Respiratory Medications Flashcards
Methods of medication delivery:
MDI, DPI, nebulizer, oral, IV, and SQ
Goals of respiratory meds:
Minimize symptoms, increase capacity to exercise, improve overall health, reduce number of exacerbations, reduce lung remodeling, minimize side effects, and treat co-existing medical problems
Corticosteroids:
Most effective asthma therapy drug, most potent and effective anti-inflammatory medications: decreases inflammation, reduces bronchial hyper-responsiveness, blocks late phase reaction, and inhibits migration of inflammatory cells, 1-2 weeks for complete therapeutic effect
Corticosteroids: delivery routes:
IV: hydrocortisone (solu-cortef) and methylprednisolone (solu-medrol); systemic: prednisone; inhaled: long term, prophylaxis, little systemic effect
ICS- inhaled corticosteroids:
Give on a fixed schedule, long term-prophylactic, little systemic absorption, highest dose levels> bruising and accelerated bone loss. SE: oral thrush*, hoarseness, irritated throat, dry mouth, cough, few systemic effects. Teaching: gargle and rinse after use, spacer to increase amount of med reaching lungs and decrease SEs
Inhaled corticosteroids (ICS) examples:
“-one or -ide” usually indicate a steroid of some sort. Flovent, pulmicort, asmanex, belclovent/vanceril.
Corticosteroids IV and PO:
Given PO for prompt control, take on fixed schedule in am w/ food (coincide with endogenous cortisol production), women take calcium & Vit D supplements (accelerated bone loss)
Prednisone:
Long term SE: immunisuppression, skin changes, osteoporosis, increased blood glucose, weight gain, and cushings (moon face)
Short term SE: insomnia and increased appetite.
Oral corticosteroid teaching:
DONT STOP ABRUPTLY*, taper doses until prescription complete, prednisone mimics action of cortisol, causes adrenal cortex to decrease or stop production of cortisol, results in adrenal insufficiency or crisis which is life threatening. (S/S: HA, confusion, restlessness, vomiting, shock, death)
Leukotriene modifiers:
Interferes with the synthesis of or blocks the action of leukotrines (anti-inflammatory, bronchodilator), not for acute episode* (prophylaxis), and administered PO
Leukotrines are:
Inflammatory mediators, potent brinchoconstrictors*, and produce airway inflammatory and edema
Immunomodulators: anti-IgE-
Moderate to severe asthma not controlled with inhaled steroids, decreases circulating IgE levels, not for acute attacks, SQ inj., very expensive, Xolair (risk of anaphylaxis)
Short acting beta 2 adrenergic agonists (SABAs):
Decrease broncho spasm, produces bronchodilation- stimulate beta2 adrenergic receptors in bronchioles and prevents release of inflammatory mediators from mast cells. Overuse can lead to broncho spasms, used as rescue, not long term control*, inhaled form>directly to site. Teach: always carry rescue inhaler, make sure it’s full, and goal is to never use. Stimulate SNS- contraindicated in heart patients
Long acting beta 2 adrenergic agonists (LABA):
Long term control (used to prevent acute attacks), dilates bronchioles to increase airflow, teach: use daily, only q12 hrs, do not work quickly, and not for acute symptoms.
Anti-cholinergic drugs:
Blocks broncho constricting effects of parasympathetic NS, inhibits vagal nerve stimulation, less effective than beta 2 adrenergic agonists, used when SABA not effective, slow initial onset than SABA, SE: dry mouth*