Resp Disorders 1

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Author:
annzors
ID:
174858
Filename:
Resp Disorders 1
Updated:
2012-10-02 22:43:07
Tags:
Pathophysiology
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Description:
Resp failure, COPD, restrictive lung disorders, misc. resp conditions, lung cancer
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  1. resp failure (3)

    1) hypoventilation -> leads to...
    2) impaired diffusion -> leads to...
    3) pleural disorders
    • 1) hypoventilation -> leads to hypercapnia (high CO2 in blood) and hypoxia
    • 2) impaired diffusion -> leads to hypoxemia (low O2 in blood) but not hypercapnia
  2. Hypoventilation causes (3)
    • depression of respiratory center
    • disease of resp nerves or muscles
    • thoracic cage disorders
  3. Impaired diffusion can occur as a result of... (4)
    • interstitial lung disease
    • ARDS (acute resp distress syndrome)
    • pulmonary edema
    • pnemonia
  4. hypoxemia
    PO2 < ?; leads to... (5)
    • PO2  <60 mm Hg
    • cyanosis results
    • leads to impaired function of vital centers
    • symptoms include agitated or combative behaviour, euphoria, impaired judgment, convulsions, delirium, stupor, coma
    • hypotension and bradycardia (decrease HR and CO -> decrease BP)
    • results in activation of sympatehtic system
  5. hypercapnia
    PCO2 > ?
    Respiratory acidosis leads to...
    • increase resp
    • decrease nerve firing (disorientation, coma)
    • decrease muscle contraction
    • vasodilation in the head region - headache, warm flushed skin
  6. plural space disorders (2)
    • 1) pleural effusions (fluid in the pleural cavity)
    • 2) pneumothorax
  7. pleural effusion (flluid in the pleural cavity) (4)
    • hydrothorax: serous fluid
    • empyema: pus
    • chylothorax: lymph
    • hemothorax or fibrothorax: blood
  8. hydrothorax
    serous fluid
  9. empyema
    pus
  10. chylothorax
    lymph
  11. pneumothorax
    a) ?
    b) ?; i) ? ii) ?
    • air enters the pleural cavity
    • air takes up space, restrictin glung expansion
    • partial or complete collapse of the affected lung
    • a) spontaneous: an air-filled blister on the lung ruptures
    • b) traumatic: air enters through chest injuries (intense pain on injured side)
    • i) tension: air enters pleural cavity through the wound on inhalation but cannot leave on exhalation (compression of the inferior ven cava + obstruction of blood flow thru) (clinical man >intense pressure preventing inhalation >can be fatal if intervention is delayed)
    • ii) open: air enters pleural cavity through the wound on inhalation and leaves on exhalation
  12. spontaenous pneumothorax
    an air-filled blister on the lung ruptures
  13. traumatic pneumothorax
    i) tension pneumothorax
    ii) open pneumothorax
    air enters through chest injuries (intense pain on injured side)

    i) tension: air enters pleural cavity through the wound on inhalation but cannot leave on exhalation (compression of the inferior ven cava + obstruction of blood flow thru) (clinical man >intense pressure preventing inhalation >can be fatal if intervention is delayed)

    ii) open: air enters pleural cavity through the wound on inhalation and leaves on exhalation
  14. features of pneumothorax (3)
    • tracheal shift
    • cardiac compression
    • lung deflation
  15. obstructive diseases (5)
    • (bronchial) asthma
    • COPD i) emphysema; ii) chronic bronchitis
    • bronchiectasis
    • cystic fibrosis
  16. restrictive diseases
    • chest wall - kyphosis
    • pleural - effusion, pneumothorax
    • parenchymal - occupational, ARDS-IRDS, atelectasis
  17. resp obstruction in children
    1) extrathoracic airways (upper)
    2) intrathoracic airways (lower)

    Describe the above.
    increased airway resistance = decreased airway conductance

    • extrathoracic airways (upper):
    • > prolonged inspirationl inspirational stridor (labored)
    • > inspiratory retraction as ribs are moved outward and body wall does not expand with rib cage (= insuf expansion)

