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Therapeutics > Lecture 24: Drugs used in COPD > Flashcards

Lecture 24: Drugs used in COPD Flashcards

1
Q

Chronic Obstructive Pulmonary Disease (COPD)

A

-10% of adult population (mostly smokers)
-IRREVERSIBLE airflow obstruction
-emphysema
-chronic bronchitis

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2
Q

COPD symptoms

A

-chronic cough
-sputum
-dyspnea
-barrel chest

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3
Q

Emphysema

A

-permanent enlargement of bronchioles and alveoli due to destruction of their walls
-dyspnea due to insufficient gas exchange
-cigs is major cause
-asymptomatic until later stage of life

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4
Q

Pathophysiology of emphysema

A

-tissue damage by proteases
-oxidative injury by ROS

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5
Q

Mech of tissue damage by proteases in emphysema

A

-irritants in cig smoke cause inflammation in alveoli
-neutrophils and macrophages release proteases
=tissue damage

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6
Q

Mech of oxidative injury in emphysema

A

-ROS in cig smoke deplete antioxidants in lungs
-ROS inactivate a1-antitrypsin, which normally suppress protease activites
-activated neutrophils also release ROS

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7
Q

a1-antitrypsin

A

-protease inhibitor produced in liver
-inhibits neutrophil elastase
-limits lung tissue damage

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8
Q

a1-antitrypsin deficiency

A

-rare genetic disorder
-inc neutrophil migration
-inc lung damage via inflammation and protease

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9
Q

Chronic bronchitis

A

-chronic inflammation in bronchial tubes
-mucus hypersecretion
-fibrosis and narrowing of airways
-often coexists with emphysema
-smokers

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10
Q

Chronic bronchitis symptoms

A

-producing cough
-wheezing
-SOB
-chest pain

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11
Q

Pathophysiology of chronic bronchitis

A

-initiated by exposure ot irritants
-hypersecretion of bronchial mucous glands
-hypertrophy of mucus glands
-metaplastic formation of mucin-secreting goblet cells
-inflammation w infiltration of CD8 T cells, macrophages, neutrophils (no eisonophils)

-microbial infection might play a lil part in maintaining inflammation and exacerbating symptoms

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12
Q

Tissue Remodeling in COPD

A

-fibrosis of small airways
-hyperinflation of lungs
-alveolar enlargement
-alveolar wall destruction
-mucus hypersecretion

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13
Q

Asthma v COPD

A

-proximal
-childhood
-episodic
-mast, eosinophils, CD4
-IL-4, 5, 13
-less oxidative stress

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14
Q

COPD v asthma

A

-peripheral
-late adulthood
-progressive
-neutrophils, macrophages, CD8
-IL-8, TNFa
-oxidative stress

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15
Q

nonpharma Treatment of COPD

A

-smoking cessation
-exercise
-immunization
-long-term oxygen therapy

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16
Q

Pharma treatment of COPD

A

-bronchodilators (B2 agonist or M antagonist)
-methylxanthines
-corticosteroids for patients w exacerbations
-a1-antitrypsin therapy (rare)

17
Q

B2 selective agonists

A

-SABA
-LABA
-Ultra-LABA

18
Q

SABA (short acting selective B2 agonist)

A

-albuterol
-levalbuterol
-rapid onset
-better in asthma

19
Q

LABA (long acting B2 selective agonists

A

-salmeterol
-formoterol
-q12h
-not for acute relief

20
Q

Ultra-LABA

A

-indacaterol
-olodaterol
-vilanterol
-bambuterol
-qd
-monotherapy for COPD
-combo w Fluticasone/vilanterol for asthma

21
Q

Antimuscarinic agents

A

-SAMA
-LAMA

22
Q

SAMA (short acting antimuscarinic agents

A

-Ipratropium
-as effective for COPD as albuterol

23
Q

LAMA (long acting antimuscarinic agents)

A

-tiotropium
-aclidnium
-umeclidinium
-qd
-approved for maintenance therapy of COPD
-quarternay amine salt
-combo as fluticasone furoate/umeclidinium bromide/vilanterol

24
Q

Methylxanthines

A

-replaced as main therapy for COPD by LABA and antiMuscarinics
-theophylline

25
Q

Theophylline

A

-methylxanthine
-used in patients who are intolerant to or cannot use inhaled bronchodilators
-bronchoDIALTION
-ANTI-inflammatory
-systemic admin might be beneficial on peripheral airways

26
Q

Roflumilast

A

-PDE4 inhibitor
-inc cAMP as methylxanthines
-suppress release of cytokines and chemokines
-approved for COPD but not asthma

27
Q

Corticosteroid use in COPD

A

-short-term systemic use for acute treatment
-inhalation for chronic COPD

28
Q

Corticosteroid mech

A

-dec mucus release by reducing permeability
-suppress proteaase release from immune cells
-suppress prostaglandin production

29
Q

a1-antitrypsin replacement therapy

A

-derived from donated blood
-prolastin, aralast, zemaira
-reduces lung tissue loss and destruction in patients w severe a1-antitrypsin deficiency
-v expensive

Therapeutics (78 decks)

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