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Respiratory > Obstructive lung disease > Flashcards

Obstructive lung disease Flashcards

1
Q

Define COPD in general

A

• progressive, and irreversible condition of the lung characterized by chronic obstruction to
airflow with many patients having periodic exacerbations, gas trapping, lung hyperinflation and
weight loss
• 2 subtypes (chronic bronchitis or emphysema): usually coexist to variable degrees
• gradual decrease in FEV1 over time with episodes of acute exacerbations

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2
Q

How is Chronic Bronchitis defined?

A

Defined clinically:
Productive cough on most days for at least
3 consecutive months in 2 successive years

Obstruction is due to narrowing of the airway lumen by mucosal thickening and excess mucus

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3
Q

How is emphysema defined?

A

Defined pathologically:
Dilation and destruction of air spaces distal to the terminal bronchiole
without obvious fibrosis

Decreased elastic recoil of lung parenchyma causes decreased
expiratory driving pressure, airway collapse, and air trapping

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4
Q

What are the (2) pathological types of emphysema?

A

1) Centriacinar - most common (respiratory bronchioles predominantly affected)
• Typical form seen in smokers, primarily affects upper lung zones

2) Panacinar (respiratory bronchioles, alveolar ducts, and alveolar sacs affected)
• Accounts for about 1% of emphysema cases
α1-antitrypsin deficiency, primarily affects lower lobes

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5
Q

What is the risk factor for COPD?

A

• SMOKING (#1)
• ƒ environmental: air pollution, occupational exposure, exposure to wood smoke or other
biomass fuel for cooking
ƒƒ• ƒ treatable factors: α1-antitrypsin deficiency, bronchial hyperactivity
• ƒƒƒdemographic factors: age, family history, male sex, history of childhood respiratory infections, low socioeconomic status

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6
Q

What are blue bloater and pink puffer?

A

Bronchitis - Blue Bloater

Emphysema - Pink Puffer

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7
Q

Px of Chronic bronchitis?

A

Chronic productive cough
Purulent sputum
Hemoptysis
Mild dyspnea initially

Cyanosis (2º to hypoxemia and hypercapnia)
Peripheral edema from RVF (cor pulmonale)
Crackles, wheezes
Prolonged expiration if obstructive
Frequently obese!! (c.f. emphysema)

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8
Q

Px of emphysema

A 
Dyspnea (± exertion)
Minimal cough
Tachypnea
Decreased exercise
tolerance
Pink skin
Pursed-lip breathing
Accessory muscle use
Cachectic!! appearance due to anorexia and increased work of breathing
Hyperinflation/barrel chest, hyperresonant
percussion
Decreased breath sounds
Decreased diaphragmatic excursion
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9
Q

Pulmonary function test of Chronic bronchitis vs. Emphysema

A

Chronic bronchitis:
low FEV1, low FEV1/FVC
N TLC, low or N DLCO

Emphysema:
low FEV1, low FEV1/FVC
high TLC (hyperinflation)
high RV (gas trapping)
low DLCO
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10
Q

CXR of chronic bronchitis vs. emphysema

A

Chronic bronchitis:

  • AP diameter normal
  • High bronchovascular markings
  • Enlarged heart with cor pulmonale

Emphysema:

  • high AP diameter
  • Flat hemidiaphragm (on lateral CXR)
  • low heart shadow
  • high retrosternal space
  • Bullae
  • low peripheral vascular markings
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11
Q

Ideal O2 sat for chronic CO2 retainers

A

88-92%

to prevent Haldane effect and decreased
respiratory drive.

retainers have chronically elevated CO2 levels with a normal pH.

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12
Q

What is alpha-1-antitrypsin deficiency

A

Inherited disorder of defective production of a1-antitrypsin, a protein
produced by hepatocytes.

Acts in the alveolar tissue by INHIBITING the action
of PROTEASES from destroying alveolar
tissue.

