COPD Flashcards
Chronic rsp sx caused by airway abnormalities (bronchitis) and/or alveoli abnormalities (emphysema) that cause persistent, progressive airflow obstruction
COPD
2 pathophysiologic categories of COPD
Chronic bronchitis
Emphysema
COPD typically occurs in the setting of ___ ___ that emit noxious particles/gases
combustible products
cigs, environment
____ + ____ are key physiologic markers of COPD
airflow obstruction
extensive airway destruction
Small airways are narrowed by a number of factors:
Immune cells, molecules, mucus, fibrotic tissue
The pattern of pathologic change depends on the features of the individual’s underlying disease: (3)
Chronic bronchitis, emphysema, alpha-1 antitrypsin deficiency
3 MC sx of COPD
coughing
dyspnea
sputum production
associated sx of COPD
- Weight gain
- Weight loss - has worse prognosis
- Activity limitation
- Wheezing +/- chest tightness
- Syncope
- Anxiety / depressive symptoms
- Increased respiratory rate
- Signs of heavy smoking - Yellowing of fingers / nails
risk factors of COPD
- Family history
- Smoking history - Consider age at initiation, average amount smoked per day since initiation, cessation date if applicable
- Environmental history - Secondhand smoke exposure, air pollution, occupational exposure
- History of childhood pulmonary infections, HIV, or TB
- Asthma
PE findings of mild COPD
often normal
may pick up on prolonged expiration, faint end-expiratory wheeze with forced expiration
PE findings of mod/severe COPD
Lung hyperinflation → ↑ resonance with percussion
Decreased breath sounds, wheezes
Crackles at lung bases
Distant heart sounds
Increased AP diameter
PE findings of end-stage/chronic rsp failure
- Tripod posturing
- calloused forearms, swollen bursae on extensor surface of forearms - Use of accessory muscles for breathing
- Expiring through pursed lips
- Hoover’s sign → lower intercostal interspace retraction during inspiration
- Cyanosis
- Rarely nail clubbing
presentation of chronic bronchitis vs emphysema
- Chronic Bronchitis
- Obese, stocky
- Productive cough >3 months for 2 consecutive years
- Coarse rhonchi / wheezing
- Hepatomegaly
- Increased JVP
- Peripheral edema
- complications: Cor pulmonale - emphysema
- Thin, barrel chest
- Scant cough & sputum
- Expiration with pursed lips
- Hyperresonant percussion
- Wheezing, rales
- Complications: Pneumothorax
ddx for COPD
Anemia
Heart failure
Asthma
Interstitial lung disease
Alpha-1 antitrypsin deficiency
Bronchiectasis¹
Tuberculosis
Obliterative bronchiolitis
Diffuse panbronchiolitis
when to screen for COPD? what critieria?
what is the score signifying COPD?
at least 1 of the 3 cardinal sx OR
gradual decline in activity with risk factors for COPD
CAPTURE Questionnaire
score 2-4 = COPD
Performed before and after bronchodilator administration
spirometry
how is COPD diagnosed thru spirometry
- irreversible or partially reversible airflow limitation after bronchodilator administration
- Evidence of obstruction: FVC > 80% with FEV₁/FVC < 0.7
additional testing/work-up for COPD
Pulse ox every visit
Labs - CBC, BMP, TSH, BNP/NT-proBNP, serum alpha-1 antitrypsin
CXR
Measures amount and speed of air inhaled and exhaled
PFT
Forced Expiratory Volume in 1 second
FEV1
Similar to spirometry but includes analysis of intrathoracic volume
Plethysmography
when should you use Diffusing Capacity of Lungs
- In presence of moderate / severe airflow limitations (FEV₁ ≤50% predicted)
- Resting O2 ≤92%
- Exertional hypoxemia (<90%)
- Severe dyspnea (mMRC ≥2)
is DLCO necessary for routine assessment for COPD?
naurr
Great assessment for the severity of emphysema
DLCO
as DLCO decreases, what does that say about severity of disease
more severe
indications for Arterial Blood Gas
Low FEV₁ (< 40% predicted)
Low O₂ saturation on pulse ox (< 92%)
Depressed LOC
Assessment of hypercapnia in “CO₂ retainers” who are given supplemental oxygen (risk of hypercapnic respiratory failure)
Signs of right heart failure
ABG of mild COPD
normal pCO2
ABG of mod/severe COPD
worsening pO₂ and elevated pCO₂
what components does an ABG measure?
