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submitted by cassdawg(1101),

Oral rehydration therapy commonly consists of sugar/electrolyte water because of the ability to utilize the sodium glucose symporter. Where sodium goes, water follows, so by hydrating with this mixture it allows for an osmotic "pull" of water into the intestines.

Here is an article with more detail and a pretty diagram: https://basicmedicalkey.com/therapy-of-viral-gastroenteritis/

ftr_dr_bowowers  thank you!!! and thanks for not having the answer scrambled smh +3  
i_hate_it_here  It's not even the contributor that scrambles it, it's the nbme answers owner whose trying to make a profit of the free contributions of med students! +  


submitted by anjum(17),

7-dehydrocholesterol is a form of pre-vitamin D3 synthesized in the skin from UBV. It is converted to Cholecalciferol, which is the inactive form of Vitamin D3 that is actually in first aid.

kevin  Cholecalciferol is synthesized from 7-dehydrocholesterol by UV, but yes, correct +  
i_hate_it_here  Didn't know the products of it were considered hormones my bad i guess +  


submitted by aliyah(26),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

fI a ergm clel or ositmac ecll dha teh nirloiag mt,atnoui neht e'tesrh na icsdrnaee krsi ofr enracc ni rohet tarsp fo eth obyd tf.Io o lnoy nraleit lclse ni noe eye si utdet,ma oynl atth eno eey is at rksi rfo ercanc.

i_hate_it_here  Gotta love that I can't even review the free contribution you put up. Thanks nbme answers guy +1  


submitted by corndog(8),

ME: I think I finally have these stupid storage disorders down

NBME: Not so fast, partner

my_second_membership  ^ voted “best username” in high school +2  
i_hate_it_here  Same bro +  


submitted by cassdawg(1101),

HbS homozygosity indicates Sickle Cell disease. Streptococcus pneumoniae is associated with sepsis in patients with Sickle Cell (due to autosplenectomy causing increased risk of infections with encapsulated organisms) [FA2020 p136 and 422]

Streptococcus pneumoniae is susceptible to penicillin and prophylactic penicillin can decrease risk of infection.

Sickle cell patients would also be at increased risk of infection with E.coli, H. influenzae and neisseria (as they are encapsulated, p127) but they run less of a risk than Strep pneumo than causing sepsis in sickle cell patients. Salmonella is the most common cause of osteomyelitis in sickle cell patients but again is not what we would primarily be concerned with in this baby.

https://pediatrics.aappublications.org/content/141/3/e20172182

selectuw  I believe Staph is the most common cause of Osteomyelitis in Sickle cell but Salmonella commonly causes it in them more than the general population. +  
fruitkebabs  @selectuw You have it backwards, S aureus is most common overall, while Sickle Cell patients are more likely to have Salmonella Osteomyelitis (and S aureus as well). As a separate note, I thought the answer was Salmonella because Sickle Cell patients are functionally Asplenic beginning age 2-4 (Amboss) since it takes time for all the vessels in the spleen to get occluded and undergo necrosis, esp while HbF is still around in the first 6 months. Maybe that's why this question was taken out of active rotation? +3  
i_hate_it_here  This question was annoying. Sickle cell patients are at risk for all encapsulated organisms, and penicillin is not the main-stay treatment for any of these bugs. Only got this question right because S. pneumo was the only gram positive +2  
topgunber  think that was the purpose of the q honestly, they wanted you to pick salmonella for osteomyelitis, but logically penicillin's moa is targeting the only gram positive in the list. +2  
shieldmaiden  We also have to consider the patient's age; 6 weeks old. At this age, the encapsulated bacteria that can most commonly cause pneumonia is strep pneumo, and with HbS, it can lead to an invasive infection. Prophylaxis for newborns IS penicillin. The publication shared by cassdawg has that information and I also found it in UpToDate. +  


submitted by cassdawg(1101),

This question can be answered by a process of elimination approach in my opinion: (FA2020 p638)

  • Because he has testes that formed, he has to have the SRY gene and thus the Y chromosome which eliminates 46,XX and 47,XXX.
  • This is not a normal-looking biopsy and the question asks about a chromosomal abnormality so you can eliminate 46,XY.
  • Mosaic karyotype 45,X/46,XY is associated with Turner's syndrome. These individuals present with female external genetalia and testes undescended or rarely descended into the labia majora. They would not have scrotal testes, and thus this eliminates this answer.

