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 +0  (nbme23#16)

The question is confusing because a TRUE POSITIVE test result is finding detecting cancer by US (goes to show you we gotta look at what the test is looking for).

An ABNORMAL test detecting PrCa means its NOT A POSITIVE: ie: 35 out of 50 were False Positives

An ABNORMAL test WITHOUT PrCa means its NOT A NEGATIVE: 20 out of 100 WITHOUT PrCa were FALSE NEGATIVE.

TN = 80, FP = 15. Specificity: TN/(TN+FP); 80/(80+15) = 84%. And since it says "best represents" then 84% is closest to 80%.


 +3  (nbme22#11)

Actually, I correct myself: I looked closer and the Genito femoral has an external Spermatic branch and a Lumboinguinal branch. I thought it was the Genitofemoral nerve because the genital branch passes through the deep inguinal ring, enters the inguinal canal, goes to spermatic cord and supplies the cremaster and scrotal skin.

Heres the image: https://upload.wikimedia.org/wikipedia/commons/e/e4/Gray824.png

Correct me if I am wrong please.

gh889  I think you're right, FA2019 pp444 even states that sensory to the scrotum is via the Genitofemoral nerve

 -2  (nbme22#30)

Process of elimination on this one.

  • I eliminated Carbomyl phosphate, Arginine due to urea cycle.
  • I eliminated ATP because ATP alone wouldn't change F6P into glucosamine
  • NAG I got lucky and I eliminated it due to its use in ECM and collagen so I didn't think it was relevant and I kind of remembered it being in urea cycle.
dr.xx  you mean, pure luck? :)
impostersyndromel1000  lol pretty sound logic here mate
nor16  same here, Glutamine is a NH3 (-amin) donor, so guessing made sense

 +3  (nbme22#38)

Although it’s about PPV, this researching helped me understand basic phys, I hope this helps everyone in some way.

Takeaway: During PPV, venous return decreases, cardiac output decreases, and heart pressures decrease in the right side of the heart.

Why does PPV decrease venous return?

  • intrathoracic pressure compresses heart, causing blood not to return

Causes for decreased left ventricular output during ventilation:

  • Shifting of intraventricular septum to Left due to increased RV volume
  • Decreased venous return
  • Changes in hearts ability to contract due to positive pressure
  • lack of O2 to heart

Normal compensatory mechanisms for maintaining CO and BP during PPV?

  • increased HR to compensate for decreased SV
  • increased SVR to maintain BP

Other Physiologic responses:

  • Decreased cerebral perfusion pressure (body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels)
  • Decreased renal perfusion (Increased ADH, RAAS, and Patient has renal problems so increased creatinine and uric acid)
  • Possible malnutrition (increased glucose via gluconeogenesis etc.)
meningitis  sorry about the formatting, they were supposed to be bullets not italic.
drdoom  looks good to me! ;) instead of asterisks try using the plus sign for unordered lists; the system gets confused sometimes because the asterisk is also for italics 😊
meningitis  Yeah, I noticed :s Oh, I didnt know the + sign did that! Very much appreciated, I will try that next time.

 +3  (nbme22#32)

A case control study cant assess the prevalence of a disease but a cross sectional study can.

  • A case control study is that you are setting the margins in the 2 by 2 table therefore you're deciding how many cases and controls you want to have in your study and the calculation of incidence / prevalence in this scenario would be biased.
meningitis  the prevalence of the exposure and the health outcome are measured at the same time. You are basically trying to figure out how many people in the population have the disease and how many people have the exposure at one point in time. Case Control would determine ODDS ratio Cohort would determine Relative Risk

 +3  (nbme22#30)

I thought: lower pole then cant be suprarenal nor stomach which are higher""

Duodenum and Body of pancreas (except tail) are retroperitoneal and midline


 +2  (nbme22#19)

Ewing sarcoma cells look like small blue hypercromatic cells because they are neuroectodermal origin (PNET) and are therefore undifferentiated with high N:C ratio.

Also remember 22+11 translocation (EWS gene on chromosome 22 and the FLI-1 gene on chromosome 11)

Yeah, I thought the same @praderwilli (about the concentric layers)


 +1  (nbme22#11)

"Pick your Big, Foamie, Zeibra nose with your Sphinger"

Choose options with the letter I.

SpIngomyelin, Sphingomyelinase, bIgorgans (hepatomegaly etc), zeIbra bodies, Foam cells


 +5  (nbme22#18)

Tanner stages start at TEN years old

Stage I:

  • I is flat, as in flat chest;
  • I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

  • 2 balls (testicular enlargement)
  • 2 hairs (pubic hairs now appearing)
  • 2 breast buds form

Stage III (3): starts at 13 y/o

  • If you rotate 3, it looks like small breasts (Breast mounds form);
  • If you squiggle the III they look like curly+coarse pubic hair
  • Increased penis length and size can be represented by: II --> III
    (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

  • First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
    MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
  • The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

  • V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
  • 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

meningitis  Sorry about the format, it came out wrong but I hope his helps.
drdoom  looks good to me!
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from?
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions.
endochondral1  stage 3 breast mound is for females not males btw
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females
angelaq11  this is just too funny, I LOVE it! xD

 -1  (nbme22#20)

I think the small dark area on the left head of femur and the darkened neck are the avascular sites.

Neck: http://img.medscapestatic.com/pi/meds/ckb/15/19515tn.jpg

Head: (obvious lesion on the RT femur, but similar discrete lesion on the left as seen on the practice NBME) http://radsource.us/wp-content/uploads/2005/11/1a.jpg


 +4  (nbme22#26)

hydrocholorothiazide is DOC for Nephrogenic Diabetes insipidus because it paradoxically causes an increase in BP by increasing sodium absorption and thus water absorption, Pathoma explains this nicely.

Desmopressin is incorrect because upon fasting (fluid restriction) ADH is increased meaning ADH is being released Centrally but is not working in the kidneys at the V2 receptors of the epithelial renal cells at Collecting duct.

On that note, Amiloride is used for Lithium induced nephrogenic DI.

hello  Where in Pathoma? I couldn't find it.

 +7  (nbme22#1)

I also thought the same as @bubbles, but now trying to "justify" this tricky NBME question: I think this revolves on the fact that the patient has a HIGH blood pressure meaning we should focus on an answer that explains both increased BP and Hypovolemia (i.e: increased ADH which vasoconstricts and also absorbs free-water, both of which increase BP and cause hypovolemia).

Maybe if this patient were decompensated with LOW BP, one could think more about ANP.

I still think this question is TOO tricky.

meningitis  Sorry, hyponatremia* right?

 +1  (nbme21#23)

Squamous and Small cell carcinomas are Sentral (central) and often caused by Smoking

Hilar mass C arising from bronchus; Cavitation; Cigarettes; hyperCalcemia (produces PTHrP). Keratin pearls D and intercellular bridges.

pg 669 2019 FA


 +5  (nbme21#46)

LPS found in outer membrane of gram ⊝ bacteria (both cocci and rods). Composed of O antigen + core polysaccharide + lipid A (the toxic component).

Activates Macrophages and induces TNFalpha release -> Hypotension and fever.

Pg 133 Endotoxin.


 +5  (nbme20#50)

When standing up, the body normally activates sympathetic system to avoid orthostatic hypotension.

But since there is now an additive effect of the pheochromocytoma adrenergics, it will lead to a hypertension

(i.e: Double vasoconstriction = Pheo adrenergics + Sympathetic system)

sympathetikey  Brilliant.
medschul  Would pheo have a normal resting BP though?
meningitis  I was trying to justify these tricky questions but very true medschul.. It shouldn't have normal resting BP. Sometimes it seems these NBME always have a trick up their sleeve. Im getting paranoid lol
nala_ula  The reason why the patient probably has normal HTN is because Pheochromocytoma has symptoms that occurs in "spells" - they come and go. Apparently in that moment, when the physician is examining her, she doesn't have the HTN, but like @meningitis explained, so many adrenergic hormones around leads to double the vasoconstriction when the patient stands up.
meningitis  Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing.
nala_ula  No problem! Thank you for all your contributions throughout this page!
mjmejora  I thought the pheochromocytoma was getting squeezed during sitting and releasing the epinephrine then. kinda like how it can happen during manipulation during surgery. Got it right for sorta wrong reasons then oh well.




