Path_15 split.txt

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Path_15 split.txt
2011-02-01 19:39:56

Obstructive lung disease
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  1. Where does the respiratory system develop from
    outgrowth of the ventral wall of the foregut
  2. Middle lobe equivalent on the left side
  3. Bronchiole arteries
    in the absence of cardiac failure the bronchiole arteries can sustain pulmonary parenchyma when pulmonary artery blood is blocked
  4. Distinguishing brochi form brochioles
    bronchioles lack cartilage and submucosal glands
  5. Acinus
    • distal to the terminal bronchioles
    • composed of respiratory bronchioles and alveoli ducts and sacs
    • spherical in shape
  6. site of gas exchange
    alveolar sacs
  7. pulmonary lobule
    cluster of three to five terminal bronchioles each with its acinus
  8. cells of the respiratory track
    • pseudostatified ciliated epithelial
    • the vocal cords are covered in stratified squamous
  9. glands of the respiratory track
    • many submucosal mucus secreting cells, end at the bronchioles
    • neuroendocrine cells; release seratonin, calcitonin, and gastrin releasing hormone.
  10. surfaces from blood to air in the alveoli
    • cappilary endothelium;
    • basement membrane; in thin segments the BM of the alveoli and cappilary are fused, in thick segments there is interstitum between; containing elastic fibers, collagen, fibroblast like cells, smooth muscle, mast cells and rarely lymphocytes
    • alveolar epithelium; contains type 1 and type 2 pneumocytes. Type 2 are the source of pulmonary surfactant and the main cell type involved in repair. They are identified by osmiophilic lamellar bodies where the surfactant is stored
    • alveolar macrophages; often filled with carbon
  11. structure of alveolar walls
    • they are not solid
    • perforated by numerous pores of Kohn, permits the passage of bacteria and exudate between adjacent alveoli
  12. Pulmonary hypoplasia
    • conginital anomaly
    • small lungs; weight, volume, and acing number
    • causes; oligohydraminos, congenital diaphragmatic hernia, renal cyclic disease, anencephaly
  13. Forgut cysts
    • formed by abnormal detachment of primitive forgut
    • most common are bronchogenic cysts, lines by brachial epithelium found in the mediastinum or hilum
    • can present as a mass lesion or become apparent after infection or rupture
  14. pulmonary sequestration
    • lung tissue without normal connection to the airways and has a vascular supply derived from the aorta, not the pulmonary artery
    • extralobular- found in infants as abnormal mediastinal masses
    • intralobar- found within the lung parenchyma of older children or adults. associated with recurrent infections
  15. Congenital pulmonary airway malformatin, CPAM
    • contains hamartomatous cycts, benign lesion that resemble the tissue of origin.
    • type 1 has large cysts and has a good prognosis
    • type 2 have medium cysts and has bad outcomes because it is associated with other anomalies
    • there are five types in all but others are very rare
  16. three types of atelectasis
    • incomplete expansion of collapse of the lung
    • reabsorption atelectasis; follows an airway obstruction, can be from mucus secretion in brochitits, forign body aspiration, bronchial neoplasm
    • compressive atelectasis; fluid or air enters the pleural space and compresses the lung. effusion from cardiac failure , blood from anurism rupture or cyst rupture
    • contraction atelectasis; local or general fibrotic changes that prevent the lung fro expanding fully. non reversible
  17. Acute lung injury
    can produce many lung injuries; congestion, edema, surfactant disruption, atelectasis
  18. Morphology of pulmonary edema
    • lungs become heavy and wet
    • fluid accumulates in basal regions
    • histologic findings include engorged capillaries, and airspace filled with pink granular precipitate.
