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Comments ...

 +0  (nbme15#44)

I was between these two (cytarabine and imatinib) because I couldn't point out if it was AML or CML. I learned all of the usual clues for each one but I forgot about the fundamental difference of blasts vs mature forms (and that bands are bound to appear in CML too). If they give you a CML in the blast crisis, then look for Auer rods. Anyways, got it wrong and hope that won't happen again.

Now, understanding this I can see how the pharmacology works.

Cytarabine - AML (mostly -blasts and pro-cytes)

Antimetabolite, a purine analog, S-phase specific, inhibit DNA synthesis

Potent enough for the crazy proliferation going on

Imatinib - CML (mostly -cytes and a lot of basophils)

Tyrosine kinase inhibitor of bcr-abl and c-kit tumors

Antimetabolites can also be used, but the best answer is imatinib because it's the most specific for this type of cancer, as it turns off the pro-cancer switch (bcr-abl).


 +0  (nbme15#40)

Irradiated blood destroys all nucleated cells, like in this case, we wouldn't want him to have foreign lymphocytes because it would cause GVHD for sure

Washed Blood eliminates plasma proteins, which is beneficial for patients with IgA deficiency for example


 +0  (nbme17#14)

Itraconazole is given in an encapsulated formula which depends on an acidic pH to dissolve. PPIs like omeprazole increase the stomach's pH, thus decreasing the amount of itraconazole absorbed. Poor absorption does not allow itraconazole to reach its therapeutic plasma concentration. A solution for this would be to give the itraconazole via oral solution or IV.


 +0  (nbme16#37)

The patient is exhibiting drug-seeking behavior: demanding a specific type of medication, becoming upset when alternatives are suggested, and lastly, a PE that does not match the symptoms. Once the suspicion has been identified, the first thing we have to do is gather as much information/PMHx there is on the patient EMR. which includes a Med Reconciliation.

Obtaining serum toxicology and referring the patient to a drug addiction program is inappropriate because we are assuming they are addicts.

An MRI on the spine without any positives on PE is unjustifiable, so it might not get approved by the patient's insurance; plus we should avoid unnecessary procedures.

Lastly, prescribing a limited course of narcotics is not the first thing we should do, although sometimes it what is ultimately done in these cases. However, you must take necessary precautions like using different color papers, ink, very specific instructions, and using formats that are not easily modifiable by the patient.


 +0  (nbme19#28)

Although the doctor should encourage talk between parents and patients, they have to allow for alone time with the patient for a more honest exchange. The doctor should also ask the patient their preference.

an_improved_me  Such a dumb question.. I thought doctors also encourage autonomy between younger patients. For sure you want patients to have privacy for questions regarding sexuality, but you should at least leave it up to the pt. +

 +0  (nbme19#11)

How do the h/o renal cell carcinoma and removal of one kidney/adrenal correlate with occlusion of the hepatic vein?

an_improved_me  looks like RCC may extend into the IVC with tumor thrombus leading to hepatic vein occlusion https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3193735/ +1
an_improved_me  In general though, i don't think you need to know that... I think the important things are that: tells you there is widening of hepatic venules (which one can imagine is due to increased pressure) tells you that hepatic wedge pressure (estimate of portal pressure) is 30; portal pressure should be less than 5. therefore, elevated portal pressure in the absence of RA pressure indicates obstruction before the heart (in this case, budd chiari). Compare that to cardiac cirrhosis, which would have increased RA pressures AND increased portal venous pressures. +
an_improved_me  Shit, and finally, since there are only mild increases in billi, AlkPhos, AST/ALT, i think that rules out cirrhosis. +
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +
an_improved_me  Add the fact that he doesn't have risk factors for cirrhosis (no drinking, smoking cigs, [would have loved to see a negative serology panel...], i think that also brings cirrhosis further down on your DDx +




Subcomments ...

submitted by cassdawg(1165),

Key aspects of the question:

