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A 64 year old male who spent most of his career as a missionary in Africa, has blood streaked sputum and a 1 year history of night sweats, malaise, fever, 30 lbs weight loss, and a chronic cough. A chest x-ray reveals cavitary lesions in the apices of his lungs bilaterally. Why do these lesions occur in the apices of the lungs as described in the patient above?

A - Decreased Perfusion.
B - Fenestrations in the alveolar basement membrane.
C - Higher pCO2
D - Lower pO2
E - Higher pO2
 

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Disease is M. Tuberculosis

E) Higher pO2 because its an strict Aerobic organism. Highest O2 is found in the apical area of the lung lobe.
 

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Why are the cavitating lesions of secondary tuberculosis located in the apices while the ghon complexes of primary tuberculosis don't seem to have much of a preference?
 

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Why are the cavitating lesions of secondary tuberculosis located in the apices while the ghon complexes of primary tuberculosis don't seem to have much of a preference?
Very interesting question, but I always thought it was due to the location of where it is infected first, think in Ghon's focus, it has to do with primary infection being spread to the Hilar lymph nodes first, and then spreading to the parenchyma of the lung (forming ghon's complex). Once the outcome of this has been made (granuloma, 2nd spread etc.) in order to reactivate, you need something to ''jump start'' you, that might be oxygen, being highest in apices, and therefore most commonly seen in 2ndary TB in this area (most of the time, 2ndary TB is reactivation, rather then continuous spread from primary lesion)

Im really not sure, but that was my hypothesis.
 

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I think it's just a matter of theory vs reality, much like 75% of Step 1. Primary TB likes to infect the Right middle lobe, but Step 1 tests the point about the apex because TB is a strict aerobe

Here is what I found online:

The tubercle bacilli establish infection in the lung after they are carried in droplets small enough (5 to 10 micron) to reach the alveolar space. If the innate defense system of the host fails to eliminate this infection, the bacilli proliferate inside alveolar macrophages and kill the cells. The infected macrophages produce cytokines and chemokines that attract other phagocytic cells, including monocytes, other alveolar macrophages, and neutrophils, which eventually form a nodular granulomatous structure called the tubercle. If the bacterial replication is not controlled, the tubercle enlarges and the bacilli enter the local draining lymph nodes. This leads to lymphadenopathy, a characteristic manifestation of primary TB. The lesion produced by the expansion of the tubercle into the lung parenchyma and lymph node involvement is called the Ghon complex.

In one series from Canada, 188 patients were assessed, all of whom were culture positive and had abnormal chest radiographs [4]. Thirty patients (18 percent) were classified clinically as having primary TB. The most common finding was hilar lymphadenopathy, present in 67 percent. Right middle lobe collapse may complicate the adenopathy.Several factors probably favor involvement of the right middle lobe:

  • It is more densely surrounded by lymph nodes.
  • It has a relatively longer length and smaller internal caliber.
  • It has a sharper branching angle.

BUT, if a question shows up on Step 1, I would go with Apex! :rolleyes:
 

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Guys I managed to come across the answer to this question while watching the physiology videos of kaplan.

According to the prof:

It has to do with the physiology. Normally, the V (ventilation) and Q (Flow) ratio is suppose to be at .8 (or 1), at the apex of the lung, there is less blood flow then there is ventilation (both due to affects of gravity), therefore, this excess ventilation results in a higher PO2 available at the apex (from the excess ventilation), this is why M.Tb migrates to apex!

:)
 
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