Obstructive Lung Disease Flashcards

1
Q

How is the left bronchus vs. the right bronchus?

A

Left is narrower/longer (5 cm vs. 2 cm)/more horizontal

*meaning foreign bodies more likely to enter the right bronchus

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2
Q

What is the characteristic epithelium of bronchorespiratory?

A

Pseudostratified ciliated columnar epithelium

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3
Q

What comprise the alveolar wall and what are the fxns?

A

Type I pneumocytes: cover 95% of alveolar surface

Type II pneumocytes: Produce surfactant and repair alveolar epithelium

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4
Q

What is COPD and what are examples?

A

Diseases that cause obstruction to outflow out of the lungs

Examples:

Emphysema

Chronic bronchitis

Asthma

Bronchiectasis

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5
Q

Describe Obstructive

A

Airway disorder- trachea to terminal bronchiole

Increased resistance to air fllow and limited expiratory rate son forced expiration

Reduced FEV1:FVCratio

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6
Q

Describe Restrictive

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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7
Q

What is emphysema

Causes?

Types?

A

Permanent enlargement of all or part of teh respiratory unit (respiratory bronchioles, alveolar ducts, alveoli) accompanied by wall destruction without obvious fibrosis.

Causes: Smoking/Air pollution/ Alpha1-antitrypsin deficiency

Types: Centriacinar (centrilobular) in 95% of cases and Panacinar

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8
Q

What is the pathogenesis of emphysema?

A

Increased macorphages, CD8+ T lymphocytes, and neutrophils

Tissue damage (From cigarette smoke) activate neutrophils and macrophages

Elastase and free radicals are then released. (anti-elastase [aka alpha1-antitrypsin] and anti-oxidants go down)

Destruction of elastic tissue

Consequential increased compliance and decreased elasticity

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9
Q

Why is destruction of elastic tissue as seen in Emphysema bad?

A

Because it keeps airway lumens open by applying traction. It’s destruction collapses airways on expiration.

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10
Q

What type of emphysema do you see in smoking?

A

Centriacinar emphysema

So the apical segment of upper lobes are affected.

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11
Q

How does smoking cause emphysema?

A

Free radicals deplete the normal levels of antioxidants in the lung.

This oxidative injury also inactivates native antiproteases (fxnal alpha1-antitrypsin deficiency)

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12
Q

What does alpha1-antitrypsin deficiency cause?

How does it occur?

Where does it happen?

Why does it happen here?

A

Panacinar emphysema.

This can be genetic (autosomal dominant. Phenotypes assoc with severe deficiency have marked underproduction of the enzyme in the liver)

or

acquired (cigarette smoking)

Affects the lower lobes/all parts of the respiratory unit are affected by elastic tissue destruction

There is total lack of antiproteases throughout the acinus bu thte lower lung distribution is where perfusion and neutrophil numbers are the greatest.

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13
Q

What are clinical findings of Emphysema

Chest x ray findings?

A

Severe and early onset of dyspnea

Pink puffers

Coexistence w chronic bronchitis (Smoker’s emphysema)

Cor pulmonale-less common than in chronic bronchitis

Diminished breath sounds due to hyperinflation

Increased AP diameter

Hyperlucent lung fields

Vertical heart

Depressed diaphragm

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14
Q

What are other types of emphysema?

A

Paraseptal emphysema

  • Subplueral involvement
  • Spontaneous pneumothorax
  • No COPD

Irregular emphysema

  • Localized, scar associated
  • No COPD
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15
Q

What is chronic bronchitis?

What causes it?

What is the pathogenesis?

A

Chronic Bronchitis is productive cough for at least 3 months for 2 consecutive years

Cause: smoking, Cystic fibrosis

Pathogenesis:

Inhaled smoke/irritant, causes mucous hypersecretion in bronchi, leads to airflow obstruction in termiinal bronchioles (making this more proximal than emphysema) leading to irreversible fibrosis of terminal bronchioles

Then made worse by infections these patients suffer. Maintining this disease and causing acute exacerbations.

Bronchospasms contribute to this process.

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16
Q

What are clinical findings of chronic bronchitis

Chest x ray findings?

A

Productive cough

Cyanosis

Blue bloaters

Dyspnea

Expiratory wheezing and rhonchi

Cor pulmonale (congestive heart failure occuring earlier in the disease than in emphysema)

in CXR: Enlarged heart, horizontally oriented

Increased bronchial markings

17
Q

Gross findings in morphology of chronic bronchitis?

Other findings?

A

Hyperemia, swelling and edema of mucomembranes

Mucinous and mucopurulent secretions

Chronic inflammation of airways and increased mucous glands

Thickening of walls (narrowing of bronchiolar lumina)

18
Q

What is the Reid index?

A

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

In Chronic bronchitis the reid index is closer to one due to the larger mucous gland thickness

19
Q

What is bronchiectasis

A

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

Causes: Cystic fibrosis (one of the main causes)

Infections (TB/Adenovirus/Hinfluenzae/Staph Aureus)

Bronchial obstruction

Primary ciliary dyskinesia

Allergic bronchopulmonary aspergillosis

20
Q

clinical findings and CXR of bronchiectasis?

A

Copious sputum

Hemoptysis

Digital clubbing

Cor pulmonale

CXR: **Bronchial markings extending to the periphery of the lungs **

21
Q

How does cystic fibrosis happen?

A

Autosomal recessive inheritance, mostly in caucausians few AZN or African americans

Deletion on chromosome 7, with 3 nucleotides coding for phenylalanine.

Defective CF transmembrane conductane regulator for chloride ions

Increased NA and water reabsorption from luminal secretions and decreased Cl secretions from epithelial cells into lumen. This causes dry and thick secretions.

Dehydration of body secretions due to lack of NaCl. (this affects bronchioles, pancreatic ducts, bile ducts, meconium, seminal fluid)

22
Q

What are clniical findings in Cystic fibrosis?

What ussually happens

A

Nasal polyps

Respiratory infections (p aeruginosa, staph aureus, h influenzae)

Malabsorption

Type I diabetes mellitus

Infertility in males

Meconium ileus

Secondary biliary cirrhosis

Usually the respiratory infections followed by secondary biliary cirrhosis

23
Q

GRoss and microscopic findings of Bronchiectasis (cystic fibrosis)

A

Gross: Bilateral lower lobes, distal bronchi, and bronchioles

Dilated airways which can be followed out to teh pleural surfaces

On cut surface the dilated bronchi appear as cysts filled with mucopurulent secretions

Micro: Intense acute and chronic inflammatory exudate in bronchial walls, necrotizing ulceration

Squamous metaplasia of bronchial epithelium

Lung abcesses may be present

Fibrosis of bronchial walls leading to bronchiolitis obliterans

Cultures are usually postiive