  • Hypokinesis of the posterior left ventricle with increasing activity levels - in my opinion this is the primary clue to stenosis of the right coronary artery. This is because the posterior heart is supplied by the posterior descending artery, which in most people who have right dominant coronary circulation is a branch of the right coronary artery.
  • "When climbing stairs" and the hypokinesis being present on stress testing - this helps you to know the condition is only exacerbated in exercise, and stenosis of the RCA generates symptoms in exercise because in excersise the increase in oxygen demand typically causes dilation of the coronary vessels to accomadate. When there is stenosis, the vessel cannot dilate and thus there is transient ischemia of the area the vessel supplies (this is potentially exacerbated by the coronary steal phenomenon in a stress test which can occur with administration of vasodilators) FA2020 p304

Increase in oxygen consumption is the normal response to exercise and alone is not pathologic. Extravascular compression of the coronary arteries is also considered normal and nonpathologic; this is why most coronary blood flow occurs during diastole and why the endocardium is most susceptible to ischemia.

euchromatin69  but isnt stenosis gonna cause m.infarction? we have not been told any percentage of stenosis +  
shieldmaiden  If it completely cuts off blood for too long, then yes, but as you mentioned, they don't tell us how much stenosis, so with his clinical presentation and echo, we can say it's stable angina. Like @cassdawg mentioned, here a case of transient ischemia +  


submitted by fruitkebabs(20),

Although botulism blocks ACh release, it wouldn't have effects on mpp and the response to exogenous ACh provided to the synaptic junction. The potentials would be the same as it would normally be. The epp difference was disclaimed in the question stem.

cvanh  How is it disclaimed in the question stem? Shouldn't the answer be as close to the normal readings as possible? Delivering ACh to directly depolarize the muscle bypasses the neural circuitry where botulism toxin is working. +  
djeffs1  @cvan, thats what I was thinking. This question was worded weird and i'm still trying to figure out how it was referring to testing in a different setup than the one discussed in the stem... +  
shieldmaiden  The potential frequency remains the same, however, the amplitude is diminished because the only acetylcholine reaching the end-plate is the one injected, so the response to ACh and the epp amplitude should be the same in botulism, and the mepp is out of the control oh acetylcholine or SNARE proteins. A thing to understand about the procedure they are using is that in ionophoresis they are basically forcing the positive charges inside the presynaptic neuron to go along with the injected acetylcholine, creating a bigger amplitude. This "forcing" out is not possible when the vesicles cannot fuse, like in the case of botulism. +  


submitted by trazobone(35),

He has a down and out pupil caused by CN III palsy. His gaze is due to opposed action of the lateral rectus and superior oblique; ptosis due to denervation of levator palpebrae superious.

The only injury listed that could cause a CN III palsy is aneurysm of the PCA compressing the occulomotor nucleus.

shieldmaiden  oculomotor nerve* +  


submitted by cassdawg(1165),

Based on the systemic findings (weight loss, night sweats, cachectic, looks chronically ill) and emigration from India (where TB is more common so the NBME likes to throw it in), miliary TB should be suspected. (FA2020 p140).

None of the other answers would cause the generalized illness to the same degree as TB.

whk123  "The lower thoracic and upper lumbar vertebrae" being the most common site of occurrence. +  
shieldmaiden  No one else fell for osteoblastoma? Though now that I see it, it says "thoracic spine" f*ck +  


submitted by cassdawg(1165),

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  
shieldmaiden  @pontiacfever is not only that, but the optic tract is not in the temporal lobe anyways. A lesion affecting the vision fibers in either the temporal or parietal will cause quadrantanopia +  


submitted by andro(189),

Myeloproliferative Disorders :

They are all associated with the JAK STAT mutation with the exception of CML which is associated with the fusion gene BCR:ABL ( from t(9;22 )-i.e philadelphia chromosome )

CML Tx : imatinib - BCR-ABL Tyrosine kinase inhibitor

TX of the myeloproliferative disorders - Ruxolitinib - Janus kinase inhibitor

cheesetouch  FA2018 P420-421 +  
shieldmaiden  FA2020 432-433 +  


submitted by cassdawg(1165),

Splenectomy is indicated for hereditary spherocytosis because it is an intrinsic hemolytic anemia where the spleen is destroying the red cells even though they could technically function fine. Thus splenectomy will prevent premature removal by the spleen (FA2020 p422).

