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 +1  (nbme18#41)

FA 2019 page 308. Most common cause of acute/primary pericarditis is assumed to be viral.

 +2  (free120#21)

If you didn't understand the tests in the stem, this should help:

Urine reducing substance test: https://study.com/academy/lesson/reducing-vs-non-reducing-sugars-definition-comparison.html

Glucose oxidase test: catalyzes the oxidation of glucose to hydrogen and D-glucono-delta-lactone. If there is no glucose present (i.e. with galactosemia), the test will be negative because there is nothing for the test to catalyze.

drpee  TLD-Watch? Reducing sugars include galactose, lactose, and fructose.

 +2  (free120#23)

In case anyone is curious about the other terms: I think apoptosis and necroptosis are fairly recognizable, but I had no clue what symptosis, ostosis, and oncosis were. Symptosis = ischemic cell death. Ostosis = bone formation (duh! why didn't I remember that, lol). Oncosis = emaciation.

amc  correction Oncosis= ischemic cell death Symptosis= emaciation

 -6  (nbme24#13)

So actually.... Medscape says that PSGN can progressive to a proliferative glomerulonephritis mechanism and so proliferative glomerulonephritis should be considered as a differential diagnosis for PSGN.

https://emedicine.medscape.com/article/980685-overview#a5: "The presence of acute kidney injury may suggest an alternate diagnosis (eg, membranoproliferative glomerulonephritis [MPGN], Henoch-Schönlein purpura [HSP], systemic lupus erythematosus [SLE]) or a severe or worsening APSGN, such as observed in those with crescentic glomerulonephritis or rapidly progressive glomerulonephritis... Differential Diagnosis: This includes most other types of childhood glomerulonephritides. These include IgA nephropathy, membranoproliferative glomerulonephritis, hereditary nephritis, and other forms of postinfectious glomerulonephritis."

Ironically enough, this must be what they were asking, i.e. complications of PSGN, because AMBOSS (another Step resource) directly linked the above article I found before looking farther and coming across the AMBOSS section.

 +4  (nbme24#42)

So... I didn't know what it was so I looked it up... and legit, granum is part of plants.......... really?! lol

cinnapie  We out here treating plants!!

 +2  (nbme24#33)

Does anyone have a good explanation for why decreased levels of inhibin is wrong? From my understanding, inhibin and activin work together, in that inhibin binds and blocks activin leading to decreased feedback on hypothalamus and activin increases FSH and GnRH production.. thus, if you decrease inhibin then you would have increased activin which would lead to increased GnRH and FSH, right? I found one article talking about it in regards to puberty, but it seems to be a hypothesis/not confirmed at this point... is that why? But still... how do I rule it out on a test?

yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt
artist90  Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH
usmile1  Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense!

 +1  (nbme24#28)

Dysmetria = discoordination of planned, voluntary movements (my own words for the different findings and used specifically to help me remember location) controlled by the posterior lobe of the hemisphere which does planned voluntary movement. Also, the hemisphere is the periphery of the cerebellum, and it deals with planned, voluntary movements of the periphery (i.e. limbs). I got this from this image with memory tips: https://www.medicowesome.com/2013/04/cerebellum-mnemonics.html.

Other helpful links:

  1. Pretty detailed anatomy: http://www.fmritools.com/kdb/_Media/image002-3_med_hr.png

  2. Interactive site all about the cerebellum (https://nba.uth.tmc.edu/neuroscience/m/s3/chapter05.html), but the most helpful picture for me was this one (https://nba.uth.tmc.edu/neuroscience/m/s3/images/copyright_marked_images/5-3_NEW.jpg)

 +6  (nbme24#24)

I just thought of a way to (hopefully) avoid getting these types of answers wrong. First, when I read them I always look for the least "asshole" answer. Then, if you're still stuck, try to put the statement into a quote that you would say to a patient as a physician, remembering that open-ended, non-judgmental questions are ideal.

The answer for this could be phrased as a question/statement by the doctor, to the family, as "Tell me more about how this impacting your family and daily life." Had it been phrased like that, I DEFINITELY wouldn't have gotten it wrong. I would have never even had the opportunity to make an assumption about the family's fighting being due to diet concerns and thus needing a nutritionist referal (which is what I chose).

usmile1  I think the reason dietician was incorrect is because she has had diabetes for 6 years and her diabetes was well controlled that entire time. Then for the past two months her glucose control has been poor. This is pointing towards the issue NOT being that they don't know how to manage the diabetes so referring to a dietician wouldn't be useful.
tiredofstudying  99.99/100 times the answer will never include referral. The only reason I do not say 100/100 is because there may be an answer one day that is to refer, but through all of UW, Rx, and NBME it has never been to refer, so do with that info what you will

 +0  (nbme24#41)

Does anyone know how to rule out E? I've never learned about microorganisms specifically activating a cell's CAMs, but when I looked it up, I found this article (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC395703/). The article doesn't specifically mention plasmodium as using it, but several of the resources for the article does.

