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Comments ...

 +4  (nbme16#4)

This seems like NADPH oxidase deficiency, as the patient has history of multiple cutaneous abscess with Staph aurues during past 9 months. Therefore, a catalase positive organism is the likely cause, besides microbiological characteristics befitting Nocardia

cheesetouch  FA18 p 117 chronic granulomatous disease (NADPH oxidase deficiency), FA18 p139 Nocardia +

 +2  (nbme16#44)

Large embolus obstructing pulmonary blood flow = Perfusion defect There is no capillary bed around smaller bronchi/bronchioles and they form the anatomical dead space. Since embolus also obstructs blood flow, the supplied alveoli which are ventilated, turn into dead space as no exchange of gases can occur through them.

Shunt = Ventilation defect


 +5  (nbme16#10)

Copied from NBME 22 for completeness sake:

"A good pic showing anomalous arteries in horseshoe kidney

https://www.researchgate.net/figure/A-case-of-horseshoe-kidney-with-accessory-renal-arteries-Posterior-aspect-of-the_fig1_313729399"


 -1  (nbme16#25)

Child has albinism. Defective melanin synthesis due to deficiency of enzyme tyrosine hydroxylase. FA 2020, page 476

topgunber  tyrosinase. tyrosine hydroxylase would make L-dopa +2
sabrooza  It is Tyrosinase deficiency not (Tyrosinase hydroxylase ) +1

 +2  (nbme16#47)

Uworld QID: 1733 explains the functions of all rotator cuff muscles.

Abduction = Supraspinatous. External rotation = Infraspinatous, Teres minor. Internal rotation = Subscapularis. Adduction = Teres minor, Subscapularis.


 +0  (nbme16#24)

Also, morphine-6-glucuronide is excreted renally. So, morphine would cause toxicity in patients with reduced renal functions.


 +0  (nbme16#42)

Patient is suffering from Schizophrenia (1 year of symptoms). Treatment is with anti-psychotics (Risperidone: Atypical antipsychtic)

nbmeanswersownersucks  In case anyone considered Lithium because you thought she had Bipolar with psychotic features, her depressed and sad mood is more likely explained by the negative symptoms of schizophrenia and she would also need current symptoms of/a past history of mania for a diagnosis of Bipolar. +1
drdoom  ah, interesting: so you cannot diagnose bipolar without an episode of mania (either at presentation or some point in the past). nice. +

 +1  (nbme16#12)

Response to EPO is typically measured by rise in plasma hemoglobin concentration over following weeks.

This article elicits the same


 +1  (nbme16#30)

The process explains Interferon Gamma Release Assay (IGRA) testing. FA 2020 page 140


 +1  (nbme16#7)

10^5 bacterial colonies/mL indicates lab diagnosis of UTI. Rest of the question is pretty explanatory: oxidase positive gram negative rods, producing green pigment is characteristic of Pseudomonas aeruginosa. This is a pretty common pathogen to cause nosocomial UTI with indwelling catheters.


 +3  (nbme16#25)

Drug X alone has an increase in blood pressure, so it must be an agonist. When you use Angiotensin + Drug X pressure increases but not as much as would increase with Angiotensin alone. This indicates that drug x is probably a partial agonist, since a partial agonist in the presence of a full agonist works as an antagonist [No effect of Angiotensin and only raise in BP is due to effect of Drug X]


 +2  (nbme16#29)

Western blotting detects proteins. Since the number of proteins detected has increased, without any change in the mRNA (detected by Northern blot) or DNA (by PCR), there has been an increase in the translation of ferritin mRNA


 +3  (nbme19#40)

Amniotic fluid phospholipid analysis is used for testing fetal lung maturity via measuring surfactant production.

Fetal echocardiography would reveal any congenital heart defects if present, but would not be diagnostic of Downs syndrome

Fetal ultrasound First-trimester ultrasound commonly shows increased nuchal translucency and hypoplastic nasal bone. But I feel this is used more commonly in older women who might have chromosomal dysgenesis as the cause of downs syndrome

Fetal biopsy Pretty invasive technique, when we have a lesser invasive and more specific test available.

drdoom  [system mailer] your account has been upgraded: FORMAT NINJA +

 +1  (nbme22#19)

In addition to amazing explanation by k_tron_3000, I'd like to add that patient also has numbness and tingling in both legs. So, all sensations to the spinal cord are impaired, hinting towards damage to dorsal horns and hence sensory neuropathy.


