Obstructive lung disease Flashcards

1
Q

What is the function of the clara cells/club cells?

A

1) They form the defensive Clara cell secretory proteins

2) Repairs ciliated and secretory cells

3) Metabolizes xenobiotic compounds

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2
Q

How can infections travel from one alveoli into another?

A

Through the pores of Kohn, which are perforations in the wall of the alveoli

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3
Q

What is the importance of the surfactant?

A
  • Made of lecithin (lipid) secreted by type-2 alveolar cells

The alveoli are soaked in blood, and thus the surfactant will reduce the surface tension created by the extravasation of blood

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4
Q

What are the two main functions of the respiratory system?

A

1) Ventilation (depends on the respiratory center, neural tracts, & respiratory muscles)

2) Perfusion (depends on the equal distribution of blood and air in the lungs)

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5
Q

what happens in case of hypoventilation and what are its main causes?

A
  • Hypoxia + hypercapnia

1) Obstructive Hypoventilation

2) Restrictive hypoventilation

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6
Q

What are the causes of obstructive hypoventilation?

A

1) Upper airway obstruction

  • Like laryngeal edema

2) Lower airway obstruction

  • COPD
  • Bronchial asthma
  • Bronchiectasis
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7
Q

What are the causes of restrictive hypoventilation?

A
  • The alveoli lose the capability of expanding and recoiling due to:

1) Decreased compliance of:

  • Lungs
  • Pleura (pneumothorax, or fluid)
  • Chest wall (in extreme obesity)

2) Disorders of the neuromuscular apparatus

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8
Q

Why do we not feel dyspnea in hypoventilation?

A

Due to the accumulation of CO2 which will depress the respiratory centers

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9
Q

How can lung perfusion be affected?

A
  • Impaired perfusion = hypoxia + normo and sometimes hypocapnia (so patient will present with dyspnea)

1) Emphysema
2) Pulmonary edema
3) Pneumonia
4) Interstitial lung disease

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10
Q

What is meant by diffuse lung disease?

A

Lung diseases the affect the whole lung

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11
Q

What are the types of diffuse lung disease?

A

1) Obstructive lung disease

2) Restrictive lung disease

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12
Q

What is meant by obstructive lung disease?

A

It is characterized by the reduction of airflow, causing shortness of breath in exhaling air, due to increased resistance and thus it will decrease the FEV1 and FVC, increasing the total lung capacity and residual volume

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13
Q

What are some examples of obstructive lung diseases?

A

1) COPD (Emphysema, Chronic bronchitis)

2) Bronchial asthma

3) Bronchiectasis

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14
Q

What is meant by chronic emphysema?

A

It is a chronic lung disease that is characterized by abnormal, irreversible dilatation of the airspace distal to the terminal bronchiole, there is wall destruction but no fibrosis

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15
Q

What are the types of emphysema?

A
  • According to the location within the lobule:

1) Centriacinar (dilatation of the central part of the respiratory bronchiole), common in the upper lobes of smokers

2) Panacinar (all airspace beyond the terminal bronchiole are dilated, more common in the lowe lobes, associated with a1-anti-trypsin-deficiency)

3) Paraseptal (distal acinar, affecting distal airspace at the periphery, adjacent to the pleura and more in the upper respiratory lobes)

4) Irregular (scar emphysema, occurring near healed inflammatory process like TB scars)

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16
Q

What are the causes of emphysema?

A

1) Environmental factors

  • cycles of inflammation and proteolysis of the ECM (due to the exposure of the epithelium to toxic substances like cigarette smoke)
  • Defective in anti-inflammatory mechanism
  • Airway infection

2) Genetic factors

  • Deficiency of a1-antitrypsin (PiZZ gene causing the misfolding of protein preventing it from being secreted into the blood, increasing inflammation leading to liver cirrhosis)
  • Polymorphism of the TGF-b gene, causing an inadequate synthesis of ECM
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17
Q

Describe the morphology of emphysema

A

1) Gross

  • Affects the upper 2/3 of the respiratory system
  • Bullae/blisters in irregular and distal acinar emphysema

2) Microscopically

  • Abnormally large alveoli separated by thin septa
  • The number of alveoli capillary is diminished
  • The terminal and respiratory bronchioles are diminished
  • No interstitial fibrosis
18
Q

What are the complications of emphysema?

A

1) Pulmonary hypertension

2) Hypoxia (due to decreased number of pulmonary caps, hypoventilation, expansion of the alveolar wall)

3) Reduction in the pulmonary vascular beds

4) Lung collapse, if the bullae rupture into the pleural space

19
Q

What is the meaning of chronic bronchitis?

A

Its clinical definition is persistent cough + sputum production for 3 months at least for 2 consecutive years

20
Q

What are the causes of chronic bronchitis?