Subcomments ...

submitted by yotsubato(286),

Although acetaminophen (Tylenol) is not considered an NSAID, it too may provoke an aspirin-like sensitivity.

meningitis  For that same reason (not an NSAID) it doesn't reduce inflammation so it cant be used for Gout. +1  
meningitis  And I think Indomethacin is associated with anaphylactic reactions in patients with aspirin-sensitive asthma and aspirin allergies. Can anyone confirm? +  
link981  How many other's like me didn't see "allergic to aspirin"? FML +1  
hyperfukus  OMFG me too i just got so mad and questioned my whole life at least its cuz i can't read not bc i don't understand :((((( +1  


submitted by yotsubato(286),

Although acetaminophen (Tylenol) is not considered an NSAID, it too may provoke an aspirin-like sensitivity.

meningitis  For that same reason (not an NSAID) it doesn't reduce inflammation so it cant be used for Gout. +1  
meningitis  And I think Indomethacin is associated with anaphylactic reactions in patients with aspirin-sensitive asthma and aspirin allergies. Can anyone confirm? +  
link981  How many other's like me didn't see "allergic to aspirin"? FML +1  
hyperfukus  OMFG me too i just got so mad and questioned my whole life at least its cuz i can't read not bc i don't understand :((((( +1  


submitted by mousie(84),

A hemangioma is a type of benign (non-cancerous) tumor in infants. This abnormal cluster of small blood vessels appears on or under the skin, typically within one to three weeks after birth. - www.childrenshospital.org Hemangioma is a BV/capillary birthmark

sympathetikey  Probably a Strawberry Hemangioma since she's a baby +2  
meningitis  Can anyone explain what is option A? +1  
redvelvet  bc, it's a benign "capillary" hemangioma, we can see "thin-walled blood vessels with narrow lumens filled with blood and separated by connective tissue". It sounds similar to "arterioles in a fibrous stroma" but it's capillary. +  


submitted by joonam(8),

Acute or chronic inflammation of gallbladder. Murphy sign: inspiratory arrest on RUQ palpation due to pain. Pain may radiate to right shoulder (due to irritation of phrenic nerve).􏰁ALP if bile duct becomes involved (eg, ascending cholangitis).

meningitis  To make sure, palpable Gallbladder is more in cholangiocarcinoma and Pancreatic Cancer? And if it were non-tender, could palpable gallbladder mean gallstones? +2  
yb_26  @meningitis, it is a Courvoisier sign of pancreatic adenocarcinoma: jaundice + palpable, nontender gallbladder +1  


submitted by docred123(3),

Are all interstitial/restrictive lung diseases indicative of a LOW DLCO?

nlkrueger  only if it's an interstitial lung disease i believe. like polio can cause a "restrictive lung disease" but it's due to muscle effort and would expect to see a decrease in diffusing capacity (FA 2018 pg 657.2) +  
meningitis  Construction worker, Diffuse reticular opacities screamed restrictive and low DLCO for me. Anything that either adds fibrosis to alveoli, or thickens the diameter between alveoli and alveolar capillaries will cause low DLCO. +1  


submitted by shaydawn88(4),

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. +  


submitted by sympathetikey(316),

Per FA (pg. 636): Concerning breast cancer...

"Amplification/overexpression of estrogen/ progesterone receptors or c-erbB2 (HER2, an EGF receptor) is common; ER ⊝, PR ⊝, and HER2/neu ⊝ form more aggressive."

sympathetikey  FA 2019 +1  
meningitis  Why others not it: Anticipation: Trinucleotide repeats; CAG (Huntington), CTG (Myotonic dyst), GAA (ataxia telangiectasia), CGG(Fragile X) Chromosomal rearrangement: Many but can think of Trisomy 21, BCR-Abl, etc Imprinting: Prader willi, angelman Loss of heterozygosity: loss of a single parent's contribution to part of its genome. A common occurrence in cancer, it often indicates the presence of tumor suppressor gene in the lost region. +1  
kai  trinucleotide repeats are not associated with breast cancer Neither are chromosomal rearrangements BRCA1,2 tumor supressor genes are associated with breast cancer, which is why I chose E, but I guess I should have bought the new First Aid.......... +  
charcot_bouchard  GAA is Freidrich Ataxia +1  


submitted by sajaqua1(214),

The marrow shows precursors to erythrocytes, as well as megakaryocytes. This is to show you that the issue isn't underproduction, which means that we are losing RBC and platelets somewhere ie destruction. That rules out D and E. There is nothing to indicate tha the child has disseminated tuberculosis (B). At this point we are left with A or C. A would indicate Disseminated Intravascular Coagulation (DIC) or something similar, which would result in low platelets and RBC but we would also see abnormal RBC like schistocytes ("helmet" cells). We are explicitly told that the erythrocytes are normochromic and normocytic. However, immune destruction of platelets explains it all- the destruction of platelets leads to some hemorrhaging and so a drop in RBC, and ITP classically arises after a recent upper respiratory tract viral infection.

meningitis  Just in case anyone is wondering like I did, the low platelet count explains thethose multinucleated cells. They are Megakaryocytes in Bone Marrow Biopsy. +1  
nwinkelmann  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. +1  


What are we supposed to be looking at? I see multinucleated giant cells. I also see infiltrate (can’t tell if this is mononuclear or not).

methylased  Young child following URI with TCP is pretty classic ITP. Sometimes they throw in extra stuff on purpose, but I didn’t see much on the bone marrow aspirate either. +1  
mousie  I was also thinking ITP but the bone marrow image kind of threw me off too, not sure what I'm supposed to see but still think ITP is best choice ... +  
meningitis  It also almost threw me off, but then I remembered he had low platelet count and I guessed those multinucleated cells were Megakaryocytes (I looked for Megakaryocyte Bone Marrow Biopsy in google and they are the same). +1  
what  Bone marrow shows increased megakaryocytes -> ITP +  


Androgens cause acne. Testosterone is a better answer than Androstanediol b/c the Testosterone is associated with puberty, Androstanediol is more associated with the adrenal glands.

meningitis  I chose Testosterone but I almost chose GnRH because it is surged when starting puberty and therefore increases everything downstream. +1  
temmy  When answering the question, i thought to myself that if GnRH is correct, LH will be too cos GnRH stimulates the Leydig cells via LH to release testosterone. That left testosterone as the best answer because it had the most direct effect. +1  


submitted by sympathetikey(316),

I see what they're saying (this was my second choice) but at the same time I feel like a backup of blood would activate the baroreceptors and cause decreased sympathetic activity to the SA & AV node.

sympathetikey  (choice E) +  
meningitis  Could you elaborate? Is this related to: less "preload" from mother circulation causes lowered HR? +  
meningitis  Or backflow of blood and causes a Reflex Bradycardia? still confused on this question. +  
kentuckyfan  So I think the subtle difference in choice E is that there would be a negative CHRONOTROPIC effect, no inotropic effect (contractility). +5  
maxillarythirdmolar  if anything, inotrophy could go UP not down as diastole prolongs and LVEDV increases --> Starling equation bullshit +  


submitted by sympathetikey(316),

I see what they're saying (this was my second choice) but at the same time I feel like a backup of blood would activate the baroreceptors and cause decreased sympathetic activity to the SA & AV node.

sympathetikey  (choice E) +  
meningitis  Could you elaborate? Is this related to: less "preload" from mother circulation causes lowered HR? +  
meningitis  Or backflow of blood and causes a Reflex Bradycardia? still confused on this question. +  
kentuckyfan  So I think the subtle difference in choice E is that there would be a negative CHRONOTROPIC effect, no inotropic effect (contractility). +5  
maxillarythirdmolar  if anything, inotrophy could go UP not down as diastole prolongs and LVEDV increases --> Starling equation bullshit +  


submitted by sajaqua1(214),

Serum sickness is a Type 3 hypersensitivity reaction, in which the body responds to antigenic medical substances and produces antibodies. These antibodies in circulation then bind to the antigenic drugs and set off the complement cascade. Rheumatoid arthritis is also a Type 3 hypersensitivity reaction.