- pO₂ - oxygen pressure in arterial blood
- pCO₂ - amount of CO2 in arterial blood
- pH - acidity or alkalinity of arterial blood
- SaO₂ - oxygen saturation
- HCO₃ - bicarb
- Base excess - amount of acid or base required to restore a liter of blood to its normal pH at a PaCO2 of 40 mmHg
- Base excess increases in metabolic alkalosis and decreases (or becomes more negative) in metabolic acidosis
T/F: Imaging is required for diagnosing COPD
F
which imaging choice has a greater sensitivity in detecting disease
CT > CXR
indications for imaging in COPD
- Dyspnea/cough etiology is unclear
- R/o complicating process during acute exacerbations
- Pneumonia, pneumothorax, HF - Evaluate for comorbidities
- Lung CA, bronchiectasis, pleural disease, ILD, heart failure
CXR of chronic bronchitis vs emphysema
- Chronic Bronchitis - likely normal unless complications or comorbidities are present
- Emphysema
- Hyperinflation
- Flattened diaphragm
- Increased retrosternal air space
- Long, narrow heart shadow
3 stagings for COPD
- GOLD
- mMRC
- CAT
COPD staging is based on what 3 factors
Staging is multidimensional:
1. Airflow limitations
2. Symptom severity
3. Exacerbations
GOLD Staging for COPD
mild - FEV1 > 80%
mod - 50-80%
severe - 30-50%
very severe - <30%
which staging assess severity of breathlessness
Modified Medical Research Council Dyspnea Scale (mMRC)
which staging assesses multitude of sx present
COPD Assessment Test (CAT)
> 2 moderate exacerbations or >1 leading to hospitalization lands them at what stage?
E
0-1 moderate exacerbations (not leading to hospital) lands them at what stage
A or B
A = mMRC 0-1, CAT <10
B = mMRC >2, CAT >10
goals of COPD therapy
Improve sx
Decreased number of exacerbations
Improve patient functioning and quality of life
COPD therapy goals must be achieved with both __ and __
pharm + nonpharm management
nonpharm management for COPD
- SMOKING CESSATION
- Ask every patient at every visit!
- Pharm: NRT, Bupropion, Varenicline - Behavioral counseling
- Vaccinations
- Influenza, COVID-19, PCV-20 OR PCV-13 followed by PCV-23, Tdap , Zoster in pts >50 - wt loss & nutrition
- BMI, vit. D - Regular, progressive exercise
- Oxygen therapy
- pulm rehab
indications for oxygen therapy
pO2 ≤ 55 mmHg on ABG
O2 sat ≤ 88%
pO2 55-60 + RHF or erythrocytosis
pulm rehab is indicated in what COPD class
B and E
components of pulm rehab
- Exercise training
- Promotion of healthy behaviors
- Smoking cessation, regular exercise, healthy nutrition, proper medication use, adherence to prescribed medications, and disease self-management - Psychological support
- Providing coping strategies for chronic illness
what med is Used for immediate relief of dyspnea
short-acting bronchodilator
3 categories of meds for COPD pharm management
- short-acting bronchodilator
- long-acting bronchodilator
- inhaled corticosteroids
SE of SABA
Tachycardia
Tremor
Cardiac arrhythmia
SABA meds
Levalbuterol
albuterol
SE of SAMA
Dry mouth / eyes, metallic taste, prostatic symptoms
Ipratropium Bromide
SAMA
med of SABA + SAMA
Albuterol + Ipratropium
SE of LABA
Tachycardia
Tremor
Headache
LABA meds
Arformeterol (both QD and BID)
Salmeterol
Formeterol
SE of LAMA
Dry mouth, constipation, urinary retention
Tiotropium
LAMA
Umeclidinium
LAMA
Revefenacin
LAMA
Aclidinium
LAMA
Glycopyrrolate
LAMA
Meds of LABA+LAMA
Olodaterol /Tiotropium
Vilanterol/Umeclidinium
Formoterol/Glycopyrrolate
Formoterol/Aclidinium
LABA + ICS meds
Salmeterol/Fluticasone propionate
Vilanterol/Fluticasone furoate
Formoterol/Budesonide
LABA+LAMA+ICS meds
Fluticasone furoate/Umeclidinium/ Vilanterol
Beclometasone/Formoterol/ Glycopyrronium
Budesonide/Formoterol/ Glycopyrrolate
initial meds for COPD
E = LABA + LAMA (+ ICS if blood eos >300)
A = a bronchodilator
B = LABA + LAMA
how do you change management for dyspnea
choose another LABA or LAMA
may need LABA + LAMA
switch inhaler devices or molecules, implement/escalte nonpharm management, investigate other causes
how do you change management for exacerbations
choose another LABA or LAMA
