chronic obstructive diseases Flashcards
- Structural changes of the airway and/or alveoli that results in chronic respiratory symptoms and airflow limitation
- Progressive and disabling
- Non-reversible** (how to distinguish from asthma)
- Chronic bronchitis and emphysema
- Usually a history of smoking, sometimes other significant inhalation history
- In other parts of the world it is more common from biomass fuel cooking
- Other implicated contributors: air pollution, airway infection, environmental factors, allergy, hereditary factors, reactive airway disease
- Exposures early in life: poor lung growth in childhood and expiratory flow limitation—may not manifest clinically until mid-life
COPD
- Normal: lung function declines with age after about 40
- Usually present in 50s or 60s–progressive
- Cough
- Sputum production
- SHOB—starts with exertion and eventually at rest
- “pink puffers” and “blue bloaters”
- Really a mix of both
COPD symptoms
cough and sputum production for ≥ 3 months per year for ≥ 2 consecutive years in the absence of
other conditions that might cause symptoms
chronic bronchitis
a pathological term describing destruction of gas exchanging surfaces of the lung (alveoli), resulting in a reduction of normal elastic recoil of the lung parenchyma
emphysema
- lower body mass index
- fewer cardiovascular comorbidiites
- fewer metabolic comorbidities
- less muscle mass
- hyperinflation
- low diffusion capacity for CO
- more dyspnea
- decreased exercise capacity
- worst health status
- lower serum levels of sRAGEs
- dry cough
- barrel chest
pink puffer (emphysema)
- higher body mass index**
- more metabolic co morbidities
- cardiac compromise
- OSA-COPD overlap
- less hyperinflation
- more chronic bronchitis
- increased exacerbations
- more normal diffusion capacity
- higher serum levels of inflammatory markers (IL-6 and CRP)
- wet cough
blue bloater (chronic bronchitis)
COPD exacerbations are Often precipitated by
infection or some sort of environmental exposure
late stages of COPD
PNA, Pulmonary hypertension,
Right sided heart failure***, chronic respiratory failure
why do people get right sided heart failure with COPD
pulmonary vasculature is under pressure so right side has to work harder
- May have no specific findings early on
- Possible findings:
- Barrel chest- lungs fill with air and are unable to fully breathe out
- The use of accessory respiratory muscles
- Pursed-lip breathing
- Reduced chest expansion
- Reduced breath sounds
- Wheezing
- Hyperresonance
- An expiratory time ≥ 4 second***
COPD physical exam
how to diagnose COPD
spirometry:
Reduced FEV1 and the ratio of FEV1/vital capacity show airflow obstruction
Severe COPD: significant FVC reduction (not exchanging air well)
measures how effectively the lungs transfer oxygen from inhaled air
to the blood
DLCO
what to do if patient has COPD with hypoxemia or hypercapnia
FEV1 or DLCO is less than 40% of predicted
ABG
COPD EKG
sinus tach
COPD XR
chronic bronchitis vs emphysema
emphysema—hyperinflation with diaphragm flattening or peripheral arterial deficiency
COPD chest CT
bronchitis vs emphysema
thickened walls and air trapped
COPD Advanced disease
pulmonary HTN
COPD: Complications
- Acute bronchitis
- PNA
- Pulmonary thromboembolism
- Abnormal atrial rhythms
- Severe:
- Pulm HTN
- RHF
- Chronic respiratory failure
- Small risk of spontaneous PNX
COPD treatment
- Smoking cessation
- Flu, COVID, Pneumococcal vaccines
COPD daily treatment
- Daily: Based on severity of symptoms
- Identification of high risk patients: 1) FEV1 less than 50% of predicted
2) more than two exacerbations in the previous year 3) one or more
hospitalizations for COPD exacerbations in the previous year - GOLD criteria
Short Acting Muscarinic Antagonist
* Reduce bronchoconstriction and mucous secretion
SAMA (COPD medication)
Short-Acting Beta2-Agonist
* Relax muscles in the airways
SABA
Long-Acting Beta2-Agonist
LAMA
elaxes the smooth muscle of the bronchial airways and
pulmonary blood vessels and reduces airway responsiveness
theophylline
Brochodilator and anti-inflammatory
phosphodiesterase type 4 inhibitor
COPD management: outpatient
- O2
- Inhaled bronchodilators
- Corticosteroids
- Theophylline
- Abx
- Pulmonary rehab
- Phosphodiesterase type 4 inhibitor
- Other
- do not alter the course of decline
- improve symptoms, exercise tolerance, FEV1, and overall health
status - match medication to disease severity
- if Pts don’t get symptomatic improvement with these, discontinue
- SAMA–Short Acting Muscarinic Antagonist
- SABA–Short-Acting Beta2-Agonist
- LAMA–Long-Acting Beta2-Agonist
inhaled bronchodilators
- for Pts with PaO2 less than 56mm hg—resting hypoxemia