A) Apoptosis of macrophages- apoptosis is generally not a type of hypersensitivity reaction. B) Mast cel degranulation- this is part of a Type 1 hypersensitivity reaction/anaphylaxis, in which mast cells bind IgE on their surface, and IgE binding to the target antigen induces a conformational change in the IgE that sets off mast cell degranulation. C) Natural Killer Cell killing- plays a variety of roles, including cancer suppression and destruction of virally infected cells. If they play a role in hypersensitivity, it is part of Type 2 HSR in which they would respond to Ig on the cell surface. E) Wheel and flare reactions- This is also a Type 1 HSR.

meningitis  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. +  
youssefa  Goljan: RA is a mixed type III and type IV immune reaction +1  
dinagohe23  I though NK cell killing was similar to T cell so and RA is also Type IV +  
nephcard  ,blll sdouof +  


submitted by dr.xx(45),

right. he absolutely must remain in the waiting area so that he is at hand to attack his wife whenever her exam ends. go NBME!

meningitis  I guess it was all about not offering battering information in order to not make matters worse since he will figure out that the wife told on him.. Also, its a HUGE STRETCH but the only reason I thought he should stay in the waiting room was just in case the wife died they could detain him and call the police for questioning. +3  
temmy  Also, he should stay there because his wife did not grant him the permission to see him. Patients requests trumps. +  
nephcard  Doctor should not believe what wife told her. There may be some other reason for injury so batttering information should not be provided. But her wish of not letting her husband in should be fulfilled +  
charcot_bouchard  No. In real life patient lies. In Board ques they always tell the truth. Unless they make it very obvious. in fact its a board ques rule. So u believe her untill proven otherwise. +1  
drdoom  The prevailing rule of American medicine and law is individual autonomy. No other person is granted “default access” or privilege to another person’s body—that includes the physician! The physician must receive consent from a (conscious) “person” before they become “a patient”. In the same way, the person (the patient) must give consent before anyone else is permitted to be involved in her care, spouses included! +  


Malaria can impair hepatic gluconeogenesis and can also consume glucose for its own metabolic demands.

yotsubato  Truly a bull shit question... Its not in FA, Sketchy or Pathoma +16  
meningitis  I will try to remember this by associating it with P. vivax, that stay in the liver (liver=gluconeogenesis). Thank you @thomasalterman. +2  


submitted by sympathetikey(316),

Dexamethosone suppresses ACTH = Pituitary Adenoma Dexamethosone fails to suppress ACTH = Ectopic ATCH (ex - Small Cell Lung Cancer)

sympathetikey  *ACTH +  
meningitis  If im not mistaken, Dexamethosone also fails to suppress ACTH = Adrenal Gland Adenoma +1  
therealloureed  I think an adrenal gland tumor would have low/undetectable ACTH? aka no dex suppression +1  
bigjimbo  Low ACTH = adrenal adenoma High ACTH, suppressible = Pituatary adenoma High ACTH, non-suppressible = SCLC +  


submitted by meningitis(161),

Tanner stages start at TEN years old

Stage I:

  • I is flat, as in flat chest;
  • I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

  • 2 balls (testicular enlargement)
  • 2 hairs (pubic hairs now appearing)
  • 2 breast buds form

Stage III (3): starts at 13 y/o

  • If you rotate 3, it looks like small breasts (Breast mounds form);
  • If you squiggle the III they look like curly+coarse pubic hair
  • Increased penis length and size can be represented by: II --> III
    (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

  • First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
    MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
  • The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

  • V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
  • 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +1  
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +  
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +  
endochondral1  stage 3 breast mound is for females not males btw +  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +  


PTH is increased because serum calcium is low. Because PTH is increased, phosphorous is decreased. The woman in unable to absorb vitamin D (a fat soluble vitamin), so calcitriol is decreased (no vitamin D for the kidney to activate into calcitriol).

gabeb71  What does this have to do with the Celiac Sprue? +1  
medpsychosis  I believe they were explaining the reason for the mentioned "mild osteopenia" in the pt presentation. +  
meningitis  No, I think this person got confused with another question about celiac sprue, PTH, Calcitriol, and Vit D (it was an arrow type question). +  


submitted by docred123(3),

Why is the answer to this question not Adhesivie Capsultiis...

hayayah  Adhesive capsulitis causes severe restriction of both active and passive range of movement of the glenohumeral joint in all planes (especially external rotation). +5  
catch-22  Adhesive capsulitis is aka "frozen shouder" so you can expect exactly that. The entire shoulder will be hard to move in all directions. +1  
meningitis  Since it says there is NO impingement sign, it cant be rotator cuff tendinitis correct? What other signs eliminate this option? +  


She just completed the course of rituximab, which targets CD20 receptors. B-cell deficiency can predispose to bacterial infections.

b) BM failure is not associated with rituximab c) wrong d) wrong e) this occurs w/in 7-10 days of starting treatment, and would not occur after completing a 4-month course of rituximab.

meningitis  Forgot the time frame for Serum sickness and got it wrong.. thanks @thomasalterman +4  
stinkysulfaeggs  Same. Crap. +1  


submitted by beeip(63),

The best I can understand, they're describing endometrial hyperplasia, a result of excess estrogen, a steroid hormone that translocates to the nucleus and binds its transcription factor.

mousie  My exact thinking also! +2  
sympathetikey  Ditto. +  
meningitis  My thought as well but the answer says: "Binding of ligand to Nuclear transcription factor" and I thought to myself: "Estrogen Receptors aren't transcription factors.. they are receptors with Transcription Factor function that bind to the ER Element and recruit more Transcription Factors". Can anyone explain what I am missing? Am overthinking things? +  
criovoly  You are overthinking it, Steroid hormones receptor is found intracellular in the cytoplasm then they are translocated to the nucleus where they regulate gene transcription. HOPE THIS HELPS +  


submitted by mcl(220),

Since you're losing all your bicarb into your pee, you would expect the pH to be more alkaline. Also, since there is decreased Na+/H+ antiport, there is less sodium reabsorbed and therefore increased loss of free fluid to the urine.

mcl  useful figure http://users.atw.hu/blp6/BLP6/HTML/common/M9780323045827-036-f002.jpg +  
joker4eva76  Why wouldn't this be similar to a Type 2 RTA where urinary pH <5.5? +1  
mcl  I can't remember exactly what the question was asking off the top of my head, I think it was asking about relative to normal? But I think you're right in that the alpha intercalated cells (AIC) can still dump H+ into the urine and acidify it to an extent. And, like in RTA2, I don't know that the action of the AIC would be able to overcome the bicarb and acidify the urine enough for it to be the usual pH, so the urine should still be more alkaline compared to baseline. Kinda sucks, pH less than 5.5 should technically be acidic but it's alkaline for pee. +  
mcl  JK, normal urine pH is around 4-8, but I guess they consider closer to 5.5 on the more alkaline side...? I guess I would go more off that the alpha intercalated cells can't completely compensate for the amount of bicarb in the pee due to the CA inhibitor, not so much the actual pH. +  
meningitis  Anhydrase inhibitors also affect the anhydrase inhibitors that are used in the AIC in order to excrete the H+. Here is a link:**http://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/uploads/distal_0.png** +3  
mcl  ohhhhhhhhhhhhhhhhhhhhhhh my god duh yes thank you <3 +1  
meningitis  Lol yw!! +  


submitted by meningitis(161),

When standing up, the body normally activates sympathetic system to avoid orthostatic hypotension.

