use
5 steroid admin routes
IV; PO, IM, SQ, topical
steroid admin precautions x3
w/ food (to limit GI ulcers); QOD to limit side effects; before 9 AM to work with endogenous; rotate IM sites; avoid topical coverings & mucous mems
steroid interactions x6
ASA & NSAIDS (GI bleeds); phenobarbital etc (prot binding); estrogens (action on endogenous); K+ depleting drugs; vaccines (suppressed immune); antidiabetic agents (glucocorticoid effect)
client teaching x8
take w/ food, milk; before 9AM; no quick stop; incr K+; beware wt gain 2-3 lb/wk; bracelet; effects diabetes; caution w/ pregnancy