This leaves only 47,XXY which is Kleinfelter's syndrome and is associated with testicular atrophy and extensive fibrosis and hyalinization leading to infertility.

i_hate_it_here  Kleinfelter's = fibrosed testis = decreased leydig and sertoli cells Turner's = fibrosed ovaries = decreased theca and granulosa cells +3  


submitted by cassdawg(1101),

Neural crest cells migrate to form the aorticopulmonary septum and abnormalities associated with neural crest migration in the heart include tetrology of fallot, transposition of the great arteries, and persistent truncus arteriosus. Fusion of the aorticopulmonary septum with the muscular ventricular septum is what forms the membranous septum, so patients with a persistent truncus arteriosus will have VSD as well. (FA2020 p280)

i_hate_it_here  Neural Crest derivatives: Melanocytes Odontoblasts Tracheal cartilage Enterochromaffin cells Leptomeningies (pia & arachnoid) PNS Adrenal medulla Schwaun cells S aorticopulmonary Septum Endocardial cushions (defects resulting in asd & vsd) Skull bones FA2020 pg 613 +  
i_hate_it_here  MOTEL PASSES +1  
cheesetouch  fa18 p 298 Persistent truncus arteriosus +  


submitted by cassdawg(1101),

Neural crest cells migrate to form the aorticopulmonary septum and abnormalities associated with neural crest migration in the heart include tetrology of fallot, transposition of the great arteries, and persistent truncus arteriosus. Fusion of the aorticopulmonary septum with the muscular ventricular septum is what forms the membranous septum, so patients with a persistent truncus arteriosus will have VSD as well. (FA2020 p280)

i_hate_it_here  Neural Crest derivatives: Melanocytes Odontoblasts Tracheal cartilage Enterochromaffin cells Leptomeningies (pia & arachnoid) PNS Adrenal medulla Schwaun cells S aorticopulmonary Septum Endocardial cushions (defects resulting in asd & vsd) Skull bones FA2020 pg 613 +  
i_hate_it_here  MOTEL PASSES +1  
cheesetouch  fa18 p 298 Persistent truncus arteriosus +  


submitted by cassdawg(1101),

I think this is Strongyloides stercoralis (threadworm) is a roundworm whose larvae live in soil and who can cause pulmonary disease. It has the ability to penetrate skin from the soil but can also be obtained by ingesting feces contaminates soil (FA2020 p159) https://www.cdc.gov/parasites/strongyloides/gen_info/faqs.html

Most intestinal roundworms are fecal-oral route except strongyloides which can also penetrate skin, hookworm (necator americanus) which only penetrates skin, and trichinella which can come from undercooked meats (especially pork) but whose symptoms do not match that of the patient. Trichinella larvae enter the blood stream and infect muscle and can also cause trichinosis with fever, nausea, vomiting, periorbital edema, and myalgia.

shervinbd  I think it is Ascaris, not Stringlyloides. The symptoms could be explained by Loeffler syndrome, caused by Ascaris larva migration. Ascaris is transmitted through fecal oral route, so ingestion of feces contaminated soil could cause the problem. Per FA, Strongylides is transmitted by larva penetrating skin. +15  
drmifta  Its Ascaris. Fecal oral transmission -> Larvae penitrate GIT -> Blood Stream -> Lung {Maturation, Respiratory Symptom} -> Coughed up and swallowing -> Adult Warm in GIT -> Egg release -> Egg in stool. +1  
i_hate_it_here  Didn't the stem mention that roundwarm larvae were found? I thought Ascaris is diagnosed by bile coated eggs in feces? +1  
sexymexican888  I actually think @cassdawg is right. Its strongyloides. They found larvae in the feces (you find eggs in feces with ascaris) you can get pulmonary sx in both. Ascaris is also usually fecal oral transmission so its more likely to come from someone making food with contaminated hands. Strongyloides is transmitted through soil or sand and the larvae penetrate your feet so this makes more sense. +  
sexymexican888  You can find this is FA 2020 Pg 159. Also if you look at the table strongyloides is assoc. with pulmonary sx. However I think its both cause according to sketchy micro ascaris presents with respiratory sx +  


