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Comments ...

 +1  (nbme24#21)

This is a case of lingual thyroid, a persistence of thyroid tissue at the base of the tongue due to failure of migration.


 +0  (nbme23#7)

Helpful image to understand that its isomerization:

https://www.viapath.co.uk/sites/default/files/upload/Newsletter/jaundice%20fig2.png

drzed  That made me want to vomit tbh; I forgot about NMRs until just now. I hated those things.

 +2  (nbme22#37)

Dr. Sattar says that decreased blood flow --> atrophy. Fibromuscular dysplasia of the left renal artery is essentially renal artery stenosis --> atrophy of the left kidney


 -1  (nbme22#47)

Pentad of TTP = FAT RN

  • Fever
  • Anemia (MAHA)
  • Thrombocytopenia
  • Renal failure
  • Neurologic symptoms

This is TTP not ITP

makinallkindzofgainz  I seem to have commented on the wrong question, sorry! I wish I was able to delete my comment, but I can't.

 +1  (nbme22#42)

Androgenetic alopecia is a progressive, nonscarring alopecia that affects the regions of the scalp with the most androgen-sensitive hair follicles, resulting in a characteristic pattern of balding (bitemporal scalp in men and vertex and frontal scalp in women).

Follicular miniaturization: Androgen shortens the anagen phase of hair growth → vellus hair formation (thin, short hair)

  • Vellus hair does not cover the scalp adequately. As the anagen phase shortens further, the hair shaft does not grow long enough to reach the scalp.

TL;DR - DHT can lead to baldness


 +0  (nbme22#28)

Isolated gastric fundal varices are seen in splenic vein thrombosis.

Thrombosis increases pressure in the short gastric veins --> gastric varices only in the fundus

  • Seen in pancreatic inflammation (ex. pancreatitis, pancreatic cancer), which can cause a blood clot within the splenic vein, backing up blood into the short gastric veins (gastrocaval shunt - drained by the inferior phrenic vein) when ruptured causes gastric bleeding, hemoptysis (seen in stem), and melena

 +3  (nbme22#7)

It's D because you're being compassionate and every other answer makes no sense:

  • A: You can't promise that things will be okay.
  • B: Being a dick.
  • C: Being a dick.
  • E: Being a dick.




Subcomments ...

submitted by mahesh(0),

Osteosarcoma histological appearance. Paget disease is one of risk factor

spow  Looking back, I know it's osteosarcoma but the lung metastases made me think of Ewing's +  
makinallkindzofgainz  Ewing sarcoma is common in boys <15 years old. This patient is a 70 year old woman. The stem notes elevated periosteum and a sunburst pattern which are characteristic of osteosarcoma. +  


submitted by neonem(371),

General theme of pathology: hypoxia impairs oxidative phosphorylation --> less ATP --> less Na-K pump activity so sodium builds up in the cell, causing swelling. This is the first step. Then you'd get the calcium buildup in the cell and eventual anaerobic glycolysis, causing lactic acid production and lowered pH... but this happens later and isn't the direct cause of cellular swelling, which is what the question is after.

aneurysmclip  can we have a moment of appreciation for Dr Sattar +2  
makinallkindzofgainz  blessed be His name +1  


submitted by yb_26(124),

My simple understanding is that pt's heart contractility is decreased due to MI => heart can't pump a lot of blood => increased backup flow into pulmonary vasculature => increased PCWP.

More blood in pulmonary vasculature => they will dilate in order to just keep all these blood => decreased pulmonary vascular resistance

Decreased cardiac output => peripheral vasoconstriction => increased systemic vascular resistance

susyars  The question says “ST elevation in the anterior leads“ so, in some way I was thinking of the most anterior part of the heart which is the right ventricle, and not the left one. +1  
makinallkindzofgainz  Anterior STEMI = ST elevations in V3, V4 which is supplied mostly by the LAD. RV is mostly supplied by the RCA, which would show up on an EKG with ischemic changes in II, III, and avF +1  


submitted by m-ice(184),

HMG CoA Reductase inhibitors prevent the liver from synthesizing its own cholesterol. In order to maintain its need for cholesterol, the liver has no choice by to increase its LDL receptor expression in order to take cholesterol from the blood.

suckitnbme  Not sure why NBME felt like they needed two questions on statin MOA on this form. +4  
makinallkindzofgainz  because they didn't even realize it because they make insanely low effort practice exams with awful formatting and vague vignettes, yet here we are paying 60 bucks a pop for "high quality" exams, gimme a break. ok i'm done venting +2  


submitted by neonem(371),

This patient isn't hypoventilating, they're HYPERventilating, hence the PCO2 < 40 mm Hg.

Let's walk it backwards: They are hyperventilating to compensate for the metabolic acidosis caused by widespread hypoxia. Hyperventilating allows you to blow off more CO2.

Why are they hypoxic? The person is hypoxic due to inflammation and acute respiratory distress syndrome from the pneumonia. All the cytokines from the inflammatory cells cause increased pulmonary capillary leakage, which blocks up the alveolar membrane so that O2 can't get through to the blood.

Why do they have metabolic acidosis in the first place? No oxygen --> no electron transport chain and no TCA --> lactic acidosis.

diabetes  no pneumonia it is UTI +1  
makinallkindzofgainz  The infection from the UTI spread to her lungs +  
makinallkindzofgainz  this is essentially urosepsis, one of the leading causes of sepsis +  
cmun777  UTI -> Sepsis -> ARDS (exudative pathophysiology d/t increased pulmonary vasc permeability) +1  


submitted by neonem(371),

This patient isn't hypoventilating, they're HYPERventilating, hence the PCO2 < 40 mm Hg.

