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Pulmonology Exam > Asthma & COPD > Flashcards

Asthma & COPD Flashcards

1
Q

obstructive lung diseases: diseases with narrowing of airways

A

*COPD
*asthma

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2
Q

obstructive lung diseases: diseases with DILATION of airways

A

*cystic fibrosis (CF)
*non-CF bronchiectasis

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3
Q

asthma - defined

A

*a disease of CHRONIC inflammation of the airways
*intermittent obstructive lung disease often triggered by allergens, viral URIs, and stress

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4
Q

asthma - variable symptoms

A

*variable and recurring dyspnea, wheezing, cough, and/or chest tightness
*reversible airflow obstruction (bronchodilator response)
*resolution of an exacerbation
*diurnal symptoms (worse symptoms at night) frequently present

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5
Q

bronchodilator reversibility in asthma

A

*obstruction is reversed with the use of a bronchodilator, defined by:
an increase in FEV1 or FVC by 10% or more after use of a bronchodilator

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6
Q

asthma phenotypes

A

*Th2 asthma (allergic asthma)
*non-Th2 asthma (non-allergic asthma)

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7
Q

allergic asthma (Th2): features

A

*atopic (rhinitis, eczema, asthma)
*allergens: dust mites, seasonal pollens, pet dander
*occupational asthma: workplace allergens

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8
Q

allergic asthma: pathobiology

A

*Th2-driven pathobiology: allergen → stimulates an antigen presenting cell → activates Th2 cells, which release IL-4, IL-5, IL-13 → activation of eosinophils, mast cells, and B cells → release of leukotrienes, histamine, etc

*leads to atopic phenotype
*eosinophils, mast cells, and B cells are the MAIN EFFECTOR CELLS
*UNCONTROLLED INFLAMMATION LEADS TO AIRWAY REMODELING

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9
Q

airway inflammation in allergic asthma

A

*inflammation of terminal bronchioles (smooth muscles, no cartilage)
*Th2 cells are activated by an antigen → release of IL-2, IL-4, IL-5, and IL-13 → activation of eosinophils, mast cells, and IgE from B cells
*bronchial submucosal edema and smooth muscle contraction
*bronchial obstruction from edema, cellular debris, airway smooth muscle hypertrophy, bronchospasm

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10
Q

hypersensitivity in allergic asthma

A

*chronic underlying inflammation of asthma: type IV Th2 hypersensitivity
*acute exacerbation of asthma is acute inflammation in addition to chronic inflammation: type 1 (IgE-mediated) hypersensitivity

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11
Q

non-allergic asthma (non-Th2): features

A

*common triggers: viral infections, cold air, exercise, sinusitis, gastric reflux, stress
*inhaled irritants: tobacco, solvents, chemicals

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12
Q

non-allergic asthma: pathobiology

A

*not entirely known
*triggers are not allergens (they are something else)
*NEUTROPHILS play a key role as an effector cell
*uncontrolled inflammation leads to airway remodeling

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13
Q

airway remodeling due to chronic inflammation

A

*smooth muscle hypertrophy & hyperplasia
*goblet cell hyperplasia
*combined, these hypertrophies cause a narrowed lumen, causing OBSTRUCTION of airflow

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14
Q

diagnosis of asthma: testing airway responsiveness

A

*assess bronchial responsiveness to see how the airways “respond” to stimuli using:
1. short-acting beta agonist (bronchodilator): responsive = 10%+ increase in FEV1 or FVC
2. bronchoprovocation to induce hyper-responsiveness by: short-acting cholinergic (e.g. methacholine)

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15
Q

classic asthma symptoms

A

EPISODIC symptoms of:
1. COUGH (esp after exertion, breathing cold air, at night, after colds, paroxysmal)
2. WHEEZING (chest tightness, noisy breathing)
3. BREATHLESSNESS (esp if intermittent, after exertion, or at night)

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16
Q

physical exam: asthma (during acute exacerbation)

A

*tachypnea
*use of accessory muscles to breathe
*markedly prolonged expiration with wheezing
*no air movement, “silent chest”
*intercostal retractions in childen

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17
Q

lab studies & pathology for workup of asthma

A

*CBC (looking for eosinophilia)
*allergy testing
*sputum samples:
-Cruschmann spirals (mucous plugs from epithelium)
-Charot-Leyden crystals (eosinophilic crystals)
-Creola bodies (desquamated epithelial cells)

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18
Q

CXR findings in asthma

A

*CXR rarely demonstrates any abnormalities in asthma
*advanced disease from airway remodeling or acute exacerbation can cause hyperinflation

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19
Q

asthma therapies: short-acting beta agonists (SABA)

A

*used for RESCUE (sudden onset symptoms)
*examples: albuterol, levalbuterol, pirbuterol