blood eos <300 = LABA+LAMA
>300 = LABA+LAMA+ICS
add rodflumilast - FEV1 <50% + chronic bronchitis
add azithromycin - for former smokers
when to add an ICS
- strongly favors
- hx of hospitalization for exacerbations
- >2 moderate exacerbations/yr
- hx asthma - favor
- 1 moderate exaceration/yr
- blood eos 100 - <300 - against use
- repeated pneumonia events
- blood eos <100
- hx mycobacterial infection
indications for ICS removal
- pneumonia
- inappropriate indications
- lack of response
- trial de-escalation
MOA of Roflumilast
suppresses cytokine release and inhibits pulmonary neutrophil infiltration → reduces inflammation, pulmonary remodeling and mucociliary malfunction
class of Roflumilast
phosphodiesterase-4 (PDE-4) inhibitor
indications for Roflumilast
reduce exacerbations in severe COPD
SE of roflumilast
- Psychiatric reaction → anxiety, depression, insomnia
- Avoid if possible in pts with mental health history - N/V/D, weight loss, and dyspepsia
class of theophylline
non-specific phosphodiesterase inhibitor
MOA of theophylline
relaxes smooth muscle → suppresses airway response to noxious stimuli → increased diaphragm contraction force
indication for Theophylline
refractory COPD
SE of Theophylline
Anxiety, tremors, insomnia, nausea, cardiac arrhythmia, and seizures
TOXICITY CAN OCCUR
caution with Theophylline
avoid with liver impairment
f/u for COPD
1-3 months initially
3-6 months once stable
spirometry annually/PRN
risk factors for acute COPD exacerbations
Advanced age
Chronic productive cough
Duration of COPD
History of prior antibiotic therapy
COPD-related hospitalization within past year
Comorbid conditions (CAD, CHF, DM)
Respiratory infections (trigger ~70% of exacerbations)
presentation of COPD exacerbation
similar to regular but happening over hrs-days +
rsp compromise
decreased mental status
wheezing and tachypnea
for COPD exacerbations you must ask about: (4)
Time course of the symptom
Baseline level of symptoms
Severity of respiratory compromise
Sputum characteristics
most COPD exacerbations (80%) are managed where?
outpatient
when to consider inpatient management
- Severe sx → sudden worsening of resting dyspnea, high respiratory rate, decreased O2 sat, confusion, drowsiness
- Acute respiratory failure
- Onset of new PE findings (cyanosis, peripheral edema)
- Failure to respond to initial medical management
- Presence of serious comorbidities (CHF, arrhythmias)
- Insufficient home support*
acute COPD exacerbation outpatient management
- Adjust bronchodilator therapy
- Consider spacers / nebulizer therapy
- Consider oral glucocorticoid therapy - prednisone
- Abx for increased cough, sputum production, and purulence
- azithromycin, clarithromycin
- cefuroxime, cefdinir
- Amoxicillin-clavulanate
- levofloxacin, moxifloxacin - maybe non-invasive mech vent
COPD exacerbation inpatient management
- Supplemental O2 (target → 88-92%)
- Reverse obstruction → SABA +/- SAMA q4h; systemic corticosteroids
- IV abx → Levaquin, Ceftriaxone, or Piperacillin-Tazobactam
- Initiate pulmonary rehab
when to consider inpatient management ICU admission
Not responding to initial emergency therapy
Mental status changes
worsening hypoxemia (pO2 <5.3 kPa or 40 mmHg) +/- severe or worsening respiratory acidosis (pH<7.25) despite O2 and NIV
Invasive mechanical ventilation needed
Hemodynamically unstable
hospital DC and f/u timeline
1-4 wks
then
12-16 wks
an enzyme naturally produced by the liver and migrates to the lungs via the blood
protects the lungs from neutrophil (elastase) damage
Alpha-1 Antitrypsin
ATT deficiency occurs when there is a ___ preventing its release from the liver
genetic defect of ATT
2 pathophysiologic processes for ATT deficiency
ATT deficiency in the lungs leads to loss of elastin in the alveolar wall and early onset emphysema
An accumulation of ATT in the liver leads to destruction of hepatocytes and liver disease
presentation of ATT def
Same as emphysema in COPD at much younger age
Symptoms of chronic hepatitis, cirrhosis, or hepatocellular carcinoma