Sickle cell disease causes autosplenectomy/splenic infarct/sequestration but splenectomy is not indicated because the spleen is not contributing to the symptoms of sickle cell, the symptoms are caused by the vasoocclusive disease.

jzbjzb  why not thalassemia major? splenectomy reduces the need for blood transfusions and greater Hb levels +  
shieldmaiden  Because of the NBME law of the "Best Answer". Splenectomy is what "cures" HS, because that is the organ that prematurely targets it for removal leading to hemolysis. As for thalassemia, you could do it, but it is not indicated at this time for this 10-year-old. Splenectomy is only indicated for thalassemia when an enlarged spleen increased the frequency of transfusions and/or chelation therapy is not enough to control iron levels. +  
shieldmaiden  For the exam, only consider splenectomy for spherocytosis, refractory autoimmune hemolytic anemia, or massive trauma +  


submitted by cassdawg(1165),

Splenectomy is indicated for hereditary spherocytosis because it is an intrinsic hemolytic anemia where the spleen is destroying the red cells even though they could technically function fine. Thus splenectomy will prevent premature removal by the spleen (FA2020 p422).

Sickle cell disease causes autosplenectomy/splenic infarct/sequestration but splenectomy is not indicated because the spleen is not contributing to the symptoms of sickle cell, the symptoms are caused by the vasoocclusive disease.

jzbjzb  why not thalassemia major? splenectomy reduces the need for blood transfusions and greater Hb levels +  
shieldmaiden  Because of the NBME law of the "Best Answer". Splenectomy is what "cures" HS, because that is the organ that prematurely targets it for removal leading to hemolysis. As for thalassemia, you could do it, but it is not indicated at this time for this 10-year-old. Splenectomy is only indicated for thalassemia when an enlarged spleen increased the frequency of transfusions and/or chelation therapy is not enough to control iron levels. +  
shieldmaiden  For the exam, only consider splenectomy for spherocytosis, refractory autoimmune hemolytic anemia, or massive trauma +  


submitted by cheesetouch(140),

Azoles (including itraconazole) and omeprazole are both P450 inhibitors. (p450 interactions FA2018 P247, azoles FA2018 p199.

shieldmaiden  They inhibit different isoenzymes +  


submitted by cassdawg(1165),

Wegener granulomatosis, also called granulomatosis with polyangiitis, is a vasculitide that commonly presents with the triad of focal necrotizing vasculitis, necrotizing granulomas in the lung and upper airway, and necrotizing crescentic glomerulonephritis (FA2020 p 314 and 596)

Wegener is associated with chronic sinusitis, hemoptysis, and PR3-ANCA (antineutrophil cytoplasmic antibody, formerly called c-ANCA).

None of the other answers are associated with ANCA except Churg-strauss syndrome. Churg-strauss syndrome (also called eosinophilic guanulomatosis with polyangiitis) is associated with MPO-ANCA (formerly called p-ANCA). However, Churg-strauss does not have lower respiratory involvement, hemoptysis, or patchy lung opacities on CXR.

j44n  All ANCA's are against proteins in the cytoplasm, they were intentionally vague and wanted you to ddx this off of clinical pres +1  
jurrutia  Churg-Strauss can affect the lungs, but not the upper airway. +2  
shieldmaiden  Actually Churg-Strauss does affect the upper airway (sinusitis); you are confusing it with microscopic polyangiitis which is also associated with MPO-ANCA like CS and with lower airway involvement like Wegener. A way to tell these apart is that (1) CS includes asthma, granulomas, eosinophils, while (2) MPA has no granulomas and does not involve nasopharynx, and (3) W has granulomas in both upper and lower airways and involves PR3-ANCA instead. +  