A

1) Cigarretes (90% of patients are smokers)

2) Air pollutants (like nitrogen dioxide)

3) Toxic inhalants

4) Infection (S.pneumonia, H.influenza)

21
Q

Describe the pathogenesis of chronic bronchitis

A

1) The irritants will cause hypersecretion of mucus, which will lead to the hypertrophy of the submucosal glands in the trachea and bronchi thickening the alveoli and narrowing the lumen, and hyperplasia of goblet cells “metaplasia in small bronchi”

2) The irritants will also lead to inflammation which will lead to the infiltration of the alveoli by the CD8 lymphocytes (releases IL-13), macrophages (releases metalloproteinases), and neutrophils (releases elastase)

3) Cigarette smoke will damage the airway epithelium, increase the production of mucin, and elastoproteases from the neutrophils

22
Q

What are the types of chronic bronchitis?

A

1) Simple chronic bronchitis (white sputum)

2) Chronic mucopurulent bronchitis (yellow sputum)

3) Chronic asthmatic bronchitis (intermittent bronchospasm and wheezing)

4) chronic obstructive bronchitis (chronic irreversible airway obstruction)

23
Q

Describe the morphology of chronic bronchitis

A

1) Gross: 1. Thickened bronchial wall, 2. Hyperemia and swelling of the mucous membrane, 3. mucus in the lumen

2) Microscopy:

  • Hypertrophy of the mucus-secreting glands measured by the Reid index, which measures the distance from the epithelial wall to the cartilage >0.4 = chronic bronchitis
  • Mixed inflammatory cells
  • Increased amount of goblet cells in the surface epithelium
  • Chronic bronchiolitis, when the inflammation affects small airways
24
Q

What are the clinical features of chronic bronchitis?

A
  • Blue Bloaters
  • Hypoxemia (central cyanosis)
  • Pulmonary hypertension
  • Hypercapnia (no dyspnea)
25
Q

What are the complications of chronic bronchitis?

A

1) Progression to COPD

2) Cor pulmonale with cardiac failure due to pulmonary HTN

3) Dysplasia of the respiratory epithelium (cancerous transformation)

26
Q

What are some other forms of emphysema?

A

1) Bullous emphysema

  • Dilated airspaces >1 cm, if they rupture they might cause pneumothorax

2) Senile emphysema

  • Homogenous enlargement of the alveolar airspace, due to alveolar wall weakness

3) Compensatory hyperinflation

  • Dilation of the alveoli due to compensate the loss of lung substance

4) Obstructive overinflation

  • Obstruction of the lung due to air-trapping

5) Interstitial emphysema

  • The entry of air into the connective tissue stroma of the lung, mediastinum, or subcutaneous tissue
27
Q

What is meant by bronchial asthma?

A

chronic inflammation disorder of the bronchial tree with reversible bronchoconstriction, breathing is very difficult due to the widespread narrowing of the bronchi, it is present with wheezes, dyspnea, and cough

  • Episodes of reversible bronchoconstriction
  • Chronic inflammation of the bronchial wall with eosinophils and smooth muscle hypertrophy
  • Increased mucus production
  • No hypercapnia mafi waqt for CO2 accumulation, only hypoxia
28
Q

What are the types of bronchial asthma?

A
  • According to the type of allergen

1) Atopic (allergic “extrinsic”)

  • Predisposed in Family history of asthma/allergic disease
  • Type-1 IgE-mediated hypersensitivity rxn
  • Caused/initiated by exogenous substances like, house dust, mites, pollens, animal dander, foods, contact with feathers, wool
  • Skin test = immediate wheal-flare rxn

2) Non-atopic (intrinsic)

  • No allergen sensitization
  • Negative skin test
  • Might be due to the hyperirritability of the bronchial tree, triggered by viral infection, inhaled air pollutants, emotional stress, exercise, exposure to cold
  • According to the agent that triggered the bronchoconstriction

1) Seasonal
2) Exercise-induced
3) Drug-induced (aspirin, NSAID, BB)
4) Occupational asthma (FUMES, chemicals, gases)
5) Asthmatic bronchitis (smokers)

  • Hygiene hypothesis
29
Q

Describe the pathogenesis of atopic asthma

A
  • INITIAL EXPOSURE

1) Genetic predisposition to type-1 hypersensitivity

2) Introduction of allergen, Th2 will produce IL-4 (IgE production), IL-5 (activates eosinophils), IL-13 (simulates mucus secretion)

3) B-cells will produce IgE, which will cover the mast cells by binding to the FceR1

4) Development and activation of eosinophils

5) Mucus secretion

  • RE-EXPOSURE TO THE SAME ANTIGEN

– Immediate response

1) DEGRANULATION OF THE MACROPHAGES RELEASING HISTAMINE AND OTHER MEDIATORS

2) This will lead to vasodilation, increased vascular permeability, edema, smooth muscle spasm, glandular secretion

3) Resolves in 60 minutes by histamine, enzymes contained in the granule matrix (chymase, tryptase), and PGD2, LTC4, LTD4, LTE4

– Late phase reaction (2-8 hours “denovo synthesis and release of secondary mediators”)

1) Occurs without exposure to antigen

2) Eosinophils, neutrophils, basophils, monocytes, and T-cells all of them are involved, which are recruited by lipid mediators

30
Q

Describe the morphology of asthma

A

1) Gross

  • The bronchi and bronchioles are occluded by thick mucus
  • Overinflation of the lungs with areas of collapse (atelectasis), in patients who die

2) Microscopic

  • Mucus plug in the bronchi and bronchioles
  • Numerous eosinophils (charcot-leyden crystals, derived from eosinophils)
  • Airway remodeling (structural changes in the bronchial wall, increase in size and number of the submucosal glands, hypertrophy and hyperplasia of the bronchial wall smooth muscle, increased vascularity, deposition of subepithelial colagen and fibrosis
31
Q

How to diagnose asthma?

