Secondary TB - apices

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Phloston

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UWorld, in QID# 1219, says, in the second paragraph of the explanations, that the aerophilic TB prefers the apices (for secondary infection) because ventilation is greatest there.

That's wrong. Both perfusion and ventilation increase from apex --> base. I wrote them a comment (not that it matters).

But that also got me thinking: ventilation is less at the apices, so why does TB still prefer to grow there? Is it because the lesser perfusion means that less O2 diffuses into the capillaries (due to earlier saturation), so increased deadspace means increased O2 available to the TB?

Cheers,
 
UWorld, in QID# 1219, says, in the second paragraph of the explanations, that the aerophilic TB prefers the apices (for secondary infection) because ventilation is greatest there.

That's wrong. Both perfusion and ventilation increase from apex --> base. I wrote them a comment (not that it matters).

But that also got me thinking: ventilation is less at the apices, so why does TB still prefer to grow there? Is it because the lesser perfusion means that less O2 diffuses into the capillaries (due to earlier saturation), so increased deadspace means increased O2 available to the TB?

Cheers,

Yeah that's true. Probably bad wording. Oxygen content is higher but ventilation is still lower.

Edit: Whoops, sorry I didn't answer your question. I think it's because V/Q is still higher at the apex relative to the bases = higher O2.
 
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Makes sense. I'm not even sure why I had to think twice about that. Because if we have a pulmonary embolus, for instance, PAO2 increases (and PaO2 decreases) because less diffusion takes place. So in the apices, where V/Q is greater than at the bases, lesser relative diffusion must take place, thereby increasing the relative PAO2.
 
Sorry to bump up an older thread, but reactivation TB does not occur at the apices due to the hyperoxic environment up there. According to our lecturer (who also happens to be an ID specialist), that's a load of BS -- the difference in oxygen content between the base and apex is not significant enough for this to be the explanation for reactivation TB. A lot of resources use this as their explanation and they're wrong (surprisingly, I think even Harrison's uses this explanation).

According to the latest theory, reactivation TB tends to occur in the apex because of deficient lymphatic flow at the apices. Respiratory motion at the apex (particularly the posterior apices) is minimal, so Mycobacteria tend to be retained in the lymph up in the apices whereas, in the rest of the lung, where respiratory motion is greater, there's efficient lymphatic drainage. Deficient lymph flow at the apex favors retention of Mycobacteria and thus, reactivation TB tends to occur there.

This latter explanation is also supported by "Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 7th ed." on page 3139.
 
According to Robbins Basic Pathology, 9E: "... The reason is obscure but may relate to high oxygen tension in the apices...". So, like you've said, this is probably not correct, but if somehow this question were to pop up in Step I, I'd still be inclined to choose high oxygen.
 
According to Robbins Basic Pathology, 9E: "... The reason is obscure but may relate to high oxygen tension in the apices...". So, like you've said, this is probably not correct, but if somehow this question were to pop up in Step I, I'd still be inclined to choose high oxygen.

Agreed. They're unlikely to even list deficient lymph flow as an answer choice. That would be evil if they did and you had to pick between the two.

I just mainly posted to point out that the "high oxygen tension in the apices" theory is currently considered wrong and less plausible than the lymph flow one. Since even the big boys like Robbins and Harrison's continue to use that incorrect explanation, we're unlikely to see any changes regarding the correct answer on standardized exams anytime soon. :meanie:
 
UWorld, in QID# 1219, says, in the second paragraph of the explanations, that the aerophilic TB prefers the apices (for secondary infection) because ventilation is greatest there.

That's wrong. Both perfusion and ventilation increase from apex --> base. I wrote them a comment (not that it matters).

Just to elaborate on the concept, while both V & Q increase from apex to base, Q increases relatively more than V as we move from apex to base.
 
Sorry to bump up an older thread, but reactivation TB does not occur at the apices due to the hyperoxic environment up there. According to our lecturer (who also happens to be an ID specialist), that's a load of BS -- the difference in oxygen content between the base and apex is not significant enough for this to be the explanation for reactivation TB. A lot of resources use this as their explanation and they're wrong (surprisingly, I think even Harrison's uses this explanation).

According to the latest theory, reactivation TB tends to occur in the apex because of deficient lymphatic flow at the apices. Respiratory motion at the apex (particularly the posterior apices) is minimal, so Mycobacteria tend to be retained in the lymph up in the apices whereas, in the rest of the lung, where respiratory motion is greater, there's efficient lymphatic drainage. Deficient lymph flow at the apex favors retention of Mycobacteria and thus, reactivation TB tends to occur there.

This latter explanation is also supported by "Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 7th ed." on page 3139.

Very interesting. Just for the sake of discussion, couldn't the apex compensate for the lack of motion by draining downwards rather than upwards as seen in the bases?
 
Very interesting. Just for the sake of discussion, couldn't the apex compensate for the lack of motion by draining downwards rather than upwards as seen in the bases?

Reduced afferent lymphatic and blood flow at the apices likely follows the same physics (i.e. less inflow due to redistribution to the bases secondary to gravity). Therefore it's not a matter of clearance or compensatory changes in efferent flow, but instead one of mere lymph availability in those regions.
 
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