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iwht PCT uyo ear pesuspdo ot idoav seeeviscx gulnshit dna VU su.opreex tesxhoMelan mkase yruo ksin reom ssbtlceeipu ot UV hti.gl

notadoctor  Wouldn't UV light also be contraindicated in Vitiligo? +5  
sweetmed  Phototherapy with photochemotherapy (PUVA) is a well-known and well-studied modality for the treatment of psoriasis, which involves systemic or topical administration of chemicals known as psoralens and administration of ultraviolet light in increasing dosages after requisite time gap. PUVA is also used in the treatment of widespread vitiligo with moderately good results, though it is being surpassed by ultraviolet B (UVB), which is equally or slightly more efficacious with fewer side effects. +8  
dashou19  Honestly, I didn't even know what Methoxsalen is, just chose the right answer because I know you can not give UV light to people with PCT... +11  
sarahs  what about tcell lymphoma which also has cutaneous lesions? +  
shieldmaiden  @notadoctor UVB from the sun is contraindicated. PUVA is actually used for vitiligo therapy +  


submitted by cantaloupe5(77),
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Ss’eh nkigiatn 450 msmO epr ady os seh ensde to erxtece 450 mmsO rep day to ntanamii uii.qbmulire ouY ’anct ujst teercex ’mssmO by esvestmelh -- tyeh vhae ot eb sevsoildd ni esom aomutn of a.erwt

L’set ays uyo etrecex 054 Omsm wthi 500 Lm of werat -- htat nmsae royu iydksen era niatcrcngeotn uenir t:o

405 smOm ÷ 005 Lm = 900 mLmO/s

utB hte immaxum tish dyasl’ dnykise nca tenrnccoate unrie ot is 054 ,mOmL/s so seh ash to ecretxe rmeo aewtr ot egt ti tath .tdileu aTht nmutao of rewta is 1 ,L saceube 045 msm1O/ L = 405 sO.mm/L

oNw h’eerst noitgnh ipotspgn her ofrm exegntirc hte 045 mssOm in na even rmeo detlui eniur -- fro eaxlpem fi hes rnadk na retax L of wreta noe d,ay hte ekynsid ducol teg rdi fo ttha rxate L ithw hte sema noutma fo 504 smOm yb ildnigut het nireu ot 054 msmO ÷ 2 L = 225 /LOmsm. tuB teh siquonet saks ofr hte mnimumi atoumn fo ertaw -- whhic is 1 L yb teh sinkdye (+ 1 L mfro eht teroh fsutf ofr a ttloa of 2 ).L

shieldmaiden  Thank God you explained where that liter came from because Flashvoyger just took it out a magic hat and I was completely lost +  


submitted by jotajota94(14),
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Hhgi lsogecu lades to omer nnuisil opodnucirt in teh etsfu raelcl( atht hte reohonm lniunsi is ica)olbna ---gt;& eglar tseuf )-;g-&-z,bt(9lo1 brelomsp in ba.olr

tinydoc  I thought that was technically a problem with the fetus and wasnt considered an obstetric complication. +3  
shieldmaiden  Because shoulder dystocia is the obstetric complication, it describes the event of the baby getting stuck in the mother's pelvic bone and regressing a bit into the canal. As a consequence, both baby and mother can suffer complications like Erb's palsy for the neonate and post-partum bleeding for mom. +  


submitted by uslme123(66),
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ryve uitspd eso.unqit heT uirsv was eniadlh -- tbsa hagn dsuiep when they eples and .rlodo oS ti psrdsea to het arinb ydicrtle ofmr hte yooartcfl smtsey via rretrdoeag rsnotatpr oguthrh eesnrv.

niboonsh  yea, aeresol transmission via bat poop in caves +  
len49  How do you know the virus was inhaled? Doesn't mention it. Moreover, non-bite/scratch transmission is extremely rare. +  
makinallkindzofgainz  You get rabies by being bitten, not by inhaling it +  
drzed  She was probably bitten by a bat; many times the bite is not recognized ('unapparent bites'), and thus the CDC recommends that even if you think you have been bitten by a bat (or that you COULD have been bitten), you should go and get active/passive immunization immediately. +  
mangotango  Sketchy (and Zanki) says you can get rabies via animal bites OR aerosol transmission. In the U.S. it's most commonly through bats. It could also be through skunks (Western U.S.) or foxes/raccoons (Eastern U.S.). I remember this by thinking about how skunks smell so bad! +  
shieldmaiden  But the question is "how it got to the brain" not how she got it, so the best answer is through the nerves +  


