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Comments ...

 +1  (free120#13)

For reference FA 2019 pg 613 has a good image to see this

 +4  (free120#31)

Incase anyone else was thinking the same:
I was stuck between this and variant of unknown significance. However, variant of unknown significance is a sequence not a single nucleotide

nbme4unme  Thank you for explaining, I selected the unknown significance answer as well!

 +2  (free120#9)

This question is asking about VDJ rearrangement which happens in the bone marrow. The genes are all chopped up because the B cell is trying to generate a unique combination for its receptor
simple concepts... odd wording

Chapter 3 of "how the immune system works" - awesome book

varunmehru  in the question stem, they are asking about a constant region. VDJ rearrangement is for the variable. It doesn't make sense :(
sallz  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.

 +3  (nbme23#45)

This is ridiculous but I could never keep these straight so meet my family:
Achey grandpa Meynert
Dope cousin VT with a side Ho* (who's names are just initials) SNc
Uncle and aunt Raphe and sara Cousin Gabby always screaming Na-Na-Na
norepi reminds me of the color blue, so locus ceruleus

paulkarr  LOL. Achey Granpa Meynert. I'm gonna steal this from you.

 +6  (nbme23#41)

always remember them in order with formula, SITS=AEEI
and the two on the END are AD-DUCTION

 +1  (nbme18#44)

FA 2019 pg 555
cause of metabolic alkalosis vomiting in someone whos a bulemic, hypokalemia and hypochloremia are common.
anion gap formula Na-(Cl+bicarb) Since we have excessive bicarb there shouldn't be a large gap. Normal is 8-12.

 +0  (nbme18#25)

https://www.ncbi.nlm.nih.gov/pubmed/7714464 common issues in type 1 and type 2 diabetics

 +0  (nbme18#15)

FA 2019 Pg 373
chronic gastritis mucosal inflammation leading to atrophy

 +0  (nbme18#27)

FA 2019 Pg 120
cyclosporine causes hypertension and nephrotoxicity

 +0  (nbme18#40)

the deeper the melanoma goes the worse the prognosis

wishmewell  isn't the basement membrane the deepest?
wishmewell  nvm! lol
lilyo  I also picked basement membrane but unlike you I haven't had a "nvm" moment. Help please.
mcdumbass  @lilyo Basement membrane is between the epidermis and dermis; beneath the dermis is the subcutaneous tissue

 +0  (nbme18#45)

bnb video - ventilation and perfussion.
underventilated but well perfused = aspiration, mucus plug, atelectasis. this causes physiologic shunting.

 +0  (nbme18#48)

Cholesterol ester hydrolase is needed for reverses cholesterol transport, not pancreatic enzymes.
- I missed this

 +0  (nbme18#13)

Heparin induced thrombocytopenia: IgG against platelet factor 4
FA 2019 page 427

 +0  (nbme18#3)

FA 2019 pg 242 & bnb video
DA at low doses d1 dilates renal vessels,
medium b1 agonist = ionotropic and chonotropic
high doses a1 agonist = vasoconstriction

 +1  (nbme18#33)

FA 2019 pg 59-61
X linked muscular dystrophy. The chance that the mom III-1 is a carrier is 1/2. XY (normal grandpa II-1) * XaX (carrier grandmom II-2) You know that III-1 is a female, so only look at half, so 1/2 chance.
The chance that III-1's mate is a carrier is near zero. So we make him normal. XY (normal Dad) * XaX (carrier mom III-1) Since we know its a boy you only look at half, so the chance of him having it is 1/2.
so 1/2 * 1/2= 1/4
These are two independent events, the chance the mom is a carrier * the chance the kid gets the affected X.

 +1  (nbme18#47)

Inability to flex at the DIP is called "Jersey finger"


 +0  (nbme18#6)

4th pharyngeal pouch gives rise to superior parathyroids.
FA 2019 pg 607

riyadh  What he want to know about choice B?