 +2  (nbme22#14)

UWorld QID: 11747 option A.

"The VVP also communicates with the azygos vein in the chest, which explains in part why breast and lung cancers frequently metastasize to the thoracic spine."

Breast → Intercostal veins → Azygous vein → Vertebral venous plexus (VVP) → Vertebrae


 -1  (nbme21#29)

Is there any drug which would cause enhancement of cell membrane permeability to chloride? It seems like the MOA of ETEC & V. cholerae adenylate cyclase toxins and somewhat that of Ivacaftor used in cystic fibrosis.

kevin  For the purposes of STEP 1 I don't think there is an antibiotic that would do that. If you wanted to really stretch the definition of enhanced cell permeability you could go with a polymixin which is essentially a detergent for bacterial membranes and can be used rarely for pseudomonas and other bacteria +

 +0  (nbme21#49)

Can anyone explain what does "lost her pep" means?

drdoom  `pep` actually comes from `pepper`; to `pepper` something (including a food dish!) is to make it more vigorous, to give it more kick, to vitalize it. so, to “lose one’s pep” is to lose one’s vitality, feel fatigued, feel lackluster, etc. https://www.etymonline.com/word/pep +1




Subcomments ...

submitted by cassdawg(1145),

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. +8  
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 cassdawg(1145),

Vinblastine works by binding tubulin and inhibiting microtubule formation. This inhibits cell division.

Basically, this question is asking which of the following cell types is nondividing/would not need functioning microtubules.

Enterocytes in crypts (which divide to replace intestinal epithelium(, keratinocytes of the stratum basale (which divide to to replace skin), and erythroblasts (blasts are stem cells) are all dividing cells and thus could be affected by vinblastine. Cortical thymocytes are also dividing cells, as they will divide to create progeny T-cells through the process of T-cell maturation.

Thus, the only non-affected cell is ventricular cardiomyocytes.

the_enigma28  Cortical thymic epithelial cells (cTECs) [aka cortical thymocytes] form unique parenchymal cell [& therefore proliferating] population of the thymus which critically contribute to the development of T cells +3  
cheesetouch  Pathoma Ch 1.1 mentions permanent tissues include: cardiac muscle, skeletal muscle & nerve - only can grow by hypertrophy. +2  


submitted by bingcentipede(257),

Grade refers to the differentiation, whereas stage refers to the TNM decriptions

This is high-grade because of the "poorly demarcated... cells growing in sheets" wit a high N:C ratio. Means it's got low differentiation.

This is low-stage because there is NO METASTASIS. Even though there is invasion (and thus, a cancer), M for the TNM is most important.

the_enigma28  Excellent explanation. For additional info, look up at Page 220, FA 2020. +  


submitted by cassdawg(1145),

The key here is this man has no history of bleeding problems yet he has an extremely prolonged PTT (associated with the intrinsic coagulation cascade pathway). This is suggestive that he is deficient in the "unnecessary" factor of the intrinsic pathway, factor XII. (FA2020 p412)

Factor XIIa (Hageman's factor) of the intrinsic pathway activates prekallikrein to kallikrein.

Histamine release, phagocytosis, and C5a generation are not associated with the intrinsic coagulation cascade. Platelet aggregation impairment could be associated with increased PTT (i.e. vWF deficiency, p428), but not that extreme of prolongation without symptoms of bleeding issues.

the_enigma28  Adding to this, XII activates prekallikrein → kallikrein. And, kallikrein converts plasminogen → plasmin. Plasmin causes fibrin degradation. https://upload.wikimedia.org/wikipedia/commons/thumb/2/28/Kinin-Kallikrein_System_Simplified_.jpg/200px-Kinin-Kallikrein_System_Simplified_.jpg +3  


submitted by cassdawg(1145),

Fragile X syndrome is X-linked dominant inheritance associated with a trinucleotide repeat in FMR1 (FA2020 p62).