But since there is now an additive effect of the pheochromocytoma adrenergics, it will lead to a hypertension

(i.e: Double vasoconstriction = Pheo adrenergics + Sympathetic system)

sympathetikey  Brilliant. +1  
medschul  Would pheo have a normal resting BP though? +  
meningitis  I was trying to justify these tricky questions but very true medschul.. It shouldn't have normal resting BP. Sometimes it seems these NBME always have a trick up their sleeve. Im getting paranoid lol +  
nala_ula  The reason why the patient probably has normal HTN is because Pheochromocytoma has symptoms that occurs in "spells" - they come and go. Apparently in that moment, when the physician is examining her, she doesn't have the HTN, but like @meningitis explained, so many adrenergic hormones around leads to double the vasoconstriction when the patient stands up. +5  
meningitis  Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing. +1  
nala_ula  No problem! Thank you for all your contributions throughout this page! +1  
mjmejora  I thought the pheochromocytoma was getting squeezed during sitting and releasing the epinephrine then. kinda like how it can happen during manipulation during surgery. Got it right for sorta wrong reasons then oh well. +  


submitted by meningitis(161),

I also thought the same as @bubbles, but now trying to "justify" this tricky NBME question: I think this revolves on the fact that the patient has a HIGH blood pressure meaning we should focus on an answer that explains both increased BP and Hypovolemia (i.e: increased ADH which vasoconstricts and also absorbs free-water, both of which increase BP and cause hypovolemia).

Maybe if this patient were decompensated with LOW BP, one could think more about ANP.

I still think this question is TOO tricky.

meningitis  Sorry, hyponatremia* right? +  


submitted by meningitis(161),

Although it’s about PPV, this researching helped me understand basic phys, I hope this helps everyone in some way.

Takeaway: During PPV, venous return decreases, cardiac output decreases, and heart pressures decrease in the right side of the heart.

Why does PPV decrease venous return?

  • intrathoracic pressure compresses heart, causing blood not to return

Causes for decreased left ventricular output during ventilation:

  • Shifting of intraventricular septum to Left due to increased RV volume
  • Decreased venous return
  • Changes in hearts ability to contract due to positive pressure
  • lack of O2 to heart

Normal compensatory mechanisms for maintaining CO and BP during PPV?

  • increased HR to compensate for decreased SV
  • increased SVR to maintain BP

Other Physiologic responses:

  • Decreased cerebral perfusion pressure (body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels)
  • Decreased renal perfusion (Increased ADH, RAAS, and Patient has renal problems so increased creatinine and uric acid)
  • Possible malnutrition (increased glucose via gluconeogenesis etc.)
meningitis  sorry about the formatting, they were supposed to be bullets not italic. +1  
drdoom  looks good to me! ;) instead of asterisks try using the plus sign for unordered lists; the system gets confused sometimes because the asterisk is also for italics 😊 +1  
meningitis  Yeah, I noticed :s Oh, I didnt know the + sign did that! Very much appreciated, I will try that next time. +1  


submitted by bubbles(31),

Just to be crystal clear (because I've gotten more thyroid axis questions wrong than I should):

T4 --> T3 is possible but T3 --> T4 isn't?

meningitis  Exactly. I know there are papers saying there is some conversion of T3 to T4 but I try to keep it simple and think of it as once you break it apart (T4->T3), you cant put it back together. Only thyroglobin etc can put another I on it, so any T3 cant become T4 because you need it to be done in thyroid. +1  
angelaq11  I honestly don't know about this, but the way I reasoned this was: she is taking a whole lot of T3, so on top of already having hypothyroidism, she is just making things worse, so TSH is going to be decreased because of feedback inhibition, and hence T4 (Which is the main one produced by the thyroid) is also going to be decreased. I think the high T3 is the exogenous T3. +  


submitted by mattnatomy(22),

I believe they're referring to compression of branches of the Ilioinguinal Nerve (possibly the Anterior Scrotal Nerves.

Source: https://en.wikipedia.org/wiki/Anterior_scrotal_nerves

armymed88  Ilioingual covers part of the medial thigh, base of penis and anterior scrotum Posterior scrotal nerves are a branch of pudendal and cover said area Doral nerves cover the dorsum of the penis which are also from the pudendal +1  
meningitis  I thought it was the Genitofemoral nerve because the genital branch supplies the cremaster and scrotal skin, but I looked it up and: The genital branch passes through the *deep inguinal ring* and enters the inguinal canal; also, Ilioinguinal wraps around the spermatic cord just like the question stem says. +1  
jean_young2019  "The structures which pass through the canals differ between males and females: in males: the spermatic cord[6] and its coverings + the ilioinguinal nerve." from wiki "Inguinal canal", which means the ilioinguinal nerve lies on the external surface of spermatic cord. https://en.wikipedia.org/wiki/Inguinal_canal The contents of spermatic cord includes, "nerve to cremaster (genital branch of the genitofemoral nerve) and testicular nerves (sympathetic nerves). It is worth noting that the ilio-inguinal nerve is not actually located inside the spermatic cord, but runs along the outside of it, in the inguinal canal." from wiki spermatic cord. https://en.wikipedia.org/wiki/Spermatic_cord +  


submitted by bubbles(31),

Has anybody found a good explanation for this histology? I genuinely have no idea what I'm looking at.

meningitis  This is common in Klinefelter.. think of the equivalent of Streaked ovaries seen in Turners. White streaks, red/pink material of hyaline, and hyperplasia of Leydig cells. Just remember: It doesn't look like normal structured testicle histology (No organized seminiferous tubules with Sertoli cells around) +5  
niboonsh  https://www.pathologyoutlines.com/topic/testisklinefelter.html these pictures are kinda similar +1  


submitted by aesalmon(37),

Leydig cell hyperplasia, should also see fibrosis and hylinazation of the tubules but i'm not seeing it... ¯_(ツ)_/¯

meningitis  I think its there.. I thought it was the lighter red/pink material (hyaline material) And I thought the white streaks were the fibrosis like "streaked ovaries"in Turners. +  


submitted by meningitis(161),

Although it’s about PPV, this researching helped me understand basic phys, I hope this helps everyone in some way.

Takeaway: During PPV, venous return decreases, cardiac output decreases, and heart pressures decrease in the right side of the heart.

Why does PPV decrease venous return?

  • intrathoracic pressure compresses heart, causing blood not to return

Causes for decreased left ventricular output during ventilation:

  • Shifting of intraventricular septum to Left due to increased RV volume
  • Decreased venous return
  • Changes in hearts ability to contract due to positive pressure
  • lack of O2 to heart

Normal compensatory mechanisms for maintaining CO and BP during PPV?