Let's walk it backwards: They are hyperventilating to compensate for the metabolic acidosis caused by widespread hypoxia. Hyperventilating allows you to blow off more CO2.

Why are they hypoxic? The person is hypoxic due to inflammation and acute respiratory distress syndrome from the pneumonia. All the cytokines from the inflammatory cells cause increased pulmonary capillary leakage, which blocks up the alveolar membrane so that O2 can't get through to the blood.

Why do they have metabolic acidosis in the first place? No oxygen --> no electron transport chain and no TCA --> lactic acidosis.

diabetes  no pneumonia it is UTI +1  
makinallkindzofgainz  The infection from the UTI spread to her lungs +  
makinallkindzofgainz  this is essentially urosepsis, one of the leading causes of sepsis +  
cmun777  UTI -> Sepsis -> ARDS (exudative pathophysiology d/t increased pulmonary vasc permeability) +1  


submitted by nwinkelmann(187),

I found a picture showing the transmission by two heterozygous alpha thalassemia trait asian (cis-deletion) parents, and modified it to also show the inheritance by two heterozygous alpha thalassemia african (trans-deletion) parents. Here you go: https://drive.google.com/open?id=1HQU1VuhI4Jc9WJR2POwnTq9T8wEdv7dw

makinallkindzofgainz  broken link +  


submitted by sajaqua1(347),

Plasma membranes are a lipid bilayer, typically with phosphate heads on each surface and long carbon tails on the inside. These carbons are neutral, and undergo hydrophobic interactions for an energetically favorable state.

Integral membrane proteins pass through this lipid bilayer, and so must be capable of interacting both with the polar solvents of intracellular and extracellular space, as well as the hydrophobic core of the layer. The transmembrane portion often has alpha-helical secondary conformation, with hydrophobic residues like glycine on the outside towards the carbon tails with polar amino acid residues tucked in.

makinallkindzofgainz  "high school biology" lmao we really out here +2  


submitted by sugaplum(122),

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

makinallkindzofgainz  The supraspinatus AB-ducts. The Subscapularis ADDucts +  
makinallkindzofgainz  disregard my comment, I misread what you meant +  
drzed  How are you supposed to remember which S is which? +1  
drschmoctor  @drzed "Supra" = on top, so the 1st S is for supraspinatus. +  


submitted by sugaplum(122),

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

makinallkindzofgainz  The supraspinatus AB-ducts. The Subscapularis ADDucts +  
makinallkindzofgainz  disregard my comment, I misread what you meant +  
drzed  How are you supposed to remember which S is which? +1  
drschmoctor  @drzed "Supra" = on top, so the 1st S is for supraspinatus. +  


submitted by yogi(11),

ITP - Platelet + Ab goes to spleen - Lysed - Low plt count.After splenectomy - usually plt count improve and Peripheral blood smear show - HJ bodies as a sign of asplenia ( nuclear remnants in RBC usually removed by spleen). If there was an accessory spleen (which was not functional when the main spleen was working) will take over the function gradually - HJ bodies will disappear and Plt starts to lyse - which has happened in this case scenario.

spow  But why are there no bite cells? Question stem states that there is normal morphology? That's why I didn't pick accessory spleen +2  
makinallkindzofgainz  Bite cells are seen when splenic macrophages take "bites" out of hemoglobin precipitates in G6PD deficiency, which doesn't have to do with our question. This patient had a splenectomy 3 months ago, 6 weeks later showed Howell-Jolly bodies (asplenia), and then today now has normal erythrocytes (spleen is working again somehow = accessory spleen) +1  


Strongyloides penetrates the skin (usually the feet), travels into the bloodstream, enters the lungs/trachea where it is usually coughed up and then swallowed into the GI tract. They can lay eggs in the intestines, and when the larvae hatch, they can penetrate the intestinal wall and enter the bloodstream again.

makinallkindzofgainz  Strongyloides is fucking metal holy shit +3  


The rhombencephalon would be on the actual fetus so just get rid of (D). The "black hole" that the fetus is floating in is the gestational sac so get rid of (C). Now I am no ultrasound expert but I know that the amniotic cavity eventually expands to fuse with the chorion thereby eliminating the chorionic cavity (B). In terms of where the amniotic cavity is shown in this image, I am not sure, so maybe someone can help but this leaves the yolk sac which typically appears within the gestational sac around 5.5 weeks.

kateinwonderland  At the end of the fourth week, the yolk sac presents the appearance of a small pear-shaped opening (traditionally called the umbilical vesicle), into the digestive tube by a long narrow tube, the vitelline duct. (Wiki) +3  
tallerthanmymom  But why does it look completely detached from the fetus? I eliminated yolk sac first because of this +  
makinallkindzofgainz  If you look reeeeeeeally closely, you'll see some signal between the yolk sac and the baby. Although you can't see the entire connection, they are connected. +1  
thotcandy  Pt is roughly 8 weeks pregnant so and typically by 9th week, Amniotic cavity has expended to fill entire volume of Gestational sac. So the entire black part around the fetus is GS/AC. +1  


incorrect question. PPIs are associated with diarrhea and c diff which would cause acute onset severe diarrhea https://www.mayoclinicproceedings.org/article/S0025-6196(17)30841-8/fulltext

makinallkindzofgainz  PPIs don't usually directly cause diarrhea. The stem mentions nothing about potential C. diff. Misoprostol directly causes diarrhea. I also put PPI, but I can see why I was wrong. +1  


submitted by haliburton(141),

medbullets has a nice pneumonic for the killed vaccines:

