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That other exam …
=> Step 2 CK (CCSSA) Form 6
=> Step 2 CK (CCSSA) Form 7
=> Step 2 CK (CCSSA) Form 8

Recent comments (see more)

... niboonsh made a comment (nbme21)
 +42  submitted by niboonsh(296) if ur lazy like me, this is a good refresher video

d_holles  Amazing video dude. Somehow never learned this in neuro lol. +5
aag  Awesome video! Is this why you can give Mg2+ to eclampsia patients, because if so, mind goddamn blown. +1
... drdoom made a comment (nbme24)
 +42  submitted by drdoom(681)

The duodenal lumen (and pancreatic proteases like CHYMOTRYPSIN) is the site where pancreatic enzymes (“endopeptidases”) cleave large polypeptides into smaller bits (=dipeptides,tripeptides). It is at the BRUSH BORDER where the smallest kinds of peptides (dipeptides,tripeptides) are broken down into their amino acids, which finally can be co-transported with Na+ into the intestinal cell.

I think about it this way:

  • stomach acid denatures and “opens up” proteins (without specific cleavage);
  • pancreatic enzymes then cleave denatured polypeptides into smaller bits;
  • brush border enzymes finally break down tiniest peptides into absorbable amino acids.
regularstudent  Isn't the brush border still part of the intestinal lumen? Don't the amino acids enter into the intestinal cell (the "intestinal mucosa")? +
drdoom  @regularstudent No, the lumen is literally the cavity—the empty space. +
... niboonsh made a comment (nbme24)
 +41  submitted by niboonsh(296)

this question makes me want to eat an e coli cookie and hope i bleed out

... yotsubato made a comment (nbme23)
 +36  submitted by yotsubato(837)

Was it just me, or did "age at onset in years" appear RIGHT above the number of patients, rather than the mean. Which confused me for a good 3 minutes.

fulminant_life  Definitely was the same for me. I was so confused for like 5 mins +13
d_holles  dude i almost didn't get the question bc of this ... i thought the age of onset was the actual age of onset (36) +6
mellowpenguins  Are you serious. NBME strikes again with shitty formatting. +6
yex  OMG!! Now I just realized that. Super confused and also thought onset of age was 36. :-/ +5
monkey  what is 36 supposed to be? +
thomasburton  Think the number of people in that group +4
paulkarr  Yup...was looking at it for a good 3 min before just doing the "fuck's gotta be 99" +3
arcanumm  Age of Onset is the Title of the table, which I didn't figure out until after exam was over. What terrible formatting. +3
... ferrero made a comment (nbme23)
 +36  submitted by ferrero(38)

A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.

seagull  The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +14
mousie  Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +2
sympathetikey  My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +31
cr  the main difference between the 2 cases is that in this case the patient has high BP +1
link981  So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +6
hello  @ferrero what are you talking about? lymphatic drainage is the wrong answer... +1
hello  ok never mind. i got it. hard to understand b/c it was a big block of text. +2
asteroides  I think they may be talking about the myogenic compensatory mechanism: "Increased arterial or venous pressure also induces myogenic constriction of arterioles and precapillary sphincters, which raises arteriolar resistance (thereby minimizing the increase in capillary pressure) and reduces the microvascular surface area available for fluid exchange. For example, because vascular smooth muscle in arterial and arteriolar walls contracts when exposed to elevated intravascular pressures, this myogenic response increases precapillary resistance and protects capillaries from a concomitant rise in their intravascular pressure." +2
... lsmarshall made a comment (nbme24)
 +36  submitted by lsmarshall(369)

Urea Cycle Disorders > Isolated severe hyperammonemia (> 1000; i.e., no other severe metabolic disturbances

Ornithine transcarbamylase deficiency > (most common urea cycle dis.) orotic acidemia/aciduria, hyperammonemia

Organic Acidemias > Hyperammonemia, anion-gap acidosis, ketosis (from hypoglycemia)

Medium-chain acyl-CoA dehydrogenase deficiency > Hyperammonemia, hypoketotic hypoglycemia (seen in β-oxidation disorders, EXCEPT adrenoleukodystrophy)

Liver dysfunction > Hyperammonemia, LFTs messed up, older pt.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +6
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +3
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +2
charcot_bouchard  if it was mitochondrial disorder no one would escape +2
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +2
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +3
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +1
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +8
... hayayah made a comment (nbme21)
 +36  submitted by hayayah(994)

the majority of carbon dioxide molecules are carried as part of the bicarbonate buffer system. In this system, carbon dioxide diffuses into the RBCs. Carbonic anhydrase (CA) within RBCs quickly converts the carbon dioxide into carbonic acid (H2CO3). Carbonic acid is an unstable intermediate molecule that immediately dissociates into bicarbonate ions (HCO3-) and hydrogen (H+) ions.