Even if you did not know this fact, fragile X syndrome (a disease affecting the X chromosome) should be X-liked of some sort.

Knowing the disease is X-linked, you can get to the answer because in the couple, the father is the only one with a family history of the disease. Whether the disease was X-linked recessive or X-linked dominant, if the father had the diseased X-chromosome he would have the disease (as males only have one X chromosome). Since the father does not have the disease, he does not have the chromosome and thus cannot pass it on. Thus, the chance of their child having the disease is 0%

the_enigma28  Any reason why II-2 & II-3 females are not shown to be affected?? +2  
yhm17  Possibly due to X-inactivation leading to mosaicism so they wouldn't demonstrate the phenotype. +11  


submitted by bingcentipede(257),

Dudes and dudettes, let me tell you how high yield Pathoma Ch. 1-3 are. Dr. Sattar is the freaking man.

Anyway, this is reversible cell injury because of swelling. If the Na/K ATPase is not working, Na is not leaving. Na follows water, so water is getting stuck in the cell, leading to swelling.

Most important is recognizing that it's reversible cell injury - everything else (except PFK lol) is talking about cell death

cassdawg  Love this explanation lol Dr. Sattar for president. FA2020 p207 for anyone who wants more details. +6  
the_enigma28  Ribosomal disaggregation (detachment) does occur in reversible cellular injury, but that is not the mechanism of cellular swelling! +3  
topgunber  this last comment is extremely important to recognize when asking about reversible injury +  


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adidCna si a tapr fo het ralomn rfloa fo sin,k luocd auecs maitnonctinoa of a elrncta nvesou tcrh.etae Teh ieonsqtu estsat ahtt eth msnrgiao si perlp,u ,iddbnug ddi otn nposder ot bdora mpsrectu nitboiicats aak( hyet didn't ues nfucleozoal ro tiiocmrehanp ).B ,Laylst tyhe odehws ti ldtpae on olbdo rgaa nda erthe asw no ihosysmle hicwh nlmtisieea hpats het( oyln ohert bsiplose ecnrnoedt eer)h.

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hungrybox  Also, the yeast form of Candida is gram (+) +30  
dr_jan_itor  I got thrown off by the part where they said "ovoid" and thought they were implying a cigar shape. I chose sporothrix for the morphology in spite of knowing that it clincally made no sense. +1  
lilmonkey  I chose S. aureus before reading the question (looks like b-hemolysis). Then I saw "budding organisms" and picked the correct one. +  
the_enigma28  I think, elliptical budding yeast forms kind of excluded cryptococcus since its almost round -_- +  
the_enigma28  I think, elliptical budding yeast forms kind of excluded cryptococcus since its almost round -_- +  
lowyield  cryptococcus also doesn't take up gram stain because the shell is too thiqq +2  


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idCaand is a patr fo teh nolamr lafro of is,nk ulcdo acuse ictaoanminont fo a altrenc ouensv ette.rach hTe qiunotse atsste atht the ormiasgn is e,pprul bgdin,ud idd tno oedspnr ot orbda ecsumrpt btnicoiisat kaa( yteh nid'td use coeulaznlof ro ircimepantho B). ,sLlaty teyh howsed it epladt on bdloo agra dan ereth asw no heosslyim icwhh nasiielmte athsp h(et nlyo roeht elsiosbp dnncroete )eer.h

cpcuysctrooC ausluly lsnevoiv gsntiinemi in irposmmnioomemudc .tps E. lcio si gmar oeriagtixovnsrhte p is lysaluu entttmraisd by a thnor no a oser ro esomeno whit a oyirhts of dinrggnae

hungrybox  Also, the yeast form of Candida is gram (+) +30  
dr_jan_itor  I got thrown off by the part where they said "ovoid" and thought they were implying a cigar shape. I chose sporothrix for the morphology in spite of knowing that it clincally made no sense. +1  
lilmonkey  I chose S. aureus before reading the question (looks like b-hemolysis). Then I saw "budding organisms" and picked the correct one. +  
the_enigma28  I think, elliptical budding yeast forms kind of excluded cryptococcus since its almost round -_- +  
the_enigma28  I think, elliptical budding yeast forms kind of excluded cryptococcus since its almost round -_- +  
lowyield  cryptococcus also doesn't take up gram stain because the shell is too thiqq +2  