 +2  (nbme20#21)

B Hensele- Cat Scratch in immuno-compotent - http://www.pathologyoutlines.com/topic/lymphnodescatscratch.html Bartonella henselae in Immuno-compromised- Baciliary angiomatotsis Looks like kaposi sarcoma "Diffuse neutrophilic infiltrate" FA 2019 177

almondbreeze  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?
almondbreeze  Got it after seeing that she's immunocompetent

 +0  (nbme20#15)

Synthetic codeine analog, has mild Opioid effects when used in high concentrations. Hence constipation FA 2019 671

 +1  (nbme20#34)

These always tripped me up:
+ Polydipsia= responds to water deprivation, low serum Na
+ Central= responds to vasopressin, high serum Na
+Nephrogenic = responds to nothing, normal serum Na

 +1  (nbme20#26)

This is apparently congenital thyroid binding globulin deficiency

"Thyroxine-binding globulin deficiency — Thyroxine-binding globulin (TBG) deficiency is characterized by low serum total T4 but normal free T4 and TSH; the diagnosis is confirmed by measuring TBG concentrations. These infants have normal thyroid function and do not require treatment." - uptodate *can't find in FA, maybe it is in there somewhere?

hhsuperhigh  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...

 +0  (nbme23#41)

FA 2019 pg 612 Endocervix-simple columnar epithelium

hopsalong  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.

 +4  (nbme23#12)

phenylpropanolamine is an alpha agonist that stimulates urethral smooth muscle contraction. - from uptodate, however, it also says it is not recommended treatment anymore

ugalaxy  α1 stimulation (via α1 agonist) constricts the bladder sphincter thereby, preventing sudden bouts of micturition during coughing/sneezing (abdominal stress).
sammyj98  I thought that B3 stimulation stopped urination
adong  @sammyj98 B3 would facilitate bladder relaxation

Subcomments ...

Below the dentate line, anal cancer drainage is superficial inguinal. Above the dentate line, superior rectal (then iliac).

sugaplum  above the dentate line superior rectal drains into inferior mesenteric then goes into the portal system http://www.surgicalcore.org/popup/420229 +  
sugaplum  my mistake, the question is asking lymphatic drainage not venous +  

Below the dentate line, anal cancer drainage is superficial inguinal. Above the dentate line, superior rectal (then iliac).

sugaplum  above the dentate line superior rectal drains into inferior mesenteric then goes into the portal system http://www.surgicalcore.org/popup/420229 +  
sugaplum  my mistake, the question is asking lymphatic drainage not venous +  

Narcotic use for acutely painful conditions is both reasonable and important. Short-term use (immediately post-surgical) does not lead to long-term dependence (or so people have thought…). And yes, drugs addicts should also receive narcotics to control pain.

drdoom  prefer “patients with hx of substance abuse” over more conveniently typed but less redemptive “drug addict” +4  
sugaplum  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. +13  
nbme4unme  @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! +5  
sushizuka  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. +2  
angelaq11  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... +  
houseppary  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. +  
anastomoses  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. +1  
llamastep1  I agree with anastomoses, cmon guys have you ever had serious pain? oral acetaminophen is NOT enough for that type of pain. +  

Note that the question is not asking what cells fight URIs. The question asks what lab finding would be consistent with decreased immune activity (and thus the only choice that matches “decreased” with an immune cell is the best answer).

sugaplum  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. +  

Leydig cells make testosterone. Leydig cell tumors aren’t always physiological active, but those that are can cause masculinization. Granulosa cell tumors, on the other hand, sometimes produce estrogen (which can lead to precocious puberty in young girls but otherwise may be occult). Teratomas are oddballs that typically have fat, hair, teeth, etc. Thecomas will not be on your test. Ovarian carcinoid is highly unlikely to show up on your test, but if it did, it would likely present with a classic carcinoid syndrome.

sugaplum  FA 2019 page 632 +  

sympathetikey  Makes total sense looking back. Just didn't know that was a thing :) +3  
sugaplum  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 +8  

submitted by step420(22),

This is mullerian agenesis. Normal ovaries but absent uterus.

endochondral   why not androgen insensitivity? +  
shaeking  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? +  
swb  Androgen insensitivity has the same presentation and symptoms. What's the clue that it is mullerian agenesis instead ? +1  
sugaplum  Testosterone would be high if it was androgen insensitivity FA 2019 Pg 625 +7  
charcot_bouchard  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 +  
dickass  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. +2  

submitted by hayayah(517),

Most restriction enzymes bind palindromes.