Rest In Peace Always:

Rabies
Influenza
Polio (Salk)
Hepatitis A

paulkarr  Also, the nice little puppet show from sketchy for those visual learners like me. +  
makinallkindzofgainz  just remembered that MMR is a live attenuated vaccine +  


submitted by monkd(6),

Am I crazy or did Uworld not have a question that stated Statins are the most effective drug regardless of baseline lipids. This logic threw my off.

adisdiadochokinetic  You are not crazy. I got this question wrong for the same reason but here's why I think NBME was going with fibrates. You can use the Friedewald equation to calculate LDL cholesterol from the values they give. This equation is LDL= Total Cholesterol-HDL Cholesterol-(Triglycerides/5). The Triglycerides/5 term is an estimate for VLDL. If you calculate it in this case you get an LDL of 120 which is firmly normal and thus the patient would ostensibly not benefit from statin therapy. +8  
hello36654  omg when the hell am I going to remember this equation? Jesuusssssss, this kind of details makes me want to give up on STEP +2  
almondbreeze  Her goal LDL should still be <100, bc she has 3 CHD risk equivalents (https://www.aafp.org/afp/2002/0301/p871.html#afp20020301p871-t3) CHD risk equivalent=the major risk factors that modify LDL goals 1) age(M>45, F>55), 2) smoking status, 3) hypertension(>140/90), 4) ow HDL level (<40), and 5) family history. (https://www.aafp.org/afp/2002/0301/p871.html#sec-4) +  
almondbreeze  *low HDL level (refer to table 3 of the article) +  
makinallkindzofgainz  These guys are hitting up attending-level cardiovascular risk factor calculations, meanwhile I picked statins because I think I remember that they help the heart +4  


submitted by wired-in(46),

Maintenance dose formula is (CssCltau)/F where Css is steady-state target plasma conc. of drug, Cl is clearance, tau is dosage interval & F is bioavailability.

Neither dosage interval nor bioavailability is given, so ignoring those & plugging in the numbers (careful to convert units to mg/kg/day): (12 ug/mL * 1 mg/1000 ug) * (0.09 L/hr/kg * 1000 mL/1 L * 24 hr/1 day) = 25.92 mg/kg/day

...which isn't any of the answer choices listed. They must have rounded 0.09 L/hr/kg to 0.1 L/hr/kg, and doing so gives exactly 28.8 mg/kg/day (choice C)

lispectedwumbologist  That's so infuriating I stared at this question for 20 minutes thinking I did something wrong +35  
hyoid  ^^^^^ +5  
seagull  lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that. +5  
praderwilli  Big mad +4  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +7  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +10  
bigjimbo  JOKES +  
cr  in ur maths, why did u put 24h/1day and not 1day/24h? if the given Cl was 0.09L/hr/kg. I know it just is a math question, but i´d appreciate if someone could explain it. +  
d_holles  LMAO games NBME plays +1  
hyperfukus  magic math!!!!! how TF r we supposed to know when they round and when they don't like wtf im so pissed someone please tell me step isn't like this...with such precise decimal answers and a calculator fxn you would assume they wanted an actual answer! +1  
jean_young2019  OMG, I've got the 25.92 mg/kg/day, which isn't any of the answer choices listed. So I chose the D 51.8, because 51.8 is double of 25.9......I thought I must have make a mistake during the calculation ...... +2  
atbangura  They purposely did that so if you made a mistake with your conversion like I did, you might end up with 2.5 which was one of the answer choices. SMH +1  
titanesxvi  I did well, but I thought that my mistake was something to do with the conversion and end up choosing 2.5 because it is similar to 25.92 +1  
makinallkindzofgainz  The fact that we pay these people 60 dollars a pop for poorly formatted and written exams boggles my mind, and yet here I am, about to buy Form 24 +3  
qball  Me after plugging in the right numbers and not rounding down : https://i.kym-cdn.com/entries/icons/original/000/028/539/DyqSKoaX4AATc2G.jpg +1  
frustratedllama  Not only do you feel like you're doing sth wrong but then that feeling stays for other questions. sucks so baad +  


submitted by rainlad(8),

my approach to this question was to eliminate all the answer choices that mentioned specificity or sensitivity, since the data here did not provide information about any sort of screening test.

that left me with two possible answer choices: I eliminated the one about consistency of other studies, since no other studies were mentioned in the question stem.

not sure if I oversimplified things, but it led me to the right answer!

makinallkindzofgainz  this is exactly how I reasoned through it. Were we correct in our line of thinking? We'll never knooooow +  
qball  But will you ever know on the real thing? +1  


submitted by aladar50(30),

For the ECG, I initially thought it was 2nd degree Type 1 because it seemed that the PR intervals were increasing until a beat was dropped, but if you look at it closely, some of the P waves were hidden in the QRS complexes. If you notice that, then you can see that there were regular P waves and regular QRS complexes, but there was a complete dissociation between them which means it was 3rd degree heart block, so the answer was ablation near the AV node.

yotsubato  answer was ablation near the AV node. No it wasnt. It was ablation OF THE AV node itself. Which faked me out. +5  
makinallkindzofgainz  The tangent by user "brbwhat" says that there is "pr lengthening progressively" but there is not. This is 3rd degree AV block. The P waves march out consistently at their own rate, and the QRS complexes march out at their own rate. There is complete dissociation between the P waves and QRS complexes. They have no relationship. This is exactly what you would see if you ablated the AV node. The SA node would continue to to create P waves. The bundle of His would continue to generate junctional (normal looking) QRS complexes. +2  


Seems like I did what most of you did. I read the "symptom" as pain and went for PGE2.

