Welcome to sugaplum’s page.
Contributor score: 323
holy cow you are crushing it right now. frickin POWER SESSION
adding to this. kid also has poor growth which reflects poor pancreatic function
Does T2DM cause weight loss? I interpreted this older man with weight loss and new-onset T2DM as having pancreatic cancer.
i guess if you dont get the anabolic benefit of insulin, you can't build up your weight- at least that's how i took it
This patient's mitral opening snap and diastolic murmur are due to her mitral stenosis. Long-standing MS leads to elevated left atrial pressures which transmit to the pulmonary artery -> secondary pulmonary hypertension (not primary idiopathic PAH)
I think she more likely has asthma. Cough is worse at night and worse with physical activity. Key findings on exam: end-expiratory wheezes bilaterally. Responsive to b2-agonists.
I was gonna get up and find the broom but then I got high ..
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.
The constant region does not undergo recombination. That's why it's called constant. It's just right next to the variable region though, so they get expressed together as one protein. That's why the constant-labeled DNA region is variable length here.
LOL. Achey Granpa Meynert. I'm gonna steal this from you.
Achey grandpa Meynert = ACh / Basal Nucleus of Meynert
Dope Cousin VT = Dopamine / Ventral tegmentum, SNc
Uncle and aunt Raphe and Sara = Serotonin / Raphe nuclei(medulla, pons)
Cousin Gabby always screaming NA-NA-NA = GABA / Nucleus Accumbens
Norepi = Locus ceruleus.
ACHey GRANDPA MEYNERT TREMBLES in the BASEment; DOPE cousin VT SNaCks DOWNstairs by the kitchen TAP; NANA GABBY ROCKS and ANXIOUSLY cooes...; "NENENENE... NENENENE...NENENE...NENE" to CRYING BLUE-eyed baby ELSIE; aunt SERO and uncle RAPHE DULLY PARK in the DOWNpour. CAPS = relevant info, lowercase = irrelevant. Includes diseases: DOWN, ANXIOUSLY, CRYING, DOWN = anxiety/depression; TREMBLES, TAP, ROCKS, PARK = movement disorder; GRANDPA = Alzheimer's. Note: ELSIE = LC = Locus ceruleus
The extended "NENE" series is just for humor - shorten if you like ;)
Also, ANXIOUSLY applies to both NTs in that sentence: GABA and NE.
I almost didn't even look at this review but then I thought "maybe someone has a cool mnemonic." and would you look at this.
How are you supposed to remember which S is which?
@drzed "Supra" = on top, so the 1st S is for supraspinatus.
according to Physeo :
wow, sugapulm, that mnemonic is gold. you are gold.
That article does not once mention the word diarrhea.
I would also add that I think they are specifically trying to get us to think of pernicious anemia here, where parietal cells are destroyed/lose their fxn. In that case, ECL cells may hypertrophy to encourage acid secretion because the parietal cells are not responding to their usual signals. All the other answer choices are quite clearly incorrect, and Zollinger-Ellison is a gastrinoma, which causes hypertrophy of the gastric mucosa so that is also wrong.
it can also cause gingival hyperplasia
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
I think some people might have picked basement membrane because we're taught once cancer goes through the BM it turns from in situ to invasive. This is correct, but subcutaneous as the others pointed out are deeper so the prognosis is worse (BM + deeper 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?
Got it after seeing that she's immunocompetent
I think serum Na+ only depends on the patient's access to water. FA19 pg 344 says serum osm is high in both and doesn't mention Na specifically. Spent a while double checking for DI, but low serum Na for polydipsia is definitely correct.
In general, SIADH or polydipsia will cause HYPOnatremia, and DI (central or nephrogenic) will cause HYPERnatremia, but in the latter--as you stated--water access change the serum Na.
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...
Goljan talks about this (around 33 mins into his endocrine lecture) in relation to increased androgens causing decreased TBG
why isnt it maternal antithyroid ABs?
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
@sammyj98- were you thinking of oxybutynin? (thats what I thought of!) According to FA, its used for urge incontinence not stress.
Nah he/she's talking about Beta-3 receptors which are Gs coupled. Gs increases cAMP thus it would cause smooth muscle relaxation -> bladder relaxation!
From Mayo: "There are no approved medications to specifically treat stress incontinence in the United States. The antidepressant duloxetine (Cymbalta) is used for the treatment of stress incontinence in Europe, however."
@hvancampen oxybutynin is an M3 muscarinic antagonist, not B3.
I thought about B3 agonist as well and got this wrong.
I think maybe B3 agonist can be used for bladder (URGENCY incontinence) where the main issue is detrusor over reactivity. In STRESS incontinence however the problem has nothing to do with detrusor, so we use α1 agonist to constrict the sphincter.
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.
I r/o oral acetaminophen b/c she's post-op for major GI surgeries so you might want to avoid PO meds for a while
As argument against the oral acetaminophen answer choice, it says "switch the patient to oral acetaminophen boldas soon as she can take the medication orallybold" This means you're just waiting for her swallowing inability from the facial fracture surgery to come back, which might not have much to do with her pain, and so it seems somewhat arbitrary.
Maybe logically/clinically A is true, but this seems like a "patient communication" question to me and I could NEVER imagine A being a good way to phrase this point IRL.
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.
because................"Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen"
NBME 24 -#13 Qs explanations/comments on this website, has led me to choose this answer! :D
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
have gotten at least 10+ NBME or Uworld questions correct because of grey's anatomy
LOL got this right because of Grey's anatomy too
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.
Also AIS has paradoxically large boobs-> tanner stage 5 and thats not mentioned anywhere
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
To add to the palindrome part, many restriction endonucleases actually function as dimers. Each individual subunit usually has a nickase, so to create a double-stranded break in DNA, they must bind a palindrome so that each enzymatic domain creates a single-stranded break (thus a double-stranded break).
Why do we start from CCGG? Why not CGGG or TACC?
Why do we start from CCGG? Why not CGGG or TACC?
I think its due to the palindrome requirement?
Maybe I'm missing a part here, but the substrate that the enzyme will bind to will be the DNA. I went with the line that was from the questions stem, as it is the mtuated DNA will be recognized by the restriction enzyme. I didnt see the need to convert it into base pairing. Let me know what you guys think.
@bbr I agree. I'm definitely not an expert in these lab tests, but the question asks "substrate specificity." I was thinking that it would recognize the abnormal DNA; nothing to do with RNA. I didn't know about the palindromic preference of restriction enzymes, but I don't think there's any need to figure out base-pairing and whatnot here. (At least for this question it didn't work out that way!)
sugaplum, I'd give you an award if this was Reddit
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 got this question wrong but I really like because it helped me get past a confusion I hadon this subject. If it were a tear, you'd see the loss of motor function that sugaplum was taling about(FA 444 2019). But if it's a herniation, like in this case, you see Radiculopathy/Sciatica symptoms that are on 446.
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 thought this too but it seems like Strep pneumo is just more specifically associated with infection in asplenic/sickle cell patients than E. Coli is. Just one of those classic associations. There's a sickle in the Sketchy Strep pneumo sketch, vs. no sickle in the E.Coli sketch.
E. coli causes pneumonia by aspiration, for which this patient had no risk factors. For USMLE, if they don't say the patient is vaccinated, you can assume they are NOT. Just because she has a history of splenectomy following trauma does NOT mean she had to been vaccinated--don't fill in the history for the patient, only use the information they give you.
also DIC more often seen with G- bacteria right???? That's why I chose E.coli instead of S.pneumonia
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.
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.