Can anyone explain why bicipital tendonitis is incorrect?

shieldmaiden  Tendonitis from this tendon will have point tenderness on the anterior side of the joint or closer to the coracoid process. Inflammation is usually caused by impingement (@bicipital groove), which it says here there isn't +  


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anttisS earsi DHL nda ecederas LLD dan G.sT erihT ftfeec on LDL is by far the mots et,npot tub hety do a ltteil oogd no grie.tenyvh

shieldmaiden  Statins increase HDL and decrease LDL/Cholesterol and TG (less of an effect than with chol) +  


The gravid female pinworms (Enterobius vermicularis) migrate through the colon towards the rectum at a rate of 12 to 14 cm per hour.They emerge from the anus, and while moving on the skin near the anus, the female pinworms deposit eggs either through (1) contracting and expelling the eggs, (2) dying and then disintegrating, or (3) bodily rupture due to the host scratching the worm. After depositing the eggs, the female becomes opaque and dies.The female emerges from the anus to obtain the oxygen necessary for the maturation of the eggs.

lakshmi  Rectal exam showed no abnormalities. Wouldn't it more likely be a hookworm? +  
shieldmaiden  Still Ascaris +  


submitted by lpp06(30),

Treated with a thiazide diuretic for HTN with measured hypokalemia, hypotension and decreased Hgb

Thiazide increases Na+ delivery to collecting ducts, increases K+ secretion, causing hypokalemia - which will lead to muscle weakness.

Low blood pressure may be sign of volume depletion from the diuretic

Low Hgb/Anemia due to chronic alcohol abuse (macrocytic, non-megaloblastic anemia)

ootscoot  Does anyone know why she would be presenting NOW after being on the thiazide for 10 years? +6  
nnasser33  This question was frustrating because it is clear that she is volume depleted given her orthostatic BP presentation, which could be caused by both the Thiazide and alcohol use (suppression of ADH release). You can certainly say her presentation is the result of an "adverse drug effect" but how can you completely rule out orthostatic hypotension and dehydration as possible answers? +2  
cbreland  Orthostatic hypotension would refer to a significant decrease in blood pressure when standing. Her BP is low sitting and standing +1  
cbreland  @nnasser33 I was stuck between the two answers as well, but I remembered a similar question on another NBME related to that explanation ^ +  
mmizell  Her BP also only dropped by 6 systolic/1 diastolic from sitting to standing. Orthostatic hypotension is defined as a drop >20/10. +4  
helenwei  I also think with dehydration her Hct would be higher +1  
shieldmaiden  @ootscoot The longer you are exposed to Thiazide diuretics the higher the probability of adverse effects +1  


submitted by cassdawg(1165),

Ondansetron is a powerful antiemetic that works by antagonizing serotonin 5HT3 receptors. It is given for postoperative nausea and chemotherapy-induced nausea (FA2020 p400)

sexymexican888  Alo scopolamine is for motion sickness (sea sick) +  
shieldmaiden  Between scopolamine and ondasteron, ondasteron starts providing relief in 30 minutes while scopolamine needs several hours to work +  
sexymexican888  @shieldmaiden yeah thats a valid point, but I think the main reason you would use odansetron is because it is specifically for chemotherapy induced nausea while scopolamine is for motion sickness +1  


submitted by barbados(5),

Did anyone else feel like the question should have been more specific as in saying "just before the consumption of a meal"? As in saying she has high ghrelin = high hunger just before she eats so point B?