submitted by aoa05(23),

First, the boy had ophathalmoplegia (eye muscle problem) and hypotonia (muscle weakness), indicating that he had muscle related problems. Second, all the problems appeared to come from his mother’s side and the symptoms from different individuals of the family appeared to be very heterogeneous and diverse. All these strongly suggest heteroplasmy, a mitochondrial genetic disease, which is known to show varying degrees of expressivity owing to heterogeneity in genetic mutations in mitochondria. All the mitochondria of one person are inherited from mother’s side (from fertilized eggs) and are different from nuclear chromosome inheritance mechanism. Heteroplasmy is caused by the fact that in each human cells, there are several hundreds mitochondria. In different mitochondria, they may contain different genetic mutations. During genetic transmission, different mitochondria may end up in different eggs / fertilized eggs, leading to mitochondrial genetic disease in the offspring with varying degrees of expressivity owing to heteroplasmy

How to exclude other possibilities: In the narrative, there are genetic diseases two generations in a row in the family. Thus, it is not recessive disease. It came from his mother’s side but affected both sexes. It does not look like a penetrance issue, Additional information - MERRF syndrome (or myoclonic epilepsy with ragged red fibers) is a mitochondrial disease MERRF syndrome affects different parts of the body, particularly the muscles and nervous system. The signs and symptoms of this disorder appear at an early age, generally childhood or adolescence. The primary features displayed on a person with MERRF include myoclonus, seizures, cerebellar ataxia, myopathy, and ragged red fibers (RRF) on muscle biopsy, leading to the disease's name. Secondary features include dementia, optic atrophy, bilateral deafness, peripheral neuropathy, spasticity, or multiple lipomata. Mitochondrial disorders, including MERRFS, may present at any age

nbmeanswersownersucks  I agree with everything you said though I don't think the disease in the question is MERRF. unless I misunderstood you and you weren't saying it was MERRF but were just describing an example of a mito disease? +6  
nbmeanswersownersucks  I think it is more in line with MELAS d/t the lactic acidosis and stroke +4  
i_hate_it_here  Username checks out +  
cheesetouch  FA18 p 57 Heteroplasmy and p59 MELAS syndrome +  


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!

notyasupreme  Lol, never mind I realize, it's a scar and that's type III collagen! +4  
meryen13  type III is whats usually present but then it gets replaced by collagen I in the scar tissue to add more strength. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352699/ +1  
i_hate_it_here  It is also the disulfide bonds that add to tensile strength of collagen, while the inter-chain fibril cross-linking that leads to elastins elasticity FA2020 pg: 51&52 +  
xw1984  I think the Q emphasized postoperatiive. Maybe the production of elastin does not increase much comparing to collagen. +  
topgunber  i think they would refer to elastin in cases of arteriolar compliance +  


nutmeg_liver  Is penile urethra damage not a risk factor when doing the TURP procedure? I guess this difference in likelihood should just be memorized... +5  
nutmeg_liver  Sorry, looks like the TURP procedure is more for BPH, not necessarily an adenocarcinoma! +2  
i_hate_it_here  I guess that makes sense cuz the prostatic plexus is more peripherally located which is the case for prostatic adenocarcinoma, while BPH is centrally locating impeding on the penile urethra. +3  


submitted by cassdawg(1101),

This is eclamsia because of the hypertension in pregnancy with symptoms of end-organ damage and failure combined with siezures (FA2020 p643).

None of the other answers are consistent with the presentation. Epilepsy alone does not cause the symptoms of end organ damage (elevated liver enzymes, lactate dehydrogenase, and inability to urinate), renal disease alone likewise would not cause the combination of symptoms. Sepsis and septic shock causes hypotension not hypertension as seen in this patient. There is no specific drug toxidrome that matches the combination of symptoms.

the_enigma28  Its HELLP syndrome. Hemolysis, Elevated Liver enzymes, Low Platelets. Eclampsia was the closest answer. +6  
i_hate_it_here  HEELLP syndrome is a condition that presents with preclampsia and eclampsia is just preclampsia with seizures +  
cheesetouch  FA18 625 HELLP +  


submitted by bingcentipede(243),

The stem is describing bullous pemphigoid, which produces IgG antibodies hemidesmosomes. (PV is IgG antibodies aginst desmoglein-1 and desmoglein-3, in the oral mucosa).