Turns out if I had just read the 2008 paper Undiscovered role of endogenous thromboxane A2 in activation of cardiac sympathetic afferents during ischaemia I would have known that TXA2 MAY be a cause of MI pain. https://www.ncbi.nlm.nih.gov/pubmed?term=18483073

There are also theories that the pain is from adenosine/bradykinin/acid/ROS/5-HT which you can read about here:

https://www.ncbi.nlm.nih.gov/pubmed?term=10099685 https://www.ncbi.nlm.nih.gov/pubmed?term=10222339 https://www.ncbi.nlm.nih.gov/pubmed?term=11458709 https://www.ncbi.nlm.nih.gov/pubmed?term=12411532

I found these via the UpToDate page Angina pectoris: Chest pain caused by coronary artery obstruction which does say the mechanism is "complex and not entirely understood."

makinallkindzofgainz  this is all irrelevant. the dude is having an MI so the answer is Thromboxane A2 +  
drschmoctor  Bruh, you gotta read all the 2008 papers. It was a fire year for obscure shit you need to know in 2020. +  


Patient is current breast-fed, so we can eliminate fructose (fructose is found in honey and fruits and some formula, but not in breast milk). Patient has reducing substances but no glucose in the urine, so he must some non-glucose sugar. My differential for reducing non-glucose sugars in the urine is disorders fructose metabolism or galactose metabolism. We have eliminated fructose, so that leaves us with galactokinase deficiency or classic galactosemia.

sympathetikey  & Galactokinase deficiency would be much milder. +5  
smc213  Big was soybean formula not giving any issues. Soy-milk can be used as a substitute formula in patients with Classic Galactosemia since it contains sucrose (->fructose and glucose). +1  
oslerweberenu  Why can't this be glucose 6 phosphatase deficiency Confused me +  
almondbreeze  @oslerweberenu G6PD - increased RBC susceptibility to oxidant stress (eg, sulfa drugs, antimalarials, infections, fava beans) -> hemolysis; has nothing to do with presence of reducing sugar +  
makinallkindzofgainz  @almondbreeze; Glucose-6-phosphatase deficiency is Von Gierke disease, they are not referring to G6PD deficiency (an entirely seperate disease) +1  


submitted by yotsubato(520),

Pancrealipase is basically "Pancreatic Enzymes" in fancy pants NBME world

makinallkindzofgainz  "Pancreatic enzymes, also known as pancrelipase and pancreatin, are commercial mixtures of amylase, lipase, and protease. They are used to treat malabsorption syndrome due to certain pancreatic problems. These pancreatic problems may be due to cystic fibrosis, surgical removal of the pancreas, long term pancreatitis, or pancreatic cancer, among others. The preparation is taken by mouth." +  


This question in it's essence is asking that after inserting the catheter in the femoral artery, which landmark should we use beyond which superiorly lies the renal artery, and the answer is the origin of the testicular artery. What a weirdly worded question though. :?

makinallkindzofgainz  I don't think it's worded that weirdly. The guide wire should be advanced superiorly just beyond the testicular artery to approach the right renal artery. +  


Pentad of TTP = FAT RN

  • Fever
  • Anemia (MAHA)
  • Thrombocytopenia
  • Renal failure
  • Neurologic symptoms

This is TTP not ITP

makinallkindzofgainz  I seem to have commented on the wrong question, sorry! I wish I was able to delete my comment, but I can't. +1  


submitted by thirdaid(5),

The initial presentation looks like cancer: weight loss and progressive dyspnea over the course of months in a heavy smoker. Then, the question describes extra-pulmonary symptoms and a paraneoplastic syndrome.

More acutely, there is development of edema of the face and jugular venous distention. Because this is localized to upper body, we should think of a mechanical obstruction to venous flow as opposed to some cardiogenic reason. This is an extra-pulmonary symptom of lung cancer.

[ Superior Vena Cava Syndrome caused by the medial spreading of the tumor. Can be exacerbated in the physical exam by asking patient to raise both arms. ]

Finally, there is a single highlighted lab value -> hyponatremia. Small cell lung cancer can release inappropriate levels of antidiuretic hormone -> SIADH. ADH will retain water and decrease sodium concentration possibly leading to cerebral edema and seizures.

[ Syndrome of Inappropriate ADH (due to small cell carcinoma, a neuroendocrine tumor of the lung) decreases sodium concentration. Paraneoplastic syndrome. ]

In SketchyPath: SVC syndrome is the red balloon near the mediastinum ship and SIADH is the guy trying to carry the water cooler and getting water all over himself.

makinallkindzofgainz  I agree! Superior sulcus tumors is a lung carcinoma that occurs in the apex of the lung and can cause SVC syndrome. +  


Ambiguous question but in because it is early shock, there is not enough time to activate the RAAS to increase kidney perfusion.

makinallkindzofgainz  This is not an ambiguous question. It makes perfect sense. +  


submitted by imgdoc(72),

I think alot of people might have over emphasized how important ANP and BNP really are, yes it is important to know these peptides get secreted by the atrial/ventricular myocardium during heart failure. However their overall effectiveness in treating heart failure is zilch, a preceptor told me that if ANP and BNP were so useful in natriuresis then why do we give diuretics? It's because RAAS overpowers this system hence causing negative effects and the endless loop of heart failure. AKA why we give ACE inhibitors.

