Pharmacology-Asthma & COPD Flashcards
What factors contribute to development of asthma?
Genetic (cytokine dysregulation), Age and Envirionment (infection, pollution and allergens)
How can asthma be triggered?
Extrinsically (increased serum IgE levels from allergens, infection, environmental exposure, stress, meds and food). Intrinsically (Normal IgE. Exercise & cold air hyper-responsiveness).
What three factors contribute to closure of the airways during and asthma attack?
1) Epithelial inflammation (induced by mast cells, basophils, eosinophils, T-cells, macrophages & neutrophils). 2) Mucus plugging. 3) Smooth muscle constriction.
Which of the images seen below is from an asthmatic patient?
The bottom image is from the asthmatic patient with permanent remodeling. Note loss of PCC, goblet cell proliferation, smooth muscle hypertrophy and hyperplasia, increased collagen depositions and inflammatory cells.
What different inhalers are used for asthma medication delivery? Where does most of the inhaled medication go?
Metered-dose inhalers w/a spacer, nebulizers and dry powder inhalers.
What is the preferred therapy for bronchoconstriction?
B2 adrenergic agonists. They relax smooth muscle, reduce mast cell secretions, reduce permeability and entry of inflammatory cells and increase mucociliary clearance.
Why are beta-2 adrenergic agonists now combined with steroids for asthma management?
Just giving beta-2 agonists only relieves the symptoms and not the underlying inflammation.
What drugs might you considering a patient who has asthma that is poorly controlled by albuterol alone?
Anticholinergics. These are muscarinic competitive antagonists that limit vagal stimulation of bronchospasm that could also be causing asthma.
What patient population is best at clearing theophylline? Who is the worst?
Young children are better than adults, however, children under 1 year are the worst.
How are corticosteroids beneficial for patients with asthma?
The block the late phase asthma reaction that causes airway remodeling, reduce hyper responsiveness of the airway, inhibit cytokine production, inhibit arachadonic acid release (reducing PG and leukotriene synthesis) and inhibit inflammatory cell activation and migration.
What cells are mostly affect by corticosteroid binding to the glucocorticoid receptor?
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Why do inhaled corticosteroids have fewer side effects?
They are inactivated when absorbed orally, they are lipid soluble (stay in the lung longer with less systemic absorption).
Which corticosteroid is inhaled as a prodrug?
Ciclesonide. It is activated by esterase’s on the airway epithelium, which makes it bind fatty acids and remain in the lung longer.
How do patients with asthma benefit from leukotriene receptor antagonists and synthesis inhibitors?
LTB4 is chemotactic for neutrophils. LTC4 and LTD4 induce bronchoconstriction and mucosal hyper secretion. Note that LTD4 is 300-6000x more potent than histamine as a bronchoconstrictor.
How do patient with aspirin-induced asthma develop asthma from taking aspirin? What drugs would you prescribe to someone having an aspirin-induced asthma attack?
Aspirin inhibition of COX sends extra AA down to leukotriene synthesis. This causes over-stimulation of the LTD4 receptor and causes an asthma attack.
What drug will have zero efficacy if you give it to a patient with intrinsic asthma?
Omalizumab. It is a human IgG1 monoclonal anti-IgE antibody against IgE’s Fc region. Patients with intrinsic asthma do not have symptoms due to IgE production.
Why is smoker’s cough so wet?
Smokers produce a different, longer-lasting type of mucin than the average bear.
What effects to PDE4 inhibitors have on patients with COPD?
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