lee280  I agree, at the start, I got a bit confused because I felt like the question was probably less specific than it would have been, but NBME being NBME this is really expected. When you think about it more closely, once you consume the meal then ghrelin will peak and start dropping. +11  
notyasupreme  I agree, I had B at first but then thought too deep into it. I thought if she ATE a meal, she'd be full and low ghrelin. Annoying to get a question wrong on something so simple. +1  
radzio1  Also got this question wrong. A really bad explanation what they want from the curve... +1  
shieldmaiden  Basically she is eating at peak ghrelin (B) its drops, then she likely eats a snack on E +  


submitted by cassdawg(1165),

This man presents with classic features of Parkinson Disease which is caused by degeneration of dopamine producing neurons in the substantia nigra (FA2020 p520)

ibpstepprep  most likely Chronic traumatic encephalopathy (CTE), Parkinson like symptoms and history of boxing/ traumatic sport. Repetitive trauma results in neuronal degeneration and Tau deposition. +6  
shieldmaiden  The problem with a diagnosis of CTE here is that it shares more sxs and etiological features with Alzheimer's, making it a cognitive-heavy disease rather than movement, like what is seen in this patient. The repeated trauma might have played a part but in this case, where a person is having trouble with movements, not memory, behavior, personality, or mood, I think is more accurate to say that it's Parkinson's and thus neuronal degeneration and not a tauopathy. +2  
msula  Why is this not a ALS ? +  
shieldmaiden  @msula I think ALS is not associated with sleep disturbances, pain, or tremors. Furthermore, the question points you to a defect in the patient's brain, so that also r/o ALS +  


submitted by ace9yak(7),

fa 2019 pg 662, Inhalation injury and sequelae. in the inhalation injury and sequelae part they say signed nasal hairs or soot in the oropharynx -> decreased activity of airway cilia as there is soot overlying them and cant function properly tobacco has silica (fa 2019 pg 663) - silica can disrupt phagolysosomes and impair macrophages -> decreased alveolar macrophage function as for the increased mucus production and secretion - idk i figured there is an irritant and your body will be trying to clear it some how, i guess think about COPD

meryen13  i was so confused by the "1 week" i was thinking is one week enough to decrease the macrophages? or are they gonna be hyper active to clean the smoke particles. smh +3  
shieldmaiden  Acute cigarette smoking "behaves" differently than chronic. While acutely you would see decreased number and function (phagocytic and proinflammatory) of alveolar macrophages (AM), chronic smokers have shown an increased number of AMs, likely as an adaptive mechanism to offset the epithelial changes. +1  


submitted by cassdawg(1165),

Polyarteritis nodosa is a medium vessel vasculitis associated with different stages of transmural inflammation with fibrinoid necrosis of vessels. [FA2020 p314]

Because this is a vasculitis that affects medium vessels, it can affect the arteries supplying the muscles and thus cause segmental ischemic necrosis from loss of blood supply.

radzio1  I thought that segmental is a key word for Burgers dz. +1  
radzio1  *Buerger +  
feochromocytoma  Beurger is characterized by segmental thrombosis with nerve involvement. +2  
cheesetouch  So he has both PAN and Buerger's? +  
pakimd  polyarteritis nodosa is characterized by segmental (different stages) of transmural inflammation with fibrinoid necrosis causing narrowing of vessel lumen and increased risk of thrombosis leading to tissue ischemia/infarction FA2020 pg314 +  
shieldmaiden  The problem in Buerger is segmental thrombosis while PAN is ischemia from immune complexes with hepatitis antigens and it is also segmental (a string of pearls) +  


submitted by melanoma(13),

fluoxetine is the only antidepressant medication approved by the FDA for the treatment of BN.

shieldmaiden  Just never choose bupropion, always an SSRI for BN +  


submitted by cassdawg(1165),

This man presents with classic features of Parkinson Disease which is caused by degeneration of dopamine producing neurons in the substantia nigra (FA2020 p520)