Knowing that ANP gets neutralized by the RAAS system, we can shift our focus back to heart failure in this patient, where cardiac output is decreased, leading to ADH secretion and finally dilutional hyponatremia.

almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +  
almondbreeze  good work done! +  
raffff  why does the body make anp at all since its so useless +2  
makinallkindzofgainz  @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +  
mdrahimi7  Also read my answer mdrahimi7. I think it seems logical... +  


Please can you kindly share NBME 22 and 23 Questions with me . I only see the answers but I do not have the full question? Thanks in advance

makinallkindzofgainz  I think you may have this website confused with nbmequestions.com +2  


submitted by rogeliogs(6),

This Question its about respiratory burst

Patients with NADPH deficiency=chronic granulomatous disease (CGD)

Even though patients with CGD can't make Superoxide, they can use it from the bacterias and convert it to bleach HCLO and kill the bacterias.

BUT bacterias with catalase enzymes neutralize their own superoxide and thats why the CGD patient can't kill them.

Catalase positive bacterias: S. aureus - Aspergillus

thomasburton  I thought E.coli was catalase positive too? Why can that not be correct? +4  
mb10  (FA 186) Catalase (+) microbes, especially S aureus +4  
makinallkindzofgainz  @thomasburton - because First Aid said so, so suck it +  


Not 100% sure on this one, but here’s how I approached it: histamine causes arterial dilation (=decreased arteriolar resistance), but all of that blood has to go somewhere since you now have more blood flowing through the arteries and that somewhere is the capillaries (increased capillary hydrostatic pressure). Histamine causes increased permeability of the post-capillary venules (one of Dr. Sattar’s favorite facts) so you’d have increased capillary filtration rate.

taediggity  Totally agree, arterial dilation--> increases blood flow into capillaries/increases capillary hydrostatic pressure + increasing permeability of the post-capillary venules= Increased Capillary Filtration Rate +1  
makinallkindzofgainz  I love you explanation, but I don't think filtration rate is dependent upon permeability of the post-capillary venules. I think the filtration rate is increased simply due to the increased blood flow; this is similar to how increased renal blood flow will increase Glomerular Filtration Rate (GFR). +2  


submitted by moloko270(47),

loss of fluid triggers aldosterone production, so patient will have hypernatremia and hypokalemia as a result

makinallkindzofgainz  dat RAAS +1  


submitted by usmleuser007(220),

Mother is Rh-neg --> she will generate RH-antibodies 1) fetus affected by Anti-Rh if it is Rh-positive 2) even if O-Rh-Positive is given, then still mother's Rh-antibodies will attack transfused blood due to its cells containing Rh+ 3) therefore, O-Rh-negative is best

makinallkindzofgainz  you're not wrong, but I think it's better to have put O-negative because that's the preferred type of RBC for transfusion unless you've type and crossed your patient +  


submitted by aesalmon(61),

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. +5  
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 +4  
makinallkindzofgainz  If you are obese, it's because you have consumed calories in excess of your energy expenditure, end of story. (there are factors that affect your energy expenditure, but the simple statement is 100% true, unless you want to argue against the laws of thermodynamics). A is the only correct answer. +1  
tulsigabbard  This answer hit too close to home. +1  


submitted by marbledoc(0),

Why would you ask the patient to identify the pros and cons? I don’t get the approach here!

someduck3  There was a question about this in Uworld. for *stubborn* patients who are "not ready to quit" just yet you use the motivational approach. The technique acronym is OARS: Open ended questions, Affirmation, Reflect, Summarize. +4  
yotsubato  Additionally the guy himself says "I know smoking is bad for me" Like he knows its bad, he doesnt care, but give him nicotine replacement and maybe he'll quit... +1  
usmleuser007  I didn't think nicotine replacement was a good answer choice b/c if he isn't ready to quit then why would he agree to use alternatives. +  
usmleuser007  People who smoke and are addicted like the feel of the cigs and environmental ques. Using replacements would be more challenging. The second best answer choice would have been Rx. +  
titanesxvi  why not detail the long-therm health effects of smoking? +  
seracen  @ titanesxvi: I assume because they always like the most "open ended" response. If you start detailing the long term effects, the patient might interpret that as attempting to convince, and might resist or feel pressured. By having the patient elucidate what they consider pros and cons, you allow it to be an open discussion. +  
suckitnbme  Also because the patient states he already knows smoking hurts him in the long run so it may come off as lecturing on something he already knows. I view this as what is the least-judgmental way to facilitate the patient moving on to the next step of the stages of change model largely of their own volition. +2  
usmlehulk  i choose the option c which is initiate a pulmunary function test. why is that a wrong choice? +2  
makinallkindzofgainz  @usmlehulk - he's asymptomatic, knows it is not good for him in the long run, but is not quite ready to make a change. It is best to talk with him about the pros/cons of cessation so that maybe he will make the decision to quit smoking soon. Ordering a pulmonary function test is not going to be useful. Let's say it's decreased. Ok, so what? It doesn't change management in this patient right now. +1  
rainlad  Think of it as motivational interviewing +  
tulsigabbard  Still don't like the answer given that the patient already stated that he knows that it can do him harm in the long run. It seems like overkill. +1  


submitted by meningitis(269),

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

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

makinallkindzofgainz  I ruled out duodenum because it's towards the right side, and I ruled out body of pancreas because that's basically midline. We are talking about the left lower kidney, which is by the spleen and splenic flexure. Idk if this logic checks out, but I got it right +  


makinallkindzofgainz  upvote for credible source +5  


submitted by welpdedelp(138),

This is Lambert-Eaton, which improves with movement as compared to Myesthenia gracias whichh worsens with movement

sbryant6  Lambert-Eaton is typically associated with Small Cell Lung Cancer. Since there was no mentino of that, I was thrown off. Such is the difference between UWorld and NBME I guess. +  
makinallkindzofgainz  I'm laughing about Myasthenia "gracias" lmao +3  


submitted by someduck3(33),

Fat soluble vitamins are A,D,E,K. So both D & E could be decreased in this pt. But you have to know that Vitamin E deficiency is associated with demyelination & has been associated with posterior column demyelination. Also Vit E can be given with Alzheimer patients as it helps with free radicals..?

