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Contributor score: 462
that was my reasoning as well. guess not.
Shitty NBME grammar strikes again.
No. No guys. Bundle of his located below AV node and it can generate impulse. it calls junction escape rhythm and narrow complex. Below this is purkinje, bundle branch & ventricular muscle. those are wide complex
The atria and ventricles beat independently of each other. P waves
and QRS complexes not rhythmically associated. Atrial rate >
ventricular rate. Usually treated with pacemaker. Can be caused
by Lym3 disease
I am embarrassed by these typos.
No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?!
The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum.
He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites.
For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy)
For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN".
@paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis.
cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken.
Cirrhosis (most likely due to alcoholism in this patient) leads to an increase in sex hormone binding globulin, causing a relative increase in estrogen compared to androgens. Cirrhosis doesn't always have to present with ascites and adema. I agree with @catch-22 that liver disease is a spectrum. This patient does not have ascites because his liver is still able to produce enough albumin to maintain oncotic pressure in the blood.
Just in case anyone is wondering like I did, the low platelet count explains thethose multinucleated cells. They are Megakaryocytes in Bone Marrow Biopsy.
Also, don't forget that autoimmune thrombocytopenia purpura has 2 demographics: young kids, which generally resolves spontaneously fairly quickly, and then young adult females which is a true autoimmune condition that doesn't resolve. Patient's age + thrombocytopenia + essentially normal rest of heme pannel = autoimmune thrombocytopenia purprua in child.
That is exactly how I approached this question. Normal heme panel and a decreased Platelet count in a young boy after an infection just made me intuitively select ITP.
You wouldn't use Standard error with Confidence Interval? (pg. 262 FA 2019)
Great explanation, except that there was a question in NBME 22 in which the prostatic carcinoma was osteolytic. One of the commenters here looked it up and apparently it's like that 30% of the time or something. So I guess you would have to use the high output HF, normal Ca, high ALP, and mosaic pattern to "play odds" as Goljan would say.
At least they were nice enough to put Paget disease because I had no idea what osteitis deformans is.
USMLE seems to be moving away from using eponymous names... so it's a good idea to see if there is a descriptive name for diseases. For example, they don't use the word "Wegener" anymore if you have noticed, since it turns out that guy was a nazi. So now they call it by what it is -- granulomatosis with polyangitis.
I didn't pick this one because I thought Serum sickness was too systemic and RA was a more localized Type 3. Again, im overthinking things.
Goljan: RA is a mixed type III and type IV immune reaction
I though NK cell killing was similar to T cell so and RA is also Type IV
NK cell killing would be a type of innate immunity, not similar to memory T cells. because they did not give an example of a type 4 HSY, the answer must be serum sickness.
Perfringens is also usually a delayed response, can help in vignettes!
His glycogen concentration is high, since he's been hyperglycemic with lots of insulin until birth.
Also explains why he's 12 pounds.
Also, think of it like this:
Insulin causes hypoglycemia, thus this baby must have increased insulin. It is also an anaobolic hormone which is clear by the babys weight.
Insulin increases glycogen synthase activity, and causes an increase in concentrations of glycogen. Decrease in insulin would do exactly the opposite
fetus of a mom with DM will develop pancreatic beta cell hyperplasia, which leads to insulinemia trying to reduce the blood glucose. after birth, the excessive blood glucose will be automatically withdrawn while the insulin at that moment is still high, which leads to hypoglycemia.
But isn't statin associated with hepatotoxicity too? FA 2019 page 320
@qfever. I think thats why OP said that statins are not metabolized in the liver.
amazing, thank you!
sensation to pinprick is DCML tract. SCD affects spinocerebellar (not spinothalamic), corticospinal, and DCML. otherwise good explanation.
Sensation to pinprick is not dorsal column-medial lemniscal tract, it's spinothalamic tract. So this patient has a lesion of the dorsal columns, spinothalamic tract hypersegmented neutrophils, and anemia. What the hell is going on? How is this just posterior cord syndrome? Spinothalamic is not posterior cord.
Pretty infuriating that this question has the standard R and L label while the other spinal cord question had it flipped.
A and J represent the gracile fasciculus, while B and I represent the cuneate fasciculus. Together they make up the dorsal column-medial lemniscal tract, responsible for pinpoint perception, proprioception, vibration, and pressure. Input is ipsilateral.
C and H make up the lateral corticospinal tract (also called the lateral cerebrospinal fasciculus), responsible for motor command of ipsilateral limbs.
D and G represent the lateral spinothalamic tract. It is responsible for pain and temperature conduction. The input arises in a limb (left lower extremity in this case), enters through the dorsal root (pictured between J and H), decussates and ascends at the anterior commissure (just behind E and F), and finally synapses on the second order neuron in the lateral spinothalamic tract. So the spinothalamic tract is responsible for contralateral pain and temperature sensation. Because our patient has lost sensation on the left, the lesion is in the right.