ibpstepprep  most likely Chronic traumatic encephalopathy (CTE), Parkinson like symptoms and history of boxing/ traumatic sport. Repetitive trauma results in neuronal degeneration and Tau deposition. +6  
shieldmaiden  The problem with a diagnosis of CTE here is that it shares more sxs and etiological features with Alzheimer's, making it a cognitive-heavy disease rather than movement, like what is seen in this patient. The repeated trauma might have played a part but in this case, where a person is having trouble with movements, not memory, behavior, personality, or mood, I think is more accurate to say that it's Parkinson's and thus neuronal degeneration and not a tauopathy. +2  
msula  Why is this not a ALS ? +  
shieldmaiden  @msula I think ALS is not associated with sleep disturbances, pain, or tremors. Furthermore, the question points you to a defect in the patient's brain, so that also r/o ALS +  


submitted by bingcentipede(260),

The patient has a brain cancer, which is 50/50 between primary cancer and metastasis (lung most common; also breast, colon).

The answer is small cell carcinoma of the lung versus a primary brain cancer because there are cells staining positive for carcinoma marker (cytokeratin) and neuroendocrine markers (chromogranin and synaptophysin), which is what SCLC is.

cassdawg  Another reason this is small cell lung cancer is the weakness of the proximal upper and lower extremities while also having augmentation (increasing) of strength with repetitive stimulation. This is characteristic of Lambert-Eaton myasthenic syndrome [where strength increases with stimulation; opposite of myasthenia gravis]. Lambert-Eaton can be caused by a paraneoplastic syndrome of small cell lung cancer (FA2020 p228 and 472) +10  
passplease  What about the fact that it is a single well-demarcated mass. Wouldnt metastatic cancer present as multiple masses? This made me think primary brain cancer. +7  
jaeyphf  @passplease I originally thought this way too and it fucked me. I think the easiest way is elimination + staining. Pt is an adult - eliminate neuroblastoma, ependymoma as both are more common in kids Pt is not immunocompromised - eliminate CNS lymphoma GBM does not stain positive for cytokeratin, chromogranin, synaptophysin - eliminate GBM Left with Small cell carcinoma +2  
shieldmaiden  @passplease Yeah I know! I basically came down to showdown of what was more likely and the metastatic small cell lung cancer won. The only thing a primary brain tumor had on its side as "unique" was that it was a solitary lesion, and that's just not enough. +  


submitted by cassdawg(1165),

She has a microcytic anemia with no major symptoms, normal vital signs, no history of illness, and normal other cell counts. Of the answers, iron deficiency anemia is the only one that fits that description and makes sense because she is a premenopausal woman (women are at risk of iron deficiency anemia due to monthly bleeding).

Aplastic anemia would have low platelets and leukocytes as well. Sickle cell and thalassemia would lokely present with a hemolytic anemia and jaundice or some other symptoms (plus they are present from birth). B12 deficiency is megaloblastic anemia and has neurological symptoms.

jackie  I feel like this is a really unfair question because beta-thalassemia minor would also present as microcytic and asymptomatic. They should have at least added HbA levels or iron levels +3  
shieldmaiden  Iron deficiency has low HCT (like in this case), while Beta-Thalassemia will more likely have a normal HCT value +  


submitted by shakakaka(4),

Why not N.meningitidis ? Penicillin and ceftriaxone are treatment chooses for N.meningitidis and it's encapsulated.. If I'm not mistaken macrolides and ceftriaxone are treatment for S.pneumo , not penicillin

shieldmaiden  This is prophylactic treatment, and penicillin is the one recommended by the AAP and CDC +  


submitted by cassdawg(1165),

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 +3  
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(1165),

B labels the spleen, which is removed in ITP because the splenic macrophages are responsible for phagocytosing platelets (FA2020 p427)

sightful  A = pancreas B = spleen C = left kidney D = right kidney E = liver +4  
shieldmaiden  C and D are the kidneys unless they ask you about adrenals... then these are it +  


submitted by peteandplop(30),

https://www.ncbi.nlm.nih.gov/pubmed/22559853

While not traditionally discussed, the kidneys' contributions to maintaining glucose homeostasis are significant and include such functions as release of glucose into the circulation via gluconeogenesis, uptake of glucose from the circulation to satisfy their energy needs, and reabsorption of glucose at the level of the proximal tubule.

