chronic obstructive diseases Flashcards

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

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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

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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

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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

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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)

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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)

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7
Q

COPD exacerbations are Often precipitated by

A

infection or some sort of environmental exposure

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8
Q

late stages of COPD

A

PNA, Pulmonary hypertension,
Right sided heart failure***, chronic respiratory failure

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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

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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

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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)

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11
Q

measures how effectively the lungs transfer oxygen from inhaled air
to the blood

A

DLCO

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12
Q

what to do if patient has COPD with hypoxemia or hypercapnia

FEV1 or DLCO is less than 40% of predicted

A

ABG

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13
Q

COPD EKG

A

sinus tach

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14
Q

COPD XR

A

chronic bronchitis vs emphysema
emphysema—hyperinflation with diaphragm flattening or peripheral arterial deficiency

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14
Q

COPD chest CT

A

bronchitis vs emphysema
thickened walls and air trapped

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15
Q

COPD Advanced disease

A

pulmonary HTN

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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
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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

18
Q

Long-Acting Beta2-Agonist

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