The newly synthesized bicarbonate ion is transported out of the RBC into the plasma in exchange for a chloride ion (Cl−); this is called the chloride shift. When the blood reaches the lungs, the bicarbonate ion is transported back into the RBC in exchange for the chloride ion. The H+ ion dissociates from the hemoglobin and binds to the bicarbonate ion. This produces the carbonic acid intermediate, which is converted back into carbon dioxide through the enzymatic action of CA. The carbon dioxide produced is expelled through the lungs during exhalation.

hungrybox  Amazing explanation. Thank you!! +1
namira  in case anyone wants to visualize things... +4
ergogenic22  CO2 is carried in the blood is bound to hemoglobin, known as carbaminohemoglobin (HbCO2) (5%), dissolved CO2 (5%), bicarb is 90% +3
pg32  Nice explanation, but can anyone clarify how we know from the question that we are measuring HCO3 rather than dissolved CO2? +1
qball  @pg32 This question is asking about what accounts for the LARGER amount of co2 and the HCO3 buffer is about 85% of this transport and dissolved C02 is about 5-7%. +1
teepot123  fa 19 pg 656 +1
... sajaqua1 made a comment (nbme23)
 +35  submitted by sajaqua1(471)

A and J represent the gracile fasciculus, while B and I represent the cuneate fasciculus. Together they make up the dorsal column-medial lemniscal tract, responsible for pinpoint perception, proprioception, vibration, and pressure. Input is ipsilateral.

C and H make up the lateral corticospinal tract (also called the lateral cerebrospinal fasciculus), responsible for motor command of ipsilateral limbs.

D and G represent the lateral spinothalamic tract. It is responsible for pain and temperature conduction. The input arises in a limb (left lower extremity in this case), enters through the dorsal root (pictured between J and H), decussates and ascends at the anterior commissure (just behind E and F), and finally synapses on the second order neuron in the lateral spinothalamic tract. So the spinothalamic tract is responsible for contralateral pain and temperature sensation. Because our patient has lost sensation on the left, the lesion is in the right.

E and F are the anterior corticospinal tract. It is involved in motor control of proximal muscles, typically of the trunk.

nor16  good job +5
jimdooder  Pretty infuriating that this question has the standard R and L label while the other spinal cord question had it flipped. +3
larry  A and J represent the gracile fasciculus, while B and I represent the cuneate fasciculus. Together they make up the dorsal column-medial lemniscal tract, responsible for pinpoint perception, proprioception, vibration, and pressure. Input is ipsilateral. C and H make up the lateral corticospinal tract (also called the lateral cerebrospinal fasciculus), responsible for motor command of ipsilateral limbs. +1
larry  D and G represent the lateral spinothalamic tract. It is responsible for pain and temperature conduction. The input arises in a limb (left lower extremity in this case), enters through the dorsal root (pictured between J and H), decussates and ascends at the anterior commissure (just behind E and F), and finally synapses on the second order neuron in the lateral spinothalamic tract. So the spinothalamic tract is responsible for contralateral pain and temperature sensation. Because our patient has lost sensation on the left, the lesion is in the right. E and F are the anterior corticospin +1
... seagull made a comment (nbme22)
 +34  submitted by seagull(1167)

Which of the following reasons is why this question is bull?

1) Using the word "cyclic" instead of tricyclic for clarity

2) Knowing all of epidemiology of all drugs

3) having to reason out that anticholinergic effects are probably the worst over alpha1 or H1 effects to no certainty.

4) The crippling depression of studying for days-to-weeks on end to probably do average on the test.

nlkrueger  yo, re-fucking-tweet +15
aesalmon  I agree, I picked H1 because such a common complaint for those on TCAs is Sedation, I figure it might be so commonly seen as to be the "most common" reason for noncompliance. I suppose the "hot as a hare...etc" effects would be more severe/annoying, but I didn't think they were more common. +4
fcambridge  I just like to pretend that there's a reason this question is now in an NBME and no longer being used for the test. Hopefully they realized the idiocy of this question like we all do +1
link981  Since it said cyclic, I thought of using, discontinuing, then using again. These people who write these questions need take some English writing courses so they can write with CLARITY. Cyclic is not the same as Tricyclic. +5
waterloo  Incredibly awful question. one thought I did have when deciding between anticholinergic and antihistaminic - nortriptyline and desipramine are secondary amines that have less anti-cholinergic effects (from Sketchy Pharm) so maybe that's what they were getting at? That someone went out and made a new TCA drug that would have less anticholinergic effects. +
... hayayah made a comment (nbme23)
 +34  submitted by hayayah(994)

Coloboma is an eye abnormality that occurs before birth. They're missing pieces of tissue in structures that form the eye.

