UWorld Step 1 Qbank: Your world of learning. Subscribe now.
Welcome to castlblack's page.
Contributor score: 8

Comments ...

 +0  (nbme21#9)

https://academic.oup.com/qjmed/article/107/11/945/2890493 PCT = vampires!

similar or same disease = Gunther's disease NSFL https://www.google.com/search?q=gunther+disease

 +3  (nbme21#18)
  • Pemphigus vulgaris is vulgar in that the blisters rupture and it's gross. + Nikolsky sign. (Its also more vulgar to use your mouth which is why only vulgaris has oral blisters.) Desmosomes are shot.
  • bullous pemphigus is therefore not vulgar and doesn't pop = - Nikolsky sign. Hemidesmosomes are shot.

  • lets rule everything else out for completeness

  • Collagen type VII (i know wtf) = basement membrane btwn epidermis & dermis. NBME language synonyms = Basal Lamina, Reticular Lamina, Extracellular Matrix. Hemidesmosomes, which are made of integrin, fibronectin/laminin, bind to this collagen so it is close to correct but still wrong.

  • cytokeratin is that intracellular intermediate filament in epithelial cells used in stains to distinguish cancers.

  • Desmoplakin is apparently a part of desmosomes, which makes etymological sense. They are going for paraneoplastic pemphigus here. Sucks for them cuz we never learned that one haha. Gottem.

  • Aside here--FA 2020 just mentions desmosomes are made from desmoglein I and III. Antibodies against desmoglein I and III are seen in pemphigus vulgaris and against I is seen in scalded skin syndrome from Staph aureus via exfoliative toxin AKA exfolitoxin. That is why both diseases are + Nikolsky. Good old nikolsky

  • plakoglobin? nobody cares.

https://en.wikipedia.org/wiki/Nikolsky%27s_sign https://en.wikipedia.org/wiki/Desmoplakin https://en.wikipedia.org/wiki/Exfoliatin https://en.wikipedia.org/wiki/Plakoglobin

 +0  (nbme22#32)

I have read all the comments, but none explain why hyponatremia is wrong. There is definitely Na+ in stool....thats why sugar+salt is rehydration for peds diarrheal sickness. Low Na+ causes low EVV explaining the low BP, high HR, pallor, and dehydration. Is it correct but just not as correct as C?

waterloo  I Dont know what you mean by low EVV. But here's my thought process. This pt lost lots of water, and when someone takes a laxative causing them to have diarrhea that will lead to metabolic acidosis. A buffering mechanism for the decreased bicarb in the blood is for H+ to leave cells and K+ to go into the cells. So he has to have hypokalemia (low K+ in serum). They gave him IV fluids, so his BP should be headed back to normal. I would think his RAAS will chill out. But it takes time to correct the acidosis, you're kidney won't just immediately stop reabs bicarb so you're body will still be buffering against the acidosis (H+ out of cell, K+ in).
waterloo  sorry, I wrote increased bicarb, I meant DECREASED bicarb in the blood. And also should have written "you're kidney won't just immediately START reabs new bicarb" My Bad, wasn't trying to add to confusion.
drdoom  i think by `EVV` author meant `ECV` (extracellular volume). @waterloo, appreciate the explanation but think something is off: loss of HCO3- via diarrhea should result in acidemia, which would oppose the presumption of ‌``H+ leaving cell, K+ going in´´.
waterloo  hey so sorry, I must have been super tired posting this. Can't believe I made so many mistakes. Read over it again, and it sounds like gibberish. Wish there was a way to delete. My bad.
waterloo  I think I tried to explain too hard. Looking at this question again, I think really the only this is when you lose that much volume, you lose bicarb and K+. Nothing really to do with acid-base. My b.
drdoom  no worries!

 +0  (nbme22#11)

Huh. Who else thought this was Gaucher until you had to pick D?

elephantbuddy  I think that the hepatosplenomegaly is definitely a common characteristic but you would see more bone abnormalities in Gaucher. This patient has no bone crises and exhibits developmental delay, HSM, and foam cells which is more characteristic of Niemann-Pick.

 +0  (nbme22#17)

Highest yield drug combo to avoid on NBME, Kaplan, and UWorld.