BP produces the tense blisters that have a negative Nikolsky sign (don't rupture with rubbing). This is because they're supepidermal. Surprised they didn't ask about hemidesmosomes, but I think that that the BP antigen is part of the hemidesmosomes and recruits the autoantibodies.

i_hate_it_here  New stem was describing Bullous pemphigoid, just never heard of BP antigen lol +1  


submitted by hungrybox(1026),

ACUTE alcohol inhibits CYP → Increased bioavailability of acetominophen

CHRONIC alcohol induces CYP → Induction of cytochrome P450 enzymes that activate acetaminophen to a hepatotoxic metabolite


I got this wrong because I assumed chronic alcohol meant years and years. I guess a weekend will suffice?

Honestly, fuck this problem.

lfcdave182  Yeah fuck this question. 2-3 days of something would never be considered chronic in anything else. +4  
pontiacfever  Drink a lot for a week makes you a chronic alcoholic? +  
pontiacfever  That means alcohol abuse = chronic alcoholism +1  
skilledboyb  Why would increased bioavailability of acetaminophen place the patient at increased risk of liver injury? What's dangerous about that? +  
i_hate_it_here  Metabolism of acetaminophen turns it into toxic metabolites (NAPQI) that inhibit glutathione in the liver forming toxic tissue products. FA2020 pg: 485 +1  


submitted by bingcentipede(243),

It's a little bit of anatomy, a little bit of knowing what the question wants us to know.

Here's a nice pic of the ureter under the ovary: https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary-alt:20180930192054-59433-mediumThumb-66713fig4_6.jpg?pub-status=live

Specifically, you want to protect the ureter during surgery. "Bridge over water" kind of applies here, knowing that uterine artery is also being ligated during ovary removal. It's so important for surgeons to be able to differentiate the arteries (which are ok to be sacrificed if you're doing a hysterectomy/oophorectomy) but the ureter must be kept intact.

i_hate_it_here  Isn't the round ligament of the uterus inferior to the ovary? Why would that not want to be preserved as well? +1  
flvent2120  It is inferior, but I think it comes down to what the question is trying to ask. To me I was stuck on that fact as well, but it came down to "what has a significant function and therefore needs to be protected?". The round ligament doesn't have any arteries and whatnot, whereas damaging the ureter has significant consequences. With that, the question seemed to be hinting at "ureter" +  


submitted by cassdawg(1101),

I definitely did not know this, but apparently smoking can worsen GERD due to tendency of nicotine to cause relaxation of the lower esophageal sphincter. Smoking is also linked to stomach ulcers due to interference with gastric mucosa and acid production. Just don't smoke kids. Don't do drugs. Stay in school forever like med students.

i_hate_it_here  don't tell me what to do +  
trazobone  Don’t you just love it here +  


submitted by cassdawg(1101),

The burnt almond smell and noncyanotic dyspnea is characteristic of cyanid poisoning. Cyanide poisoning is treated with nitrites because nitrites oxidize hemoglobin to form methamoglobin which binds cyanide, allowing less toxicity. Thiosulfate is often added to increase renal excretion as thiocyanate. Cyanide toxicity may also be treated with hydroxycobalmin, which binds cyanide.

FA2020 p667 has differentiation of cyanide from CO poisoning.

drippinranch  is there a circumstance where you would treat cyanide poisoning first with hyperbaric oxygen before hydroxy/nitrates/thiosulfate? +1  
prosopagnosia  If the patient had concomitant carbon monoxide poisoning, then I think the hyperbaric oxygen would help. But in order to reverse cyanide poisoning, hyperbaric oxygen will not help because the cells are unable to use oxygen since the cyanide directly inhibits oxidative phosphorylation. +1  
i_hate_it_here  Another thing to know about this is that unlike with CO poisoning, your O2 saturation of hemoglobin, total O2 content, and oxygen-hemoglobin dissociation curve would all be normal. FA2020 pg: 666 +1  
trazobone  Thank you i love it here +  
cheesetouch  FA18 p 648 +  


submitted by cassdawg(1101),

A furuncle is a boil, typically caused by staphylococcal infection. Thus, it can be deduced that the food poisoning is due to staphylococcus aureus, which forms a heat stabile enterotoxin not destroyed by cooking. Ingestion of the preformed enterotoxin causes vomiting.

i_hate_it_here  Oh, i guess I thought the preformed toxin would lead to hella diarrhea and then shock... silly me +  
cheesetouch  I think the right answer might be more related to letting a meatloaf with raw hamburger sit for 12 hours at room temp. E coli the hamburger toxin! (although that's associated with uncooked meat and 350 for an hr should be plenty of time to cook it unless it's real thicc) +  


submitted by cassdawg(1101),

Here is my take: a ventricular septal defect in infancy allows for left to right shunting of blood in the ventricles. This causes an increased pressure in the right ventricle (due to more blood being pushed into it) and a decreased pressure in the left ventricle. Because there is more blood in the pulmonary circulation from the shunt, I think the left atrial pressure would also be increased in an early VSD.

