Coupon Accepted Successfully!



Asthma Is Characterized By Episodic Air-Flow Obstruction In:
  1. Patients typically have paroxysms of wheezing, dyspnea and cough.
  2. Severe acute asthma unresponsive to therapy is termed status asthmaticus.
  1. Divided into extrinsic (allergic) and intrinsic (idiosyncratic) categories.
  2. Bronchospasm is induced by inhaled antigens, usually in children with a personal or family history of allergic disease.
  3. After exposure to an inciting factor (e.g., allergens, drugs, cold, exercise), inflammatory mediators released by activated macrophages, mast cells, eosinophils, and basophils induce bronchoconstriction, increased vascular permeability, and mucous secretion. Q
The changes are -
  1. In a sensitized person, an inhaled allergen interacts with TH2 cells and IgE antibody bound to the surface of mast cells.
  2. TH2 cells and mast cells release mediators of type I (immediate) hypersensitivity, including histamine, bradykinin, leukotrienes, prostaglandins, thromboxane A2, and platelet-activating factor (PAF), as well as cytokines such as interleukin (IL)-4 and IL-5.
  3. The inflammatory mediators lead to
  1. smooth muscle contraction,
  2. mucous secretion, and
  3. increased vascular permeability and edema.
  1. IL-5 causes terminal differentiation of eosinophils in the bone marrow.
Allergic Asthma
  1. Patients with asthma have known or suspected reactions to pollens, animal hair or fur, and house dust contaminated with mites. Q
  2. It is strongly correlated with skin-test reactivity. Q
Infectious asthma:
  1. Viral respiratory tract infection.
  2. In children under 2 years, RSV is the usual agent; in older children, rhinovirus, influenza, and parainfluenza.
  1. On gross examination, the lungs are remarkably distended with air and airways are filled with thick, tenacious, adherent mucous plugs.
  2. Microscopically, these plugs contain strips of epithelium and many eosinophils. Charcot-Leyden crystals, are also seen.
  3. In some cases, the mucoid exudate forms a cast of the airways (Curschmann spirals), which may be expelled with coughing.
  4. Compact clusters of epithelial cells (Creola bodies) also are seen in the sputum.
Clinical features
  1. A typical attack of asthma begins with a feeling of tightness in the chest and nonproductive cough. Both inspiratory and expiratory wheezes appear, the respiratory rate increases and the patient becomes dyspneic. Q
Status asthmaticus
  1. Refers to severe bronchoconstriction that does not respond to the drugs.
  2. The cornerstone of asthma treatment includes administration of Beta-adrenergic agonists, inhaled corticosteroids, cromolyn sodium, methylxanthines, and anticholinergic agents. Systemic corticosteroids are reserved for status asthmaticus or resistant chronic asthma. The inhalation of bronchodilators often provides dramatic relief. Q