FA2019 p78 - [Gluconeogensis] occurs primarily in the liver; serves to maintain euglycemia during fasting. Enzymes also found in kidney, intestinal epithelium.

... seems like a silly thing to test... shrugs shoulders laughs in NBME

shieldmaiden  especially silly since they also list the small and the large intestine +1  


submitted by drdoom(885),
unscramble the site ⋅ remove ads ⋅ become a member ($39/month)

aliinIytb ot tniaanmi na certonei = lereitce nfoudsytnci. So now het uqniotse si hW?""y

eaFu,igt tffcuiyild igepln,es fcldfyiuit nornitncatgec si irantstg ot odnsu klie eiosnesrpd. yitifluDcf" enaroticgtn"cn gmith be tdeietenrrp as arpmdiie vceteueix coiuntnf or teh ggbisninen of rvseteacalldaur- eiteandm inaeetmd( erladte ot almls ubt musueorn ecerrabl ,fncta)sir utb on pteS 1 naeidtme will eb abltnta (,i.e. to"ls his ayw mo,"he ir,e"wgn"adn ).tc.e

Desrnsepio si alaytucl mmoocn aftre a abtigtiednil entev klei etrs,ok sa uoy higmt t.pexce tiWh ereodnspsi seocm a lsso of selaxu ntretsei dan eieshtrdta— is eeddecsar ilidbo.

Oen anc akem het mtnueagr atht a sravc"ula tne"ipta ithgm haev some sseisu ithw sih ""ppsei eitasosr,irl(ocrse ipyasmtiehceayathsam/trppct sofnuyidcnt) da,n for tish oean,rs unarctlno ecneirot soldhu be sdcrdeaee; but tnoe taht nnthogi si dnonmtiee auotb ilnag-stgonnd rvucaals sdeasie o(n hx fo tynpeo.hrsin)e

sA a us,elrt eth btse ernwas hiccoe heer is C. idobL(i edcdseare ubt raonultcn ectrnsioe r)maln.o eTh ibg oeinuqst I ehva ,is ohw het khce dseo iths gyu wkon es'h radh nweh sh'e ?l!s!apee :p

cbay0509  thank you +1  
ilikedmyfirstusername  there are several UWorld questions about psychogenic ED with the answer being normal libido and normal nocturnal erections, idgi +11  
djeffs1  Yeah NBME says its C, but I still think with a recent stroke you can't bank on normal nocturnal erections... +  
drdoom  @djeffs nocturnal erections happen at the level of the spinal cord (S2–S4)! a “brain stroke” (UMN damage or “cortical damage”) would not kill your ability to have nocturnal erections! https://en.wikipedia.org/wiki/Nocturnal_penile_tumescence#Mechanism +  
drjo  fatigue, difficulty sleeping and concentrating could be depression or hypothyroidism both of which can cause decreased libido +  
jurrutia  @djeffs1 when you say NBME say's it's C, how do you know that's the official answer? Did NBME post the answers somewhere? +  
djeffs1  in the versions I purchased from them they highlight the correct answer in the test review +1  
shieldmaiden  For me the keyword in the stem is "maintain"; he can maintain an erection, therefore nocturnal erections must be normal. Libido, on the other hand, is psychologically driven, so if he is depressed (trouble sleeping, concentrating, fatigue, recent major health problem) then the strength towards any kind of desire, including sexual, will be low +  


submitted by baja_blast(113),

Anyone know why this was Hydronephrosis and not Staghorn Calculus??

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. +2  
prosopagnosia  Personally, I couldn't tell that the ureter was dilated without a comparison image. But what I did notice was the dilation of the renal calyces and severe renal atrophy which clued me into some ureteric obstruction --> Hydronephrosis. +1  
trazobone  OK so I put ARPKD bc of chronic renal insufficiency and also i thought the dilated parts were cysts +2  
shieldmaiden  Remember that for ARPKD both kidneys will be affected and it will involve the cortex as well as the medulla. If you notice, the cortex is intact +3  
taylor5479  Also, it's my understanding that ARPKD typically presents much younger with a lot of really small cysts, kind of with a spongelike appearance. +