Symptoms of panniculitis → inflammation of subcutaneous tissue
consider diagnostic testing for ATT def with these factors:
In patients <45
Non-smokers or minimal smoking (<10-15 years)
FH of emphysema and/or liver disease
Adult onset asthma that does not respond to bronchodilators
Panniculitis or unexplained liver disease
work up for ATT def
- Low serum alpha-1 antitrypsin levels
- Genetic testing needed to confirm phenotype - PFT, CXR should be assessed
management for ATT def
Refer to provider specializing in disease
Aggressive lifestyle modifications
Pharmacotherapy, O2 therapy, vaccinations as indicated in COPD
Prompt management of acute respiratory infections
Pulmonary rehab
An irreversible focal or diffuse dilation and destruction of the bronchial walls
Bronchiectasis
pathophys of Bronchiectasis
multifactorial
1. Infectious insult in addition to impaired draining/obstruction and impaired host defense
- Often results from recurrent inflammation or infection of the airways
2. Leads to inflammation, mucosal edema, cratering, ulceration, and neovascularization of airway
presentation of Bronchiectasis
- Chronic daily productive cough
- Copious, foul-smelling, thick, purulent sputum is characteristic - Rales/rhonchi/wheezing on exam
- Acute exacerbations
- Increased sputum volume and purulence
imaging for Bronchiectasis
CXR to r/o pneumonia
Not always sensitive but “tram tracks”
CT - Ballooned or “honeycomb”
work-up for bronchiectasis
Sputum cx → directs abx in infectious exacerbations
Bronchoscopy → assess for underlying mass or FB in focal disease
tx for bronchiectasis
- Non-pharm management as in COPD
- Empiric antibiotics for acute exacerbations
- Amoxicillin, Amoxicillin-clavulanate, Doxycycline, TMP-SMX
- Consider long-term abx for pts with ≥ 3 exacerbations/yr - Bronchial hygiene
- Mucolytic therapy, bronchodilators, chest physiotherapy - Surgical resection → indicated in poorly controlled focal disease
- Lung transplant (definitive) → indicated when FEV₁ <30% predicted
Most common sleep-related breathing disorder
OSA
OSA is MC in who?
More common males, Asians and young African Americans
Increased prevalence in U.S. due to obesity
risk factors for OSA
Increasing age, male, obesity, smoking, craniofacial or upper airway abnormalities
Comorbid conditions such as pregnancy, ESRD, CHF, COPD, hx of stroke (CVA)
pathophys of OSA
Recurrent, functional collapse of pharyngeal airway during sleep → reduced airflow → intermittent disturbances in gas exchange and fragmented sleep
presentation of OSA
Signs of disturbed sleep
Daytime somnolence secondary to disturbed sleep
Obstructive apneas, hypopneas, or respiratory-related arousals
work up for OSA
- Sleep Apnea Questionnaire - Berlin Questionnaire, STOP-BANG
- Polysomnography - first-line
- Home sleep apnea testing
- Overnight oximetry
OSA criteria
- ≥5 obstructive respiratory events (apneas, hypopneas, or respiratory-related arousals) per hour of sleep plus one or more of the following:
- Sleepiness, non-restorative sleep, fatigue, insomnia
- Waking with breath-holding, gasping, or choking
- Habitual snoring or breathing interruptions
- HTN, mood disorder, cognitive dysfunction, CAD, CVA - ≥15 or more predominantly obstructive respiratory events per hour of sleep, regardless of associated symptoms or comorbidities
complications with OSA
Excessive daytime sleepiness, inattention, fatigue
Drowsy driving and associated MVA
Cardiovascular morbidity (HTN, pulmonary HTN, CAD, arrhythmias, CHF, CVA)
Metabolic syndrome and DM2
Nonalcoholic fatty liver disease (NASH)
Perioperative complications
Increased all-cause mortality (2-3x’s general population)
goals of OSA therapy
Reduce or eliminate apneas, hypopneas, and/or oxygen desaturations during sleep
Improve sleep quality and daytime function
management for OSA
- Wt loss is paramount
- Continuous positive airway pressure (CPAP) or Automatic positive airway pressure (APAP) - mainstay of therapy
- Oral appliances
- Upper airway surgery (UPPP², tonsillectomy, adenoidectomy)
- Hypoglossal nerve stimulation³
