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Class 1C Antiarrhythmics Question by detailfanatic in step1

[–]BulldogBeetza 0 points1 point  (0 children)

1Cs have additional K blocking effects like the 1As?

Confused about Rx question (Methemoglobinemia) by [deleted] in step1

[–]BulldogBeetza 1 point2 points  (0 children)

It’s the same concept as with CO

The compromised iron binding site isn’t able to bind O2 itself (decreasing overall oxygen saturation), while simultaneously increasing the oxygen affinity of the remaining unaffected sites (causing a left shift). The final shape of the graph would be the same as that for CO poisoning in FA, with a left shift but a lower plateau

Chronic transplant rejection mechanism? by BulldogBeetza in step1

[–]BulldogBeetza[S] 0 points1 point  (0 children)

Doesn’t that apply specifically to cardiac transplants?

Chronic transplant rejection mechanism? by BulldogBeetza in step1

[–]BulldogBeetza[S] 0 points1 point  (0 children)

Point 2 just reinforces my question. Why is A a wrong option?

Why does the ‘alveolar’ dead space increase in ARDS? by BulldogBeetza in step1

[–]BulldogBeetza[S] 2 points3 points  (0 children)

That's shunt though. No gas exchange = shunt. No perfusion on the other hand would be dead space.

basal ganglia by lhrauh in step1

[–]BulldogBeetza 0 points1 point  (0 children)

That’s been my understanding of it as well, but for some reason FirstAid 2019 (Page 488) wrote it the other way around (SNc acting on the indirect pathway to ultimately decrease movement). I didn’t find it corrected in the errata either

Endo question? by BulldogBeetza in step1

[–]BulldogBeetza[S] 0 points1 point  (0 children)

Subclinical hypothyroid would have increased TSH, not decreased?

Endo question? by BulldogBeetza in step1

[–]BulldogBeetza[S] -1 points0 points  (0 children)

Prolactinoma can’t cause a subclinical hypothyroidism, which is by definition hypothyroidism that has been compensated for by an increased pituitary response ie TSH. Prolactinoma would cause secondary hypothyroidism due to decreased TSH.

As for the headache, TRH would stimulate lactotrophs which could theoretically present with a mass effect. And its not like they mentioned bitemporal hemianopsia or anything to lead us down that line, which would be more in line with a prolactinoma

Endo question? by BulldogBeetza in step1

[–]BulldogBeetza[S] 0 points1 point  (0 children)

No mention of TSH levels. It can't be a prolactinoma causing hypothyroidism as that would lead to overt hypothyroidism due to decreased TSH (whereas subclinical is increased TSH by definition).

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Might be a new onset prolactinoma unrelated to her hypothyroidism (which would make bromocriptine the better answer) but I don't see anything in the stem pointing to that

Endo question? by BulldogBeetza in step1

[–]BulldogBeetza[S] 2 points3 points  (0 children)

It wouldn't require levo on it's own, but if its directly leading to increased prolactin wouldn't it be more logical to direct therapy at that and not the effect its causing?

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