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While L gastroepiploic would make more sense than the other answers, considering it has an anastomosis (and therefore an outlet for the increased blood) I think it would have much less risk of varices/bleeding than the short gastric would
Same, except in my case I was the person who was tricked and who did the tricking though. Thx for the link.
Sir Dan, my boi.
Does the obviously darkened area not point at all towards ischemia of any kind? Maybe I am blind, but I don't see anything that remotely looks like an obstructive diverticulum in this picture. I feel like I would have gotten this question correct if no picture had been provided at all because the symptoms described absolutely pointed towards diverticulitis otherwise. I actually changed my answer because of the image lol
Picture is a bullshit distractor
From what I've seen on practice tests and advice i've gotten is that often if the picture is given along with an already complete clinical picture it's often a distractor. I also was going between ischemia and diverticulitis but then remembered that clinical signs in the vignette trump everything else.
they dont give a fuck about pictures
Famotidine is an H2 blocker which really only stops acid secretion via the stimulation of H+/K+ ATPase by histamine, but it still has vagus and gastrin stimulation.
If you use Omeprazole, you get irreversible inhibition of the pump itself which stops the secretion of acid even if there is histamine, gastrin, vagus stimulation.
what about the healing of her mucosa. Is that not the action of prostaglandin?. That threw me off cos according to FA, misoprostol increases secretion of the gastric mucosa
I guess because misoprostol is more associated with treatment of NSAID related ulcers and PPIs are 1st line DOC for GERD?
@temmy, I think that Omeprazole is a better answer because although Misoprostol would promote healing of her esophageal mucosa, it wouldn't do anything to relieve the symptoms of GERD (due to acidic contents in the esophagus)
In short, cortisol upregulates adrenergic receptors and makes them more sensitive
that video was sick
How is that NOT posterior to middle concha? bad question
@yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw)
Sphenoethmoidal RECESS not sphenoethmoidal SINUS
the atrioventricular bundle is also called the bundle of his
What if it had said "AV node", that's in the interaatrial septum as well, right? I'm wondering, that could be answer as well. (FA 2019 pg291)
I know you're right. I was just so uncomfortable picking an answer with "inferior rectus" because damage to the inferior rectus does nothing to explain the clinical findings of impaired upward gaze. Unless the muscle is physically stuck and can't relax or something
Agreed. Why would a dysfunctional inferior rectus contribute to impaired upward gaze??? I eliminated that answer choice and got it wrong :(
in the last sentence it asks you to assume an "entrapment", so it is actually the inferior rectus which is the cause of the upward gaze palsy. The entrapped muscle is functionally trapped in it's shortened position, thereby not allowing the orbit to gaze upward.
bam! dr_jan_itor just cleaned up that confusion
Thought this was a trick question as C1 esterase deficiency also results in a decrease in C4. However, the second answer choice was not referring to C4 but to C4 binding protein, which I now know is different. I also didn't realize C1 esterase was technically a complement protein.
Based on many sources hereditary angioedema does NOT cause a rash (urticaria) which is a main differentiating point between angioedema and allergy. This mislead me in this question. Any clarification?
+1 on the above because uptodate states that c1 esterase inhibitor deficiency, both acquired and nonhereditary, are both non-urticarial, non-pruritic, and that is confirmed by the above linked article
Question writer probably didn't know the difference between cutaneous urticaria and subcutaneous edema.
same. got it wrong bc the pt didn't have sx of hereditary angioedema - swollen lips and eyelids
According to Amboss "Mast cell-mediated angioedema
Often associated with urticaria and pruritus
Other associated with clinical findings of allergic reactions (see type 1 hypersensitivity reaction)
Presents within 30 minutes to 2 hours after exposure and resolves over hours to days"
Im mad at how simple this question actually is
Incidence is measured from those AT RISK. People with the disease are not considered to be at risk. So 2500 - 500 = 2000 people at-risk. Of those 2000, within one year 200 develop the disease. So 200/2000 of the at-risk population develop the disease. 20/2000 = 10% = incidence
Wow. I hate this. I only looked at the number of participants and completely ignored the Diastolic BP readings
Everyone commented how to get the mode right. But there is an easier way to realize that the median in Y is higher without all the calculations. If you see, the last Diastolic BP in group X is 110 (as there are ZERO people with 120). While group Y has 8 people with 120 DBP. This automatically shifts the median to the higher side.
I got this wrong though at first I didn't pay attention to the "0" number at group X for 120 DBP
I think there's another easy way to find the median without writing out every value. There are 100 total people in each group, so that means the median (if the DBPs are written in ascending order, which they are) is the 50th person.
Group X: 8 + 12 + 30 = 50, so median is 70
Group Y: 2 + 8 + 10 + 20 +10 = 50, so median is 90
I did it the way @brasel explained. The way @ma_rad did it could give the incorrect answer in some cases (e.g. Group X had 0 ppl with 120 BP but a ton of ppl for 110 BP etc. + Group Y had 10 ppl with 120 BP but basically none with 110 BP etc.). In this question that way worked but it's not always guaranteed since median doesn't sway with outliers, but mean does. // FA 2019 pg. 261
I agree! Also, At the end of the stem, the question is which of the following best explain the patients symptoms? Not physical exam findings. Since this patient is coming in with a chief complaint of SOB while playing sports exercise induced asthma is the best choice. Hopefully that helps.
