• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/20

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

20 Cards in this Set

  • Front
  • Back
Codeine
binding in CNS. Cough suppression by direct central action in the medulla (cough center); partial (weak) mu agonist

Adverse effects: Sedation/drowsiness, constipation, vomiting
Pharmacogenetic variation: Codeine is converted into morphine by the cytochrome P450 enzyme CYP2D6. Genetic variation of CYP2D6 allows for ultra-fast accumulation of morphine leading to increased adverse effects.
Expectorants
Derived from Latin to mean "from the chest"
Drugs that allow sputum to more easily be coughed up are considered expectorants
Guaifenesin
Thin and liquefy sputum by reducing adhesivenss and surface tension

Thought to act as an emetic and is given in subemetic doses; gastric irritation promotes an increase in mucus secretion by cholinergic reflex mechanism
Amantadine
Tx or prevent influenza A

Amantadine blocks M2 proton ion channel of the virus, thereby interferes with fusion of the virion coat to vacuolar membranes and thus inhibits the uncoating of the viral RNA within infected cells. (Prone to resistance strains developing and being maintained.)

Adverse effects - mostly in CNS, driven by accumulation of dopamine); nervousnes, difficulty concentrating, insomnia
Zanamavir
Neuraminidase inhibitor; prevent/tx influenza

Inhibition of viral neuraminidase destroys receptors for the viral hemagglutinin and so interfere spread of infection within respiratory tract. Effective against both influenza A and B.
Acetylcysteine
Mucolytics; tx pts w cystic fibrosis

Sulfhydryl groups react w difulside linkages in mucoproteins in bronchial secretions; decrease viscosity of mucus secretions of the lungs and aids in removal of these secretions through coughing, mechanical mechanisms, or postural drainage
MOA of albuterol, salmeterol, ipratropium and theophylline
Albuterol
 Short-acting β2 agonists: (Albuterol) cause bronchodilation by increasing cAMP which brings about smooth muscle dilation through a cascade of phosphorylation events.
Salmeterol
 Long-acting β2 agonists: (Salmeterol), pharmacodynamics appear to be the same as for short-acting β2 agonists but pharmacokinetic differences allow for much longer beneficial effects without significant accumulation of adverse effects.
Iprotropium
o Muscarinic cholinergic antagonists: (Iprotropium) cause bronchodilation by competing with acetylcholine that is released by the parasympathetic nervous system in the bronchiole smooth muscle. Cellular mechanisms of action potentially involved both decreasing the production of cAMP and ion channel opening to decrease cellular contraction.
Theophylline
o Methylxanthines: (Theophylline) presumed or partial mechanisms of actions include
 Antagonists to adenosine receptor in bronchiole smooth muscle which acts analogously to muscarinic cholinergic receptors of bronchiole smooth muscle.
 Inhibitors of cyclic AMP phosphodiesterase in bronchiole smooth muscle and thus acting analogous to β2 agonists.
Beclomethasone
o Corticosteroids: (Beclmethasone) cause a variety of anti-inflammatory responses that lead to decreased immune reactivity (decreased infiltration of lymphocytes, eosinophils and mast cells) and decreased engorgement of blood vessels in the bronchial mucosa.
Cromolyn
o Cromolyn: This agent’s mechanism of action is not completely clear. It is known to alter a delayed chloride channel of the cell membrane and decrease cellular activation. In its actions in asthma it is known to decrease mast cell activation and thereby inhibit the early phase response to antigen challenge and to decrease eosinophil activation and thereby inhibit the inflammatory response to inhalation of allergens.
Montelukast
 Leukotriene D4 antagonists: (Montelukast) inhibition of the production of leukotriene D4 diminishes the effects of that agonist to cause bronchoconstriction, increased bronchial reactivity, mucosal edema and mucus hypersecretion.
Zileuton
 5-lipoxygenase inhibitor: (Zileuton) by blocking the first step in the production of leukotrienes (5-lipoxygenase) there is diminished production of leukotriene B4, C4, and D4. Leukotriene B4 is a potent neutrophil chemoattractant while leukotriene C4 and D4 cause bronchoconstriction, bronchial reactivity, mucosal edema and mucus hypersecretion.
Omalizumab
o Anti-IgE monoclonal IgG: (Omalizumab) binds to the portion of IgE that binds to its receptors on mast cells (and other inflammatory cells). Thus IgE is blocked from binding to mast cells and so diminish the degranulation of mast cells.
Asthma tx protocols
Consider the role of leukotriene receptor antagonists as an alternative for inhaled corticosteroids.
LTRA – oral
Less efficacious the ICS on symptoms airway caliber, reactivity & inflammation but about equal in reducing exacerbations overall
Few adverse effects – new one: increased neuropsychiatric events (agitation, abn dreams etc)
Consider the role that anti-IgE (omalizumab) might have in the tx of severe asthma
Reserved for moderate to severe persistent allergic asthma not adequately controlled by ICS.
Most effective at this stage
Administered - Subcutaneous injection
Adverse effect profile –
increased risk of CV events
Black Box warning - Anaphylaxis