Subcomments ...

submitted by tinydoc(157),

Type 1 Familial Dyslipidemia (pg. 94 FA 19 )

increased TG ---> pancreatitis Eruptice / pruritis Xanthomas and HSM

Can be caused by Lipoprotien lipase or Apoprotien CII deficiency

they said that LPL is fine so its APO CII

Heparin seperates LPL from Herparin Sulfate Moeity on Vasc Endothelium allowing us to test its function in the lab.

I got it wrong too - Stupid Rote memorization recall Question.

masonkingcobra  I think you need to know that ApoCII activates LPL not necessarily know the disease +7  
yotsubato  Knowing the disease makes it easier to remember the details though +1  
pg32  Mnemonic for these 4 types of dyslipidemias and their causes: 1 = LP meaning LPL is deficient (or anything associated with activating LPL, like C-II) 2 = LD meaning LDLR is deficient (or anything involved in interacting with LDLR, like B-100) 3 = E meaning ApoE is defective and 4 for more (VLDL) ("more" just meaning more letters in the cause (VLDL oversecretion)) +1  
castlblack  One too many chylomicrONs, two much cholesterol, threE apo E gone, 4 put the fork down fatty +1  

submitted by chillqd(19),

The primary mechanism of action of colchicine is tubulin disruption. This leads to subsequent down regulation of multiple inflammatory pathways and modulation of innate immunity.

castlblack  FA mnemonic = Microtubules Get Constructed Very Poorly: Mebendazole (antihelminthic), Griseofulvin (antifungal), Colchicine (antigout), Vincristine/Vinblastine (anticancer), Paclitaxel (anticancer). A = dont confuse colchicine with celecoxib. celecoxib is a 'celective' COX inhibitor B = ziLEUton = leukotriene inhibitor for asthma +1  

submitted by sbryant6(92),

To remember Baclofen is a GABA agaonist and muscle relaxant, I always think of "Greek Baklava". Greek for GABA, and Baklava for Baclofen.

castlblack  Thanks. Baklava is from Armenia though. Go us +  
athenathefirst  No it's actually Arabic/Turkish. That's why it's called Baklawa. +  

submitted by hungrybox(585),

Huntington's disease

  • anticipation: she has a similar disorder as her father but died earlier

Remember "HUNT 4 an animal, put it in a CAGe". Huntingtin gene found on Chromosome 4. CAG is the trinucleotide repeat:

  • Chorea, caudate nucleus
  • Ataxia
  • Gloomy (depression)
sbryant6  Side note: atrophy of the caudate nucleus leads to a widened anterior horn of the lateral ventricle. I've seen it worded both ways in UWorld. +8  
sbryant6  Side note: atrophy of the caudate nucleus leads to a widened anterior horn of the lateral ventricle. I've seen it worded both ways in UWorld. +  
foulari112  How would you differentiate this from Frontotemporal lobe dementia +  
temmy  Foulari 112..the ageof the patient and the anticipation cos her dad had it too. Also in frontotemporal pick, you will see personality changes where they act completely different vs huntington where they are aggressive and depressed. +  
castlblack  CAG = Caudate loses ACh and GABA (from FA) also points you to caudate +  

submitted by drmohandes(52),
  • DIC, unlikely: PT/PTT normal; wouldn't just see gum bleeding
  • hypersplenism: would cause anemia
  • iron deficiency: anemia
  • vitamin C deficiency: wouldn't cause thrombocytopenia
  • von Willebrand disease: mixed platelet/coagulation disorder → would cause deep joint bleeding instead of mucosal membrane bleeding. Inherited (Autosomal Dominant), would see symptoms before. PTT can be normal/high.
beto  Bleeding symptoms in von Willebrand disease tend to occur in mucous membranes. deep joint bleeding is rare +1  
castlblack  New onset bleeding? Immediately rule out vWD! +  
waterloo  Vit C def I thought was super tricky. My knee jerk reaction was oh easy bruising, bleeding from gums that's what it has to be. But yeah, I think low platelet is key here. +  
nafilnaf  Platelet count would be normal in vWD because there's nothing wrong with the platelets themselves. +  

FYI this is nth* question I've seen that wants to see if you know that the CFTR mutation results in a misfolded protein that gets stuck in the rER.

