Obstructive Lung Disease Flashcards

1
Q

Where is pseudostratified ciliated columnar epithelium found in the lung?

A

Airways proximal to RBs lined by pseudostratified ciliated columnar epithelium

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2
Q

Where does the normal acinus start?

A

starts distal to terminal bronchiole

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3
Q

What types of cells are in the alveolus?

A

Type I pneumocytes:
cover 95% of alveolar
surface and are the diffusion surface

Type II pneumocytes: Produce surfactant & Repair of alveolar
epithelium

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4
Q

What are pores of Kohn?

A

alveola septa are not continuous but have the pores of Kohn

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5
Q

Define OPD:

A

Diseases that cause obstruction to airflow out of the lungs

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6
Q

What are the types of COPD?

A

– Emphysema
– Chronic bronchitis
– Asthma
– Bronchiectasis

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7
Q

What is FVC?

A

Forced vital capacity (FVC)– Lungs are forcibly emptied at maximal speed from point of full inspiration

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8
Q

What is FEV1?

A

Forced expiratory volume in 1 second

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9
Q

What is the FEV1:FVC ratio used for?

A

useful for detecting obstruction and differentiating obstructive from restrictive lung disease

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10
Q

What happens in obstructive airway disease?

A
  • Airway disorder – trachea to terminal bronchiole
  • Increased resistance to air flow and limited expiratory rates on forced expiration
  • Reduced FEV1:FVC ratio
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11
Q

What happens in restrictive airway disease?

A
  • Parenchymal disorder -respiratory bronchiole, alveoli and alveolar ducts
  • Decreased expansion with reduced Total Lung Capacity, O2 diffusing capacity, Lung Volumes and compliance
  • Increased FEV1:FVC ratio
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12
Q

What is Emphysema?

A

Permanent enlargement of all or part of the respiratory unit (respiratory bronchioles, alveolar ducts, alveoli) accompanied by wall destruction without obvious fibrosis due to a protease imbalance

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13
Q

What are some causes of emphysema?

A

– Smoking (tobacco, marijuana)
– Air pollution
– α1-antitrypsin deficiency

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14
Q

What are the two types of emphysema?

A

– Centriacinar (centrilobular) – 95% cases

– Panacinar

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15
Q

What is the pathogenesis of emphysema?

A

Increased numbers of macrophages, CD8+ T lymphocytes and neutrophils activated by tissue damage from cigarette smoke

Elastase and free radicals derive from neutrophils and macrophages –> Destruction of elastic tissue –>Increased compliance and decreased elasticity

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16
Q

What is a disease of Elastic tissue → keeps airway lumens open by applying traction → elastic destruction causes collapse of airways on expiration → prevents exit of air → trapped air distends part of respiratory unit that has lost the elastic support → dilatation and destruction of alveoli and alveolar ducts (also distal/terminal bronchioles)?

A

Emphysema

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17
Q

What is Centriacinar emphysema?

A

Smokers’ emphysema in Apical segments of upper lobes

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18
Q

How does smoking cause Centriacinar emphysema?

A

Tobacco smoke contains “free radicals” which deplete these antioxidants and Oxidative injury also inactivates native antiproteases – “functional α1-antitrypsin deficiency”

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19
Q

What is Panacinar emphysema?

A

α1-antitrypsin deficiency: Lower lobes All parts of the respiratory unit are affected by elastic tissue destruction

20
Q

What causes Panacinar emphysema?

A

genetic or aquired (smoking)

genetic is autosomal dominant with phenotypes associated with severe deficiency of α1-antitrypsin enzyme production in the liver

21
Q

What are the clinical findings with emphysema?

A

– Severe and early onset of dyspnea
– Pink puffers
– Coexistence with chronic bronchitis (smokers’ emphysema)
– Cor pulmonale – less common than in chronic bronchitis
– Diminished breath sounds due to hyperinflation

22
Q

What can you see on a chest xray of emphysema?

A

– Increased AP diameter
– Hyperlucent lung fields
– Vertical heart
– Depressed diaphragm

23
Q

What are some other types of emphysema?

A
  • Paraseptal emphysema (Subpleural involvement, Spontaneous pneumothorax, No COPD)
  • Irregular emphysema (Localized, scar associated, No COPD)
24
Q

What is chronic bronchitis?