 +1  (nbme24#41)

Found this great document with slides about the different pathogens: http://ncasmbranch.org/meetings/2019SprPpts/2019-03_Spring_Garcia.pdf

 +1  (nbme23#1)

Here's a GREAT video explaining ultrasound findings of pregnancy. @9:57 is a great picture so far with labels of the yolk sac, gestational sack, fetal pole, and amnion. One thing the person explaining said that I thought would be good to keep in mind is that the yolk sac looks like a cheerio inside the gestational sac. Also, this site has a bunch of pictures as well: https://radiopaedia.org/articles/first-trimester?lang=us.

zpatel  what video?
usmlecharserssss  porn video how they make this embryo and yolk sac
samsam3711  Shorter video that explains this pretty well: https://www.youtube.com/watch?v=01mMBDEthV8
focus  @samsam3711 that video is BOMB. Thank you!!!

 +0  (nbme23#4)

So... I've been trying to figure this out and I think I got it...

One of the main clearance techniques by the body is extravascular hemolysis by the RES. Hemolysis of RBCs leads to elevated serum LDH (because RBCs have high amounts of lactate dehydrogenase which is released into serum after hemolysis). Increased LDH can then lead to increased pyruvate to lactate conversion, which would deplete the body of pyruvate and lead to increased anaerobic glycolysis. As the process continues, hypoglycemia results due to overutilization of serum glucose.

I agree with @yotsubato that this is a bullshit question for Step 1 (hopefully it was retired because it was an experimental question at the time and no one knew it, lol). I'm glad that I was able to try to figure out possible pathogenesis, though. That is probably why it was asked, when it was asked, to determine if students could VERY critically think about all of the complications of malaria and what complications those original complications could lead to, just by know normal physiology/pathophysiology of the body. I came to these conclusions based on putting together information from several of Armando Hasudagun's videos (@4:00-4:37 https://www.youtube.com/watch?v=wxzf_rg_Wd4, https://www.youtube.com/watch?v=oQmL6XqCKSU&list=PLqTetbgey0acuF2wsTispLDzZVKDyOEev&index=16).

 +2  (nbme23#41)

The things that confused me/I forgot: horizontal gaze and dysarthric speech.

The horizontal gaze is a combination of signals between PPRF (paramedian pontine reticular formation), MLF, and other vision cranial nerves. PPRF is closely located to the MLF, which is in the dorsal pons, so a basillar artery infarct, i.e. ventral pons infarct, won't completely inhibit the PPRF, and thus why some horizontal gaze function is available.

Dysarthric speech = defect in articulation of speech mainly due to motor movements of speech, so because CST and CBT are impaired in basillar artery lesion, it makes sense that the motor function of speech would also be impaired.

 +5  (nbme23#33)

I found a picture showing the transmission by two heterozygous alpha thalassemia trait asian (cis-deletion) parents, and modified it to also show the inheritance by two heterozygous alpha thalassemia african (trans-deletion) parents. Here you go: https://drive.google.com/open?id=1HQU1VuhI4Jc9WJR2POwnTq9T8wEdv7dw

makinallkindzofgainz  broken link

 +10  (nbme23#32)

FA 2019 page 453: Ganglion cyst = Fluid-filled swelling overlying joint or tendon sheath, most commonly at the dorsal side of the wrist. Arises from herniation of dense connective tissue..

FA doesn't discuss long-term prognosis/course.

Per this article (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682407/), the ganglion cysts fluid is due to extra-articular mucin droplet accumulation. It also indicates 50% undergo spontaneous resolution. On examination, wrist ganglion are usually 1–2 cm cystic structures, feeling much like a firm rubber ball that is well tethered in place by its attachment to the underlying joint capsule or tendon sheath. There is no associated warmth or erythema and the cyst readily transilluminates.

To rule out the other options:

A. Per the above article, these aren't really cysts because there is no lining: "It should be emphasized that since no synovial lining exists in these structures, they cannot be classified as true cysts. Though there are focal areas of mucinous degeneration in the cyst wall, neither significant global degenerative changes, necrosis nor inflammatory changes within the pseudocyst or surrounding tissues have been demonstrated" = A is wrong as it wouldn't have malignant potential.