So both 5'CCGG or 3'GGCC would have been acceptable in this scenario.

meningitis  Yes, correct. The 5'GGCC option could cause some confusion. +  
guillo12  I really don't understand the question nor the answer. Can someone explain it for dummies like me? +2  
whossayin  yes please.. I'm with guillo12 on this +  
sugaplum  @guillo12 @whossayin 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 +11  

submitted by sympathetikey(444),

Choice A. would have been correct if this patient was immunocompromised. Per First Aid, "If CD4 <100, Bartonella...Findings: Neutrophilic Inflammation.

However, as this patient has a competent immune system, buzz words are stellate necrotizing granulomas.

yotsubato  Everyones choice A is different. +  
sugaplum  they mean- Diffuse neutrophil infiltration +  
macrohphage95  what does stellate necrotizng granuloma means ? +  
krisgsxr600  always with the details! losing dumb points :( +1  
futuredoc12345  @sympathetikey Doesn't the biopsy finding vary with the biopsy location: Lymph nodes have stellate granulomas and Bacillary Angiomatosis (skin lesion) has neutrophilic inflammation. What do you think? +  
chextra  @sympathetikey Pathoma chapter 2 says cat scratch disease forms non-caseating granulomas +  
almondbreeze  @ chextra Same with FA 2019 pg. 218 +  
almondbreeze  Sketchy micro: Immunocompetent: regional LN in axilla in one arm (like our pt here) Immunocompromised: bacillary angiomatsis is transmitted by cat scratches +  

submitted by strugglebus(85),

Also, Meckels would have describe hematochezia or failure to pass meconium

sugaplum  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 +  

submitted by stepbystep(0),

does some mind explaining why this isn't a tear in the sciatic nerve?

sugaplum  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 +  

submitted by yotsubato(390),

This question is bullshit. The woman would most likely be vaccinated to Strep pneumo, especially if she had a splenectomy.

E coli is also an encapsulated bacterium that causes pneumonia, so that is more likely IMO.

sugaplum  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 +  
lmfaoayeitslit  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. +  

submitted by whossayin(7),

why can't "organification defect in T3 and T4" be the answer?

sugaplum  I think if it was organification defect you wouldn't have a normal T4 level in the serum. +3  
divya  because there would be an overall decrease in serum T3, T4 and increase in serum TSH levels. +  

submitted by hayayah(517),

Little finger = ulnar nerve.

C8-T1 are the roots of the ulnar nerve, which is a branch of the medial cord. The ulnar nerve is not found in the carpal tunnel (the medial nerve is).

Ulnar n. damage can lead to loss of wrist flexion and adduction, flexion of medial fingers, abduction and adduction of fingers (interossei), actions of medial 2 lumbrical muscles. Loss of sensation over medial 1 1/2 fingers, including hypothenar eminence.

sugaplum  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 +2  
thefoggymist  shouldn't the other nerves of the same roots be affected? +  
thefoggymist  shouldn't the other nerves of the same roots be affected? +  
charcot_bouchard  Not really. In klumpeke paralysis ulnar nerve s/s dominates (Almost same cause) +  

submitted by hayayah(517),

With chronic vomiting, you lose electrolytes and a lot of acid. It triggers metabolic alkalosis which is why all the serum values are low (or on the lower end of the normal range) except for bicarbonate.

ergogenic22  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 +3  
sbryant6  Wouldn't increased RAAS lead to increased Na+? The answer shows decreased Na+. +1  
sbryant6  Also, remember Bulimia Nervosa is associated with hypokalemia. +1  
sugaplum  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" +2  
dbg  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 +  

submitted by namira(14),

Possible explanation:

If the pt is taking a thiazide (which is K depleting), it might have also been given with a K sparing drug such as spirinolactone.

Spirinolactone has endocrinologic effects such as gynecomastia and galactorrhea.

sugaplum  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 +2  

submitted by hayayah(517),

Methanol is toxic by two mechanisms:

First, methanol can be fatal due to its CNS depressant properties in the same manner as ethanol poisoning.

Second, in a process of toxication, it is metabolized to formic acid via formaldehyde in a process initiated by the enzyme alcohol dehydrogenase in the liver. Methanol is converted to formaldehyde via alcohol dehydrogenase (ADH) and formaldehyde is converted to formic acid (formate) via aldehyde dehydrogenase (ALDH).