  • Colobomas affecting the iris, which result in a "keyhole" appearance of the pupil, generally do not lead to vision loss.

  • Colobomas involving the retina result in vision loss in specific parts of the visual field.

  • Large retinal colobomas or those affecting the optic nerve can cause low vision, which means vision loss that cannot be completely corrected with glasses or contact lenses.

mousie  thanks for this explanation! +
macrohphage95  can any one explain to me why not lens ? +
krewfoo99  @macrophage95 Lens are an interal part of the refractive power of the eye. Without the lens the image would not be formed on the retina, thus leading to visual loss +4
qfever  Do anyone know why not choroid? +1
adong  @qfever, no choroid would also be more detrimental to vision since it supplies blood to the retina +2
irgunner  That random zanki card with colobomas associated with a failure of the choroid fissure to close messed me up +7
mamed  Key here is that it doesn't affect vision- the only thing would be the iris. All others are used in vision. Don't have to know what a coloboma actually is. +1
azibird  The extra section of that Zanki card specifically says that a coloboma "can be seen in the iris, retina, choroid, or optic disc." Don't you dare talk trash about Zanki! +1
Some notes
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Help your fellow humans! (see more)

meryen13 asks (nbme13):
i was so confused by this question. is this because the rest are human antigens, so why would we have antibodies against them? but HPV is antibody toward E6 is foreign...? help answer!
motherhen asks (nbme18):
Are these gottron's papules from dermatomyositis? Pareaneoplastic syndrome from adenocarcinoma, esp ovarian? help answer!
endochondral1 asks (step2ck_form7):
why not myastehnia for this one? They put some LE weakness in the stem as well so that before respiratory depression made me skeptical of it being a pure descending paralysis and I went with MG instead . help answer!
meryen13 asks (nbme21):
pt had high indirect bilirubin with high reticulocyte count---> hemolytic anemia. which one in the options is showing hemolytic anemia? pyruvate kinase def. help answer!
yotsubato asks (step2ck_form7):
The indications for blood transfusion for pelvic fracture patients are systolic blood pressure of <90 mmHg, heart frequency >130 bpm and clinical symptoms of shock. In an emergency, combined transfusion of red blood cells, plasma and platelets (6-4-1) is preferred (19). So...... This question is bullshit? help answer!
yotsubato asks (step2ck_form7):
Lactose Intolerant I guess? Not Celiac. Kind of a bullshit question. help answer!
nnasser33 asks (nbme15):
My understanding is that H. pylori actually decreases the risk for esophageal disorders (ex. adenocarcinoma) How would a chronic H. pylori infection lead to healing ulcer/ stricture formation or adenocarcinoma? help answer!
b1ackcoffee asks (nbme23):
I don't know this is weird grammar or I overthought! They asked 'whose expression is regulated by which of the following hormones?" I knew defect is in GPCR - adrenergic receptors, whose transcription is regulated by corticosteriods. So chose hydrocortisone. What was the defect in thought process? help answer!
b1ackcoffee  Oh, I get it now. defect in signal transduction by GPCR, not in GPCR itslef +1
lovebug asks (nbme21):
really curious about why not (C) Suggest that the couple to a therapist together.? T.T help answer!
drdoom  thou shall not punt nor refer thy patient to another +1
lovebug  Oh, thank you! +
drdoom  yeah, think about it this way: the Step exams are here to certify “this person can practice medicine in your state without supervision.” even the most worshipped and glorified neurosurgeons have to pass the Steps. that’s because, at the end of the day, all responsibility (and liability) falls on the physician of record. “the buck stops here,” as they say. so, the Step needs to assess that you can make a decision when no one else is around. it couldn’t do that if it allowed you to choose “refer this problem to someone else.” +1
csalib2  @drdoom fantastic point. never thought of it that way. +
lovebug  @drdoom THX! very sweet explanation! +
anechakfspb asks (nbme23):
Why couldn't it be inhibition of gastric muscarinic (M1) receptors? Wouldn't that be the most effective overall? help answer!
shutch94 asks (nbme22):
I get that bleeding time is a measurement of platelet function. Is clotting time a measurement of the coagulation cascade (PTT/PT)? help answer!
drdoom  yes, that's correct. +
rohan225 asks (free120):
Why is the answer carrier status unknown? Why can't the mother be homozygous? Duchennes is X linked recessive. help answer!