SO when you repair the VSD, the left ventricle pressure will be increased compared to when the shunt was present (it is no longer losing blood), the right ventricle pressure will be decreased (it is no longer getting blood from the shunt), and the left atrial pressure will be decreased (there is no longer overload of the pulmonary system returning to the left atrium).

FA2020 p298

epiglotitties  ily cassdawg +5  
i_hate_it_here  epiglotitties 😂 +  


submitted by lola915(35),

I compared the two progenies that had .8 +AC/-AC (NY-SF/2 &3) which is equivalent to being sensitive to ammonium chloride as described in the stem. The ratio stayed the same with HA and NA being SF while the rest changed to NY in either 2 or 3. The ratio changed significantly when HA was switched to NY in NY-SF/6(.008) while NA stayed at SF.

This question took me way too long to solve -- too much mental gymnastics, classic NBME.

i_hate_it_here  <-- +2  


submitted by hungrybox(1026),

Excess pattern repeats lead to strand slippage/errors due to an unstable region (in this case, excess Cytidine bases).

It could be a repeated pattern as well (ie the trinucleotide repeat CAG in Huntington's).


here's a more in depth explanation (from wikipedia article on Slipped-strand mispairing):

A slippage event normally occurs when a sequence of repetitive nucleotides (tandem repeats) are found at the site of replication. Tandem repeats are unstable regions of the genome where frequent insertions and deletions of nucleotides can take place, resulting in genome rearrangements.

hungrybox  Anyone know why it's not Transposon insertion? I was thinking maybe because transposons have to be longer than one nucleotide, but I'm not sure. +3  
bingcentipede  @hungrybox I think it's because transposons are usually gene segments rather than a single nucleotide insertion - plus w/ what you said about the repeated pattern, I think slipped-strand mispairing (which is a concept the NBME loves) more likely. +22  
i_hate_it_here  cool so why do I need to know this +2  


submitted by cassdawg(1101),

From what I can tell, the gist of this question is that he has SCID and since the SCID child has basically no immune system (particularly because the lack of T-cell immunity) there is a higher chance of transfusion-associated graft versus host disease (TA-GVHD) so blood products have to be irradiated.

Here is a medscape reference with who requires irradiated RBCs due to increased risk of TA-GVHD for your perusing.

i_hate_it_here  Just curious, are you a student? Your answers are always much appreciated. +2  


How do you know for sure that this is incomplete penetrance and not gonadal mosaicism? Dont both allow an AD disease to be transmitted by a phenotypically non-expressing carrier?

nissimhazkour1  my line of thinking is that gonadal mosaicism is much less likely considering there is a family history of the disease. If there was no family history then a gonadal mutation causing mosaicism is possible, but taking into consideration how there is a clear AD inheritance, it must be that the person inherited the disorder but is not expressing the phenotype. hope this helps! +2  
mittelschmerz  Yes thanks! That feels like it should have been so obvious in retrospect, ugh. +  
i_hate_it_here  Don't sweat it fam, I hate it here too +1  


submitted by cassdawg(1101),

She has left homomynous hemianopia, which can be due to lesion of the contralateral optic tract or as in this case lesion to the contralateral occipital lobe. It is not mentioned explicitly but this causes macular sparing. (FA2020 p542 gives the visual field defects)

bbr  tricky tricky +1  
pontiacfever  Left homonymous hemianopia w/o macular sparing can also occur due to damage to parietal and temporal lobes. But occipital lobe damage is more common. +  
i_hate_it_here  <-- +  
pakimd  macular sparing will only occur if there is an infarct of the posterior coronary artery supplying the occipital lobe. this is because the macular region of the visual cortex has a double blood supply from the middle cerebral artery and the posterior cerebral artery. this woman has breast cancer hence the mets are probably directly to the occipital lobe causing left homonymous hemianopia WITHOUT macular sparing. FA pg 542 look at the illustration: it says number 3 (left homonymous hemianopia WITHOUT macular sparing) and 6 (if PCA infarct when there is left homonymous hemianopia WITH macular sparing) +1  


submitted by andro(188),

First question : They tell us its a lymphocytic leukemia

Second question : Deciphering whether it is a B cell or T cell.