aesalmon  I actually thought that the posterior column findings were likely due to B12 deficiency - "subactue combined degeneration", due to malabsorption, as we see in this pt (. Turns out vitamin E can also cause symptoms which look like subacute combined degeneration: https://www.ncbi.nlm.nih.gov/pubmed/9012278, as does Copper (TIL): https://www.ncbi.nlm.nih.gov/pubmed/15249607 +3  
jooceman739  Vitamin E deficiency causes posterior column findings and hemolytic anemia :) +3  
nwinkelmann  The way I think about it is that essentially, vitamin E is an anti-oxidant. Vitamin E deficiency = LOTS of oxidation, i.e. free radicals, which are toxic to most cells in the body (particularly myelination and RBCs). That's why it can be used with Alzheimer's patients. +3  
makinallkindzofgainz  Vitamin E presents like B12 deficiency but without megaloblastic anemia +  


submitted by privwill(11),

Step by step:

  1. pH = low = acidosis
  2. HCO3 = low = acidosis
  3. CO2 = high = acidosis

So, what I've learned is that, in essence, metabolic acidosis always takes priority in these scenarios. It's evident that the person is not compensating, but you want to calculate anyway by using Winter = 1.5 (HCO3) + 8 .
If you calculate you will see that the expected is 30.5.

  1. If CO2 is higher than expected = concomitant respiratory acidosis
  2. If CO2 is lower than expected = concomitant respiratory alkalosis

Here it is higher than expected (65) so concomitant respiratory acidosis.

I guess if you wanted to start with the respiratory acidosis you would've taken into consideration that bicarbonate should've gone up to compensate. It didn't so it's uncompensated. Not sure if there's a formula to calculate the other stuff

makinallkindzofgainz  don't forget to add the +/- 2 to the end of Winter's formula. You have a tiny range in which CO2 can fall within +1  


submitted by armymed88(29),

Glucose is co-transported into enterocytes of SI via sodium

toxoplasmabartonella  That makes that glucose needs to be given with sodium. But, what about bicarb? Isn't the patient losing lots of bicarb from diarrhea? +2  
pg32  Had the same debate. I knew glucose/sodium was the textbook answer for rehydration but also was wondering if we just ignore the bicarb loss in diarrhea...? +2  
makinallkindzofgainz  @pg32 - Sure, they are losing bicarb in the diarrhea, and yes this can effect pH, but it doesn't matter that much. You're not going to replace the bicarb for simple diarrhea in a stable, but hydrated previously healthy 12 year old. You're gonna give him some oral rehydration with a glucose/sodium-containing beverage. Don't overthink the question :) +  
makinallkindzofgainz  *dehydrated +  


submitted by armymed88(29),

Glucose is co-transported into enterocytes of SI via sodium

toxoplasmabartonella  That makes that glucose needs to be given with sodium. But, what about bicarb? Isn't the patient losing lots of bicarb from diarrhea? +2  
pg32  Had the same debate. I knew glucose/sodium was the textbook answer for rehydration but also was wondering if we just ignore the bicarb loss in diarrhea...? +2  
makinallkindzofgainz  @pg32 - Sure, they are losing bicarb in the diarrhea, and yes this can effect pH, but it doesn't matter that much. You're not going to replace the bicarb for simple diarrhea in a stable, but hydrated previously healthy 12 year old. You're gonna give him some oral rehydration with a glucose/sodium-containing beverage. Don't overthink the question :) +  
makinallkindzofgainz  *dehydrated +  


submitted by armymed88(29),

Down syndrome 2nd trimester screen (usually around 16-18wks) shows decreased AFP, estriol and increased hCG and inhibin A.

Of trisomy 13/18/21, Down Syndrome is the only to have an eleveted hCG

makinallkindzofgainz  "Down Syndrome has high HI (hCg and inhibin)" the relationship between the words down/high really stuck for me +  
drzed  An easy way to remember the other aneuploides is that the "lower" ones (e.g. lower than 21 = 13,18) have "lower" values (e.g. LOW hCg and LOW inhibin) +1  


DKA is a state of decreased insulin; since we know that insulin causes a shift of K+ into the cells low levels of insulin will prevent this and result in hyperkalemia. In addition, due to hyperglycemia and high ECF osmolality water will shift out of the cells into the ECF and K+ shifts out with the water which will futher increase the hyperkalemia

dentist  I know Insulin cause shift K+ into cells due to closing of ATP-sensitive K channels (blocking K from leaving)? Does it increase K in the cells by another mechanism? +  
makinallkindzofgainz  @dentist - Insulin stimulates the Na+-K+-ATPase pump, this drives K+ into the cell (Source: Amboss) +  


submitted by fenestrated(18),

For this one I think what you had to know is that Transcription (DNA-->RNA) is performed by RNA polymerase. It was not DNA polymerase because this one replicates (DNA-->DNA)

fenestrated  between increased or decreased binding I picked decreased because it was a mutation which affected the hydrogen bonds which is how nucleotides bind to each other +  
makinallkindzofgainz  this is how I got it right +  


submitted by yotsubato(520),

In biology, phase variation is a method for dealing with rapidly varying environments without requiring random mutation. It involves the variation of protein expression, frequently in an on-off fashion, within different parts of a bacterial population. As such the phenotype can switch at frequencies that are much higher (sometimes >1%) than classical mutation rates. Phase variation contributes to virulence by generating heterogeneity. Although it has been most commonly studied in the context of immune evasion, it is observed in many other areas as well and is employed by various types of bacteria, including Salmonella species.

