COPD Flashcards
Describe process that leads to COPD
inflammation -> small airway disease (airway remodeling) and parenchymal destruction (loss of alveolar attachments; decrease of elastic recoil ) -> airflow limitation
- think paper bag
what are the clinical subtypes of COPD
- chronic bronchitis
- emphysema
differentiate between chronic bronchitis and emphysema patients in terms of appearance
- chronic bronchitis: blue bloaters
- cyanosis; overweight
- hypoxemia; respiratory acidosis, cor pulmonale more common
- emphysema: pink puffers
- pursed lip breathing
- thin body habitus
define chronic bronchitis
- chronic productive cough x 3 months, during 2 consecutive years with no other cause
structural changes associated with chronic bronchitis
- mucous gland enlargement -> hypersecretion
- bronchial squamous metaplasia
- loss of ciliary transport
chronic bronchitis: inflammation of bronchial wall and infiltration of sub mucosal layer by what types of cells
neutrophils
in chronic bronchitis, the obstruction is inspiratory or expiratory?
inspiratory and expiratory -> leads to hypoxemia and hypercapnia
which subtype of COPD has more parenchymal damage
emphysema : more alveolar sac damage
define emphysema
- pathologic enlargement of the air spaces distal to the terminal bornchioles due to desctruction of the alveolar walls
- reduced alveolar surface area
- decreased elastic recoil
- loss of alveolar supporting structures -> airway narrowing
destructive process in emphysema is due to
- too much elastase
- breaks down elastin and destroys elasticity of lung
- too little antitrypsin
- inhibits elastase
in emphysema, airflow obstruction occurs mostly during inspiration or expiration?
exhalation
which COPD subytpe is associated with hypoxemia
- chronic bronchitis
- emphysema: not associated with significant hypoxemia until later in disease severity
asthma is a chronic inflammatory disorder of the airways that is primarily mediated by what cell type
eosinophil
define asthma and explain why is it different from COPD
- airway hyper-reactivity -> increased secretions, mucosal edema -> constriction of bronchial smooth muscle -> aiway obstruction
- reversible
name the risk factors for COPD
- cigarette smoking
- air pollution
- genetic: alpha-1 antitrypsin deficiency
- premature emphysema
how does cigarette smoking increase risk for COPD
stimulates elastase activity, causing degenerative changes in elastin and alveolar structures
alpha 1 antitrypin deficiency causes an early onset of
emphysema
- <1% of US cases
- develops in smokers at age 40 yo; nonsmokers 53 yo
what are the cardinal symptoms of COPD
- dyspnea
- chronic cough
- sputum production
when does COPD typically present (what age)
50-60s
clinical presentation
- accessory muscle use
- increased AP diameter
- pursed lip breathing
emphysema
function of pursed lip breathing
- ordinary breathing in COPD allows early bronchial collapse on exhalation
- pursed lip breathing achieves resistance to outflow at the lips -> raises intrabronchial pressure -> bronchi stay open -> more air expelled
what do you expect to hear on percussion of COPD patients
hyper-resonant: due to air trapping
what test is used to establish the diagnosis and determine the stage of COPD
- spirometry
what do you expect to see in the spirometry results for COPD patents
- FEV1/FVC < 0.7 -> obstruction
- decreased FEV1
- increased TLC
- FEV1 predicted that is not reversible
Why could CBC show polycythemia in COPD patients
- polycythemia: abnormally increased concentration of hemoglobin in the blood
- increase in RBC due to hypoxemia of chronic bronchitis
when should you get an arterial blood gas
pulse oximetery shows O2 < 92%
what imaging is used for routine workup of COPD
- CXR
- high resolution CT: greater sensitivity and specificity than CXR for the diagnosis of COPD but is not necessary for routine workup
These CXR findings are consistent with
- hyperinflation (possibly with bullae)
- flattening of diaphragms
- enlargement of retrosternal air space
emphysema
These CXR findings are consistent with
- cardiac enlargment
- pulmonary congestion
- increased lung markings
chronic bronchitis
list the GOLD strategy for staging of COPD
-
determine if obstructive pattern
- FEV1/FVC <0.7
-
determine severity
- FEV1 %
-
assess symptoms
- patient rating scale: mMRC
-
determine exacerbation risk (in past yr)
- 0-1 exacerbations
- > 2 exacerbations OR 1 or more hospitalizations
goals of disease managment of COPD
- prevent progression
- smoking cessation
- relieve symptoms
- improve exercise tolerance
- reduce mortality
what is the mainstay of therapy for COPD
- bronchodilators: inhaled B2-agonists and anticholinergics
SABA: protype drug and dosing
- albuterol (B2 agonist
- 2 puffs q 4-6 hrs
side effect of B2 agonists
- palpitations
- tachycardia
- insomnia
- tremors
name two LABA (long acting beta 2 agonists)
- Salmeterol
-
Formoterol
- both given q12 hr
Name two short acting anticholinergics used for COPD and dosage
- Ipratropium bromide (atrovent)
- Ipratropium plus albuterol (Combivent)
- 2 puffs BID-QID
Name one long acting cholinergics used for COPD and dosage
- Tiotropium bromide (spiriva)
- once a day
side effects of anticholinergics
- dry mouth
- metallic taste
function of corticosteroids in the treatment of COPD
- reduces mucosal edema/inflammation by inhibiting prostaglandins
- increases responsiveness to beta-adrenergics
- SE: oral candidiasis, bruising
what is Roflumilast? Function?
- PDE-4 inhibitor
- for refractory cases as adjunct to bronchodilator
- anti-inflammatory effect
side effects of Roflumilast
- Nausea
- Diarrhea
- abd pain
- weight loss
- HA
what is the first line treatment for COPD: Stage A
short acting bronchodilator
- doesnt matter if beta 2 agonist or anticholinergic
- used as rescue inhaler
what is the first line treatment for COPD: Stage B
long acting bronchodilator
what is the first line treatment for COPD: Stage C
- inhaled corticosteroid +
- LABA or long-acting anticholinergic
what is the first line treatment for COPD: Stage D
- inhaled corticosteroid +
- LABA and/or long acting anticholinergic
tx for patients with alpha1-antitrypsin deficiency
- antiprotease therapy
- weekly or monthly injections
some patients with COPD wear supplemental oxygen a minimum of 12 hours a day. When is it indicated? Purpose?
- indicated if chronic dyspnea at rest
- PaO2 < 55 mmHg or SaO2 < 88%
- prolongs survival
what is the concern for patients with COPD to wear supplemental oxygen
concern that high flow O2 may reduce drive to breath and cause respiratory acidosis (maintain O2 sat 90-92%)
what two things should patients with COPD get to minimize complications and exacerbations
- annual influenza vaccine
- pneumococcal vaccine (PPV23)
signs of an acute COPD exacerbation
- cough increases in frequency or severity
- sputum production changes
- dyspnea increases
most common triggers for acute COPD exacerbation
- viral infection: rhinovirus and influenza
outpatient treatment/management for acute COPD exacerbation
- SABA
- oral steroids
- antibiotics?
when should abx be given in outpatient treatment/management for acute COPD exacerbation
- if 2/3 cardinal symptoms are present
- increased dyspnea
- increased sputum production
- increased sputum purulence
What makes a COPD patient at a higher mortality risk
- BODE index
- cigarette smoking
- BMI < 21
- male
- FEV1
- mMRC score
- exercise capacity