  • increased HR to compensate for decreased SV
  • increased SVR to maintain BP

Other Physiologic responses:

  • Decreased cerebral perfusion pressure (body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels)
  • Decreased renal perfusion (Increased ADH, RAAS, and Patient has renal problems so increased creatinine and uric acid)
  • Possible malnutrition (increased glucose via gluconeogenesis etc.)
meningitis  sorry about the formatting, they were supposed to be bullets not italic. +1  
drdoom  looks good to me! ;) instead of asterisks try using the plus sign for unordered lists; the system gets confused sometimes because the asterisk is also for italics 😊 +1  
meningitis  Yeah, I noticed :s Oh, I didnt know the + sign did that! Very much appreciated, I will try that next time. +1  


submitted by welpdedelp(75),

Increased intracranial pressure that results in Cushing's triad of increased blood pressure, irregular breathing, and bradycardia. Thus, high CO2 induces cushing triad and if you give PP then it will reduced CO2, and then down regulate the sympathetic vasoconstriction. Originally the brain had so much CO2 that it spazzed out and tried to increase the BP in order to push more oxygenated blood to the brain.

https://pbs.twimg.com/media/CK3J5kZUsAAqSf-.jpg:large

lispectedwumbologist  "Bradycardia" 84 bpm lol +  
lispectedwumbologist  The hypertension in obstructive sleep apnea is due to increased sympathetic tone not increased intracranial pressure lmao +  
meningitis  @lispectedwumbologist : Be mature enough to correct him/her and move on, not laugh at him/her. +7  


submitted by mattnatomy(22),

Severe hypertension often leads to hyperplastic arteriolosclerosis (onion-skin appearance). Also see proliferation of smooth muscle cells.

meningitis  and explains the flame hemorrhages (Goljan) caused by malignant HTN +1  


submitted by k_tron_3000(11),

Just a random factoid (as far as I know), in patients with pancreatitis the most likely vessel for thrombosis is the splenic vein due to close “anatomic ties” with the pancreas. This would also cause gastro-splenic varices, explaining the vomiting of blood.

meningitis  Also explains the splenomegaly. If you have thrombosed splenic vein, the blood will pool in the spleen, can also cause expansion of red pulp of spleen. +  


submitted by aesalmon(37),

FA pg. 607 - failure of fusion of the maxillary and merged medial nasal processes (formation of primary palate)

meningitis  I think Cleft palate could also be due to failure of fusion of lateral and medial nasal prominences.. but since the baby had lip involvement and the lateral nasals can be seen, I went with failure of Maxillary and medial nasal fusion. Someone correct me if im wrong. +1  
redvelvet  a helpful photo +  


submitted by meningitis(161),

A case control study cant assess the prevalence of a disease but a cross sectional study can.

  • A case control study is that you are setting the margins in the 2 by 2 table therefore you're deciding how many cases and controls you want to have in your study and the calculation of incidence / prevalence in this scenario would be biased.
meningitis  the prevalence of the exposure and the health outcome are measured at the same time. You are basically trying to figure out how many people in the population have the disease and how many people have the exposure at one point in time. Case Control would determine ODDS ratio Cohort would determine Relative Risk +2  


submitted by aesalmon(37),

I feel dumb for asking but can someone explain this? If his parents are of close to normal BMI and are concerned about his weight why would they be allowing his calorie consumption to exceed his energy expenditure? ( AKA letting the kid eat too much and not exercise enough)

meningitis  That's a modern day mystery. +  
drdoom  The prompt is only asking "what's the likely cause of obesity?" It's not that they're "allowing" him to eat more than exercise. (Few parents can monitor their kids that closely!) The prompt is only asking what's the most likely explanation for his 95th percentile weight and BMI (given that he otherwise appears normal); in the United States, the most likely explanation is eating way more than you expend. +  
niboonsh  aka 'merica #firstworldproblems +  


submitted by mattnatomy(22),

I believe this is referring to midgut malrotation. Due to improper positioning of bowel (on the right side). Ladds bands connect the large intestine to the liver.

Can lead to:

  1. Volvulus

  2. Duodenal obstruction

3. SMA Occlusion -- I'm guessing based on the answer to the question

meningitis  Yes, the question clicked for me when I realized the ligament was on the RT side instead of LT so I thought of Volvulus. Image of ligament of treitz: https://media.springernature.com/original/springer-static/image/chp:10.1007/978-3-642-13327-5_17/MediaObjects/978-3-642-13327-5_17_Fig3_HTML.gif +1  
hyperfukus  So Volvulus regardless in baby or adult is gonna cause SMA prob + Duodenal Obstruction: d/t Ladd bands im gonna go back and remember those associations :) +  


Niemann-Pick Disease presents with mental retardation, lipid laden (foam cells) in bone marrow and cherry red spot on macula. No sphingomyelinase results in buildup of sphingomyelin which builds up in macrophages.

meningitis  "Pick your **Big** **Foamie** **Zeibra** nose with your Sphinger" Choose options with the letter I. SpIngomyelin, Sphingomyelinase, bIgorgans (hepatomegaly etc), zeIbra bodies, Foam cells +  


submitted by seagull(437),

True vocal cords are often damaged in singing or yelling. THis allows HPV to enter the underlying nucleated cells. HPV 16 and 18 are common subtypes that may cause SCC.

meningitis  Out of all of the virus', HPV has a predilection for stratified squamous epithelium and there is no indication of vesicles(HSV) or linear ulcers (CMV)in the question stem. But with HPV you usually get a big/small (depending on time) unilateral nodule. You are correct to say singing and yelling can cause nodules but these would be bilateral in the and would appear differently. So if a question stem could easily have included that as an option: maybe irritation or something like that. +5  


submitted by meningitis(161),

Tanner stages start at TEN years old

Stage I:

  • I is flat, as in flat chest;
  • I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

  • 2 balls (testicular enlargement)
  • 2 hairs (pubic hairs now appearing)
  • 2 breast buds form

Stage III (3): starts at 13 y/o

  • If you rotate 3, it looks like small breasts (Breast mounds form);
  • If you squiggle the III they look like curly+coarse pubic hair
  • Increased penis length and size can be represented by: II --> III
    (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

  • First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
    MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
  • The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

  • V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
  • 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +1  
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +  
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +  
endochondral1  stage 3 breast mound is for females not males btw +  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +  


submitted by armymed88(15),

emphysema leads to CO2 trapping leading to increase paCO2 in the blood, which gives you a respiratory acidosis Proper renal compensation will increase bicard reabs and decrease excretion- giving you increased bicarb in the blood

meningitis  Increased blood HCO3 could have easily been interpreted as increased blood pH aswell. FOllowing your explanation, since the pt had acidosis, the increased HCO3 will just make it a normal pH. Another way to think of the question is: if there is decreased exhalation due to COPD --> increased CO2 --> increased CO2 transported in blood by entering the RBC's with Carbonic Anhydrase and HCO3 is released into blood stream. So increased CO2 -> increased HCO3 seeing as this type of CO2 transport is 70% of total CO2 content in blood. +8  
drmohandes  I thought you could never fully compensate, so your pH will never normalize. Primary problem = respiratory acidosis → pH low. Compensatory metabolic alkalosis will increase blood HCO3-, but not enough to normalize pH, it will just be 'less' low, but still an acidosis. +  


submitted by hayayah(416),

Growth hormone releasing hormone acts via G-coupled receptors. G coupled receptors need GTP to become activated and GTPase to become inactivated.

No GTP-ase --> chronically active growth hormone releasing hormone receptor --> constant activation of adenylyl cyclase / cAMP pathway and release of growth hormone.

mcl  This figure is useful https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png +  
mcl  [link](https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png) +  
meningitis  How did you knkow it was GHRH and not GH perse? +3  
meningitis  nevermind; I just read down below. Thank you +1  


submitted by hayayah(416),

Growth hormone releasing hormone acts via G-coupled receptors. G coupled receptors need GTP to become activated and GTPase to become inactivated.

No GTP-ase --> chronically active growth hormone releasing hormone receptor --> constant activation of adenylyl cyclase / cAMP pathway and release of growth hormone.

mcl  This figure is useful https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png +  
mcl  [link](https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png) +  
meningitis  How did you knkow it was GHRH and not GH perse? +3  
meningitis  nevermind; I just read down below. Thank you +1  


submitted by welpdedelp(75),

So I think that issue of wrist extension and/or finger drop would be more radial nerve. However, there was more proximal weakness, so it would be C7.