E and F are the anterior corticospin
Suicide attempts are also commonly seen with Borderline
Great explanation - just one addition. The retroperitoneal fibrosis could also be a direct consequence of the external beam radiation. It's linked to both causes. Either way, it's a better fit than urothelial carcinoma (in retrospect).
Why would the onset be 15 years later though?
I was thinking the same thing @spow. I had put urothelial carcinoma, thinking that a field defect would result in bilateral tumor.
SCHIZOTYPAL = Included on the schizophrenia spectrum.
Pronounce schizO-TYPE-al: Odd-TYPE thoughts.
Another way to approach it is to think about MHC class I processing. Basically, if you inhibit the proteasome, peptides will not be generated and nothing is available to be loaded onto MHC I (remember MHC I has to be loaded before it's transported to the cell surface). Cells that don't express MHC I get killed by the natural killers.
"In conclusion, we have demonstrated that the proteasome inhibitor bortezomib down-regulates class I and enhances the sensitivity of myeloma to NK cell–mediated lysis" from the conclusion of the NIH paper
another mechanism is by blocking proteosome u even decrease degration of proapoptotic proteins...so it enchances apoptosis(from uworld)
But CD8+ and NK cells kill via perforin! Why is this answer wrong? Is it because it's not the primary effect?
"The proteasome is the major source of proteolytic activity involved in the generation of peptides for presentation by major histocompatibility complex class I molecules. We report the new observation that bortezomib down-regulates HLA class I on MM cells, resulting in increased NK cell–mediated lysis."
It doesn't explain the sudden death, but I suppose they aren't asking for that!
also, a liver infarct is unlikely due to rich dual blood supply.
@divya Rather, if there was an infarct, it will be hemorrhagic, not pale.
Multiple solid lesions on a healthy liver = meta. I assumed breast wouldn't meta to liver (it's usually GI cancers) but it makes sense since all the blood gets filtered by the liver at some point. TIL!
Also, VZV causes pneumonia (what this patient probably had) and encephalopathy in the immunocompromised.
What threw me off was that it didn't mention the synchronicity of the rash. I stupidly took failure to mention to mean that the rash was synchronous, which doesn't fit VZV because chickenpox rash is characterized as a dyssynchronous rash (i.e. all stages of the macule to papule to vesicle to ulceration are seen at the same time). MUST REMEMBER: don't add information not given!
If anyone wants to refresh info on Vaicella-Zoster virus, page 165 in FA 2019.
if this isn't a globe rupture than idk what is tbh
the air in the center of the globe made me think rupture too .....
There may be some global rupture, but impairment of one of the ocular muscles causing diplopia would still be the best explanation for this patient's double vision.
Globe rupture leads to entrapment of the IR muscle which causes diplopia. The question is asking what is causing his visual complaints, which is diplopia, not loss of vision.
I am embarrassed by these typos.
Why can it not be arterial hypertension?
I think Arterial HTN is referring to Pulmonary Artery HTN which would be present in LT HF in the long run with RT HF and edema. Pulm HTN would cause a backflow, and doesn't really answer the question "explain the patients Dyspnea". At least, that's how I saw it. Hope this helped.
the question has 2 murmurs, so does she have aortic stenosis too?
i guess it is not relevant since it asked for what is causing her SOB
I guess pulmonary HTN would happen in response to increased pressure after the edema happens, and would cause backflow (to the RV) over pulmonary edema.
There's a really great diagram in UWorld (QID 234) that explains what happens as a result of mitral stenosis. Very similar sounding to the patient in this question.
@sugaplum, yes rheumatic heart disease can cause mitral and aortic stenosis. Rheumatic aortic stenosis can be distinguished from degenerative aortic stenosis by 1)coexisting mitral stenosis and 2)fusion of the commisures.
Yeah haha I had the same conundrum.
If she's breathing deep as she breathes fast, then oxygen is still reaching the alveoli , so arterial pO2 would not be effected.
lmao i'm so freaking dumb i thought she was having alcohol withdrawals because it was relieved by alcohol
Maybe Po2 is unaffected bc its perfusion (blood) limited not difusion limited (under normal circumstances).
PErioral tingling- due to transient hypocalcemia induced by resp alkalosis.
I believe CO2 diffuses ~20x faster than O2, so increases in her respiratory rate have more effect on her PCO2 than her PO2
adding onto Charcot_bouchards comment, I found this:
Respiratory alkalosis secondary to hyperventilation is probably the most common cause of acute ionised hypocalcaemia. Binding between calcium and protein is enhanced when serum pH increases, resulting in decreased ionised calcium. Respiratory alkalosis can induce secondary hypocalcaemia that may cause cardiac arrhythmias, conduction abnormalities and various somatic symptoms such as paraesthesia, PErioral numbness, hyperreflexia, convulsive disorders, muscle spasm and tetany.
