Obstructive lung disease Flashcards

1
Q

two major causes of airflow obstruction

A

Intrinsic airway narrowing (bronchospasm, plugging, inflammation/edema) or “Floppy” airways – decreased radial tethering or decreased airway integrity
Intrinsic airway narrowing (bronchospasm, plugging, inflammation/edema) or “Floppy” airways – decreased radial tethering or decreased airway integrity
Intrinsic airway narrowing (bronchospasm, plugging, inflammation/edema) or “Floppy” airways – decreased radial tethering or decreased airway integrity

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2
Q

Total work of breathing = ?

A

work done against resistance to airflow (resistive work)vPLUS work done against the elastic recoil of the respiratory system (elastic work).

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3
Q

How do obstructive diseases affect airflow and lung volumes and diaphragm

A

Airflow is decreased and lung volumes increase (due to incomplete emptying of alveoli causing air trapping). Diaphragm is flattened to allow hyperventilation which then reduces inspiratory pressure and inspiratory capacity

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4
Q

What location of airway does bronchitis, asthma, bronchiectasis, bronchiolitis and emphysema affect?

A

Bronchitis: Bronchi. Asthma and bronchiectasis: bronchi/bronchioles. Bronchiolitis: respiratory bronchioles. Emphysema: alveolar sacs

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5
Q

Asthma definition

A

Asthma is a chronic, reversible inflammatory disorder of the airways associated with airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing particularly at night or in the early morning

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6
Q

Two types of asthma

A

Extrinsic (type I hypersensitivity rxn to outside agent) and intrinsic (non immune rxn to aspirin, infection, stress, exercise).

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7
Q

Subtypes of extrinsic asthma

A

atopic or allergic asthma, occupational asthma, and allergic bronchopulmonary aspergillosis.

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8
Q

Factors that influence asthma development

A

–genetic predisposition to atopy or airway hyper responsiveness, obesity, and sex. Exposure to allergens, infection, occupational exposures, smoke, pollution, diet

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9
Q

Describe airway inflammation in asthma and cells involved

A

airway inflammation in asthma is persistent even though symptoms may be intermittent. Involves mast cells (histamine, prostaglandin), Eosinophils, Th2 (cytokine release), dendritic cells, macrophage, neutrophils

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10
Q

Structural changes in asthma

A

Increase in airway smooth muscle cells due to hypertrophy and hyperplasia, Blood vessel proliferation, Mucus hyper-secretion in the context of increased number of goblet cells and increase size of submucosal glands.

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11
Q

Key clinical features of asthma

A

Intermittent (PFTs can be normal btw), reversibility of obstruction, cough, dyspnea, wheezing, exacerbations to exercise, cold air, allergens, nl to increased DLCO

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12
Q

Test used to detect asthma

A

Bronchoprovocation with methacholine (or exercise alone) will show decreased FEV at lower conc than healthy people. The PC20 is the concentration required to lower airflow FEV by 20%

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13
Q

Signs of acute asthma

A

hyperinflation, decreased tension and pressure from diaphragm, Breathing at flatter part of P-V curve so more pressure required to get similar change in volume, accessory muscles, increased work of breathing

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14
Q

Asthma severity levels

A

intermittent (2X/ week), moderate persistent (daily symptoms, multiple exacerbations per week), severe persistent (continual symptoms, frequent exacerbations)

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15
Q

Vocal cord dysfunction

A

•Inappropriate vocal cord adduction during inspiration results in airflow obstruction. Symptoms mimic asthma

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16
Q

Stridor

A

Wheezing sound upon inhalation (seen in vocal cord dysfunction)

17
Q

Vocal cord dysfunction bronchoprovocation

A

FEV and the 20% change concentration will not change in VCD, but VCD may worsen

18
Q

COPD definition

A

fixed airflow limitation- includes emphysema and chronic bronchitis

19
Q

Chronic bronchitis defn

A

•Productive cough at least 3 months over the past 2 years without other cause. Increased airway resistance due to changes in airway structure (edema, mucus, fibrosis). May have overlapping features with asthma. Impaired ventilation

20
Q

chronic bronchitis airways

A

hypertrophied submucosal glands and increased in number, with increased ratio of glands to bronchial wall thickness. Goblet cells increased in number. Airway lumen is narrowed

21
Q

P-V curve in chronic bronchitis

A

shifted upwards

22
Q

Chronic bronchitis is a disease of ________________ while emphysema is a disease of _____________________

A

airways, parenchymal disease (loss of tissue elastic recoil)

23
Q

Emphysema pathogenesis

A

Loss of normal alveolar spaces with enlargement of distal airspaces. Increased lung compliance (lung is less stiff due to decreased elastic tissue, alpha-1-antitrypsin deficit, apoptosis of alveolar cells, impaired repair). Impaired gas exchange

24
Q

types of distal airspace enlargement in emphysema

A

pan-acinar involves entire distal airspace (acinus), seen in older patients and alpha1 antitrypsin deficiency. Centri-acinar involves respiratory bronchioles and is smoking related

25
Q

What causes airflow obstruction in emphysema

A

dynamic airway collapse- loss of elasticity in surrounding tissue of airways

26
Q

P-V curve in emphysema

A

Curve is steeper and shifted upwards

27
Q

Distinguish chronic bronchitis and emphysema on physical exam

A

Chronic Bronchitis: Cough, Rhonchi, Wheezing. Emphysema: diminished breath sounds, hyper-resonant. Common: Prolonged expiratory phase, Pursed-lip breathing, Tri-pod position

28
Q

COPD acute exacerbation -signs, precipitated by, treatment

A

increased cough, Sputum volume and purulence
Increased wheezing. Worsening obstruction on PFTs, Unchanged CXR. Precipitated by infection, pollution, PE, unknown factors. Increased work of breathing due to hyperinflation, increased airway resistance. Treated with bronchodilators, steroids, antibiotics
increased cough, Sputum volume and purulence
Increased wheezing. Worsening obstruction on PFTs, Unchanged CXR. Precipitated by infection, pollution, PE, unknown factors. Increased work of breathing due to hyperinflation, increased airway resistance. Treated with bronchodilators, steroids, antibiotics

29
Q

Causes of death from COPD

A

Respiratory failure, Right ventricular failure, Pneumonia, Spontaneous pneumothorax, Pulmonary embolism

30
Q

compare DLCO in asthma, chronic bronchitis and emphysema

A

asthma: nl to increased. Chronic bronchitis: nl to increased. Emphysema: decreased b/c alveolar capillary bed is destroyed

31
Q

Chronic bronchitis and emphysema response to bronchodilators

A

bronchitis: minimally reversible. Emphysema: not reversible

32
Q

Bronchiectasis

A

Abnormal Dilation of Proximal Bronchi due to destruction of muscular and elastic components of their walls

33
Q

Presentation of bronchiectasis

A

cough with purulent sputum (often copious), wheezing, hemoptysis(bronchial arteries enlarge to supply the inflamed airway), mild airflow limitation

34
Q

Pathophys of bronchiectasis

A

Combo of infectious insult and impaired drainage, obstruction or immunodeficiency. Loss of airway wall integrity with dilation. Recurrent infections worsen bronchiectasis (CF, PCD, immunodeficiency).Dilated, collapsible airways result in obstruction that May be compounded by inflammation

35
Q

Management of bronchiectasis

A

Airway clearance (promote secretion clearance), antibiotics, treat reactive airway disease

36
Q

Bronchiolitis signs and causes

A

inspiratory squeaks on exam. Caused by infection (RSV in kids, mycoplasma in adults), toxins, collagen vascular disease, etc