- the only trx known to lengthen life*
- also reduces hospitalizations and increases quality of life
- O2 for at least 15 hours a day
- there are specific Medicare guidelines for coverage
O2
- used for Pts who don’t improve enough with other medications
- requires monitoring d/t toxicity
- last resort, d/c w/o improvement
theophylline
- reduce frequency of exacerbations and improve functional status
- weigh benefits vs risks
- Cataracts, bone density, bacterial PNA
- use in severe disease w/ frequent exacerbations, eosiniophilia > 300
cells per mcL, concomitant asthma or h/o hospitalization for
exacerbations - after Pts are stable for 2 years, may consider discontinuing
- oral corticosteroids only used for exacerbations, not long-term
corticosteroids
1) *acute exacerbation
* increased sputum production or purulence, increase dyspnea
2) acute bronchitis
3) prophylaxis for exacerbations of chronic bronchitis
Abx
- Choice of Abx
- local resistance, recent use, certain individual risk factors
physical exercise programs
pulmonary rehab
Roflumilast: for moderate or severe COPD and chronic bronchitis and
frequent exarcerbations and who are taking LABA/ICS and/or LAMA
phosphodiesterase type 4 inhibitor
other COPD management
- Hydration
- Helps manage secretions
- Cough training methods, flutter device and postural drainage, chest
percussion or vibration
COPD management: inpatient
* Acute exacerbations:
- O2—90-94%
- Inhaled beta 2 agonists w/ or w/o inhaled ipratropium (SAMA)
- Corticosteroids
- Broad-spectrum Abx
- Sputum bacterial cultures are usually negative—more often triggered by viral infections
- Sometimes chest physiotherapy
COPD: When to Admit
- Severe symptoms or acute worsening that fails to respond to
outpatient management - Acute or worsening hypoxemia, hypercapnia, peripheral edema, or
change in mental status - Inadequate home care, or inability to sleep or maintain
nutrition/hydration due to symptoms - high-risk comorbid conditions
COPD management: other
* Procedures
- Lung transplant
- Lung reduction
- Bullectomy
genetically inherited condition characterized by the impaired production of the alpha-1 antitrypsin protein
- This protein protects the body from neutrophil elastase, an enzyme
released during inflammation and infection - Leads to the destruction of alveoli and resulting in conditions such as
emphysema and bronchiectasis - Symptoms appear much earlier—as early as 20yo
COPD: Alpha 1 anti-trypsin deficiency
* AAT deficiency
AAT deficiency treatment
Infusion of pooled plasma-purified human alpha-1 antitrypsin is the
only licensed disease-specific therapy for AAT deficiency associated
with lung disease
- A chronic lung condition that leads to widening and scarring of airways
- Results in chronic, often progressive, suppurative lung disease
- chronic productive cough**
Caused by a variety of things:
* Cystic fibrosis**
* Severe infections that effect the lungs, expecially recurrent: severe PNA, TB, measles, whooping cough
* Immunodeficiency syndromes
* Autoimmune conditions
* Inhaled objects: can block and scar the airway
* Idiopathic
* Radiation
bronchiectasis
AAT deficiency: when to test
- Early unexplained emphysematous lung disease
- Relatives of known AAT deficiency
- Dyspnea and cough present in multiple family members across
generations - Unknown cause of liver disease
- Adults with bronchiectasis of unknown etiology should be tested
- Asthma Patients whose spirometry does not improve with treatment
- Unexplained panniculitis and anti-proteinase-3 vasculitis
- Can be present at birth but usually presents at/after middle age
- Symptoms may not develop until years after initial event
- Can coexist with COPD
- Symptoms include:
- Chronic cough
- Purulent sputum production
- Dyspnea or dyspnea on exertion
- Hemoptysis
- Chest pain (may be pleuritic)
- Wheezing
- Rhinosinusitis
- Fatigue
- Weight loss
- Failure to thrive
bronchiectasis symptoms
Bronchiectasis: Complications
Infectious exacerbations of chronic respiratory symptoms
* Clubbing
* Cyanosis
* Wheezing
* Inspiratory crackles
bronchiectasis management
- Airway clearance techniques, w/pretreatment….
- Humidifiers
- Short term exacerbations for acute worsening of symptoms
- Long-term Abx for Pts with 3 or more exacerbations a year
- Expectorants/mucolytics
- Steroids—not routine
- Long-term bronchodilators—not routine
- Lung resection
- Lung transplant
Bronchiectasis: diagnostic Testing
XR—often nonspecific or normal, possible dilated bronchi
- CT scan— bronchoarterial dilation ratio (the ratio of internal airway
lumen to adjacent pulmonary artery) > 0.8 to define abnormality in
children/adolescents instead of the adult ratio for abnormalities of >
1-1.5, mucous impaction