Not only is their WBC count low, it is not uniform. If we assume a minimum normal WBC count of 5000 cells/mL^3, and a regular range of ~60% neutrophils, then normally a person should have ~3,000 neutrophils/mL^3. This patient has a total of 2000 cells/mL^3, with 1,800 neutrophils/mL^3. Their lymphocytes and macrophages have been whiped out. This is best accounted for by HIV.
I believe that keycompany's answer comes the closest. In an MI, consider it as cardiogenic shock. The heart is a pump, and it is failing to move blood out of the heart and into vasculature. This is why PCWP increases. Because of insufficient output, the body has a sympathetic response. The catecholamines then cause vasoconstriction in peripheral vasculature to keep blood pressure up and continue flow, leading to increased SVR. Meanwhile, the sympathetic response causes vasodilation in the lungs; this would be an appropriate autoregulatory response, because the body is trying to keep up the flow of oxygen throughout the system. This decreases PVR.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715548/ Is a pretty good article on this. Of course the binding of catetcholamines changes depending on saturation and the response is not perfectly understood.
My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation.
With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel.
So ordinarily a misfolded protein does undergo ubiquitination and proteolysis. It is noteable that CFTR misfolding doesn't even allow it escape the ER, so it accumulates in the ER
83 might seem an uncommon age, but we don't know for sure her sexual history. She only recently (8 months ago) started showing some signs of mild cognitive impairment. She has all these results implying that she has syphilis, so the most likely answer is that she has syphilis, so we should speak to her privately about her sexual history. The tests don't necessarily means she got syphilis very recently, it's possible she's had syphilis for a while and never got treated.
I understand that she could possibly have syphilis but I also put repeat tests because I know there are a few things that can cause false positive VRDLs but if she also has a + RPR does this make a FP less likely? And also if she has mild cognitive impairment you still discuss with her not her daughter correct ...?
This definitely could be a false positive, but before we want to consider it to be a false positive, we should talk to the patient about it privately. Assuming that it's a false positive before asking the patient about it could delay treatment of her syphilis. There's a chance she didn't want to disclose her sexual history in front of her daughter or maybe she was embarrassed or didn't think it was important to mention.
And you're absolutely right, she only has mild cognitive impairment, so we most definitely should talk to the patient alone without her daughter first.
She has dementia. She doesn't have the capacity to determine her own care (23/20 MME). I feel the daughter should have the word on the care since Grandma likely doesn't have the capacity to understand her actions.
From what I remember, dementia is typically a combination of impaired memory *and* impaired thought processes. There is nothing to indicate that the patient has impaired thought processes, and the memory impairment is only mild. The patient can still reasonably said to be competent, and so her private information should be discussed with her alone.
Elder care homes or elderly communities actually have a high rate of STDs. Turns out, when you put a bunch of divorced/widowed adults together in a community they have sex.
Additionally, you should respect the privacy of a competent adult with "Mild memory" impairment. I know I could have mild memory impairment considering the crap I forget studying for step 1
also.... I think we can assume that "repeated tests" means repeat VRDL, not "additional tests to rule out false positives"
The combination of low blood pressure (from lack of mineralocorticoids) and low glucocorticoids (cortisol) indicate adrenal failure. Hyperpigmented skin is a sign of elevated ACTH, indicating that this is a failure of the adrenal gland and not the pituitary. In the industrialized western world, autoimmune destruction of adrenal glands is the leading cause of primary adrenal failure (disseminated tuberculoid destruction of the adrenal glands is significant outside of industrialized nations).
It also fits the time line better than Waterhouse-Friederichsen syndrome, which is sudden in onset and associated with hemorraging. Metastases to the adrenal glands *might* be a possibility, but autoimmune destruction is simply likelier.
Chronic Addisons disease.
Pretty straightforward here. Decreased gland function -> decreased Cortisol, decreased Aldosterone -> hypotension (with hyponatremic volume contraction)
Hyperpigmentation from increased ACTH (from POMC) making MSH.
(FA) Due to adrenal atrophy or destruction by disease (autoimmune destruction most common in the Western world; TB most common in the developing world).
I picked autoimmune adrenalitis but was tempted to pick Waterhouse syndrome because of the low BP (hemorrhaging). But I believe Waterhouse-Fried. syndrome is more likely associated with Neisseria infection
I think the trick here is that they don't mention that the daughter has a history of Type 1 DM, so she has no reason to be taking insulin at all. She's definitely receiving insulin, but we don't have any history implying she's a type 1 diabetic. That, combined with the fact that there have been multiple episodes like this one, favors that the mother is giving the daughter insulin when she doesn't need it.
C-peptide is produce by endogenous insulin, but is not part of exogenous insulin. She has elevated insulin, with low C-peptide, so she is receiving too much exogenous insulin. A history of recurrent episodes this year implies a behavioral issue; Factitious disorder imposed on another (also called Munchausen syndrome by proxy).
In addition to causing pulsus paradoxus, we see jugular venous distension, and muffled/distant heart sounds (hard to hear through the cardiac tamponade). https://radiopaedia.org/articles/beck-triad?lang=us