A

1) Elevated eosinophil count in the peripheral blood

2) Sputum rich in eosinophils

3) Charcot-Leyden crystals (atopic asthma), curschmann spirals, and Creola bodies are all seen microscopically

32
Q

What is meant by bronchiectasis?

A
  • Dilation of the bronchi

Local or diffused, irreversible abnormal dilation of the bronchi and bronchioles, caused by the destruction of smooth muscle and elastic tissue

33
Q

What is the cause of bronchiectasis?

A

1) Nonobstructive (diffuse, post-inflammatory)

1a) Genetic causes

  • Kartagner/immotile cilia syndrome (due to the absence of the dynein arms), secretions will accumulate, recurrent infection, sinusitis then bronchiectasis
  • Cystic fibrosis, the CFTR channel absorbers chloride and secretes it in the lungs, pancreas, and GIT in CF this channel; is mutated and thus chloride is stored along with Na and Water, which will cause the secretions to be thick which can accumulate causing infection

1b) Acquired causes

  • Postinfectious (chronic persistent necrotizing infection, bacteria “tuberculosis”, viruses “SARS”, Fungi)
  • Immunodeficiency (HIV after lung transplant)
  • Autoimmune and immune-mediated diseases (like SLE)

2) Obstructive (localized to the obstructed segment of the lung)

  • Partial obstruction allows air to enter during inspiration but doesn’t allow it to leave during expiration
  • Total obstruction, will cause negative intrapleural pressure that might lead to lung collapse
  • Causes can be, thick secretion, tumor in the wall, or pressure form outside like lymph node tumor
34
Q

What are the classification of bronchiectasis?

A

1) According to the shape of the bronchial dilation

  • Cylindrical type
  • Fusiform type
  • Saccular
  • Varicose type

2) According to the extent of involvement

  1. Generalized, Bilateral affecting the lower lobes more commonly
  2. Localized, restricted, usually with obstruction, if found in the upper lobes it is usually due to TB, right middle lobe syndrome (chronic middle right lobe collapse)
35
Q

Describe the morphology of bronchiectasis

A

1) Gross:

  • Dilated bronchi and bronchioles
  • Saccular, cylindrical or varicose, wall thickness by fibrosis, the lumen is filled with mucopurulent secretion

2) Microscopically:

  • Bronchial wall dilation and destruction, dense infiltration of lymphocytes and plasma cells, Fibrosis of the bronchial and bronchiolar wall
  • Mucosal changes including ulceration of the epithelium & squamous metaplasia which could lead to lung carcinoma
  • Staph, strep[, pneumococci, enteric organisms, H.influenza and p.aeruginosa
36
Q

What is the clinical presentation of bronchiectasis?

A

1) Severe persistent cough with mucopurulent sputum (very imp)

2) Sevre widespread bronchiectasis, obstructive hypoventilation = hypoxia + hypercapnia

37
Q

What is meant by atelectasis?

A

Loss of lung volume (lung collapse) leading to the mismatching of ventilation-perfusion (hypoxia)

  • Collapse of area of the lung, the blood brought to it will not get oxygenated and thus hypoxia, seen in the tongue as it is central
38
Q

What are the types of atelectasis?

A

1) Obstruction (resorption)

  • Complete obstruction of the bronchus (causes: thick secretion, wall tumor, asthma, bronchiectasis, chronic bronchitis)

2) Compression

  • Fluid, blood, OR AIR IN THE PLEURAL SPACE, increased intrapleural pressure, compressing the lungs (causes like pneumothorax)

3) Contraction

  • Local or diffuse Areas of fibrosis, hampering lung expansion
39
Q

What are the complications of atelectasis?

A

1) Infection

2) Abscess formation

3) Bronchiectasis

4) Fibrosis

40
Q

What are the clinical features of emphysema?

A

Pink Buffers

  • Hypoxemia (no cyanosis) with normo/hypocapnia, thus dyspnea
41
Q

What are the different clinical findings in emphysema, chronic bronchitis, and asthma?

A
  • EMPHYSEMA

1) Dyspnea

  • Bronchitis

1) Cough
2) Sputum

  • Asthma

1) COUGH
2) Wheezing
3) Dyspnea

42
Q

Differentiate between the four types of COPD based on microscopic photo

A

1) Emphysema

  • Enlarged alveoli
  • Thinned alveolar septum

2) Chronic bronchitis

  • Mucus hyperplasia
  • Wall thickening
  • Inflammatory cell infiltration

3) Bronchiectasis

  • Destruction of elastic tissue
  • Chronic inflammation
  • Mucosal damage

4) Bronchial asthma

  • Eosinophilic infiltrate
  • Mucus plugging
  • Airway remodeling