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20
Q

asthma therapies: inhaled corticosteroids

A

*goal: target underlying inflammation (maybe prevent airway remodeling)
*examples: fluticasone, budesonide, mometasone, flunisolide, etc

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21
Q

asthma therapies: leukotriene modifier therapies

A

*Montelukast [a leukotriene (LTD4) receptor (CysLT1) antagonist)

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22
Q

asthma therapies: biologic therapies for severe eosinophilic asthma

A

*monoclonal antibodies (omalizumab, reslizumab, mepolizumab, benralizumab)

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23
Q

aspirin-induced asthma

A

*patient with a history of asthma takes aspirin
*aspirin inhibits COX-1
*less COX-1 activity → decreased arachidonic acid metabolism via COX → less PGE2 (anti-inflammatory)
*increase in leukotrienes and more inflammation of the submucosa
*increased bronchial constriction/hyper-responsiveness

24
Q

status asthmaticus - overview

A

*extreme, life-threatening asthma exacerbation
*does NOT respond to bronchodilators

25
Q

status asthmaticus - clinical features

A

*tachypnea, hypoxemia, cyanosis
*signs of respiratory arrest, pulsus paradoxus (exaggerated drop in systolic BP with inspiration)

26
Q

status asthmaticus - diagnosis

A

*CBC (look for infection)
*arterial blood gas (look for increased PCO2, hypoxemia, low pH)
*peak expiratory flow measurement (FEV1 < 50% warrants ICU admission)
*CXR
*EKG

27
Q

status asthmaticus - management

A

*bronchodilation
*systemic steroids
*IV magnesium
*O2
*non-invasive ventilation or intubation
*INDICATIONS OF INTUBATION: NORMALIZATION OF PCO2 (PCO2 starts low, but then starts rising/becomes elevated)

28
Q

chronic obstructive pulmonary disease (COPD) - risk factors

A

*SMOKING
*genetic etiologies
*other

29
Q

chronic obstructive pulmonary disease (COPD) - definition

A

*characterized by PERSISTENT (CHRONIC) AIRFLOW OBSTRUCTION [FEV1/FVC is , 0.70]
*frequently progressive and disabling
*associated with a chronic inflammatory response in airways/lungs to noxious particles or gases
*damage to small airways

30
Q

chronic obstructive pulmonary disease (COPD) - phenotypes

A
  1. chronic bronchitis
  2. emphysema
31
Q

PFT findings in COPD

A

*FEV1/FVC: < 0.7 or less than LLN
*FVC: normal or decreased
*FEV1: DECREASED (used to determine severity of disease)
*RV: increased if air trapping is present
*TLC: normal or increased
*DLCO: normal (chronic bronchitis) vs. decreased (emphysema)
*NO reversal of obstruction with bronchodilator

32
Q

DLCO PFT findings of COPD: chronic bronchitis vs. emphysema

A

*if DLCO is normal: chronic bronchitis
*if DLCO is decreased: emphysema

33
Q

pathophysiology of COPD

A

*COPD is a disease of chronic inflammation
*increased NEUTROPHILS, macrophages, and lymphocytes
*goblet cell hyperplasia
*hypersecretion and impaired ciliary function
*smooth muscle hyperplasia
*loss of parenchyma (in emphysema - due to unopposed proteases)

34
Q

COPD: chronic bronchitis - overview & clinical definition

A

*“blue bloaters”
*defined by: sputum production most days for 3 months for 2 consecutive years of more (excessive mucociliary dysfunction, increased goblet cell secretion)
*most commonly caused by smoking

35
Q

COPD: chronic bronchitis - mechanism

A

*progressive obstruction → hypoventilation and V/Q mismatch → progressive respiratory acidosis and hypoxemia (BLUE)
*alveolar hypoventilation → pulmonary artery vasoconstriction → right heart failure (cor pulmonale) → fluid retention (BLOATER)

36
Q

COPD: chronic bronchitis - Reid index

A

*ratio between the thickness of the submucosal mucous secreting glands and the thickness between the epithelium and the cartilage
*ratio > 0.4 is consistent with chronic bronchitis

37
Q

COPD: emphysema - overview and clinical definition

A

*“pink puffers”
*defined by: destruction of alveoli, alveolar duct, and/or respiratory bronchioles
*DECREASED DLCO on PFTs
*INCREASED COMPLIANCE due to loss of elastic fibers and less lung recoil
*leads to barrel chest, air trapping, and hyperinflation

38
Q

COPD: emphysema - mechanism

A

*alveolar macrophages release proteases and cytokines → recruit neutrophils secrete elastase and proteases
*both terminal bronchioles/alveoli with associated capillary beds destroyed
*match V/Q deficit: HYPOXEMA & HYPERCAPNIA
*attempts hyperventilation due to hypercapnia → air trapping develops and decreased cardiac output → increasing V/Q mismatch (poor perfusion in areas of good ventilation)
*cachexia is mutifactorial: hyperventilation, increased work of breathing (PINK PUFFER), inflammatory cytokines

