2023-10-04T04:58:50+03:00[Europe/Moscow] en true <p>degradation of alveolar walls that causes air to get trapped</p>, <p>secrete chemokines to stimulate neutrophils</p>, <p>secrete proteases; this causes emphysema and mucus hypersecretion </p>, <p>less eosinophils </p>, <p>loss of cilia, airway remodeling/dyspnea, decreased oxygen exchange</p>, <p>pneumonia </p>, <p>neutrophils, macrophages, CD8+ T lymphocytes</p>, <p>LTB4, IL-8, TNF-a</p>, <p>SABA, SAMA</p>, <p>IL-5, LT-antagonist, IL-4, IgE, ICS</p>, <p>reduction of airway remodeling/dyspnea </p>, <p>indacaterol, olodaterol, vilanterol </p>, <p>true</p>, <p>false</p>, <p>anticholinergics; vagal tone may be the only reversible element in airway obstruction; decreased ACh production </p>, <p>TNF-a</p>, <p>tiotropium, aclidinium, umeclidinium, glycopyrronium, revefenacin </p>, <p>glaucoma; nebulizer</p>, <p>inhibition of PDE- bronchodilation; antagonism of adenosine- prevent bronchoconstriction; histone deacetylation- prevent transcription of inflammatory genes; IL-10 release- apoptosis of neutrophils/eosinophils</p>, <p>can increase risk of pneumonia </p>, <p>anticholinergics </p>, <p>activate GPCR adenyl-cyclase to induce smooth muscle relaxation/bronchodilation</p>, <p>inhibits PDE4; prevents cAMP degradation which decreases activity of inflammatory cells, IL-8, TNF-a</p>, <p>CYP3A4; CYP1A2</p>, <p>weight loss (N/V), neuropsychiatric </p>, <p>f; orally </p>, <p>A1-antitrypsin </p>, <p>c</p>, <p>azithromycin, erythromycin</p>, <p>n-acetylcysteine + water</p> flashcards
Pharmacology of COPD

Pharmacology of COPD

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  • degradation of alveolar walls that causes air to get trapped

    What is emphysema?

  • secrete chemokines to stimulate neutrophils

    What is the role of macrophages in COPD?

  • secrete proteases; this causes emphysema and mucus hypersecretion

    What is the role of neutrophils in COPD?

  • less eosinophils

    Why are IL-5 & IL-4 drugs NOT used in COPD?

  • loss of cilia, airway remodeling/dyspnea, decreased oxygen exchange

    What are the 3 main pathophysiological consequences of COPD?

  • pneumonia

    What can increased mucus production lead to in COPD?

  • neutrophils, macrophages, CD8+ T lymphocytes

    Which cells are involved in COPD? (3)

  • LTB4, IL-8, TNF-a

    Which inflammatory mediators are involved in COPD? (3)

  • SABA, SAMA

    What medications would be used for relief of acute symptoms? (2)

  • IL-5, LT-antagonist, IL-4, IgE, ICS

    Which drugs used in Asthma would NOT be useful in COPD? (4)

  • reduction of airway remodeling/dyspnea

    What are bronchodilators/anti-inflammatory drugs used for in COPD?

  • indacaterol, olodaterol, vilanterol

    What are the Ultra-long acting LABAs? (3)

  • true

    SABAs & SAMAs are equally effective in COPD. T/F?

  • false

    LABAs are more effective than LAMAs in COPD. T/F?

  • anticholinergics; vagal tone may be the only reversible element in airway obstruction; decreased ACh production

    Which is more effective, Anticholinergics or B2 agonists?

    Why?

  • TNF-a

    _______ induces ACh secretion.

  • tiotropium, aclidinium, umeclidinium, glycopyrronium, revefenacin

    What are the LAMAs? (5)

  • glaucoma; nebulizer

    __________ can occur when anticholinergics are taken via ________.

  • inhibition of PDE- bronchodilation; antagonism of adenosine- prevent bronchoconstriction; histone deacetylation- prevent transcription of inflammatory genes; IL-10 release- apoptosis of neutrophils/eosinophils

    MOA of Methylxanthines? (4)

  • can increase risk of pneumonia

    Why are ICS generally avoided in COPD?

  • anticholinergics

    -M3 receptor antagonist that prevent bronchoconstriction & mucus

    production.

  • activate GPCR adenyl-cyclase to induce smooth muscle relaxation/bronchodilation

    B2 agonist MOA?

  • inhibits PDE4; prevents cAMP degradation which decreases activity of inflammatory cells, IL-8, TNF-a

    Roflumilast MOA?

  • CYP3A4; CYP1A2

    Roflumilast is metabolized via ______ & ______.

  • weight loss (N/V), neuropsychiatric

    AE's of Roflumilast? (2)

  • f; orally

    Roflumilast is administered via inhalation. T/F?

  • A1-antitrypsin

    -coats lungs & protects them from neutrophil elastase.

  • c

    Where is A1-antitrypsin produced?

    a) lungs

    b) kidneys

    c) liver

    d) adrenal glands

  • azithromycin, erythromycin

    Which ABs can we give for COPD exacerbations? (2)

  • n-acetylcysteine + water

    Which mucolytic treatment can we use in COPD?