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pulmonology > chronic obstructive diseases > Flashcards

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

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
Q

Brochodilator and anti-inflammatory

A

phosphodiesterase type 4 inhibitor

21
Q

COPD management: outpatient

A
  • O2
  • Inhaled bronchodilators
  • Corticosteroids
  • Theophylline
  • Abx
  • Pulmonary rehab
  • Phosphodiesterase type 4 inhibitor
  • Other
22
Q
  • 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
A

inhaled bronchodilators

22
Q
  • 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
A

O2

22
Q
  • used for Pts who don’t improve enough with other medications
  • requires monitoring d/t toxicity
  • last resort, d/c w/o improvement
A

theophylline

23
Q
  • 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
A

corticosteroids

24
Q

1) *acute exacerbation
* increased sputum production or purulence, increase dyspnea
2) acute bronchitis
3) prophylaxis for exacerbations of chronic bronchitis

A

Abx

  • Choice of Abx
  • local resistance, recent use, certain individual risk factors
25
Q

physical exercise programs

A

pulmonary rehab

25
Q

Roflumilast: for moderate or severe COPD and chronic bronchitis and
frequent exarcerbations and who are taking LABA/ICS and/or LAMA

A

phosphodiesterase type 4 inhibitor

26
Q

other COPD management

A
  • Hydration
  • Helps manage secretions
  • Cough training methods, flutter device and postural drainage, chest
    percussion or vibration
27
Q

COPD management: inpatient
* Acute exacerbations:

A
  • 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
Q

COPD: When to Admit

A
  • 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
Q

COPD management: other
* Procedures

A
  • Lung transplant
  • Lung reduction
  • Bullectomy
28
Q

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
A

COPD: Alpha 1 anti-trypsin deficiency
* AAT deficiency

29
Q

AAT deficiency treatment

A

Infusion of pooled plasma-purified human alpha-1 antitrypsin is the
only licensed disease-specific therapy for AAT deficiency associated
with lung disease

29
Q
  • 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

A

bronchiectasis

29
Q

AAT deficiency: when to test

A
  • 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
Q
  • 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
A

bronchiectasis symptoms

30
Q

Bronchiectasis: Complications

A

Infectious exacerbations of chronic respiratory symptoms
* Clubbing
* Cyanosis
* Wheezing
* Inspiratory crackles

31
Q

bronchiectasis management

A
  • 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
Q

Bronchiectasis: diagnostic Testing

A

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 (8 decks)

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