39
Q

COPD: emphysema - 2 locations

A
  1. centrilobular/centriacinar emphysema (occurs in respiratory bronchioles)
  2. panlobular/panacinar emphysema (occurs in alveoli/alveolar ducts)
40
Q

centrilobular emphysema

A

*emphysema in the respiratory bronchioles (spares distal alveoli)
*associated with SMOKING
*commonly affects the upper lobes

41
Q

panlobular emphysema

A

*emphysema in the alveoli/alveolar ducts
*associated with A1AT (alpha1-antitrypsin deficiency)
*commonly affects the lower lobes

42
Q

chronic hypercapnic respiratory failure in COPD

A

*to maintain minute ventilation early in the disease, patients will take large tidal volumes and have a prolonged expiratory phase (due to obstruction)
*hypercapnia is due to INCREASED DEAD SPACE, which happens because of:
-as the disease progresses, air trapping occurs due to obstruction of the small airways and progressive worsening of FEV1; air is trapped in the alveoli, but its not well exchanged (ventilated) during respiration
-this leads to an overall decrease in tidal volume with a max respiratory rate, but the alveolar minute ventilation is inadequate → chronic hypercapnic respiratory failure

43
Q

COPD - clinical presentation

A

*DYSPNEA (persistent, progressive, worse with exercise)
*chronic cough that may be productive,
*recurrent infections
*patients often underreport symptoms

44
Q

COPD - physical exam findings

A

*PE is rarely diagnostic in COPD
*lung exam: hyper-resonant, wheezing, or silent chest
*cardiac exam: distant heart sounds, especially if hyperinflation is present
*physical signs of airflow limitation

45
Q

COPD: treatment - 2 major goals

A
  1. symptom reduction (relieve symptoms, improve exercise tolerance, improve health)
  2. risk reduction (prevent progression, prevent exacerbations, reduce mortality)
46
Q

COPD: non-pharmacologic treatments

A

*SMOKING CESSATION
*vaccinations (pneumococcal and influenza, COVID)
*supplemental oxygen
*pulmonary rehabd

47
Q

COPD: pharmacologic options

A
  1. bronchodilators:
    -short acting beta agonists
    -short acting anticholinergics (ipratropium)
    -long acting anticholinergics (tiotroprium, aclidinium, umeclidinium)
    -long acting beta agonists
  2. anti-inflammatories:
    -ICS + LABA
    -PDE-4 inhibitors (roflumilast)
    -oral steroids
    -chronic azithromycin
48
Q

what genetic abnormality is associated with COPD

A

*alpha 1 antitrypsin deficiency (associated with panlobular emphysema)

49
Q

alpha 1 antitrypsin deficiency

A

*genetic abnormality that is a risk factor for COPD
*Serpin superfamily (SERPINA1 gene)
*found on chromosome 14
*functions as a protease inhibitor, primarily against neutrophils elastase

50
Q

clinical vignette clue for COPD due to alpha 1 antitrypsin deficiency

A

*COPD in someone less than 50yo
*+/- cirrhosis
*basilar emphysema (at the base of the lungs; lower lobes)

51
Q

alpha 1 antitrypsin deficiency COPD - pathophysiology

A

*neutrophils release neutrophil elastase after stimulation
*lack of A1AT allows neutrophil elastase to breakdown elastin of the lungs (“tethers”)
*lower lungs are more involved

52
Q

alpha 1 antitrypsin deficiency COPD - genotypes

A

*PiMM = normal
*PiZZ = severe deficiency
*PiZZ is associated with LIVER CIRRHOSIS (due to misfolded protein can’t be excreted and accumulated in liver cells)
*ALL COPD patients should be tested
*treatment: augmentation with donor A1AT

53
Q

COPD exacerbation - defined

A

*an acute change in a patient’s baseline symptoms:
-increased dyspnea compared to baseline
-more frequent cough
-increased sputum production beyond day-to-day variability
-symptoms significant enough to warrant a change in therapy

54
Q

etiologies of COPD acute exacerbation

A

*viral infections
*bacterial infections
*environmental triggers
*non-adherence to therapy
*pulmonary embolism

55
Q

severity of COPD exacerbation

A

*assess respiratory rate, mental status, accessory muscle use, and O2 response

*MILD: no respiratory failure
-RR 20-30, no accessory muscles, normal MS, responds to O2

*MODERATE: non-life-threatening respiratory failure
-RR > 30, accessory use, normal mental status, responds to O2, elevated PCO2

*SEVERE: life-threatening respiratory failure
-moderate criteria + CHANGE IN MENTAL STATUS, no O2 response, pH < 7.25

Pulmonology Exam (36 decks)

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