"7-8 lay them straight", the pt couldn't "lay them straight" so it would be C7 root

welpdedelp  *As an addition, median nerve involvement would have leaned more toward C8 than C7. +1  
meningitis  Do you have anymore useful mnemonics for brachial plexus? +  
henoch280  FA pg 494 for mnemonics +  
winelover777  Doesn't look like there are many in FA 2019. S1/S2 - Buckle my shoe. L3/L4 - Shut the door. C5/C6 - Pick up sticks. +  


submitted by mcl(220),

Since you're losing all your bicarb into your pee, you would expect the pH to be more alkaline. Also, since there is decreased Na+/H+ antiport, there is less sodium reabsorbed and therefore increased loss of free fluid to the urine.

mcl  useful figure http://users.atw.hu/blp6/BLP6/HTML/common/M9780323045827-036-f002.jpg +  
joker4eva76  Why wouldn't this be similar to a Type 2 RTA where urinary pH <5.5? +1  
mcl  I can't remember exactly what the question was asking off the top of my head, I think it was asking about relative to normal? But I think you're right in that the alpha intercalated cells (AIC) can still dump H+ into the urine and acidify it to an extent. And, like in RTA2, I don't know that the action of the AIC would be able to overcome the bicarb and acidify the urine enough for it to be the usual pH, so the urine should still be more alkaline compared to baseline. Kinda sucks, pH less than 5.5 should technically be acidic but it's alkaline for pee. +  
mcl  JK, normal urine pH is around 4-8, but I guess they consider closer to 5.5 on the more alkaline side...? I guess I would go more off that the alpha intercalated cells can't completely compensate for the amount of bicarb in the pee due to the CA inhibitor, not so much the actual pH. +  
meningitis  Anhydrase inhibitors also affect the anhydrase inhibitors that are used in the AIC in order to excrete the H+. Here is a link:**http://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/uploads/distal_0.png** +3  
mcl  ohhhhhhhhhhhhhhhhhhhhhhh my god duh yes thank you <3 +1  
meningitis  Lol yw!! +  


submitted by meningitis(161),

When standing up, the body normally activates sympathetic system to avoid orthostatic hypotension.

But since there is now an additive effect of the pheochromocytoma adrenergics, it will lead to a hypertension

(i.e: Double vasoconstriction = Pheo adrenergics + Sympathetic system)

sympathetikey  Brilliant. +1  
medschul  Would pheo have a normal resting BP though? +  
meningitis  I was trying to justify these tricky questions but very true medschul.. It shouldn't have normal resting BP. Sometimes it seems these NBME always have a trick up their sleeve. Im getting paranoid lol +  
nala_ula  The reason why the patient probably has normal HTN is because Pheochromocytoma has symptoms that occurs in "spells" - they come and go. Apparently in that moment, when the physician is examining her, she doesn't have the HTN, but like @meningitis explained, so many adrenergic hormones around leads to double the vasoconstriction when the patient stands up. +5  
meningitis  Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing. +1  
nala_ula  No problem! Thank you for all your contributions throughout this page! +1  
mjmejora  I thought the pheochromocytoma was getting squeezed during sitting and releasing the epinephrine then. kinda like how it can happen during manipulation during surgery. Got it right for sorta wrong reasons then oh well. +  


submitted by moloko270(31),

Myofibrils are composed of smaller structures called myofilaments. There are two main types of filaments: thick filaments and thin filaments; each has different compositions and locations. Thick filaments occur only in the A band of a myofibril. Thin filaments attach to a protein in the Z disc called alpha-actinin and occur across the entire length of the I band and partway into the A band.

https://opentextbc.ca/biology/chapter/19-4-muscle-contraction-and-locomotion/

meningitis  isn't letter C the intercalated disc where the gap junctions are? +2  


johnthurtjr  FTR I had no idea this was a thing, and was pretty disappointed in myself when the google search had it in big bold letters right in my face. +2  
drdoom  via @johnthurtjr link: "Testosterone and other androgens have an erythropoietic stimulating effect that can cause polycythemia, which manifests as an increase in hemoglobin, hematocrit, or red blood cell count." https://www.medscape.com/viewarticle/773465 +  
meningitis  I guess that's another reason for steroids and doping up. +2  


submitted by oznefu(7),

how do you narrow down that testosterone increased hemoglobin concentration? just a random fact to know? i put alkaline phosphatase because i figured increased testosterone will increase bone growth and ruled out prostate-specific antigen bc it’s a woman.

hysitron  I guessed this one cause men have a higher hemoglobin than women. +1  
notadoctor  High levels of testosterone will result in amenorrhea. I guessed that since she's not menstruating she will not be losing blood and therefore hemoglobin. Therefore her hemoglobin levels will be higher than expected. +3  
meningitis  It kinda makes sense knowing testosterone causes catabolism so I was in between Alkaline phosphatase and hemoglobin... +1  
enbeemee  isn't testosterone anabolic? +  


submitted by seagull(437),

maybe someone can explain why this is avascular necrosis and not sepsis. It doesn't mention fever or absence of fever. The MRI has a small amount of hypodensity but to get avascular necrosis seems odd/

someduck3  Pg 455 of F.A. mentions that alcoholism can be a cause of avascular necrosis. +4  
meningitis  I think the small dark area on the left head of femur and the darkened neck are the avascular sites. Neck: http://img.medscapestatic.com/pi/meds/ckb/15/19515tn.jpg Head: (obvious lesion on the RT femur, but similar discrete lesion on the left as seen on the practice NBME) http://radsource.us/wp-content/uploads/2005/11/1a.jpg +1  
yotsubato  He wouldnt be playing golf if he had septic arthritis. Avascular necrosis is a more chronic condition that has a slow onset. +2  


submitted by asapdoc(20),

Patient has nephrogenic Diabetes Insipidus. One of the treatments is Hydrochlorthiazide.

meningitis  hydrocholorothiazide is DOC for Nephrogenic Diabetes insipidus because it paradoxically causes an increase in BP by increasing sodium absorption and thus water absorption, Pathoma explains this nicely. Also you shouldn't have chosen Desmopressin because upon fasting (fluid restriction) ADH is increased meaning ADH is being released Centrally but is not working in the kidneys at the V2 receptors of the epithelial renal cells at Collecting duct. On that note, Amiloride is used for Lithium induced nephrogenic DI. +  


submitted by hungrybox(241),

when diff single strand repair mechanisms are used:

  • repair newly synthesized strand: mismatch repair (Lynch syndrome)
  • repair pyrimidine dimers caused by dat UV exposure: nucleotide excision repair (Xeroderma pigmentosum)
  • repair spontaneous/toxic alteration: base excision repair
meningitis  Brca: recombinant repair +  


Arthropod for sure, but for the record I'm pretty sure this was Chikungunya Virus. Only got this from a UWorld question as I hadn't seen it until then, but apparently the arthralgia is really bad, which is what drew me to the answer.

https://www.cdc.gov/chikungunya/index.html

meningitis  More like Zika Virus (Same a. aegypti vector) since it says she has rash associated to her bone and muscle pain. I had Zika one time (i live in Puerto Rico). Remember also dengue and Zika are Flavivirus. Dengue can cause hemolysis (hemorrhagic), and Zika is associated with Guillen Barre and fetal abnormalities. +6  
nala_ula  I'm shocked that I found a fellow puerto rican on this site! Good luck on your test! +  
namira  dont be shocked! me too! exito! +1  
niboonsh  Dengue is also known as "bone break fever" which makes me think its more likely to be dengue due to the "excruciating pains in joints and muscles". https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242787/ +2  
dr_jan_itor  I was thinking that its Murine typhus transmitted by fleas +  
monique  I would say this is more likely scenario of either Dengue or Chikungunya, not Zika virus. Excruciating pain is common in those, not in Zika. Zika has milder symptoms of those three infection. +  


submitted by nosancuck(38),

Dam son this lil b got some UMBILICATED Molluscum all up in her bizness

drdoom  tru. +  
meningitis  Pg 164 FA 2019 +  
dr.xx  likely not "lil b" as 2-4 times as many cases are found in whites than in persons of other races +  
drdoom  lil b not a referent of race; cf. lil boo, lil baybay, lil bowow, &c. +  
dr.xx  I disagree. Google "lil b" for images. See what you may discover. +  


submitted by egghead(0),

This is one of those questions I was never going to get. It's not in FA, I don't think I've seen it in class.

