Flashcards in COPD/Emphysema Deck (57):
What are some things that characterize COPD?
-Fibrosis of airways walls
-Inflammation with lymphocytes, neutrophils, and macrophages
-Smooth muscle hyperplasma
-hyper-secretion of mucus
Which disease of airway limitation is fully reversible?
Which parts of the breathing cycle are hindered in COPD?
T or F. COPD is progressive
What is the most common cause of COPD in the WORLD?
Wood smoke exposure
Risk factors for COPD?
-Occupational dust and chemicals
What protein is usually deficient in COPD?
What does alpha-1 antitrypsin do?
protect the lungs from neutrophil elastase, an enzyme that can disrupt connective tissue
What cells promote Asthma inflammation?
mast cells, eosinophils, CD4, macrophages
What cells promote COPD inflammation?
neutrophils, CD8, macrophages
What mediators promote Asthma inflammation?
LTD, histamine, IL-4/5, ROS
What mediators promote COPD inflammation?
LTB, IL-8, TNF-a, ROS
Steroids in COPD mainly target what cell and what mediator?
macrophages and ROS
How does COPD limit airway flow?
-small airway disease via inflammation, fibrosis, and increased resistance
-parenchymal destruction via loss of alveolar attachments and decrease in elastic recoil
What is emphysema?
loss of alveolar attachments
T or F. The amount of residual air in COPD patients is higher
T. Leading to a barrel chest appearance (so the tendency for the airways to collapse is higher)
What are the two parts of COPD?
chronic bronchitis and emphysema
What is chronic bronchitis?
chronic or recurrent cough present on most days for a minimum of 3 months in a year and for not less than 2 straight years
What is the Reid index?
bronchial gland depth /total bronchial wall thickness (normally higher than 0.4)
How does the Reid Index change in chronic bronchitis?
increases, bronchial gland hypertrophy and goblet cell metaplasia lead to excessive mucous production
What kinds of airway changes accompany chronic bronchitis?
squamous metaplasia of airway epithelium, loss of cilia, and ciliary function, and increased smooth muscle and connective tissue
What cells make up the inflammation in chronic bronchitis?
CD8 and neutrophils
What do you see in small airways (less than 2mm) in CB?
-formation of goblet cells and mucus secretion
-fibrosis and collagen deposition
-this is the MAJOR site of airflow resistance
What is emphysema?
an abnormal enlargement of air spaces distal to the terminal bronchioles
What is centrolobular emphysema?
dilation and destruction of the respiratory bronchioles
What mainly causes centrolobular emphysema?
mostly an upper lobe process associated with smoking
What causes panlobular emphysema?
destruction of the entire acinus, predominantly a lower lobe process associated with A1AT deficiency
What are bull?
emphysematous spaces greater than 1cm in diameter
Common complication of emphysema?
small airway collapse during exhalation (dynamic airway collapse)
What things lead to IRREVERSIBLE airflow limitation in COPD?
-loss of elastic recoil
-destruction of alveolar attachments
What things lead to REVERSIBLE airflow limitation in COPD?
-accumulation of inflammatory cells and mucus in bronchi
-smooth muscle contraction
What are 'pink puffers' (Type A COPD)?
-good spiratory drive
-intense dyspnea; purse-lip breathing
-thin and often elderly
-small sputum volume
What are 'blue bloaters' (Type A COPD)?
-poor respiratory drive
-large sputum volume
often associated with CHF
When should COPD be suspected?
considered in any patients with those complaining of dyspnea, chronic cough or sputum production, or risk factors
How is COPD diagnosed?
spirometry with FEV1/FVC less than 0.70 after bronchodilation with drugs
T or F. FEV1 AND FVC decrease in COPD
T. But FEV1 decreases more (both in chronic bronchitis and emphysema)
T or F. Lung volumes, compliance, elastic recoil, and diffusing capacity for CO (DLCO) are normal in pure chronic bronchitis
T. Note that DLCO is low in pure emphysema due to destruction of alveoli
In Emphysema, are lung volumes and compliance increases or decreased
Increased because elastic recoil decreases
How does COPD present?
-wheezing during auscultation on slow breathing
-pursed lip breathing
Cor pulmonale is seen in COPD. What is this?
split of S2, JVD, peripheral edema
How are the symptoms of suspected COPD rated?
mMRC ratio or FEV1:FVC ratios
Grade 0- only SOB with strenuous exercise
Grade 1- SOB when hurrying
Grade 2- walks slower than normal and gets SOB
Grade 3- Stops to breath after 100 m when level
Grade 4- too SOB to leave house
FEV1:FVC criteria in COPD severity
GOLD 1: 80+%
GOLD 2: 50-80%
GOLD 3: 30-50%
GOLD 4: less than 30%
Exacerbations in COPD rating (most important)
Two or more within 1 yr or an FEV1 less than 50% are HIGH risk
One or more hospitalizations= HIGH risk
Co-morbidites of COPD?
-Anxiety and Depression
What vaccines should be considered with COPD?
Influenza and Pneumococcal
Treatment for Group A COPD Patients?
SAMA or SABA
Treatment for Group B COPD Patients?
LABA or LAMA
Treatment for Group C COPD Patients?
ICS+ LABA or LAMA
Treatment for Group D COPD Patients?
ICS+LABA and/or LAMA
What do B2-agonists do to bronchodilate?
-act through PKA (increased cAMP)
Side effects of B2 agnosts?
How do muscarinic antagonists combat broncho-constriction?
Side effects of muscarinic antagonists?
-dryness of mouth
How do corticosteroids work in asthma?
Inflammatory genes are activated by inflammatory stimuli (IL-1β, TNF-α, etc.), resulting in activation of IKKβ (inhibitor of I-κB kinase-β), which activates the transcription factor nuclear factor κB (NF-κB). A dimer of p50 and p65 NF-κB proteins translocates to the nucleus and binds to specific κB recognition sites and also to coactivators, such as CREB-binding protein (CBP), which have intrinsic histone acetyltransferase (HAT) activity. This results in acetylation of core histones and consequent increased expression of genes encoding multiple inflammatory proteins.
Cytosolic glucocorticoid receptors (GR) bind corticosteroids; the receptor-ligand complexes translocate to the nucleus and bind to coactivators to inhibit HAT activity in two ways: directly and, more importantly, by recruiting histone deacetylase-2 (HDAC2), which reverses histone acetylation, leading to the suppression of activated inflammatory genes.
What is there rescuer bronchodilator of choice in COPD?