1
Q
- 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
A
COPD
2
Q
- 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
A
COPD symptoms
3
Q
cough and sputum production for ≥ 3 months per year for ≥ 2 consecutive years in the absence of
other conditions that might cause symptoms
A
chronic bronchitis
4
Q
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
A
emphysema
5
Q
- 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
A
pink puffer (emphysema)
6
Q
- 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
A
blue bloater (chronic bronchitis)
7
Q
COPD exacerbations are Often precipitated by
A
infection or some sort of environmental exposure
8
Q
late stages of COPD
A
PNA, Pulmonary hypertension,
Right sided heart failure***, chronic respiratory failure
9
Q
why do people get right sided heart failure with COPD
A
pulmonary vasculature is under pressure so right side has to work harder
9
Q
- 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***
A
COPD physical exam
10
Q
how to diagnose COPD
A
spirometry:
Reduced FEV1 and the ratio of FEV1/vital capacity show airflow obstruction
Severe COPD: significant FVC reduction (not exchanging air well)
11
Q
measures how effectively the lungs transfer oxygen from inhaled air
to the blood
A
DLCO
12
Q
what to do if patient has COPD with hypoxemia or hypercapnia
FEV1 or DLCO is less than 40% of predicted
A
ABG
13
Q
COPD EKG
A
sinus tach
14
Q
COPD XR
A
chronic bronchitis vs emphysema
emphysema—hyperinflation with diaphragm flattening or peripheral arterial deficiency
14
Q
COPD chest CT
A
bronchitis vs emphysema
thickened walls and air trapped
15
Q
COPD Advanced disease
A
pulmonary HTN
15
Q
COPD: Complications
A
- Acute bronchitis
- PNA
- Pulmonary thromboembolism
- Abnormal atrial rhythms
- Severe:
- Pulm HTN
- RHF
- Chronic respiratory failure
- Small risk of spontaneous PNX
16
Q
COPD treatment
A
- Smoking cessation
- Flu, COVID, Pneumococcal vaccines
16
Q
COPD daily treatment
A
- 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
17
Q
Short Acting Muscarinic Antagonist
* Reduce bronchoconstriction and mucous secretion
A
SAMA (COPD medication)
18
Q
Short-Acting Beta2-Agonist
* Relax muscles in the airways
A
SABA
18
Q
Long-Acting Beta2-Agonist
A
LAMA
19
Q
elaxes the smooth muscle of the bronchial airways and
pulmonary blood vessels and reduces airway responsiveness
A
theophylline
20
Brochodilator and anti-inflammatory
phosphodiesterase type 4 inhibitor
21
COPD management: outpatient
* O2
* Inhaled bronchodilators
* Corticosteroids
* Theophylline
* Abx
* Pulmonary rehab
* Phosphodiesterase type 4 inhibitor
* Other
22
* 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
22
* 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
22
* used for Pts who don’t improve enough with other medications
* requires monitoring d/t toxicity
* last resort, d/c w/o improvement
theophylline
23
* 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
24
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
25
physical exercise programs
pulmonary rehab
25
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
26
other COPD management
* Hydration
* Helps manage secretions
* Cough training methods, flutter device and postural drainage, chest
percussion or vibration
27
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
27
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
28
COPD management: other
* Procedures
* Lung transplant
* Lung reduction
* Bullectomy
28
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
29
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
29
* 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
29
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
30
* 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
30
Bronchiectasis: Complications
Infectious exacerbations of chronic respiratory symptoms
* Clubbing
* Cyanosis
* Wheezing
* Inspiratory crackles
31
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
32
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
pulmonology
flashcards
Decks in class (15)
# Cards
-
intro9
-
pulm infectious disease124
-
chronic obstructive diseases45
-
DX and TX28
-
obstructive sleep apnea and obesity hypoventilation syndrome36
-
asthma23
-
pulmonary function testing22
-
croup4
-
restrictive lung disease30
-
pulmonology neoplastic disease28
-
pulmonary venous embolism24
-
ARDS8
-
pulmonary hypertension/cor pulmonale14
-
pleural diseases37
-
acute respiratory failure16