  1. The pneumoconioses are pulmonary diseases caused by dust inhalation.
  2. The specific types of pneumoconioses are named according to the substance inhaled (e.g., silicosis, asbestosis).
  1. The most important factor in the production of symptomatic pneumoconioses is the capacity of inhaled dusts to stimulate fibrosis. Thus, small amounts of silica or asbestos may produce extensive fibrosis, whereas coal and iron are only weakly fibrogenic.
  2. Particles over 10 µm in diameter deposit on bronchi and bronchioles.
  3. Alveolar macrophages ingest the inhaled particles
  4. A significant number of ingested particles accumulate in and about respiratory bronchioles and terminal bronchioles.
Silicosis Is Caused By Inhalation Of Silicon Dioxide (SILICA)
Silicosis was described historically as a disease of sandblasters.
  1. Crystalline silica (quartz) is more toxic than amorphous forms,. Particles of 0.2 to 2.0 µm are the most dangerous.
  2. After their inhalation, silica particles are ingested by alveolar macrophages.
  1. SIMPLE NODULAR SILICOSIS: This is the most common form of silicosis and is almost inevitable in any worker with long-term exposure to silica. Twenty to 40 years after the initial exposure to silica (but sometimes after only 10 years), the lungs contain silicotic nodules, which are less than 1 cm in diameter (usually 2 to 4 mm). Q
  2. On histologic examination, they have a characteristic whorled appearance. Polarized light reveals doubly refractile needle-shaped silicates within the nodule. Q
  3. Hilar nodes may become enlarged and calcified, often at the periphery of the node (eggshell calcification).
Progressive Massive Fibrosis:
  1. Progressive massive fibrosis is defined radiologically as nodular masses of more than 2 cm diameter in a background of simple silicosis. Q
  2. Most of these lesions are 5 to 10 cm across and are usually in the upper zones of the lungs bilaterally. Q
  3. Morphologically, they often exhibit central cavitation.
Clinical Features:
  1. Dyspnea on exertion and later at rest suggests progressive massive fibrosis or other complications of silicosis. Q
Coal Workers' Pneumoconiosis (CWP) Reflects Inhalation Of Carbon Particles
Workers in certain occupations, such as those who work within mines, inhale more quartz particles
  1. CWP is typically divided into simple CWP and complicated CWP (a.k.a. progressive massive fibrosis).
  2. Microscopically, a coal-dust macule exhibits numerous carbon-laden macrophages which surround distal respiratory bronchioles.
  3. Simple CWP was once thought to cause severe disability, it is now clear that at worst it causes a minor impairment of pulmonary function.
  4. Complicated CWP is defined as a lesion 2.0 cm or greater in size. Patients with complicated CWP may have significant respiratory impairment.
Caplan Syndrome
  1. Was originally described as the presence of rheumatoid nodules (Caplan nodules) in the lungs of coal miners with rheumatoid arthritis. Q
  2. The term is now also used for the association of pulmonary rheumatoid nodules with other pneumoconioses, such as silicosis or asbestosis. These nodular lesions are large (10 cm in diameter), multiple, bilateral, and usually peripheral. Q
  3. Microscopically. Rheumatoid nodules consist of large, central, necrotic areas surrounded by a border of chronic inflammation and palisading macrophages. Q
Caplan Triad
  1. Includes a group of fibrous silicate minerals that occur as long, thin fibers.
  2. Chrysotile accounts for the bulk of commercially used asbestos. Q
  3. The amphiboles include amosite, crocidolite. If coal is the classic example of much dust and little fibrosis, asbestos is the prototype of little dust and much fibrosis. Q
  4. The amphiboles, and crocidolite in particular, have a much greater propensity to produce disease than does chrysotile. Q
Asbestos-Related Lung Disease
a.    Pleural lesions
  i.    Benign pleural effusion            ii.   Parietal pleural plaques              iii.  Diffuse pleural fibrosis             iv.   Rounded atelectasis
b.    Interstitial lung disease
  i.    Asbestosis
c.    Malignant mesothelioma
d.    Carcinoma of the lung (in smokers)

  1. Asbestos fibers are long (up to 100 µm) but thin (0.5µm).
  2. They deposit in distal airways and alveoli.
  3. The smallest particles are engulfed by macrophages, but many larger fibers penetrate into the interstitial space. Q
  4. The first lesion is an alveolitis.
  5. Release of inflammatory mediators by activated macrophages and the fibrogenic character of the Free asbestos fibers in the interstitium promote interstitial pulmonary fibrosis.
  1. Asbestosis is characterized by bilateral, diffuse interstitial fibrosis, and asbestos bodies in the lung.
  2. When asbestos fibers deposit in bronchioles and respiratory bronchioles, they incite a fibrogenic response that leads to mild chronic air-flow obstruction.
  3. Asbestosis is usually more severe in the lower zones of the lung.
Asbestos bodies:
  1. Are found in the walls of bronchioles or within alveolar spaces, often engulfed by alveolar macrophages. The particle has distinctive morphologic features, consisting of a clear, thin asbestos fiber (10µm long) surrounded by a beaded iron protein coat. Q
  2. By light microscopy, it is golden brown and stains strongly with the Prussian blue stain for iron.
Pleural Plaques:
  1. Pleural plaques typically occur on parietal and diaphragmatic pleura, often 10 to 20 years after exposure to asbestos.
  2. On gross examination, pleural plaques are pearly white and have a smooth or nodular surface.
  3. Plaques may measure over 10 cm in diameter and become calcified.
  4. Pleural plaques are not predictors of asbestosis, nor do they evolve into mesotheliomas. Q
Diffuse Pleural Fibrosis:
  1. Fibrosis limited to the pleura is usually detected at least 10 years after initial exposure to asbestos.
  1. Mesothelioma is seen in workers heavily exposed to asbestos, mainly crocidolite.
  2. The major diagnostic problem is differentiation from peripherally spreading pulmonary adenocarcinoma or from adenocarcinoma metastasized to pleura from an extrathoracic primary site.
  3. Microscopically Malignant mesothelioma may be epithelioid (60% ),Sarcomatoid (20%) or can be mixed i.e biphasic histology seen.
Carcinoma of the lung
  1. 3- to 5- times more common in nonsmoking asbestos workers.
  2. In asbestos workers who smoke, the incidence of carcinoma of the lung is vastly increased: up to 60 times. Q