https://www.wikiwand.com/en/Phase_variation

whoissaad  is it the same thing as antigenic variation? +3  
dorsomedial_nucleus  No, antigenic variation involves genomic rearrangement Phase variation can be thought of as MORE or LESS of something. An on/off switch. No DNA is being rearranged, just under or overexpressed in response to the environment. +1  
makinallkindzofgainz  This isn't in Zanki, Lightyear, or First Aid, and I don't remember ever learning about this in class. Thanks NBME! :D +3  


submitted by usmleuser007(220),

In cases of child or adult abuse

1) if there is clear evidence such as if a child states that parents punish by hitting, child is showing fear of parent ---- call child protection right away ( don't need to wait and ask)

2) same thing goes for the adult but call the adult protection services

osler_weber_rendu  Does anyone not remember Dr Daugherty's lessons which said domestic violence on adults is NOT necessary to report? Instead help them find an escape route in case of an emergency and encourage them to report it themselves. +  
makinallkindzofgainz  @osler_weber_rendu: Domestic violence is not the same thing as dependent adult abuse, such as a special needs adult or an elderly adult (basically anyone who depends on others for care). What you said applies IF the adult is living independently and fully capable to make their own decisions. +1  


submitted by bubbles(45),

Chronic renal insufficiency:

1) poor phosphate clearance --> high serum inorganic phosphorous

2) high serum phosphate --> complexes with divalent cation Ca --> Ca falls

3) Ca falls --> triggers PTH axis

4) kidney failure --> decreased activity of 1-hydroxylase at the kidney --> less calcitriol

makinallkindzofgainz  this guy renals +3  
paperbackwriter  Someone please help me with this (always trips me up): PTH causes increased vit D production in kidney... are we assuming the increased PTH can't catch up with the kidney failure? Is it the level prior to PTH compensation that they want? D: +  
miriamp3  @paperbackwriter what it works for me ;;;; is find the first abnormality so CKD low calcitriol (no D vit) ---> is gonna increase PTH ---> the kidney are not working (chronic, they don't tell u recently- you can;t revert a CKD so the kidney never going to catch up) --> increase inorganic phosphorus.--> always start with the problem. I also use this for celiac and types of shocks. start with the problem, and trust yourself. +1  
paperbackwriter  @miriamp3 thank you! I will try out your strategy next time!! :) +  
snripper  I thought renal insufficiency -> inability to reabsorb phosphate at PCT -> decreased phosphate? +  


submitted by mcl(377),

CDC recommended treatment of schistosoma mansoni is praziquantel.

makinallkindzofgainz  It's also the pretzel in the Sketchy video, which I think most would agree is more reputable than whoever these "CDC" people are +3  


submitted by emmy2k21(17),

Just a mnemonic to keep track of case control w/ odds ratio and cohort w/ relative risk. Think: Case-ContORl intentionally misspelled for odds ratio CohoRRt for relative risk

makinallkindzofgainz  I like Dr. Ryan's way to remember it better: Just look at the 2nd to last letter in each word. Case ContrOl --> Odds Ratio and CohoRt --> Relative risk :) +1  


It said it was fatal to males in utero, and the question asked about live born offspring. Since the males aren’t being born in the first place, I said 50% females and 0% males.

hungrybox  fuck i got baited +19  
jcrll  "live-born offspring" ← baited +8  
sympathetikey  Same :/ +  
arkmoses  smh +  
niboonsh  why is it 50% females tho? +2  
imgdoc  felt like an idiot after i figured out why i got this wrong. +1  
temmy  oh shit! +  
suckitnbme  This isn't exactly right as males can still be born as evidenced by individuals III 6,9,11. This basically an x-linked recessive disease. A carrier mother can still pass her normal X chromosome to a son (50% chance). It's just that the other 50% chance of passing an affected X chromosome results in death of the fetus in utero. Thus all males actually born will not be affected. +2  
makinallkindzofgainz  @suckitnbme, Correct, but if you're a live-born male, you 100% for sure do NOT have the disease, so the chance of a live-born male "being affected" is 0. +1  
spow  @suckitnbme it's not X-linked recessive, otherwise every single son would be affected and therefore have died in utero. It's X-linked dominant +  
qball  Jail-baited +  


submitted by uslme123(20),

very stupid question. The virus was inhaled -- bats hang upside when they sleep and drool. So it spreads to the brain directly from the olfactory system via retrograde transport through nerves.

niboonsh  yea, aeresol transmission via bat poop in caves +  
len49  How do you know the virus was inhaled? Doesn't mention it. Moreover, non-bite/scratch transmission is extremely rare. +  
makinallkindzofgainz  You get rabies by being bitten, not by inhaling it +  
drzed  She was probably bitten by a bat; many times the bite is not recognized ('unapparent bites'), and thus the CDC recommends that even if you think you have been bitten by a bat (or that you COULD have been bitten), you should go and get active/passive immunization immediately. +  


submitted by usmleuser007(220),

If you couldn't remember which were essential; then alternative would have been to realize that growing children need cells to divide. This requires DNA replication and translation. Of which the nucleic acid thyime is important. It requires a methyl transfer.