Where n = a very big number

castlblack  I knew that but I thought the chaperone proteins counted as protein regulation :( +  

submitted by yotsubato(646),

Why cant this be laxatives? Both would cause metabolic alkalosis with hypokalemia... ?

sup  Laxatives would cause an anion gap metabolic acidosis due to loss of bicarbonate in the stool. You would see hypokalemia though as seen in this question. +1  
miriamp3  it took me a lot of time choosing between laxatives and diuretics and at the end I choose diuretics. but I didn't realize that the only thing I had to do was check if were a anion gap or not. +  
snripper  Why would laxatives cause anion gap MA? Isn't it similar to diarrhea? +  
castlblack  The above comments are incorrect. Diarrhea is a cause of normal-anion-gap metabolic acidosis (D in HARDASS from FA). Laxatives are wrong because they would lower HCO3- but in this scenario it is high. The low K+ and Cl- fits either case though. +1  

Alkylating agents (merchlorethamine) (the other drugs listed are microtubule inhibitors) increase the risk of AML.

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +23  
seagull  CML has blasts too but they tend to favor mature forms. +4  
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +3  
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +10  
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +  
sweetmed  Procarbazine is alkylating as well. +  
pg32  @keycompany how did you know the phrase "multiple blast forms" meant literally different types of blasts and not just many blast cells were seen? +2  
castlblack  this link says CLL has 'large lymphocytic variety' under the picture of the peripheral smear. I am not arguing against you, just researching here https://emedicine.medscape.com/article/199313-workup +  

submitted by aesalmon(65),

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. +9  
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  
castlblack  I think the reason they point out the average weight of the parents is because leptin disorders are inherited. It helps you eliminate that answer choice. +  

submitted by bobson150(5),

Is the grey supposed to be a suture? If not why would this not be wound healing therefore granulation tissue?

asapdoc  If you look at the picture you can see the epithelioid and giant cells. I only picked granuloma because I remember seeing a similar picture in Uworld. +5  
dentist  granulation tissue is a part of the normal wound healing process, and happens within the first week. +  
castlblack  I agree I looked at that grey blob and thought foreign body --> granuloma +  

submitted by d_holles(105),

This video explains the pediatric neurocutaneous disorders well.


Basically the key here is hypopigmented macules. NF1 has cafe au liate spots (hyperpigmented macules) while TSC has ash leaf spots (hypopigmented macules). This is a decode the buzzword style question. I felt like I didn't really understand these orders until I watched the above video.

pg32  I figured this out for a few reasons. The hypopigmented patches are ashleaf spots and the raised, flesh-colored lesion on the back is a Shagreen patch (only seen in TSC). Multiple brain lesions = hamartomas. Additionally, NF1 has 100% penetrance, though it also has variable expressivity, meaning if it were NF1 we would probably see some family history of similar symptoms. +2  
castlblack  Agree. CAFESPOTS Cafe-au-lait, Axillary Freckles, Eye (Lisch nodules), Sarcoidosis, Pheo, Optic Tumor (glioma), Seizures +  

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) +  
castlblack  Another mechansim = acidosis causes hyperkalemia due to H+/K+ antiporters. H+ is high in blood so shifts into cells via this antiporter, which shifts K+ out. --potassium section of acid/base chapter in Costanzo physiology +  

submitted by pg32(63),

How did anyone get this as T cruzi? That was literally the first answer I ruled out. She has swelling of the eye, but that is the only sx that fits. Chagas presents 10-20 years after initial infection, not two weeks later. It also doesn't present with recurrent fever, muscle aches and joint pain. I mostly ruled it out because of the time course.

castlblack  I made the same mistake. Tsetse flies only exist in africa. African sleeping sickness is named well. Chagas is only in south america/central. Leishmaniasis is found on both continents. +  
medjay7  The clinical presentation confused as hell, but I could recognize that Trypomastigote anywhere and definitely was not African sleeping sickness. +1  

submitted by joha961(35),

Maintenance dose = (Css * CL * t) / F

... where t is elapsed time between doses (not relevant here since it’s continuous infusion) and F is bioavailability (which is 100% or 1.0 here because it’s given IV).