Diffuse Alveolar Damage (Acute Respiratory Distress Syndrome)

  1. Diffuse alveolar damage (DAD) refers to a pattern of reaction to injury of alveolar epithelial and endothelial cells from a variety of acute insults.
  2. The clinical counterpart of severe DAD is the acute respiratory distress syndrome (ARDS).
  3. A patient with apparently normal lungs sustains pulmonary damage and then develops rapidly progressive respiratory failure. Q
  4. The condition reflects decreased lung compliance (usually requiring mechanical ventilation) and hypoxemia and features extensive radiologic opacities in both lungs. Q
  5. The overall mortality of ARDS is more than 50%, and in patients older than 60 years, it is as high as 90%.
Important Causes of the Acute Respiratory Distress Syndrome
Nonthoracic Trauma          Infection   Aspiration     Drugs and Therapeutic Agents
Shock due to any cause  Gram-negative septicemia  Near-drowning     Heroin
Fat embolism  Other bacterial infections
 Viral infections
  Aspiration of gastric contents
    Cytotoxic drugs
  1. DAD is a final common pathology caused by respiratory tract infections, sepsis, shock, aspiration of gastric contents, inhalation of toxic gases, near-drowning, radiation pneumonitis, and a large assortment of drugs and other chemicals. Q
  2. Although these conditions are quite diverse, they can all injure the epithelial and endothelial cells of the alveoli, thereby producing DAD. Q
  3. Injury to endothelial cells allows leakage of protein-rich fluid from alveolar capillaries into the interstitial space. Q
  4. Destruction of type I pneumocytes permits exudation of fluid into alveolar spaces, where deposition of plasma proteins results in formation of fibrin-containing precipitates (hyaline membranes) on the injured alveolar walls.
  5. Type II pneumocytes, proliferation replaces the normal epithelial lining of the alveoli. Q
  1. The earliest alveolar injury degenerative changes in endothelial cells and type I pneumocytes. Q
  2. Followed by sloughing of type I cells.
  3. Hyaline membranes begin to appear by the second day.
  4. These eosinophilic, glassy membranes consist of precipitated plasma proteins and cytoplasmic and nuclear debris from sloughed epithelial cells. Q
  5. Interstitial inflammation, consisting of lymphocytes, plasma cells, and macrophages, is apparent early and reaches its maximum in about a week.
  6. In fatal cases of DAD, the lungs are heavy, edematous, and virtually airless. Q
  7. The organizing phase of DAD, beginning about a week after the initial injury, is marked by proliferation of fibroblasts within alveolar walls. Interstitial inflammation and proliferated type II pneumocytes persist, but hyaline membranes are no longer formed. Q

Churg-Strauss Syndrome

(Allergic Angiitis and Granulomatosis) Is Defined by Asthma, Eosinophilia and Vasculitis
  1. Histologic features include eosinophilic pneumonia, vasculitis,  parenchymal necrosis, and granulomatous inflammation.
  2. The vasculitis includes diverse inflammatory cells: eosinophils, lymphocytes, plasma cells, macrophages, giant cells, and neutrophils.
Clinical Features
Churg-Strauss syndrome passes through three clinical phases.
  1. Prodrome phase:  allergic rhinitis, asthma, peripheral eosinophilia, and eosinophilic infiltrative disease.
  2. Systemic vasculitic phase: Extrapulmonary vasculitic manifestations are present, such as cutaneous leukocytoclastic vasculitis or peripheral neuropathy. Q
  3. Postvasculitic phase:

Test Your Skills Now!
Take a Quiz now
Reviewer Name