I mean... couldn't increased BP during exercise worsen his MVP and give him SOB?
(by causing slight regurg)
"Lungs are clear to auscultation"
But wouldn't choosing exercise-induced asthma leave the murmur unaccounted for?
I incorrectly chose malingering and am wondering if the fact that he presented (although it doesn't state who brought him in/confirmed his symptoms while exercising) makes this less likely despite the fact that he clearly states "I don't want to play anymore" which could be interpreted as a secondary gain? Also, regarding the MVP, I'm wondering if the fact that these are usually benign should have factored into our decision to rule it out? Thoughts?
Just noticed that he has FHx, game changer.
clear lungs, they try to say no cardiogenic Pulm. edema, means is not due to MVP
shortness of breath while doing sports and no shortness at rest makes me to think more asthma induced by exercise)
Isn't exercise induced asthma usually found in people running outside, especially in cold weather? I feel like that is how it is always presented in NBME questions, so this threw me off. Not to mention the MVP.
it took me a little; the FHx really pushed me to exercise induced. I was also looking at malingering but there wasnt a real reason to push me to this (as a doctor it would be sad to be like hes faking it becasue he doesnt want to play sports with out being sure first; led me away because there wasnt enough pointing there). Also MVP could be slightly benign and is very common and usually no Sx and his lungs were clear as was rest of exam. All pushed to Asthma
I think MVP on its own shouldnt cause SoB with cough (in a question, I'm sure it could in the real world). In the world of NBME questions where you need to follow the physiology perfectly, you would need some degree of MR that lead to LV dysfunction/vol overload, and theres no pulmonary edema nor an S3 that point us towards that. Malingering would have to be faked for gain, and theres no external gain here or evidence that he's faking symptoms. You would also need to r/o physical illness before diagnosing malingering, which hasnt been done. Cold weather is certainly known for exacerbating EIA and are the exam buzzwords, but any exercise can absolutely be a trigger
If one of the answer choices was, "that baby gon be big lol" I would have gotten it right
This is wrong. PLASMA cells (mature B cells, the ones found in multiple myeloma) secrete antibodies, but IMMATURE B cells have antibodies that haven't switched classes yet (IgM and IgD).
To clarify - immature B cells have antibodies attached to their membrane.
I should have clarified that I was speaking about mature B cells. Thank You
So because MM has mature B cells, exogenous antibodies can't attach to them. Am I getting that right?
What is an Anti-Idiotypic Antibody?
As shown in figure 1, an anti-idiotypic (Anti-ID) antibody binds to the idiotype of another antibody, usually an antibody drug. An idiotype can be defined as the specific combination of idiotopes present within an antibodies complement determining regions (CDRs). A single idiotope, is a specific region within an antibodies Fv region which binds to the paratope (antigenic epitope binding site) of a different antibody. Therefore, and idiotope can be considered almost synonymous with an antigenic determinant of an antibody.
@sahusema: almost exactly correct, but it's important to note they are talking about idiotypic antibodies specifically because by definition these bind the "idiotype" of another antibody (see definition above)
The fibrosis causes contraction, the airways are pulled open giving less resistance to airflow
Hyotension will lead to decreased arterial pressure and DECREASED stretch. This leads to decreased afferent barcreceptor firing (carotid sinus and aortic arch). This leads to an increase in efferent sympathetic firing and decreased efferent PNS stimulation. This leads to vasoconstriction, increased HR and increased BP.
The way I remember this, carotid massage slows the heart. So baroreceptor stimulation (more impulses) increases parasympathetic output.
FA 2018 pg 291 has helpful image/description
Stem actually states, “On questioning, the patient does not know the date [time], the name of the hospital [place], or the name of her nurse who had just introduced himself [person].” So, pt *is* actually disoriented to time and place (Choice A). That is definitely concerning -- as would be depressed mood (Choice E) and the other choices -- but “inability to understand severity and prognosis” is **the most concerning** since that is the very definition of capacity. Inability to understand = lack of capacity.
So by the logic of the question, if someone understands the severity of their medical condition AND happens to also be disorientated to place and time. Go ahead and do sx on them, it's fine.
To remember Baclofen is a GABA agonist and muscle relaxant, I always think of the "Greek Baklava". Greek for GABA, Baklava for Baclofen.
Also, acts on GABA receptors specifically in the spinal cord
Okay i might be retarded, but why i can’t understand that they r asking about the thing that is damaged ? 😂😂
Seriously! The question says "the goal of treatment is the protection of which of the following structures?" If too much O2 damages the retina, how is this treatment supposed to be protective to the retina?
I think too much oxygen would be with the ventilator having a high FiO2 setting, which they don't mention here but I'm guessing thats the thing they're controlling to avoid oxygen toxicity?
they didn't give the patient fio2 100%, question asks the reason for it. but in a very stupid way
Supplemental O2 may also cause bronchopulmonary dysplasia or intraventricular hemorrhage (germinal matrix, located in subventricular zone NOT choroid plexus)
92-95% isn't high, but it's enough to get everything else oxygenated. Because it's not 100% high flow the retinas don't over-vascularize and lead to damage/hemorrhage, and shit like that.