The cells have no surface bound Ig M ,Ig G or cytoplasmic chains for these antibodies , but have a rearranged gene segment( meaning active ) for the T cell Receptor . So the Cells are T Cells

Third question : Now that we know that they are T Cells , we want to know whether they are CD4 or CD 8 positive

The cells in the clinical vignette lack both CD4 and CD 8 ( double negative ) According to how T cells normally develop - They start of as being double negative ( i.e not expressing CD4 or CD 8) in the subcapsular region and progressively become
- positive for both CD 4 and CD 8 in the cortex
- and eventually acquire the TCR and CD3 by the time they get to the medulla

These cells therefore must T lymphocyte thymocytes localised to the cortex

i_hate_it_here  FA2020 pg: 102 +1  


submitted by cassdawg(1101),

I don't like this question for many reasons, but basically he has sarcoidosis (noncaseating granulomas with no pathogen found on biopsy) which according to First Aid is more common in African-American females. Since he is African-American that is his risk factor (FA2020 p676).

cheesetouch  FA2018 p658 +  
i_hate_it_here  Questions like this let me know that the ideals of racism have never left the medical system. Ok, so he's "African-American", is he of actual African descent? Is sarcoidosis just increased in american found black people, or is it black people of African descent, what about Jamaican? Afro-Latino, Europeans?? I hate that they teach us things like this and we're suppose to take it at face value. +1  
kaf  agree...medicine is full of racism, sexism and so on. Some meds work differently and diseases present differently etc...for ex., ACE inhibs in AA vs white...or MI presentation in women vs men. +  


submitted by ergogenic22(320),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

AIQNP si a ixotc tineeamitdre is erodmf yb in mlals oanstmu by taomlbmise of maphtaonecn.ie ieDeltopn fo atcehpi ilthentguao retsso by NQAIP aedls to etuac AAPP iottyxci dan ctuea rleiv jru.yni

cassdawg  Also relevant to the question: the CYP450 pathway is what turns acetaminophen into NAPQI, and chronic alcohol abuse is one of the inducers for the CYP pathway so it increases NAPQI production. Chronic alcohol abuse itself also depletes glutathione, increasing propensity for toxicity when acetaminophen is introduced. +  
specialist_jello  my probably stupid thought process was : treatment of acetaminophen toxicity is N acetyl cystine which regenerates gluathione. so toxicity will be coz of dec glutathione. +10  
i_hate_it_here  Real talk, can this site even charge for the contributions made by other people?? +1  
cheesetouch  FA18 470 & 243 +1  


submitted by ergogenic22(320),
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ehS ahs orotm nad orsnsey oytmsp.ms sihT or/ ohtb dinsk of iel.pms eHr izerssue ear not dciebrsde as lctcioinc/on mnoes,evtm nda eldicun pesdori fo imaipedr se.ucinsnocsso iThs erslu out adgielneezr cnoloni.tcic/ eehrT si a i-stpaolct est,ta ahtt ursel tou c.benesa

Aosl the pli mgikcnas si ehcairrticscta fo t,toismuaam hhwic si udofn ni elopcmx iplaart rsseeizu

bbr  Isn't is just motor symptoms, thats why its Partial? Maybe Im conflating things here. But complex partial decoded would be: Complex (lose consciousness) and partial (just 1 area of the brain, just motor). +6  
euchromatin69  simple seizure wont have altered cociousness....alt. concious = complex or generaliised +  
i_hate_it_here  What's the difference between a complex partial and an absence seizure? +  
kaf  Absence - they just gaze off as if they're daydreaming. +1  


submitted by acerj(7),

So from the definition of Michaelis-Menten Kinetics,
Km = [S] at 1/2 Vmax

For this problem Kmax = 2.0 because that's the value that the velocity maxed out at, even when the substrate [Guanine] was increased 10x.

Back to the definition above, we want to find the amount of substrate, [Guanine] at 1/2 Vmax, when Vmax = 2.0.