hungrybox  same :( +  
masonkingcobra  My issue was the stem said no skin damage (I would think pulling out your hair damages your scalp) [Turns out it does not](http://onlinelibrary.wiley.com/doi/full/10.1111/j.1529-8019.2008.00165.x) +  
gh889  FA 2019, pg 551 +3  
meningitis  Compulsively pulling out one’s own hair. Causes significant distress and persists despite attempts to stop. Presents with areas of thinning hair or baldness on any area of the body, most commonly the scalp. Incidence highest in childhood but spans all ages. Treatment: psychotherapy is first line; medications (eg, clomipramine) may be considered. +2  
step1soon  FA 2019 pg 551 +  


submitted by yo(26),

they're talking about a splenorenal shunt procedure

https://my.clevelandclinic.org/health/treatments/4950-distal-splenorenal-shunt

hungrybox  be honest did u know that before looking it up +2  
meningitis  @hungry, because you didn't know it, doesn't mean he didn't. This is a forum for answering questions and helping out, not dissing or showing off. Grow up before becoming a doctor. +1  
sympathetikey  Relax @meningitis. Hungry's just messin :) +1  
sbryant6  Looks like somebody needs an enema to get that stick out. +  
chandlerbas  ya'll are too TP/(TP+FN) lol +  


submitted by est88(13),

Retroperitoneal structures: SAD PUCKER.

Only the descending colon is part of this.

meningitis  SAD PUCKER: Suprarenal (adrenal) glands [not shown] Aorta and IVC Duodenum (2nd through 4th parts) Pancreas (except tail) Ureters Colon (descending and ascending) Kidneys Esophagus (thoracic portion) Rectum (partially) +4  
cienfuegos  I find "SAID PUCKER" to be helpful because it includes IVC +  


submitted by hungrybox(241),

jugular venous distention = left heart failure

pulmonary edema = right heart failure

Four-chamber dilation is the most likely answer.

Other answers:

  • Assymetric septal hypertrophy, myocardial disarray: these are both classic findings in hypertrophic cardiomyopathy (HCM)
  • endocardial fibroelastosis: a rare restrictive cardiomyopathy seen in infants/children
  • lymphocytic infiltration of the myocardium: seen in viral (autoimmune) myocarditis. A cause of dilated cardiomyopathy, but there was no mention of a preceding viral illness.
meningitis  I think you meant: Jugular venous distention = LT HF Pulmonary edema = RT HF +3  
hungrybox  woops yea I meant Jugular venous distention = RIGHT HF, Pulmonary edema = LEFT HF +3  


submitted by mcl(220),

PCOS is associated with abnormal production of sex steroids, including dysfunction of estrogen production and progesterone. Chronically elevated levels of estrogen can cause endometrial hyperplasia.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3917599/

meningitis  Why isnt it endometriosis? Could someone help me out on this? +  
meningitis  Sorry, I was confusing with higher risk for endometrial carcinoma. +  
vi_capsule  Estrogen is responsible for cyclical bleeding and pain associated with endometriosis hence progestin is a treatment modality. But estrogen isnt a risk factor for Endometriosis. Rather theres retrograde flow, metaplatic transformation etc theories are responsible for endometriosis. +  
sympathetikey  Tfw you get so thrown off by a picture that you don't read the question properly. +2  
hyperfukus  @meningitis idk if u still care lol but always go back to endometriosis=ectopic endometrial tissue outside of the uterus so you can rule it out since increased estrogen would cause you to have worsened endometriosis or a thicker one but not directly...you can see the clumps of the follicles in the ovaries if you look super close so that along with the presentation takes you to PCOS and anytime you don't have a baby or stay in the proliferative phase(estrogen phase) you get endometrial proliferation-->hyperplasia--->ultimately carcinoma +  


submitted by mcl(220),

PCOS is associated with abnormal production of sex steroids, including dysfunction of estrogen production and progesterone. Chronically elevated levels of estrogen can cause endometrial hyperplasia.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3917599/

meningitis  Why isnt it endometriosis? Could someone help me out on this? +  
meningitis  Sorry, I was confusing with higher risk for endometrial carcinoma. +  
vi_capsule  Estrogen is responsible for cyclical bleeding and pain associated with endometriosis hence progestin is a treatment modality. But estrogen isnt a risk factor for Endometriosis. Rather theres retrograde flow, metaplatic transformation etc theories are responsible for endometriosis. +  
sympathetikey  Tfw you get so thrown off by a picture that you don't read the question properly. +2  
hyperfukus  @meningitis idk if u still care lol but always go back to endometriosis=ectopic endometrial tissue outside of the uterus so you can rule it out since increased estrogen would cause you to have worsened endometriosis or a thicker one but not directly...you can see the clumps of the follicles in the ovaries if you look super close so that along with the presentation takes you to PCOS and anytime you don't have a baby or stay in the proliferative phase(estrogen phase) you get endometrial proliferation-->hyperplasia--->ultimately carcinoma +  


submitted by nosancuck(38),

Yo dawg we all about PVT TIM HaLL

Phenylalanine, Valine, TryptoDANK, Threonine, Isoleucine, Methionine, Histidine, Leucine Lysine

meningitis  I don't understand what the question is asking... can someone please explain it to me? Patient doesnt eat protein, shes chubby. What does methionine have to do with this? +2  
charcot_bouchard  Just basically asking which is essential amino acids. +1  
usmleuser007  Essential amino acids (something i came up with) 1. "Three HAL fans will try meth" a. Threonine = Three b. Histidine; Arginine; Lysine = HAL c. Phenylalanine = fans d. Valine; Isoleucine; Leucine = will e. Tryptophan = try f. Methionine = meth +2  
nala_ula  They're saying there is a lack of good quality protein -> slight nutritional deficiency. She may have acquired weight but it's not because of protein. So they're specifically asking what amino acid she might be missing due to her subpar diet. Since essential amino acids are those that the body cannot make itself, out off those listed, methionine is the essential amino acid. It's on page 81 of FA 2019. +6  
nala_ula  correct me if I'm wrong please :) +  
hello  For anyone confused trying to follow @usmleuser007's comment -- slightly modified Essential amino acids mnemonic "Ah, Three fans will try meth" Ah = arginine, histidine Three = Threonine Fans (phans)= Phenylalanine Vil (Will -- German accent pronouncing English word 'will') = valine, isoleucine, leucine, lysine Try = tryptophan Meth = Methionine +  


submitted by neonem(263),

This is a case of porphyria cutanea tarda. The way I remember this is that it's the only high-yield porphyria that has skin manifestations due to UV. I remember this by "After U (uroporphyrin), it's UV". Apparently it's also associated with Hepatitis C, which could be the reason why there's increased AST & ALT, or it could be due to toxic buildup of intermediates in heme synthesis.

meningitis  Why cant it be protoporphyrinogen oxidase? It was because of that reason (Increased AST and ALT) I thought it wasnt uroporphyrinogen decarb. My train of thought was: "wow, mitochondria are messed up.. there must be a lot of intermediates in there,therefore the Uroporph decarb must OK." +  


submitted by taway(7),

Does anybody understand why we are allowed to interfere with the clinical decisionmaking of two other specialists directly? Wouldn't that muddy the waters even more by adding our opinion? I don't see the underlying principle that explains the rationale in this answer.

jcrll  I think it's about adding our opinion and more about seeing what the situation is because a patient contacted you in distress. The others are about contacting management off hearsay; that could also "muddy the waters," I Is this question also addressing quaternary prevention? +1  
meningitis  I agree with jcrll. My same thought process but then I changed it to psychiatric consultation in order to first attend the patient's distress and anxiety since it was hindering her decision making. Besides, the whole ordeal about her treatments and ineffectiveness was emotionally and physically exhausting her. +2  
vi_capsule  Referral is NEVER a answer +4  
tsl19  Going straight to the chair of the ethics committee without having spoken to the other physicians would be inappropriate because it would be jumping a bunch of steps in communication first - like jcrll said, you want to get the picture of what's going on from the other physicians first. Maybe the gynecologic oncologist isn't actually as opposed to palliative measures as the patient perceives him to be and thinks he's doing what the patient wants, etc. It could just be miscommunication, which you could help clear up without getting ethics involved ... better to start there. +2  


submitted by nosancuck(38),

Yo dis B got NO INTERNAL FEMALE ORGANS

Why dat!???

