to snoo-finity ... and beyond!
Welcome to sugaplum's page.
Contributor score: 82
Thank you for explaining, I selected the unknown significance answer as well!
in the question stem, they are asking about a constant region. VDJ rearrangement is for the variable. It doesn't make sense :(
Both the constant (heavy chains) and the light chains undergo gene rearrangement. The heavy chain undergoes V(D)J random recombinations, while the light chain undergo VJ random recombinations. So gene rearrangement could work for both regions.
LOL. Achey Granpa Meynert. I'm gonna steal this from you.
isn't the basement membrane the deepest?
I also picked basement membrane but unlike you I haven't had a "nvm" moment. Help please.
@lilyo Basement membrane is between the epidermis and dermis; beneath the dermis is the subcutaneous tissue
What he want to know about choice B?
FA 177 says Kaposi has lymphocytic inflammation whereas Bartonella spp has neutrophilic inflammation. I guess this does not apply when immunocompromised? But doesn't Bartonella usually affect the immunocompromised ppl?
The only thing I can relate to this is FA P331 " TBG in pregnancy, OCP use (estrogen increases TBG) increases total T3/T4", so here is the opposite situation, which TBG decreases, and total T3/T4 decreases...
I use barrett's esophagus to remember these questions. Remember barrett's esophagus is squamous to columnar metaplasia -> this happens because of increased acid in the esophagus. What this means is that columnar cells are better for dealing with acid/internal fluids, and are a better cell type. Squamous is a better cell type for dealing with outside irritants. This means the vagina will be lined with squamous cells normally, and the cervical canal will be lined with columnar epithelium.
α1 stimulation (via α1 agonist) constricts the bladder sphincter thereby, preventing sudden bouts of micturition during coughing/sneezing (abdominal stress).
I thought that B3 stimulation stopped urination
@sammyj98 B3 would facilitate bladder relaxation
my mistake, the question is asking lymphatic drainage not venous
my mistake, the question is asking lymphatic drainage not venous
prefer “patients with hx of substance abuse” over more conveniently typed but less redemptive “drug addict”
I don't see why switching her to oral pain meds when she is ready would be incorrect. Clearly she is worried about being on the pain meds, I feel making a proclamation that she has a low risk of addiction would be profiling just because she doesn't have a history.
The opioid epidemic also affects people who didn't have a previous history of drug abuse. Just a thought, not trying to push any buttons. Maybe I am thinking to hard about this, but I don't see the clear A vs B line for this question.
@sugaplum I thought the exact same thing as you and chose the acetaminophen answer accordingly. I maintain that I am correct, my score be damned!
I had a similar question on UW and the explanation stated that the correct answer choice was the only one that addressed the patient's concern and answered her question. The rest were just alternative treatments, so they were incorrect.
But I too answered with oral pain meds.
couldn't agree more with you all. I chose acetaminophen because opioid abuse is NO joke. The crisis is still going strong because of answers like this...
I ruled out oral acetaminophen because they described in great detail the severity of her injuries, and indicated that she wasn't even fully conscious/aware when she asked this question about opioids. Rather than expose her to more pain, and possibly worsen her long-term pain prognosis, by switching to acetaminophen too early, in this case it makes sense to keep her comfortable because she's very seriously injured and not even fully lucid. It's kind to reassure her in this case.
I appreciate all of the passion for the opioid crisis, and the wording of the answer is definitely not ideal. However, PAIN is also very real, and there is no way acetaminophen alone would cut it in a case like this, not "as soon as she can take medications orally." Maybe I'm lucky to have 6 months in clinicals before STEP or had a mom who just went through urgent spine surgery for breast cancer mets, but there is a time and place for opioids and this is clearly one of them. Thank you for coming to my ted talk.
I agree with anastomoses, cmon guys have you ever had serious pain? oral acetaminophen is NOT enough for that type of pain.
So I read Lymphocyte as leukocyte (because cortisol probably)
so that is what I put. but cortisol does increase levels of neutrophils floating around in the blood right, I was going for stress demarg. Can't tell if i am thinking too hard about this.