A

Productive cough for at least 3 months for 2 consecutive years

25
Q

What are some causes of chronic bronchitis?

A

– Smoking

– Cystic fibrosis

26
Q

What is the pathogenesis of chronic bronchitis?

A

– Inhaled smoke (irritant) → mucous hypersecretion in bronchi → airflow obstruction in terminal bronchioles (more proximal than in emphysema) → irreversible fibrosis of terminal bronchioles
– Infection: Maintenance of disease andAcute exacerbations
– Bronchospasm

27
Q

How do airways look in chronic bronchitis?

A

mucous overproduction, constriction of bronchiole with bronchospasm/smooth muscle hyperplasia, edema, erythema

28
Q

What are the clinical findings with chronic broncnitis?

A
– Productive cough
– Cyanosis (due to decreased O2
saturation from hypoxemia)
– “Blue bloaters”
– Dyspnea
– Expiratory wheezing and rhonchi
– Cor pulmonale
29
Q

What would you see on a chest xray of chronic bronchitis?

A

– Enlarged heart, horizontally oriented

– Increased bronchial markings

30
Q

What about on histology for chronic bronchitis?

A

blue inflammatory cells, mucous gland hyperplasia, thickening of walls, narrow lumens

31
Q

How is mucous gland hyperplasia measured?

A

Reid Index

• Ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and cartilage

32
Q

What is Bronchiectasis?

A

Permanent destruction and dilatation of bronchi and bronchioles involves cartilage and elastic tissue

33
Q

What are some causes of Bronchiectasis?

A

– Cystic fibrosis
– Infections: TB, Adenovirus, H influenzae, staph aureus
– Bronchial obstruction
– Primary ciliary dyskinesia
– Allergic bronchopulmonary aspergillosis

34
Q

What are the clinical findings of Bronchiectasis?

A

– Copious sputum
– Hemoptysis
– Digital clubbing
– Cor pulmonale

35
Q

What would you see on a chest xray of Bronchiectasis?

A

Bronchial markings extending to the periphery of the lungs

36
Q

What are the gross findings of Bronchiectasis?

A

dilated airways filled with mucous and pus

37
Q

What are the microscopic findings of Bronchiectasis?

A

– Intense acute and chronic inflammatory exudate in bronchial walls, necrotizing ulceration
– Squamous metaplasia of bronchial epithelium
– Lung abscesses may be present
– Fibrosis of bronchial walls leading to bronchiolitis obliterans
– Cultures are usually positive

38
Q

What is cystic fibrosis?

A

Autosomal recessive Deletion on chromosome 7 causing Defective CF transmembrane conductance regulator (CFTR) for chloride ions

39
Q

What is the pathogenesis of CF?

A

Increased Na and water reabsorption from luminal secretions and decreased Cl secretions from epithelial cells into lumen so Dehydration of body secretions due lack of NaCl – bronchioles, pancreatic ducts, bile ducts, meconium, seminal fluid

40
Q

What are the clinical findings in CF?

A
– Nasal polyps
– Respiratory infections → Respiratory failure
– Malabsorption
– Type I diabetes mellitus
– Infertility in males
– Meconium ileus
– Secondary biliary cirrhosis
41
Q

A pt has recent 20 lb weight loss associated with rapid onset SOB what is the most likely diagnosis?

A

lung cancer

42
Q

Do swollen feet and significant sputum production occur in asthma?

A

Nope

43
Q

What if a pt has seasonality to their breathing symptoms?

A

probably allergies and asthma

44
Q

Asthma is usually _____ airway obstruction while COPD is usually _______

A

asthma: reversible
COPD: not reversible

45
Q

– Usually related to smoking exposure
– Obstruction generally not reversible with a beta-agonist
– Reduced gas exchange
– Emphysema
– Chronic bronchitis
– Associated diseases: Right heart failure / Congestive heart failure & Lung cancer

What’s going on here?

A

COPD

46
Q

– Usually develops early in life: Viral induction and exacerbation & Exacerbated but not caused by smoke exposure
– Associated with allergies
– Obstruction is usually reversible with a beta-agonist
– No defect in gas exchange
– Associated diseases: Allergic rhinoconjunctivitis & Atopic dermatitis

What’s going on here?

A

Asthma