Since [Guanine] = 0.5 when velocity = 1.1 and [Guanine] = 0.2 when velocity = 0.6, the [Guanine] when velocity = 1.0 must be between 0.2 and 0.5.

i_hate_it_here  why do i need to know this +2  


submitted by fruitkebabs(20),

This is Pierre Robin sequence, which presents with micrognathia, glossoptosis, cleft palate, and airway obstruction.

It is one of the First Arch syndromes, and the major tip off in the stem would be the mandibular cleft since the mandible is derived from 1st pharyngeal arch.

cheesetouch  fa2018 p602 +  
cheesetouch  Glossoptosis is a medical condition and abnormality which involves the downward displacement or retraction of the tongue. +1  
i_hate_it_here  I hate your name lmao +  
raulirios  FA2020 p620 +  


submitted by cassdawg(1101),

Deoxyhemoglobin has a higher pKa than oxyhemaglobin and thus will accept hydrogen ions more readily. This is important in the ability to "carry" CO2 as the main mechanism of CO2 transport is actually conversion of CO2 to HCO3- (CO2 + H2O -> HCO3- + H+), thus deoxyhemaglobin carries the H+ while HCO3- is transported in the plasma to the lungs. Carbaminohemaglobin is actually only about 20% of the CO2 trasnport and CO2 dissolved as CO2 is 10%; trasnport as HCO3- is around 70% of the CO2 transport.

Here is another image of the process.

Another important aspect of the process to take note of that they like to ask about is the chloride shift. Chloride moves the opposite direction as HCO3- in the RBC. Thus at tissues where we are generating HCO3- from CO2 and need to pump it out of the cell, chloride moves into the cell.At the alveoli where we need to pump HCO3- back into the RBC to turn it into CO2, chloride moves out of the cell.

Other answers:

  • 2,3BPG will bind and stabilizes deoxyhemaglobin making it less attracted to oxygen, shifting the hemaglobin dissosiation curve right.
  • Deoxyhemaglobin has a higher capacity to form carbanimohemaglobin
  • Deoxyhemaglobin has a higher pKA than oxyhemaglobin (this is why it can accept hydrogen ions more readily)
  • Competition for binding site is not a major mechanism for the ability to carry CO2 as most CO2 is "carried" by conversion to HCO3-
  • Nitric oxide binding is not a mechanism of CO2 carry.
i_hate_it_here  <-- +1  
pakimd  @cassdawg thank you for explaining so well along with explaining all the answer options. +  


submitted by cassdawg(1101),

This woman has gout which is associated with hypertension and diabetes and attacks can be precipitated by diuresis (such as with furosemide). Negatively biorefringent crystals (uric acid crystals) are also characteristic of gout. Gout is associated with kidney stones (nephrolithiasis). [FA2020 p467]

frijoles  I don't see where it says that gout is associated with kidney stones. Gout is more commonly caused by underexcretion than overproduction, yes? And this patient has renal insufficiency, yes? So if anything, they have LESS uric acid in the urine and are LESS likely to have stones. It's the reason they have gout to begin with (because it's out of the urine and into the blood). This answer would make sense if the gout was due to overproduction but there is no evidence of that here. This isn't a very good question imo. Please lmk if I'm missing something here. +2  
jt263619  uric acid stones... +2  
tyrionwill  hyperuricemia may cause kidney stone if urine turns to be acidic or condensed. so I think this question is asking a general possible complication. +  
i_hate_it_here  I think that what they were trying to ask was what could also occur due to the predisposing factor that led to gout. The patient was on a loop diuretic which can lead to hypovolemia. Kidney stones and gout occur more frequently when the substrates are able to concentrate in low volume. +1  
kard  furosemide and acetazolamid---> Nephrolithiasis! +  


submitted by cassdawg(1101),

This is feedback inhibition of the RAAS (renin-angiotensin-aldosterone system) axis. Increased aldosterone will feedback and inhibit renin secretion of the kidney. (FA2020 p588)

flapjacks  Increased serum sodium concentration is not specific enough to support the diagnosis +7  
cheesetouch  Fa2018 p332: Hyperaldosteronism - primary hyperaldosteronism seen with adrenal adenoma (Conn syndrome). High aldosterone, low renin. Causes resistant hypertension. +3  
mark0polo  Serum sodium concentration wouldn't actually change because of the aldosterone escape mechanism in primary hyperaldosteronism +7  
i_hate_it_here  <- +1  