FA 2019 page 632
Makes total sense looking back. Just didn't know that was a thing :)
Fun fact: Meredith from Grey's anatomy got her idea for Mini livers from a patient who presented with an accessory spleen.... and who said watching TV doesn't count as studying
why not androgen insensitivity?
I was wondering the same thing because doesn't androgen insensitivity also have normal female secondary characteristics. Was it the levels of hormones because she doesn't have abnormally high testosterone?
Androgen insensitivity has the same presentation and symptoms. What's the clue that it is mullerian agenesis instead ?
Testosterone would be high if it was androgen insensitivity
FA 2019 Pg 625
Testo would be high in AIS. in AIS pubic hair, axillary hair doesnt devlop because of androgen insensitivity. both have normal breast dev and primary amenorrhea
This is not androgen insensitivity because she has perfectly normal Estradiol, which means she has perfectly normal ovaries. She also has regular female levels of testosterone.
Yes, correct. The 5'GGCC option could cause some confusion.
I really don't understand the question nor the answer. Can someone explain it for dummies like me?
yes please.. I'm with guillo12 on this
questions says you've created a new cut site,
1. look at the region on the sick vs healthy. The C to G is the change
2. Write out the sick "CCGG" from 5'3'- you could write out the whole thing, but the answer only has 4 letters, so being lazy here
3. write under it, its complement, the dna base pair. So "GGCC"
4. remember both strands are going in opposite directions when you write them out on top of each other.
5. So the bottom strand actually reads 5' CCGG 3' so that is the answer
I hope that clears it up
Everyones choice A is different.
they mean- Diffuse neutrophil infiltration
what does stellate necrotizng granuloma means ?
always with the details! losing dumb points :(
@sympathetikey Doesn't the biopsy finding vary with the biopsy location:
Lymph nodes have stellate granulomas
Bacillary Angiomatosis (skin lesion) has neutrophilic inflammation.
What do you think?
@sympathetikey Pathoma chapter 2 says cat scratch disease forms non-caseating granulomas
@ chextra Same with FA 2019 pg. 218
Immunocompetent: regional LN in axilla in one arm (like our pt here)
Immunocompromised: bacillary angiomatsis is transmitted by cat scratches
I believe failure to pass meconium is Hischsprung's
Meckels don't present within the first few days of life, so meconium wouldn't be a factor
FA 2019 378
It is a very thick nerve, so I think it is hard to tear without physically cutting it. Also if it tore you would have tibial and common fibular nerve symptoms as well. You would see sensory numbness and tingling along the dermatome
also the mechanism of injury is focused on spine so a disc rupture is more likely
I agree with you, only possible logic for their answer:
the qualifier asplenic makes the "ShIN" pathogens more likely, even though Ecoli can cause gram negative sepsis and DIC. FA 2019 pg 127
Also it says s pneumo causes sepsis specifically in asplenic patients Pg 136
To be honest, the only reason I got this right (because I really was thinking E.Coli as well), is that I ended up remembering the MOPS part of the Sketchy, and I couldn't remember if he said that it was the number 1 cause of all of them or not, and ended up clicking it. It's pretty shitty they don't offer explanations for these.
I think if it was organification defect you wouldn't have a normal T4 level in the serum.
because there would be an overall decrease in serum T3, T4 and increase in serum TSH levels.
Also to add: since it is a bilateral sx it is more likely to be coming from the spinal cord then from equal compression of ulnar nerve (in guyons canal) on both sides. unless she is a cyclist
shouldn't the other nerves of the same roots be affected?
shouldn't the other nerves of the same roots be affected?
Not really. In klumpeke paralysis ulnar nerve s/s dominates (Almost same cause)
decreased K+ (from increased RAAS due to volume loss) and decreased Cl- (loss of HCl from the stomach), Alkalosis from loss of HCl and thus high bicarb.