submitted by usmleuser007(397),
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ecCifndeno atnrvile riscnseea wiht dsaderece saeplm .eizs

usmleuser007  would require a a large sample size to see if there is a true difference +  
claptain  This question is bogus. CI does not always increase with decreased sample size or vice versa. Four readings with small variation would give a narrower CI than 10 readings with greater variation. The only thing you can be certain about by adding more samples is that the CI will most likely change, but which direction is uncertain. +8  
bartolomoose  Recall the formula for 95%ci Mean +/- 1.96* (SD/sqrt(samplesize)) +1  
the_enigma28  @claptain The point you made is relevant in studies involving random data. But in case of this question, the data being collected is in fact the diastolic BP. We take several readings of BP to rule out white-coat hypertension and have as accurate reading as possible. In this case, taking more readings will actually narrow down the confidence interval. The readings here represent physiological parameter, which wouldn't vary veryyyy widely in an individual. +  
lowyield  @claptain i was thinking the same thing but ended up choosing the increased because alot of NBME seems to reward the more simplistic answer than the overthinking answer +  


submitted by divya(59),
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yhW is reteh erhonhriar in diiopo w?liarhtawd nAd ,olas if mtlsasitnu liek aeinocc cusea anlas scvinonasior,cott nuhdt'lso poiiod alwdairhtw od eht s?mae

the_enigma28  Mechanism of opioid-induced rhinorrhoea, lacrimation, stomach cramps and diarrhoea is actually muscarinic receptor effects, rather than alpha adrenergic blockade caused by cocaine, causing nasal vasoconstriction. +1  
baja_blast  Symptoms of Opioid Withdrawal can be remembered with the phrase "anxious, hot, and moist" per SketchyPharm Opiods. Rhinorrhea is one way people can be "moist" during opioid withdrawal, but they can also sweat excessively and lacrimate too. +1  


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If otbh CZTH nad olpo sduritice ewre oivrdedp as na wanser cohice, rethurf celu taht chtz ulwod eb eth nawsre occehi si hte nteetsinpora fo eth ianttpe lfegen"i .fun"yn sihT egsustgs ryaphcmeilaec atpicy(sihcr o)tenesrov hwcih si a esid etfefc uiuqen ot HCT.Z

adong  there wasn't any loop diuretics... +  
the_enigma28  Good explanation!! +  


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sihT noe is iyarfl cillago fi uoy mreermeb atth raaiebct EVLO our on.ir So ucmh so, hatt rou yodb maec pu hwti a yaw nruaod .ti Wnhe an einnftoic is cddeette by eht d,oyb ti easkm ekil a amdsdooy peeprrp and absnot dwno the cshte.ha

"All eth rnoi niot the es,nob kcuiq !)ri(fnit^er iHde ti rfmo the eisrtn!dur tGe hoest nior ridlevey ckstru ti()nrfier ffo hte aodr lo!(obd)

with eracdeeds nfrtirei coesm a erecsdae citpycaa ofr dgibnni niro in hte boold

cooldudeboy1  i like the way to remember acd but there is no bacterial etiology in Rheumatoid arthritis is there? +  
the_enigma28  The body recognises chronic inflammatory states as infections +  
fatboyslim  Ferritin is not the "iron delivery trucks", that's actually TRANSFERRIN (transfers iron to liver and bone marrow). Ferritin is the STORAGE form of iron in the liver and bone marrow. In anemia of chronic disease, there usually is an inflammatory process going (whether infectious, auto-immune [as in this case of Rheumatoid Arthritis], or cancer). During inflammation, the body releases IL-6, which releases hepcidin. Hepcidin downregulates ferroportin channels in the gut and on macrophages; therefore you absorb less iron from the GI and iron is trapped in macrophages (ferritin) and cannot be used for RBC production. All this causes INCREASED FERRITIN, decreased TIBC (if ferritin goes up, TIBC goes down and vice versa), and decreased serum iron levels and TIBC saturation (the bone marrow will suck up all the serum iron to make RBCs because it cannot make use of the iron stored as ferritin). +9