    • may get interstitial fibrosis with fibrin exudate
    • hemosiderin laden macrophages may appear
  19. Hemodynamic pulmonary edema
    • increased hydrostatic pressure; left heart failure, increased volume, pulmonary vein obstruction
    • decreased oncotic pressure; hypoalbuminemia, nephrotic syndrome, liver disease, protein losing enteropathies
    • lymphatic obstruction; rare
  20. Edema due to microvascular injury
    • infections; pneumonia, septicemia,
    • Inhaled gases; oxygen, smoke
    • lipid aspiration; gastric contents
    • drugs and chemicals; chemo, heroin,
    • shock or trauma
    • radiation
    • transfusion related
  21. What is acute respiratory distress syndrome, ARDS
    • diffuse alveolar capillary damage leading to severe pulmonary edema, respiratory failure, arterial hypoxemia refractory to oxygen theropy
    • starts in the endothelium and can progress into the epithelium
    • characterized by increased capillary permeability and edema, fibrin exudate , formation of hyaline membranes, and septal inflammation
    • mortality rate is 60%
  22. Pathogenesis of ARDS
    • activated neutrophiles aggregate in the pulmonary vasculature and damage the epithelium by secreting oxygen derived free radicals and enzymes. Also secrete arachnidonic acid metabolites that attract more neutrophils
    • activated pulmonary macrophages release oxidants , pretenses, and proinflammatory cytokines
    • Surfactant is lost or damaged. leads to atelectasis and edema
  23. Morphology of ARDS
    • acute stage; lungs are diffusely firm, red, boggy, and heavy with DAD
    • proliferative/organization stage; interstitial fibrosis and type 2 pneumocyte proliferation . Bacteria is seen in most fatal cases
  24. Acute interstitial pneumonia
    presents like ARDS but etiology is unknown
  25. Four main obstructive diseases
    • emphysema
    • chronic bronchitis
    • asthma
    • bronchiectasis
    • COPD is emphysema and chronic bronchitis
  26. Emphysema
    abnormal permanent enlargement of the airspaces distal to the terminal bronchioles with alveolar wall distraction and minimal fibrosis
  27. Two anatomical types of emphysema
    • cintriacinar; destruction and enlargement of the proximal acinus, mostly the resptitory brochiole. predominantly involves the upper lobe. seen primarily in male smokers associated with chronic bronchitis
    • Panacinar / panlobular; uniform destruction and enlargement of the acinus. lower basal zones. alpha 1 antitrypsin deficiency
    • Distal acing; involves distal acing, alveolar sacs. near the pleura and adjacent to fibrous scars. Frequently the underlying lesion in spontaneous pneumothorax.
  28. Airspace enlargement with fibrosis, irregular emphysema
    • protease-antiprotease hypothesis
    • will develop with hereditary alpha 1 antitrypsin deficiency
    • tobacco smoke will oxidize A1 antitrypsin while activating macrophages that recruit neutrophiles to the lungs. elastase activity breaks down the lung parenchyma
  29. Chronic bronchitis
    persistent cough with sputum production that lasts at least three months in at least 2 consecutive years
  30. Pathogenesis of chronic bronchitis
    • chronic irritation of the airways by inhaled substances, tobacco smoke
    • smoke causes mucus hypersecretion with gland hypertrophy
    • goblet cell metaplasia in bronchiolar epithelium
    • bronchiolitis
    • may get secondary infection
  31. Morphology of chronic bronchitis
    • hyperemia and edema of the lung mucus membranes
    • mucus secretions and casts in the airways
    • increased mucus gland cells
    • brochiole mucus plugging, inflammation, and fibrosis
    • squamous metaplasia or dysplasia of bronchial epithelium
  32. Asthma
    • chronic inflammatory disorder characterized by paroxysmal reversible brochospasms of the smooth muscle of tracheal bronchial airways. Hyper-reactivity
    • classified by triggering agents, clinical severity, response to therapy,
  33. Atopic asthma
    • allergic mediated, triggered by environmental antigens; pollen, dust, food
    • overproduction of TH2 cells with subsequent IgE production and eosinophil dominated immune responses
    • Antigen binds to IgE coated mast cell and causes leukotriene and cytokine mediator release. These cause bronchospasms, edema, mucus secretion, and leukocyte recruitment
    • in the late phase neutrophiles, eosinophiles, lymphocytes, and monocytes cause persistent bronchospasms and emema
    • leukocytes infiltrate the epithelium and cause damage
    • IL-4 secreted by TH2 cells causes Bcells to produce IgE, IL3 and 5 recruit eosinophiles
  34. Nonatropic asthma
    • non reaginic
    • triggered by resriptoy track infections, chemical irritants, drugs
    • no IgE involvment
  35. Curshman spirals
    • seen in asthma
    • spiral mucus plugs that contain epithelium
  36. Charcot- leyden crystals
    collections of crystalloid made of eosinophil membrane protein
  37. Bronchiectasis
    • chronic necrotizing infection of brooch and bronchioles leading to permanent dilation of these airways
    • Clinical features include cough, fever, obstructive respiratory insufficiency
    • can cause cor pulmonale, metastatic abscess, systemic amyloidosis
    • obstructions and infections are the major cause; secretions pool and become infected leading to inflammation, necrosis, fibrosis, and airway dilation.
    • cystic fibrosis can be complicated by a bronchiole hypersensitivity reaction to aspergillus fumigates with intense eosinophil rich airway inflammation
  38. Bronchiolectasis is associates with
    • cystic fibrosis, immunodeficiency states
    • post-infection conditions; necrotizing viral. bacterial , or fungal pneumonia
    • bronchial obstruction; tumor
  39. morphology of bronchiolectasis
    • most sever changes occur in the lower lobe distal airways
    • dilations may be of various shapes; cylindrical, fusiform, saccular