For this reason high to mid range K is wrong
Wouldn't increased RAAS lead to increased Na+? The answer shows decreased Na+.
Also, remember Bulimia Nervosa is associated with hypokalemia.
so the range they gave for K is 3-6? so 3.2 is WNL then?
or are we just operating on "it is on the lower end of normal in peds"
sodium levels in pyloric stenosis vary, nothing really classic, can be high as in this case simply due to hydration, can low in other cases if aldosterone managed to reverse that to the other extreme
I think you could only make this assumption if they said "patient is on standard htn tx" but since they gave the name hctz, would not be fair to assume they are also taking spirinolactone. I went with process of elimination on this one.
Even checked access medicine's drug adverse effect profile...galactorrhea not listed for hctz
Above is obviously incorrect because the answer is Meningeal lol.
Here is a link to a good picture:
Obviously thomas is disagreeing with the presentation of the question, and I agreed with him! This absolutely sounds like GBM, with rapid onset leading to death, and the symptoms. The question stem leads you to GBM, and the gross image to meningioma (I guess).
Furthermore, where are the meninges on the gross image form which this (meningioma) grew?! It should at least show the tissue from whence it came!
Had the same problem, got confused since it appeared that the growth was malignant :(
FA 2019 pg 514, also agree with everyone. weird presentation. Glios are malignant death within 1 year, meningioma are often asymptomatic or have focal signs.
just a gross pathology question at this point
ı think she died bc of pressure or something guys, its obviously round shaped benign lesion, its also extra axial not like GBM. she had this maybe years before death
Wouldn't Fanconi syndrome also cause hypokalemia though?
Especially considering the fact that the DCT will be working in overdrive to compensate for lost solutes???
This question did not make sense to me at all. I knew it was Fanconi syndrome yet didn't select the obvious answer because it said "follow up examination 1 week after diagnosis". I thought it would already be in treatment... I searched (now) and it says that treatment is basically replenishing was is lost in the urine. So definitely the wording is like wtf to me
I was thinking since it affected the PCT that Na resorption would be affected as well? But I guess the other segments will pick up the slack?
aka cavernous artery, that is what I was looking for. Did not realize it was also called the deep artery
Wouldn't that be more long term?
I think Epo would indicate Rcc or renal failure, she seems like she has "just" refractory HTN, and no other sx to indicate anemia.
She has Fibromuscular dysplasia which should be in your differential for a young female with hypertension ( along with Conns syndrome and pheochromocytoma). it typically causes stenosis and aneurism formation of the renal arteries leading to elevated renin.
Hypotension can also cause pre renal azotemia with a FENa <1%.... How do you know this is ischemic ATN and not hypotension induced Prerenal Azotemia?
I had the same thought as you @mousie, but I think "azotemia" and low urine output push it more towards ATN (looking back; I got it wrong too). Plus, the initially MVC / muscle damage probably caused some tubule injury by itself.
This might help clarify why the pt. has ATN rather than pre renal azotemia.
The question did mention, though subtly, that the bleeding was controlled. That most likely indicates that his hypovolemia has been corrected. Developing azotemia 24 hrs after correction of hypovolemia is more suggestive of ATN (since he doesn't have hypovolemia anymore). I hope that helps and feel free to correct me, if I am wrong.
In addition to my earlier comment, I just noticed the question also explicitly mentioned that he was fully volume restored. Which is consistent with my earlier assumption!
Although initially, hypotension causes prerenal azotemia, the volume correction pushes you away from prerenal azotemia. but they want you to remember that in hypovolemia, the kidneys are also becoming ischemic, and so development of azotemia 24 hours later is more indicative of intrarenal azotemia due to ATN
for anyone who wants to see it: FA 2019 pg591
i'm confused about one thing. if the tubules aren't working like they should, the bun:cr ratio falls right? doesn't that essentially mean azotemia reduces too?
Lets all take a moment to admire how shit this question is
"Bp 90/60.""Repeated episodes of hypotension in the OR" and still the answer is ATN
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.