    • intrathoracic airways (lower)
    • > prolonged expiration with wheezing
    • > rib cage retraction as ribs are pulled inward but air  does not leave lungs
  18. Upper airway obstructive disorders (2)
    • epiglottitis
    • croup:
    • age range 3 months - 3 years
    • brought by variety of viral infection (e.g. flu)
    • characterized by hoarseness, a brassy cough
    • fever
    • inspirational stridor
    • cough is lessened by inlhation of cold air
    • can lead to cyanosis, pallor in severe cases (restriction of blood flow; Hg decr.)
  19. Lower airway obstructive disorders
    • acute bronchiolitis:
    • incr. expiratory effects = wheezing
    • brough by viral infection
  20. Asthma (2)
    • Extrinsic (atopic): allergic reaction
    • Intrinsic (nonatopic): attacks precipitated by:
    • physical factors
    • exercise
    • psychological stress
    • chemical irritants and air pollution
    • bronchial infection
    • aspirin
  21. extrinsic (atopic) asthma
    • type 1 hypersensitivity
    • mast cells' inflammatory mediators cause acute response within 10-20 min
    • airway inflammation causes late phase response in 408 hours
  22. pathogenesis of asthma
    • IgE interacts w/ mast cells and acts as receptors for allegens
    • hisamine release triggers the change in airway walls (thicken) (from granules)
  23. histopathology of asthma
    • mucus in lumen
    • inflmmation and basment membrane thickening
    • enlarged mucous glands
    • smooth muscle hyperplasia
  24. clinical manifestations of asthma (3)
    • 1) bronchial smooth muscle constriction
    • 2) mucosal edema
    • 3) hypersecretion of mucus
    • others: epithelial injury, bronchospasm, edema
  25. intrinsic (nonatopic) asthma
    - causes
    - treatment
    • 1) resp infection: epithelial damage, IgE produced
    • 2) exercise, hyperventilation, cold air: lost of heat and water may cause bronchospasm
    • 3) inhaled irritants: inflmmation, vagal reflex
    • 4) aspirin and other NSAIDs: abnormal arachidonic acid metabolism
    • treatment: anticholinergic (preventing contraction of smooth muscles)
  26. COPD disorders (3)
    • emphysema: enlargment of air spaces and destruction of lung tissue
    • chronic obstructive bronchitis: obstruction of small airways
    • bronchiectasis: infection and inflammation destroy smooth muscle in airways, causing permament dilation
  27. mechanism of COPD (4)
    • 1) inflmmation and fibrosis of bronchial wall
    • 2) hypertrophied mucus glands -> excess mucus; obstructed airflow
    • 3) loss of alveolar tissue: decr. surface area for gas xchange
    • 4) loss of elastic lung fibers (emphysema): airway collapse, obstructed exhlation, air trapping, decr. air delivery
  28. treatment of asthma (4)
    • 1) manage enviro
    • 2) bronchodilators (Ventolin)
    • 3) antihistamine
    • 4) antiinflammatory (corticosteroid - Flovent) - synthesis of beta receptors therefore boost the effects of beta agonist
    • beta agonist: related to CV system, mimics SNS; decr. receptors locally on smooth muscle; receptor down regulation
  29. treatment of COPD
    • 1) bronchodilator
    • 2) steroid (antiinflam)
    • 3) antibiotics (decr. bacteria growth in the thickened mucus)
    • 4) flu shot
    • 5) O2 therapy
    • 6) others - quit smoking, DB & C, exercise, reposition
  30. emphysema
    - trypsin & neutrophil
    - types
    • emphysema: enlargment of air spaces and destruction of lung tissue
    • neutrophils in alveoli secrete trypsin (digestive protein) - incr. neutrophil = incr. trpysin
    • aplha-antitrypsin inactivates the trypsin before it can damage the alveoli
    • trpysin damages protein, fibers, elastin in alv. wall
    • alv loses radial fraction
    • types: centrilobular (distended resp bronchiole) and pancinar (one lumped alv)
  31. pink puffer
    (ephysema - COPD)
    • breathe in deep
    • chest muscle incr.
    • barrel chest (narrow); lean forward when breathing
    • pursed lip breathing
    • dont suffer hypoxia by incr. drawing volume of air
    • increase resps
    • dyspnea (incr. ventilatory effot)
    • use of accessory mucscles
  32. chronic bronchitis (4 char)
    • chronic irritation fo airways
    • increased number of mucus cells
    • mucus hypersecretion
    • productive cough
  33. chronic bronchitis
    • needs to sit upright
    • tachypnea (incr. resps)
    • incr. temp due to incr. metabolic demand of muscles
    • cannot increase resp enough to maintain oxygen level
    • cyanosis and polycythemia (incr. RBC)
    • cor pulmonale from think blood, incr. work for RS of heart, RS HF

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