​Contrast with loading dose:

(Css * Vd) / F

... where Vd is volume of distribution.

yotsubato  So do we just have to memorize this... +6  
gh889  yep +9  
drschmoctor  @yotsubato Not necessarily. I can't remember a formula to save my life. The Css is the amount you want in the blood. The clearance is the fraction removed per unit time. Since we want to maintain a steady state, we only need to replace what is removed. Thus, maintenance dose = amount present * fraction removed. +4  
mambaforstep  https://www.youtube.com/watch?v=gnqOUmNhmdg good & short explanation +  
castlblack  I remember CLoCk Time as in check the clock time to give the next dose Cl = clearance, C = concentration and T = half life. I have never had to use F. +1  
baja_blast  This is on p. 233 in FA 2019. +  

submitted by mcl(454),

Beta-2 receptors are coupled to Gs proteins, which activate adenylyl cyclase and increase cAMP. Cyclic AMP then increases activity of protein kinase A, which phosphorylates myosin light chain kinase, ultimately resulting in smooth muscle relaxation. Albuterol, a B2 agonist, is therefore useful in treating bronchospasm.

impostersyndromel1000  are you able to clarify that phosphorylated myosin light chain kinase from cAMP/PKA and dephosphorylated myosin light chain from cGMP both cause smooth muscle relaxation? saw this on another Q with the nitrates causing headache so now im confused +  
dubywow  @impostersyndromel1000: Here is an image that summarizes cAMP and cGMP actions in smooth muscle cell very will. Hope it helps. link +  
iwannabeadoctor2  cGMP is the use of Nitrates for endothelial vasodilation; B2 is a different action, similar end result. See this diagram for the adrenergic receptor actions. https://s3.amazonaws.com/classconnection/769/flashcards/5928769/png/screen_shot_2014-11-04_at_92935_am-1497B7358A4552ACB39.png +  
castlblack  cAMP INHIBITS myosin light chain kinase causing relaxation according to FA 2020 pg. 317 +  

submitted by sunny(-1),

why is this not a cross sectional survey? ... since we are asking at a particular time

drdoom  As Aristotle once quipped, “A ‘single-point in time’ doth not a cross-sectional study make.” The design of a cross-sectional study would not define “ahead of time” two cohorts (two groups); said another way, a cross-sectional design would not “split people into two groups.” In the design of a cross-sectional study there is only “one group”, and then you ask all members of that group some question (“Do you have asthma?”). At the end of a cross-sectional study, the authors will be able to make a statement like this: “We called 10,000 phone numbers with area code 415 at random and asked ‘Do you take Drug X?’ 500 responded ‘I don’t know’, 633 responded ‘Yes’, and 8,867 responded ’No’.” +8  
castlblack  That is interesting. I think the question is phrased ambiguously. I interpreted the question stem to say that they called random people and sorted them into hemorrhagic stroke pts vs controls after the fact using an ORAL questionnaire. Therefore the question would be " Did you have a stroke?" Yes = 702 or no = 1376. And thus would be a cross-sectional study. I see now that the questionnaire must be paper and contacted from some unstated list of drug X recipients. +  

submitted by ergogenic22(180),

Na-(Cl-+HCO3-)=anion gap = 140-(105+10) = 25 mEq/L

normal range for anion gap is 8 to 16 mEq/L...Therefore, positive anion gap.

pH = 7.25, normal range 7.35-7.45... Therefore acidosis

Normal bicarbonate 22-28, questions shows bicarb of 10. Therefore metabolic acidosis

Additionally PCO2 normally 33-45 mm Hg, question shows PCO2 of 23 with normal PO2, therefore respiratory compensation

mambaforstep  why did the stem say she had a drinking problem... is that just a distractor? +  
castlblack  I think alcohol uses up all the NAD+ in its metabolism leading to increased NADH/NAD ratio. After that, TCA cannot progress and the cell is forced to use anaerobic metabolism, which increases lactate. lactate causes anion gap metabolic acidosis (L in MUDPILES from first aid) +1  
nafilnaf  She may also have ingested methanol if she couldn't get her hands on regular ethanol which causes an anion gap metabolic acidosis (M in mudpiles). +  

UWorld Step 1 Qbank: Your world of learning. Subscribe now.