Lecture 24

Question 1

asthma site

Answer 1

proximal airways

Question 2

asthma onset

Answer 2

in childhood

Question 3

asthma symptoms

Answer 3

episodic attacks

Question 4

asthma immune cells

Answer 4

mast cells
eosinophils
CD4+ T cells (TH2)

Question 5

asthma key mediators

Answer 5

IL4
IL5
IL13

Question 6

asthma oxidative stress

Answer 6

+

Question 7

COPD site

Answer 7

peripheral airways

Question 8

COPD onset

Answer 8

late childhood

Question 9

COPD symptoms

Answer 9

progressive deterioration of pulmonary functions

Question 10

COPD immune cells

Answer 10

neutrophils
macrophages
CD8+ T cells (TH1)

Question 11

COPD key mediators

Answer 11

IL8
TNFa
IL1b
IL6

Question 12

COPD oxidative stress

Answer 12

+++

Question 13

emphysema

Answer 13

permanent enlargement of bronchioles and alveoli
leads to damages through proteases or oxidative injury by ROS

Question 14

damages through protease mechanism

Answer 14

leads to emphysema
cigarette smoke –> irritation –> inflammation in alveoli –> accumulation of neutrophils and macrophages –> protease release –> tissue damage

Question 15

oxidative injury by ROS mechanism

Answer 15

leads to emphysema
cigarette smoke –> ROS –> depletes antioxidants in the lungs –> inactivates a1-antitrypsin –> oxidative injury

Question 16

chronic bronchitis

Answer 16

mucus hypersecretion
fibrosis and narrowing of airways
initiated by the exposure of irritants
microbial infection may play secondary role to maintain inflammation and exacerbate symptoms

Question 17

chronic bronchitis mechanism

Answer 17

cigarette smoke –> irritation –> hypersecretion of the bronchial mucous glands –> hypertrophy of mucous glands –> metaplastic formation of mucin-secreting goblet cells –> inflammation with infiltration of CD8+ T cells, macrophages, and neutrophils

Question 18

ultra-LABA

Answer 18

examples - indacaterol, olodaterol, vilanterol, bambuterol
once a day
monotherapy for COPD only (not asthma)

Question 19

LAMA

Answer 19

long acting antimuscarinic agents
examples – tiotropium, aclidinium, umeclidinium
once a day
maintenance therapy of COPD

Question 20

roflumilast

Answer 20

phosphodiesterase-4 inhibitor
increase cAMP concentration to suppress release of cytokine and chemokines
COPD only

Question 21

corticosteroids

Answer 21

used in both COPD and asthma
COPD - short term systemic use for acute exacerbations

Question 22

a1-antitrypsin

Answer 22

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

Question 23

a1-antitrypsin deficiency

Answer 23

increases neutrophil migration
increases lung damage via inflammation and protease activity
especially harmful in COPD patients

Question 24

a1-antitrypsin deficiency treatment

Answer 24

prolastin, aralast, zemaira (derived from donated blood)
reduces lung tissue loss and destruction in patients
expensive