We be lookin at someone with an SRY from dere Y chromie! Dey be a Y chromie Homie so they be makin some Testis Determinin Factor which I be sure makes some nice lil ANTI MULLERIAN FACTOR so dey aint got that Female Internal Tract u know what i be sayin

And since wimminz is da DEFAULT they stil be gettin dose pussy lips and breastes

meningitis  The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering: chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities +11  
yotsubato  Turner syndrome patients are also chromatin negative as well though.... +3  
sympathetikey  I didn't know a complication post-meningitis was lack of humor. +2  
sympathetikey  Ah, didn't read the last line. Yeah, that is taking it a bit far +1  
niboonsh  yall are haters. this is the first explanation that has ever made sense to me +2  
arkmoses  https://www.youtube.com/watch?v=yuXL-3eoB-o&t=77s Interesting syndrome watching this helped me to put it into real life perspective, interesting points they have no pubic hair/body hair, they apparently also dont smell, and breast size is usually increased... +  
whoissaad  How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA? +1  
cienfuegos  According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turner’s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative. This abnormal X-chromatin negative finding in the majority of Turner’s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turner’s syndrome is found to be X-chromatin positive." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233891/ +  
hyperfukus  i really hate haters this is awesome! +  


submitted by hungrybox(241),

Hydrochlorothiazide is a thiazide diuretic => thiazide diuretics are associated with hypokalemia.

What other diuretics are associated with hypokalemia? Loop diuretics.

Why?

Inhibition of Na+ reabsorption occurs in both loop diuretics (inhibit NKCC cotransporter) and thiazide diuretics (inhibit NaCl cortransporter). All of this increased Na+ increases Aldosterone activity.

Relevant to this problem, Aldosterone upregulates expression of the Na+/K+ ATP antiporter (reabsorb Na+ into body, expel K+ into lumen). This results in hypokalemia in the body.

Hang on, there's more high yield info!

Aldosterone does one other important thing - activation of a H+ channel that expels H+ into the lumen.

So, given that this patient has hypokalemia, you know there is upregulation of Aldosterone. Do you think her pH would be high, or low? Exactly, it would be high because inc. Aldosterone => inc. H+ expelled into the lumen => metabolic akalosis.

Now you understand why both loop diuretics and thiazide diuretics can cause what's called "hypokalemic metabolic alkalosis."

hungrybox  jesus this answer was probably too long i'm sorry +1  
meningitis  I disagree. It's the complete thought process needed for many Thiazide/Loop question that can be thrown. Thanks. +5  
amirmullick3  This is what NBME should be providing with each question's correct answer! Thanks hungrybox! +  
amirmullick3  @hungrybox did you mean "All of this DECREASED Na increases aldosterone activity."? +  


submitted by calcium196(7),

Ubiquitin-mediated proteolysis is not reversibly affected by insulin. The question asks for reversible ways that insulin affects it, and ubiquitination would lead to degradation via proteases, which is not reversible. Nuclear/cytoplasmic shunting makes sense because FOXO is a transcription factor, so it can’t do its job if it is in the cytoplasm!

meningitis  Thank you for your explanation! One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated? +  
tsl19  I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes. +  
didelphus  I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question. +4  
niboonsh  yes, FOXO is affected downstream of the activation of PI3K. This is a really good video that explains the whole cascade https://www.youtube.com/watch?v=ewgLd9N3s-4 +  
alexb  According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up? +  


submitted by neonem(263),

Obstructive uropathy causes a postrenal azotemia --> when prolonged, tubular damage ensues. This leads to an acute tubular necrosis, characterized by necrotic plugs in the tubular system as seen in the image

meningitis  Does anyone know the relevance of the stem saying: "during this time she also has been crying frequently"? +6  
usmleuser007  Think the postrenal azotemia is d/t her pregnancy. With the increasing in size fetus, the pelvic cavity is being compressed and thus there is pressure on the ureters. This leading to the presentation. As per above --- the crying maybe just d/t her pain and emotional stress caused by worrying about possible complications regarding her fetus. +2  
maxillarythirdmolar  My gut tells me it must be some sort of transient change in placental size with hormonal changes. It's reminiscent of what you might expect for breast changes during the menstrual cycle, imo +  


submitted by johnthurtjr(53),

I'm not a fan of gross path images and questions that say "look, what is this thing?" - that said meningiomas are the most common brain tumor and this picture is is a good example of one. I had no idea what these things looked like and got it wrong, too. Take a look at this one

johnthurtjr  [Here's more info](http://www.pathologyoutlines.com/topic/cnstumormeningiomageneral.html) +  
meningitis  I got it wrong because I didn't see any apparent Dura mater nor other meninges (The veins aren't being covered by any "shiny layer"), so I thought the tumor was coming from inside the brain and not compressing it like meningiomas usually do. +  
meningitis  But it did follow the common aspect where they are found in between divisions of brain and are circular growths like a ball. +3  
nala_ula  Since it was basically implied that the patient died and "here look at what this is" I thought it was a malignant tumor (glioblastoma)... but I guess it's all about placement. +4  


submitted by johnthurtjr(53),

I'm not a fan of gross path images and questions that say "look, what is this thing?" - that said meningiomas are the most common brain tumor and this picture is is a good example of one. I had no idea what these things looked like and got it wrong, too. Take a look at this one

johnthurtjr  [Here's more info](http://www.pathologyoutlines.com/topic/cnstumormeningiomageneral.html) +  
meningitis  I got it wrong because I didn't see any apparent Dura mater nor other meninges (The veins aren't being covered by any "shiny layer"), so I thought the tumor was coming from inside the brain and not compressing it like meningiomas usually do. +  
meningitis  But it did follow the common aspect where they are found in between divisions of brain and are circular growths like a ball. +3  
nala_ula  Since it was basically implied that the patient died and "here look at what this is" I thought it was a malignant tumor (glioblastoma)... but I guess it's all about placement. +4  


submitted by hayayah(416),

Iron overdose is a cause of a high anion gap metabolic acidosis.

meningitis  I found this to add a little bit more explanation as to how it causes the acidosis if anyone needs it. 1. Mitochondrial toxicity - decreases aerobic respiration and shunts to lactic acid production 2. Cardio toxicity (Secondary to Mitochondrial toxicity) leads to cardiogenic shock (hypoperfusion), which causes lactic acidosis 3. Hepatotoxicity - Decreases lactate metabolism, causing lactic acidosis 4. When in trivalent form (Fe+3), it can react with 3 molecules of H2O --> FeOH3 + 3H+ This will then deplete Bicarb buffering system resulting in non-gap acidosis. Source: https://forums.studentdoctor.net/threads/iron-poisoning-anion-gap-or-non-anion-gap-acidosis.958285/ +7  
sympathetikey  None of the other choices were even metabolic acidosis. They threw us a bone with this one. +  
imnotarobotbut  Don't changes in bicarb take a few days? How did his bicarb drop down to 8 in 12 hours? +  
charcot_bouchard  its met acidsis. not compensation +1  


submitted by hayayah(416),

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? +  
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 +7