dkhan123  not sure but here is my logic: -Male sibling of patient has died from Duchenne, confirming mother MUST BE either affected or a carrier. -Mother does NOT have the Duchenne phenotype, but has elevated enzymes, suggesting she is a carrier. The Duchenne average life expectancy is 26. Also the question is written such that it implies the mother does not have the Duchenne phenotype and the elevated enzyme level is due to the carrier status of Duchenne and not an unrelated illness. -Lastly, the daughter has normal enzyme levels. This could be due to two possible scenarios, either she inherited the Duchenne gene and has inactivated it, or she never inherited the gene to begin with. +1
ilikedmyfirstusername asks (free120):
Why not superoxide dismutase? Its the step right in between NADPH (chronic granulomatous disease) and MPO help answer!
ilikedmyfirstusername  I guess that could potentially manifest as an even worse phenotype in SCID? +
masn8cc asks (nbme18):
Can someone explain how they r/o aortic stenosis? because that could enlarge the LA and give the same sx of hoarseness etc. And the murmur also fits with AS help answer!
nbmeanswersownersucks  "brisk carotid upstroke" is the description of a normal carotid pulse. Aortic stenosis has a slowly rising/late peaking upstroke since the stenosis impedes flow out of the LV. +1
chadgas asks (nbme18):
Did anyone have any difficulty deciding between C and E? I knew it was a Vitamin D deficiency, but doesn't calcitriol feedback to decrease PTH production? help answer!
nbmeanswersownersucks  I think it is because the question stem asks about the deficiency that "DIRECTLY" affects a process. Vitamin D directly affects calcium reabsorption whereas it is the rise in Calcium (caused by Vitamin D) that then negatively regulates PTH production (so Vitamin D indirectly regulates PTH). The "directly" wording has gotten the best of me more than a few times so now I've become hyper-aware of that wording. +1
boostcap23 asks (nbme24):
This mentioned anywhere in FA or other board prep resources or just supposed to be common knowledge lol? help answer!
md_caffeiner asks (nbme18):
yo sketchy veterans. do you remember that loping back and forth lop eared rabbit that was increasing the phasic segmentation and therefore icreasing stool transit time? This is it now. help answer!
peteandplop asks (nbme20):
Can anyone explain why it's not anxiolytic? My logic was this dude has a bum ticker from previous MI, and his HR was 104/min--which can't be good for the old heart. I went w/a anxiolytic to bring his HR and anxiety under control. Would an antidepressant do the same, thus, is it a better answer, or cover a wider range of symptoms? help answer!
jessikasanz asks (nbme22):
What does Zidovudine act on? It is a rev transcriptase inhibitor. Resistance often occurs at site of drug activity. help answer!
baja_blast asks (nbme15):
Anyone know why this was Hydronephrosis and not Staghorn Calculus?? help answer!
hchairston  There are no calculi in the image. The image shows a dilated ureter, you know it's a ureter because there is an opening into the hilum of the kidney. +1
anechakfspb asks (nbme22):
Why couldn't it be retroperitoneal idiopathic fibrosis? help answer!
notyasupreme asks (nbme16):
Just wondering if someone could explain the difference between collagen and elastin for this one? I thought either or could be used for tensile strength. Anyone have clarification, don't know why collagen is the best answer! help answer!
notyasupreme  Lol, never mind I realize, it's a scar and that's type III collagen! +1
azibird asks (free120):
How can we differentiate RSV from the common cold? Is it the bilateral, diffuse wheezes and expiratory rhonchi? Along with the intercostal retractions, signifying significant respiratory problems? help answer!
nbmeanswersownersucks  I was initially thinking it was rhinovirus too but in retrospect I think the wheezes etc make RSV more likely +
icedcoffeeislyfe asks (free120):
Is the decrease in baroreceptor output due to the body adapting to the hypertension? help answer!
azibird  Apparently. "Baroreceptor activity is reset during sustained increases in blood pressure so that in patients with essential hypertension, baroreceptor responsiveness is maintained." "It is a universally accepted phenomenon that vascular baroreceptors reset to operate at higher pressure levels in hypertension." Okay, so they can reset to normal levels, but wouldn't this patient already have undergone their reset? Why would the receptors further decrease? I thought that eventually their LV would hypertrophy and fail, leading to decreased stroke work. +1
azibird  From Costanzo Physiology: "The sensitivity of the baroreceptors can be altered by disease. For example, in chronic hypertension (elevated blood pressure), the baroreceptors do not “see” the elevated blood pressure as abnormal. In such cases, the hypertension will be maintained, rather than corrected, by the baroreceptor reflex. The mechanism of this defect is either decreased sensitivity of the baroreceptors to increases in arterial pressure or an increase in the blood pressure set point of the brain stem centers." +6

Tag directory (see more)
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