Formate is toxic because it inhibits mitochondrial cytochrome c oxidase, causing hypoxia at the cellular level, and metabolic acidosis, among a variety of other metabolic disturbances.

sugaplum  Good pictograph comparing methanol, alcohol, and ethylene glycol. https://wikem.org/wiki/File:Toxic_alcohol_ingestion.JPG +4  

submitted by thomas(4),

Answer is Astrocyte. Patient has glioblastoma multiforme. Although meningiomas may occur at convexities, meningiomas are benign and often asymptomatic. They may cause h/a seizures, but would be unlikely to cause death w/in 6m of onset of h/a. The size of tumor and course of illness is consistent with the course of GBM

masonkingcobra  Above is obviously incorrect because the answer is Meningeal lol. Here is a link to a good picture: http://neuropathology-web.org/chapter7/chapter7fMiscellaneous.html +5  
kernicterusthefrog  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). +2  
kernicterusthefrog  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! +1  
nala_ula  Had the same problem, got confused since it appeared that the growth was malignant :( +  
sugaplum  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 +  
garima  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 +  

submitted by celeste(43),

This sounds like Fanconi syndrome. The proximal tubular epithelial cells have a hard time reabsorbing filtrate, so you'll see a loss of phosphate, amino acids, bicarbonate, and glucose.

medschul  Wouldn't Fanconi syndrome also cause hypokalemia though? +2  
yotsubato  Especially considering the fact that the DCT will be working in overdrive to compensate for lost solutes??? +  
nala_ula  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 +  
sugaplum  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? +  

submitted by sympathetikey(444),

Hard to see due to poor picture quality, but based on what I could see, it seems like a spontaneous pneumothorax to me (based on the lack of lung marking on the left compared to the right side).

Therefore, since the lung is deflated, all you would have in the left side of the open cavity, which would make the left side hyperressonant.

sugaplum  FA 2019 pg667 +1  

submitted by lfsuarez(91),

The patient is prescribed Sildenafil which caused increased cGMP levels are therefore SMOOTH MUSCLE relaxation. In this case you would want to vasodilate the deep artery to increase blood flow into the corpora cavernosa.

sugaplum  aka cavernous artery, that is what I was looking for. Did not realize it was also called the deep artery +1  

submitted by mcl(287),

Patient with bilateral renal artery bruits and hypertension will for sure have activation of RAS system and therefore increase in angiotensin.

Although pheochromocytoma and consequent elevated catecholamines can increase blood pressure, symptoms are typically episodic and renal bruits are not likely to be heard. Elevated levels of serotonin can also cause hypertension, but we would also expect to see flushing; also, there is nothing in the stem to indicate patient is taking SSRIs or something else that could predispose her to elevated levels of serotonin. Elevated levels of thyroid hormone could also give patient hypertension, but we would also expect other signs of hyperthyroidism (tremors, weight loss, etc.).

I was a little confused if EPO would be elevated -- if there is stenosis of renal arteries (as indicated by the bruits) the kidneys could also detect this as hypoxia and ramp up production of EPO. However, I ended up going with angiotensin since it seemed more "concrete" to me that RAS would be up. Does anyone know why it's not EPO?

brise  Wouldn't that be more long term? +1  
sugaplum  I think Epo would indicate Rcc or renal failure, she seems like she has "just" refractory HTN, and no other sx to indicate anemia. +  
davidw  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. +2  

The patient has ATN secondary to renal ischemia. Due to tubular necorsis, the patient will have an elevated FeNa. The patient's urine will also be dilute, but this will be reflected by the low urine osmolality, not the FeNa

mousie  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? +2  
sympathetikey  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. +1  
ajo  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. +12  
ajo  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! +6  
gh889  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 +  
sugaplum  for anyone who wants to see it: FA 2019 pg591 +1  
divya  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? +  
osler_weber_rendu  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 +  

submitted by shaydawn88(6),

Is it intra-alveolar transudates because this patient might have HF d/t a. fib and left atrial enlargement-> inc hydrostatic pressure-> transudate pleural effusion?

sajaqua1  Basically. +1  
medschul  Why can it not be arterial hypertension? +  
meningitis  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. +2  
sugaplum  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 +  
nukie404  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. +