Hence when low/deficient -> proteases win -> destroy lung alveoli -> emphysema

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13
Q

How do you Rx stable COPD? List (3) for prolonging survival and (2) for symptomatic relief with no mortality benefit

A

Prolonging survival:
1. Smoking cessation
2 Vaccination (influenza, pneumococcal)
3. Home oxygen (prevents cor pulmonale)

Symptomatic relief
1. Bronchodilators (Inhaled corticosteroids + LABA combination, SABA)
2. Corticosteroids (as combination with LABA)
Others: lung volume reduction surgery, lung transplant, pt education, rehab

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14
Q

Define acute exacerbation of COPD

A

sustained (>24-48 h) worsening of dyspnea, cough, or sputum production leading to an
increased use of medications

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15
Q

What causes acute exacerbation of COPD?

A

viral URTI, bacteria, air pollution, CHF, PE, MI must be considered

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16
Q

Rx of acute exacerbation of COPD

A

· ABCs, consider assisted ventilation if decreasing LOC or poor ABGs
· O2: target 88-92% SaO2 for CO2 retainers
· bronchodilators by MDI with spacer or nebulizer
○ SABA + anticholinergic, e.g. salbutamol and ipratropium bromide via nebulizers x 3 back-to-back
· systemic corticosteroids: IV solumedrol or oral prednisone
· antibiotics if purulent sputum
○ simple exacerbation (no risk factors): amoxicillin, 2nd or 3rd generation cephalosporin, macrolide, or TMP/SMX
○ complicated exacerbation (one of: FEV1 ≤50% predicted, ≥4 exacerbations per year, ischemic heart disease, home O2 use, chronic oral steroid use): fluoroquinolone or β-lactam + β-lactamase inhibitor (Augmentin: amoxicillin/clavulanate)
· post exacerbation: rehabilitation with general conditioning to improve exercise tolerance

17
Q

What is BODE index?

A

Index used to predict risk of death in COPD

10 point system consisting of 4 factors:

  1. Body index
  2. Obstruction
  3. Dyspnoea
  4. Exercise capacity
  • greater score = higher probability the patient will die from COPD; score can also be used to predict hospitalization
18
Q

What are the common (4) conditions that cause airway obstruction (decreased FEV1)?

A
  1. Asthma
  2. COPD
  3. Bronchiectasis
  4. Cystic fibrosis
19
Q

What are the red flags of asthma?

A
  • severe tachypnoea, tachycardia
  • respiratory muscle fatigue
  • reduced expiratory effort
  • cyanosis
  • silent chest!!!
  • decreased LOC
20
Q

Define asthma

A
  • chronic inflammatory disorder of the airways resulting in episodes of reversible bronchospasm causing airflow obstruction
  • associated with REVERSIBLE airflow limitation and airway hyper-responsiveness to endogenous or exogenous stimuli
21
Q

Who gets asthma?

A
  • common, 7-10% of adults, 10-15% of children
  • most children with asthma significantly improve in adolescence
  • often family history of ATOPY (asthma, allergic rhinitis, eczema)
  • occupational asthma (organic allergies, isocyanates, animals, etc.)
22
Q

What are the triggers of asthma?

A

• URTIs, allergens (pet dander, house dust, moulds), irritants (cigarette smoke, air pollution), drugs (NSAIDs, β-blockers), preservatives (sulphites, MSG), other (emotion/anxiety, cold air, exercise, GERD)

23
Q

Pathophysiology of asthma

A

airway obstruction -> V/Q mismatch -> hypoxemia (type 1 RF) -> ↑ ventilation -> ↓ PaCO2 -> ↑ pH and
muscle fatigue -> ↓ ventilation, ↑ PaCO2/↓ pH (type 2 RF)

24
Q

Px of asthma

A
  • dyspnea, wheezing, chest tightness, cough (especially nocturnal), sputum
  • symptoms can be paroxysmal or persistent
  • signs of respiratory distress (see sidebar R3)
  • pulsus paradoxus
25
Q

Ix of asthma (make a comment about how CO2 levels can tell us how severe the asthma is)

A

• O2 saturation
• ABGs decreased PaO2 during attack (V/Q mismatch)
- decreased PaCO2 in mild asthma (hyperventilation)
- normal or increased PaCO2 is a dangerous sign: patient is no longer able to hyperventilate (worsened airway obstruction or respiratory muscle fatigue)

• PFTs (do when stable)

26
Q

Rx of asthma (in emergency & less severe cases)