In other words....the question is basically asking why they gave the patient a fio2 of 92-95% instead of 100%. The reason is because 100% oxygen would lead to retinopathy of prematurity. The lower 92-95% oxygen levels protect the retina from damage. The wording of the question sucks tho imo.
FA 2019 p210 under Free radical injury examples
I have a question : whats the relation then between power and P value ?
This one took me a minute and was during the last block so my brain was already fried. But my reasoning was that, as stated above, since it gave you power, it is basically just a long-winded way of asking what Power is, and how this relates to p-value. P-value is the odds that the finding was due to chance alone. Obviously a p-value set to <0.05 implies a greater than 95% chance that the finding is legit. Since the power is said to be 80%, this means that there is an 80% chance that the study finding is legit, at least insomuch that it met the pre-set criteria of being 95% non-chance related.
80% chance (power) the study correctly identifies the existence of an association in reality. If an association is determined to exist, >95% chance the study and reality agree with each other (p<.05)
Ya I think this question is trying to test your knowledge between a cortical lesion and a subcortical lesion.
Central Stroke Syndrome: Neuropathic pain due to thalamic lesions. Initial paresthesias followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysesthesia on the contralateral side. Occurs in 10% of stroke patients. FA 2018 499
Amphetamines use the NE transporter (NET) to enter the presynaptic terminal, where they utilize the vesicular monoamine transporter (VMAT) to enter neurosecretory vesicles. This displaces NE from the vesicles. Once NE reaches a concentration threshold within the presynaptic terminal, the action of NET is reversed, and NE is expelled into the synaptic cleft
Hardy Wineberg equilibrium
square root 900 = 30
1/2 of all offspring will be carriers so 30*.5 = 15
simple as that
this question is garbage. She doesnt want to be examined by a male how would the presence of her husband make any difference in that respect?
The question here focuses on a specific issue which is the patient's religious conservative beliefs vs. urgency of the situation. A physician is required to respect the patient's autonomy while also balancing between beneficence and non-maleficence. The answer choice where the physician asks the patient if it would be ok to perform the exam with the husband present is an attempt to respect the conservative religious belief of the patient (not being exposed or alone with another man in the absence of her husband) while also allowing the physician to provide necessary medical treatment that could be life saving for her and or the child. Again, this allows for the patient to practice autonomy as she has the right to say no.
I showed this question to my parents and they said "this is the kind of stuff you study all day?" smh
I totally agree this is a garbage question. I personally think there is more garbage question on new NBME forms than the previous ones...they can argue in any way. I feel like they were just trying to make people struggle on bad options when everybody knows what they were trying to ask.
This question is a3othobillah
this question is really not that garbage....actually easy points I was grateful for... yall are just clearly ignorant about Islam. educate yourselves, brethren, just as this exam is trying to get you to do. but yeah I agree there should be an option for female physician lol
I think this NBME24 is a waste of $60.
On one hand we have these types of questions, that have 0 connection to our week-month-year-long studying.
On the other hand we have "Synaptobrevin" instead of SNARE, because f*ck coming up with good questions.
@sunshinesweetheart I actually have studied the religion tremendously and there a clear consensus among all Muslims that in the case of an emergency, it is completely allowed to have someone from the opposite gender examine you. I think this actually represents how ignorant the exam writers are of Islam.
All it takes is one NBME question concerning muslims for the Islamophobia to jump out I guess
This is a very fair question. I agree with sunshinesweetheart above. That is all.
well we should wait for the question "if a man shouts I CANT BREATHE with a police knee on his neck, what is your next step? Ans- wait 8 minutes."
be kind to yourself, doc! (it's a long road we're on!)
Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency?
I think the blood smear is showing a lone lymphocyte, which should be the same size as a normal RBC. You can see the RBCs in this smear are bigger than that ->macrocytic ->B12 deficiency
maybe i'm new to the game. but isn't the answer folate deficiency and not B12? Also, i though it was anemia of chronic disease as well.
Lispectedwumbologist, please explain your mistake? Lol because that seems like a respectible answer to me...
It's a B12 deficiency
Ileum is where B12 is reabsorbed, folate is jejunum
The blood smear is showing enlarged RBCs
Methionine synthase does this conversion, using cofactor B12
Anemia of chronic disease is a microcytic anemia -- I believe this is why they put a lymphocyte on the side -- so we could see that it was a macrocytic anemia.
Thanks NBME, that really helped me....
the question was relatively easy, but the picture was so misguiding i felt! i thought it looked like microcytic RBCs. I guess the key is, that they clearly mentioned distal ileum. and that is THE site for B12 absorption.
I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF
Leave it to NBME to find the palest macrocytes on the planet.
so i guess size is more important than color cause those are hypochromatic as fuck
The NUCLEUS of a lymphocyte should be the same size as a normal RBC, which is not the case here. Under normal circumstances RBCs are not as big as lymphocytes, so this is truly extraordinary = megaloblastic anemia.