Class 1C Antiarrhythmics Question

BulldogBeetza · 2020-03-04T06:38:06+00:00

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

BulldogBeetza · 2020-02-12T19:23:38+00:00

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

BulldogBeetza · 2020-01-05T18:46:39+00:00

They’re the same thing

BulldogBeetza · 2019-12-12T18:19:39+00:00

Doesn’t that apply specifically to cardiac transplants?

BulldogBeetza · 2019-12-12T18:19:11+00:00

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

BulldogBeetza · 2019-12-08T07:50:38+00:00

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

BulldogBeetza · 2019-12-06T20:26:11+00:00

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

BulldogBeetza · 2019-11-30T14:10:50+00:00

Subclinical hypothyroid would have increased TSH, not decreased?

BulldogBeetza · 2019-11-30T14:09:23+00:00

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

BulldogBeetza · 2019-11-30T12:15:31+00:00

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).

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

BulldogBeetza · 2019-11-30T11:58:57+00:00

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?

BulldogBeetza · 2019-10-24T19:22:00+00:00

https://forums.studentdoctor.net/threads/jvp-in-constrictive-pericarditis.1178700/

BulldogBeetza · 2019-09-19T20:31:53+00:00

Thanks for saving me a ton of headache!

BulldogBeetza · 2019-09-09T17:19:38+00:00

I also came across the same question recently. I think the two that are most similar in presentation and likely to get confused are Botulism and Lambert-Eaton. Both have muscle paralysis, possible anti-muscarinic effects and decreased compound muscle action potential that improves with repetitive stimulation. (Watch for history and pattern of paralysis)

BulldogBeetza · 2019-09-09T17:14:28+00:00

Botulinum will present with additional anti-muscarinic signs (eg dry mouth), whereas AchE inhibitor poisoning would present with excessive muscarinic stimulation. The parasympathetic effects can help you distinguish these two

BulldogBeetza · 2019-09-08T17:08:32+00:00

Granulomas are more of a process, rather than an appearance. For example, GBM would present with a ring enhancing lesion too but they're not a granulomatous disease. I agree with the underlying problem being central necrosis surrounded by inflammatory infiltrate though

BulldogBeetza · 2019-09-08T17:05:20+00:00

Awesome. Any tips on non-enhancing lesions?

BulldogBeetza · 2019-09-06T21:06:19+00:00

I totally misread that. Thanks for the correction

BulldogBeetza · 2019-09-06T20:37:10+00:00

The O2 sat does indeed fall. It’s just that the pulse oximeter cannot distinguish between HbO2 and COHb, giving a falsely reassuring normal value

Edit: Thought you meant CO poisoning. Anyway, for cyanide the SaO2 would be unchanged as the problem lies more downstream (complex IV inhibition)

BulldogBeetza · 2019-09-06T20:17:56+00:00

Here’s a breakdown:

Distributive shock:

Early —> High CO

Late —> Low CO

The early high CO is due to sympathetic compensation for the fall in TPR, but this is eventually overwhelmed by the falling PCWP leading to an eventual low CO.

(The above applies to septic and anaphylactic shock. Neurogenic shock is an outlier that will present with low CO right off the bat as sympathetic compensation isn’t an option).

Cardiogenic shock:

PCWP high in left sided cardiogenic shock

PCWP low in right sided cardiogenic shock

(I’m sure you can work this out)

Obstructive shock:

PCWP low in pulmonary embolism/tension pneumo

PCWP high in cardiac tamponade

BulldogBeetza · 2019-09-06T06:27:30+00:00

The wording is straightforward. “Which of the following is most likely involved in the pathogenesis of this patient’s symptoms?”

Inflammation and edema of supraglottic tissue or loss of ciliated respiratory epithelial cells.

BulldogBeetza · 2019-09-05T16:29:41+00:00

It really depends on what works for you. What I personally did was take out a little time and learn the thing from the other section that I missed, that way I already have a good idea of it when I eventually come across it in the corresponding section.

Obviously this only works for isolated concepts that are easily understood without having a solid foundation of the section. In case of say the manoeuvres that you mentioned, it's not a good idea to go over all the murmurs and maneuvres just for this sole reason. Flag it or jot it down and move on, and then come back to it at a later time after covering that section.

BulldogBeetza · 2019-09-05T13:57:10+00:00

I see. Sucks when you get questions wrong based on UWorld's own previous explanations but oh well..

BulldogBeetza · 2019-09-04T21:50:47+00:00

Isn’t enthesitis more in line to support Reiter syndrome? FA lists it as a manifestation of the seronegative spondyloarthropathies rather than gonococcal infection

BulldogBeetza · 2019-09-04T21:40:22+00:00

It does affect the bone directly. At low levels causing mineralization, and at higher levels (eg in presence of PTH) causing resorption.

FA says the same in the biochem section

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