A
  1. inhaled β2-agonist first line (MDI route and spacer device recommended)
  2. systemic steroids (PO or IV, if severe)
  3. add anticholinergic therapy ± magnesium sulphate
  4. rapid sequence intubation in life-threatening cases (plus 100% O2, monitors, IV access)
  5. SC/IV adrenaline, IV salbutamol if unresponsive
  6. corticosteroid therapy at discharge

Less severe:

- symptomatic relief in acute episodes: short-acting β2-agonist, anticholinergic bronchodilators, oral steroids, addition of a long acting β2-agonist
- long-term prevention: inhaled/oral corticosteroids, anti-allergic agents, long-acting β2-agonists, methylxanthine, LTRA, anti-IgE antibodies (e.g. Xolair®)

patient education: features of the disease, goals of treatment, self-monitoring

27
Q

Define bronchiectasis

A
  • IRREVERSIBLE dilatation of airways due to inflammatory destruction of airway walls resulting from persistently infected MUCUS
  • usually affects medium sized airways
28
Q

What are the risk factors of bronchiectasis & what is the most common pathogen?

A
  1. Obstruction (E.g. tumour, foreign body, thick mucus)
  2. Post-infectious (pneumonia, TB, ABPA)
  3. Impaired defenses (CF, hypogammaglobulinemia)

Pseudomonas aeruginosa = the most common pathogen

S. aureus, H. influenzae and nontuberculous mycobacteria also common

29
Q

Px of bronchiectasis

A
  • chronic cough, purulent sputum (but 10-20% have dry cough), hemoptysis (can be massive), recurrent pneumonia, local crackles (inspiratory and expiratory), wheezes
  • clubbing
  • may be difficult to differentiate from chronic bronchitis
30
Q

Ix of bronchiectasis

A

• CXR
- nonspecific: increased markings, linear atelectasis, loss of volume in affected areas
- specific: “tram tracking” – parallel narrow lines radiating from hilum, cystic spaces, honeycomb like structures
• high-resolution thoracic CT (diagnostic, gold standard):
- 87-97% sensitivity, 93-100% specificity
- “signet ring”: dilated bronchi with thickened walls where diameter bronchus > diameter of accompanying artery
• sputum cultures (routine + AFB)
• serum Ig levels

• sweat chloride if cystic fibrosis suspected (upper zone predominant)

31
Q

Rx of bronchiectasis

A
  • vaccination: influenza and Pneumovax®
  • antibiotics: macrolides may be used chronically for an anti-inflammatory effect
  • inhaled corticosteroids: decrease inflammation and improve FEV1
  • oral corticosteroids for acute, major exacerbations
  • chest physiotherapy, breathing exercises, physical exercise
  • pulmonary resection: in selected cases with focal bronchiectasis
32
Q

How does cystic fibrosis present?

A

Usually presents in childhood as recurrent lung infections that become persistent and chronic.

  • results in severe lung disease, pancreatic insufficiency, diabetes and azoospermia
  • other manifestations: meconium ileus in infancy, distal ileal obstruction in adults, sinusitis, liver disease
33
Q

What organisms commonly cause chronic lung infections in CF?

A
  • S. aureus: early
  • P. aeruginosa: most common
  • B. cepacia: worse prognosis but less common
  • Aspergillus fumigatus
34
Q

Ix for CF

A

• sweat chloride test
- increased concentrations of NaCl and K+ ([Cl-] >60 mmol/L is diagnostic in children)
- heterozygotes have normal sweat tests (and no symptoms)
• PFTs
- early: airflow limitation in small airways
- late: severe airflow hyperinflation, gas trapping, decreased DLCO (very late)
• ABGs
- hypoxemia, hypercapnia later in disease with eventual respiratory failure and cor pulmonale
• CXR
- hyperinflation, increased pulmonary markings (especially upper lobes)

35
Q

Rx of CF

A
  • chest physiotherapy and postural drainage
  • bronchodilators (salbutamol ± ipratropium bromide)
  • inhaled mucolytic (reduces mucus viscosity), hypertonic saline DNase
  • inhaled tobramycin
  • antibiotics (e.g. ciprofloxacin)
  • lung transplant
  • pancreatic enzyme replacements
36
Q

What is pathophysiology of CF?

A

chloride transport dysfunction: thick secretions from exocrine glands (lung, pancreas, skin, reproductive organs) and blockage of secretory ducts

Hence increased Cl-

Respiratory (11 decks)

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