Inhalant intoxication= slurred speech, disturbed gait, drowsiness

Inhalant withdrawal= headaches and irritability

usually will present with rash around nose and mouth too

FA2020 pg 570

mittelschmerz  So mad I second-guessed myself on this. Its always PCP or huffing glue smh +1  
bingcentipede  Think I had UWorld question on this. Apparently in this age group (teens), inhalants like glue are the first drugs they try. Only ever seen this on It's Always Sunny but w/e +6  
i_hate_it_here  <- +  


submitted by cassdawg(1101),

Yellow nodules (cholesterol deposits) on the achilles tendons have a very high association with Type II familial dyslipidemia, or familial hypercholesterolemia. This is caused most often by a defect in the LDL receptor function. (FA2020 p94)

cassdawg  NOTE: This patient shows a SELECTIVE increase in LDL so it is a defect in the LDL receptor NOT a defect in ApoB100. A defect in ApoB100 would present with increased VLDL as well! +18  
ginachipotle  Note that the answer is ABSENT LDL receptors vs. partial reduction b/c LDL >700 (LDL = 980), indicating individual is likely homozygous for the trait. (FA2020 pg. 94) +6  
jdc_md  you trick me nbme. veryy veryy tricky +1  
i_hate_it_here  <- +  


FA 2020 pg 425

Porphyria cutanea tarda-- defect in UROD in the heme synthesis pathway that causes photosensitivity and blistering

bingcentipede  Most common porphyria, too +2  
brise  The thing that got me screwed was the "increases synthesis of compounds"; like what compounds? +  
i_hate_it_here  I swear they just love to say shit to throw us off smh +  
sexymexican888  @brise I think they were referring to the previous products of heme synthesis that build up (hydroxymethylbilane, uroporphynogen - or however the fk u spell it) I think those are what cause the blistering photosensitivity, im guessing it is since these dont accumulate in acute intermittent porphyria -> no skin symptoms. but yeah I agree these ppl fucking suck +  


submitted by andro(188),

Differential Diagnosis of Newborn/Neonatal Vomiting

-Benign gastroesophageal reflux ( i.e immature lower esophageal sphincter ) regurgitation of food shortly after feeding .
No further symptoms , healthy children with normal development

-Hypertrophic pyloric stenosis
Regurgitation - projectile nonbilious vomiting electrolyte imbalances ( alkalosis and hypokalemia ) * physical examination may reveal an olive mass on palpation of epigastrium
*typically starts from between 2nd and 7th week of age

-Midgut volvulus /Malrotation /Duodenal atresia * bilious vomiting * abdominal distention * Imaging may reveal signs like the double bubble sign ( duodenal atresia ) etc

Note: The list is not exhaustive as there are many more causes associated with newborn vomiiting

covid_19  To add on to Benign GER, I couldn't find anything in a cursory look through FA and also didn't know that GER was a thing in neonates, so I found this nice and concise article in UpToDate: https://www.uptodate.com/contents/gastroesophageal-reflux-in-premature-infants +  
i_hate_it_here  I don't understand why Esophageal spasm isn't right +  
topgunber  I would say esophageal spasm would cause immediate regurgitation or inability to swallow properly. so we would be looking for dysphagia. +1  
nikitasr27  In general neonates have an immature nervous system (e.g. babinski) and I think that also applies to the ANS. That’s why you see so many YouTube videos of babies vomiting out of the blue without even changing their face expression. I don’t knoow, babies are weird +  


submitted by bingcentipede(243),

A premature infant does not have mature surfactant levels until week 35. Being born at 28 weeks, his type II pneumocytes are not fully mature yet/haven't produced enough yet.

Type I and II pneumocytes line the basement membrane. Type I (C) are squamous, and type II (D) are cuboidal.

E: alveolar macrophage B: RBCs A: capillary endothelial cell?

jj375  Here is a labeled diagram that may help! A) Capillary endothelium B) RBCs C) Type I pneumocyte D) Type II pneumocyte E) I kinda think these are alveolar macrophages https://ib.bioninja.com.au/_Media/lung-tissue-diagram_med.jpeg +4  
j44n  did anyone else think D was trying to show a lamellar body that ID's a type II pneumoyte +  
j44n  my bad i meant B**** +  
i_hate_it_here  I sure did +  
prostar  Lamellar bodies are not visible in this magnification. They are viewed in Electron microscopy. +1