Patho Pulmonary.txt

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pcobb
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137657
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Patho Pulmonary.txt
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2012-02-25 17:09:39
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Patho Pulmonary
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Patho: Pulmonary
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  1. What are two causes for the development of hypoxia or hypercarbia?
    • Low alveolar oxygen
    • Diffusion Impairments
  2. Describe two causes of low alveolar oxygen?
    • Decreased inspired oxygen: high altitude or on a plane
    • Hypoventilation: decreased breaths per minute = increased CO2
  3. Which does hypoventilation cause first? hypoxia or hypercarbia?
    Both at the same time and very quickly. The other disorders usually start with hypoxia which then leads to hypercarbia.
  4. cList four causes of diffusion impairments.
    • loss of surface area
    • V/Q mismatch
    • Shunts
    • Abnormalities in the diffusion membrane
  5. Loss of surface area is a cause of diffusion impairment. Describe it.
    Cut out a lung, due to cancer perhaps
  6. V/Q mismatch is a cause of diffusion impairment. Describe it. What does a high V/Q mean, what does a low V/Q mean?
    If the V/Q is low that is a venilation issue, if the V/Q is high, that his
  7. If there is 5 liters of profusion and 2 liters of ventilation, what does that indicate?
    That would give us a low V/Q which is a ventiliation obstruction.
  8. Abnormalities in the diffusion membrane are cause diffustion impairment. Provide two examples and when we would most likely see them.
    Edema and fibrosis are examples of abnormalities in the diffustion membrane. We commonly see these with chronic disorders; they are more likely to cause hypoxia.
  9. Would abnormalities in the diffusion membrane, such as edema or fibrosis, have more of an affect on oxygen levels or CO2 levels? Why?
    Abnormalities in the diffusion membrane have more of an affect on O2 levels, becuase it is less diffusable than CO2. CO2 is 20% more diffusable than O2.
  10. Shunting is a compensatory mechanism for difussion impairment. Describe it; what is the problem with it?
    The pulmonary vessels constrict blood away from the damaged alveoli. Shunted blook will frequently bypass the lungs and go back to the heart to be profused through the body again. Gas exchange has not happened, so the 40/45 blood is bad.
  11. What is the normal lab value for PCO2?
    35-45
  12. What is the normal lab value for O2?
    80-100
  13. What is the difference between an Obstructive Disorder and a Restrictive Disorder?
    An Obstructive Disorder involves increased resistance, like blowing through the neck of a balloon. A restrictive disorder involves expansion, like if the balloon has water in it so it's harder to blow up.
  14. What is an example of an Obstructive Pulmonary Disease?
    Asthma
  15. List two types of asthma.
    Extrinsic and Intrinsic
  16. Describe Extrinsic asthma.
    Type I Hypersensitivity response to an allergen. IgE responds. It is a local response in the lungs.
  17. Describe Intrinsic Asthma. What is another name for it?
    Also called Hyperreactive Airway Disease. This is not caused by an allergen. It could be the cold, exercise, an infection...
  18. Describe the two phases of asthma. What is the predominant phase?
    • Early Phase: bronchospasms
    • Late Phase: inflammation (asthma is predominatly inflammation)
  19. What are six clinial manifestations of OPD?
    • Wheezing: the sound of air going through a small space
    • Dsypnea/chest tightness: they are having to work hard
    • Use of accessory muscles: especially intercostals
    • Cough/sputum: they have excessive mucous and its sticky
    • Tachypnea/tachycardia: due to air trapping
    • V/Q mismatch: low V/Q
  20. What is residual volume, what are complications of it and how does it relate to air trapping?
    Residual volume is the amount of air you cannot expire. It manifest on a CXR and over time it can push down on the diaphragm. It can also cause the chest to stay inflated = barrel chest.
  21. What is a PFT?
    Pulmonary Function Test
  22. What would you expect to see on an a PFT with a person who has OPD?
    Decrease in FEV (forced expiratory volume), decreased FVC (forced vital capacity)
  23. In a person with asthma (OPD), what causes the tachypnea/tachycardia?
    The air trapping is interferring with the breathing.
  24. Describe the diagnosis of OPD as it relates to the ABGs.
    Early respiratory alkalosis, later respiratory acidosis, hypoxemia
  25. What are the two types of COPD? Which is more common?
    • Chronic Bronchitis
    • Chronic Emphysema
    • usually have a combo of both
  26. In relation to COPD, what are the causes of chronic bronchitis and chronic emphysema?
    • Chronic bronchitis: smoking and occupational exposure
    • Chronic emphysema: smoking and deficiency of alpha1-antitrypsin (<1%, manifest in 20s/30s)
  27. Describe the process of chronic bronchitis.
    Chronic inflammation with hypertrophy of bronchiole walls and hyperplasia of mucous cells leading to excessive sputum. Chronic inflammation eventually leads to excessive WBC infiltration of broncial walls, fibrosis occurs = obstruction = Low V/Q. Ciliated epithelium is replaced by squamous cells.
  28. Describe the roll of elastase in emphysema.
    Chronic inflammation causes excess elastase production. Elastase breaks down the elastine in the alveolar walls. The loss of elastin results in the collapse of alveolus and walls of respiratory bronchiole upon expiration, so air is trapped behind the alveolus. Cannot stretch bronchioles.
  29. Describe some manifestation of COPD.
    • PND (paroxysmal nocturnal dyspnea = sudden night dyspnea)
    • pursed-lip exhalation (prolonged exiratory phase)
    • recurrent bacterial infections and broncospasms
    • low V/Q
    • orthopnea
    • thin or overweight
  30. What is PND and when do we see it?
    Paroxysmal Nocturnal Dsypnea: sudden nightime dsypnea - we see it with COPD
  31. What are two complications of COPD; explain how they relate to each other.
    Pulmonary Hypertension and Cor pulmonale: The obstruction in the teminal bronchioles causes shunting via vaso-constriction. The vasoconstriction causes an increase in pulmonary hypertension. The pulmonary hypertension causes righ-sided hypertrophy in the heart, that causes cor pulmonale (right-sided heart failure).

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