This is where methionine comes in. Methionine combines with ATP to form SAM (a methyl donor)

whossayin  That’s a legendary explanation. Thanks dude! +  
makinallkindzofgainz  This is exactly how I solved it! I remembered that Methionine is essential for methyl transfers, and you would need that in dividing (growing) cells. But now I'll just remember PVT TIM HaLL too :) +  


i fell for bleeding from lesion at chose psoriasis but psoriasis pts experience itching. Also, the distribution is not characteristic.

makinallkindzofgainz  Yes it is. These areas are all sun-exposed areas, and he is a farmer. Multiple years of sun-exposure can lead to Actinic Keratosis, a precursor of SCC. +  


submitted by usmleuser007(220),

just a hunch.... Omeprazole is always the right answer

nala_ula  Famotidine is an H2 blocker which really only stops acid secretion via the stimulation of H+/K+ ATPase by histamine, but it still has vagus and gastrin stimulation. If you use Omeprazole, you get irreversible inhibition of the pump itself which stops the secretion of acid even if there is histamine, gastrin, vagus stimulation. +6  
temmy  what about the healing of her mucosa. Is that not the action of prostaglandin?. That threw me off cos according to FA, misoprostol increases secretion of the gastric mucosa +4  
cry2mucheveryday  same doubt..marked miso +  
sahusema  I guess because misoprostol is more associated with treatment of NSAID related ulcers and PPIs are 1st line DOC for GERD? +1  
makinallkindzofgainz  @temmy, I think that Omeprazole is a better answer because although Misoprostol would promote healing of her esophageal mucosa, it wouldn't do anything to relieve the symptoms of GERD (due to acidic contents in the esophagus) +  


submitted by burak(21),

Orbital floor fracture:

1- Infraorbital nerve injury: Numbness and paresthesia of the upper cheek, upper lip, upper gingiva.

2- Entrapment of the inferior rectus muscle: Impaired upward gaze

3- Enophtalmosis

4- Clousing of maxillary sinus: Teardrop sign

minion7  if IR muscle is affected it is impaired downward gaze!!! +  
makinallkindzofgainz  @minion7, If the Inferior Rectus muscle is impaired (e.g. nerve dysfunction), then yes, downward gaze would be affected. However, the question states that there is ENTRAPMENT of muscles. Trapping the inferior rectus muscle essentially locks the eye into a downward gaze, therefore impairing upward gaze, as the inferior rectus muscle is essentially trapped in contraction. +1  


submitted by hayayah(603),

Catheter placement:

https://aneskey.com/wp-content/uploads/2016/08/image00804.jpeg

Recall that the lung apex extends above the first rib.

hungrybox  His expression is so blissful. U can tell they're shootin up some full u-opioid agonist codeine type of shit and not some shitty partial u-opioid agonist buprenorphine type of shit or some shit like loperamide that doesn't even act on the CNS +16  
rerdwins  even better, if you recall that the esophagus is RETROperitoneal ( its in like half the answer choices). hence, to get to it you have to go WAAYYYYY deep ( like rick and morty smuggling shit). after that, the lung option makes the most sense. +8  
hello  Also, pulmonary artery is way too far away to be damaged by internal jugular vein catherization. +  
makinallkindzofgainz  @hungrybox my mans just slipped in 3 high yield facts within a joke +  
makinallkindzofgainz  @hayayah, I have an issue with that picture unless I'm missing something. In every other source I have, the internal jugular vein lies LATERAL to the common carotid artery. The picture you provided shows the internal jugular veins medial to the common carotid artery. +1  
cmun777  Look at the other side... I think it must be the manipulation of turning the head to the opposite side that better exposes the jugular for catheterization purposes +  


submitted by hayayah(603),

Catheter placement:

https://aneskey.com/wp-content/uploads/2016/08/image00804.jpeg

Recall that the lung apex extends above the first rib.

hungrybox  His expression is so blissful. U can tell they're shootin up some full u-opioid agonist codeine type of shit and not some shitty partial u-opioid agonist buprenorphine type of shit or some shit like loperamide that doesn't even act on the CNS +16  
rerdwins  even better, if you recall that the esophagus is RETROperitoneal ( its in like half the answer choices). hence, to get to it you have to go WAAYYYYY deep ( like rick and morty smuggling shit). after that, the lung option makes the most sense. +8  
hello  Also, pulmonary artery is way too far away to be damaged by internal jugular vein catherization. +  
makinallkindzofgainz  @hungrybox my mans just slipped in 3 high yield facts within a joke +  
makinallkindzofgainz  @hayayah, I have an issue with that picture unless I'm missing something. In every other source I have, the internal jugular vein lies LATERAL to the common carotid artery. The picture you provided shows the internal jugular veins medial to the common carotid artery. +1  
cmun777  Look at the other side... I think it must be the manipulation of turning the head to the opposite side that better exposes the jugular for catheterization purposes +  


submitted by hayayah(603),

Secondary hyperparathyroidism (usually d/t chronic renal failure).

Lab findings include ↑ PTH (response to low calcium), ↓ serum calcium (renal failure), ↑ serum phosphate (renal failure), and ↑ alkaline phosphatase (PTH activating osteoBlasts).

haliburton  also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia. +1  
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +  
nala_ula  Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +1  
privatejoker  Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious. +1  
fatboyslim  @cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption +  
suckitnbme  @privatejoker ALP is included in the standard lab values +  
makinallkindzofgainz  @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values +  
pg32  Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity). +  
drzed  @pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases. +1