B. Honestly not sure how to rule this answer out because if it compressed the superficial radial nerve branches, theoretically it could cause paresthesias. That being said, the couple of articles I've read have only indicated potential paresthesia due to ganglion cyst being due to dorsal cysts, NOT volar cysts. C. Based on these pictures (http://bit.ly/30hccjo, http://bit.ly/30loCH4, http://bit.ly/30kFrBV, and http://bit.ly/30qahZN), volar ganglion cysts (as this patient has) do not cause extensor retinaculum nerve entrapment, and thus are unlikely to produce radial nerve palsy. Also, the radial nerves closes to a volar ganglion cyst, seem to be cutaneous as opposed to motor, so if they did cause compression, it would likely only lead to sensory deficit, not motor deficit.

D. Yes, 50% spontaneously regress.

E. Synovitis = no because it is not an inflammatory condition

apc  One thing to correct, this is a dorsal cyst (not volar). Dorsal normally doesn't have compression sx, but volar can be in contact with neurovascular structures (median nerve or radial artery) & may need ultrasound-guided aspiration

 +6  (nbme23#47)

Murmurs and maneuvers: 1st thought = how does it change with preload. All murmurs except HOCM, MVP, and atrial myxoma severity is directly proportional to change in preload (i.e. increased preload=worse murmur, etc.). Because of this, DDx can be narrowed down to HOCM, MVP, and atrial myxoma right away because the murmur worsened with decreased preload (i.e. standing up) when all but exceptions with improve.

Atrial myxoma = MCC primary cardiac tumor due to proliferation of connective tissue mesenchyme; a pedunculated mass connected via stalk to atrium septum that is suspended in the atrial blood volume and moves with the volume movement.

Presentation: triad of 1) mitral valve obstruction (i.e. malaise, symptoms of cardiac failure, syncope, etc.), 2) symptoms of embolism (i.e. facial and right arm hemiparesis in patient), and 3) constitutional symptoms (i.e. fever, weight loss, symptoms resembling connective tissue disease, because tumor releases IL-6). Others include neurologic symptoms, "pseudo-mitral valve disease" auscultatory findings (i.e. diastolic murmur), and atrial enlargement (which could compress underlying structures and cause symptoms also).

Not only does standing decrease preload, which means LA volume is lower so mass isn't as "suspended" but more mobile, standing also increases the downward gravitation force, which would contribute to the tumor moving towards the base of the atrial chamber, "plopping" on the mitral valve leaflets, and potentially extending through and causing a functional type of mitral stenosis (i.e. worsening diastolic murmur). This video explains it really well: https://www.youtube.com/watch?v=slIY64nViLg&t=161s

dentist  Sorry, you narrowed it down to HOCM, MVP, and LA myoxma, but I only see LA myxoma as an answer choice. Wouldn't you have been able to stop right there?
hello  @dentist, I appreciate this full answer b/c nwinkelmann is telling those of us that were wondering "how to ddx one from the other in case we need to"?
hello  @dentist btw, HOCM is an answer choice (RVOT is part of HOCM)
thotcandy  @hello but since that's pseudo-aortic stenosis, it would present with a systolic murmur, correct?

 +9  (nbme23#33)

I literally just realized why this question confused me so much (and I've tried to figure it out a couple of times, lol). I let the colloquial definition of bulimia (i.e. vomiting) stick in my mind, that I forgot the actual medical definition = normal BMI (>18) + binge eating and purging (where purging could be induced vomiting or diuretic use or laxative use or/and excessive exercise). So really, what this question was asking is simply what is the electrolyte balance of excessive diarrhea? GEEZ! I made it so much harder in my head when trying to answer it originally.

Diarrhea causes non-anion gap (i.e. hyperchloremic) metabolic acidosis. Stool predominantly contains HCO3- and K+, so excessive diarrhea = excessive loss of HCO3- and K+. Chloride levels in the serum will be increased due to the normal HCO3-/Cl- equilibrium, so as negative charge dissipates due to loss of HCO3-, Cl- will increase correcting the anion-gap.

drdoom  Bulimia comes from Greek "ravenous hunger"; the term is a literal concatenation of the words for ox (bous) + hunger (limos). So, in Greek, bou-limia is literally "ox hunger", which is a nod to how the word is used in medicine = perpetual and insatiable appetite for food (the very "opposite" of vomiting).
abhishek021196  I agree with your reasoning but the classic case description of Bulima lists electrolyte disturbance of HypOkalemia, HypOchloremia, and Metabolic Alkalosis, along with other things like parotid hypertrophy and dorsal hand calluses due to the induced vomiting. I tripped up there. :/ FA 20 Pg 567
llamastep1  Take home lesson: reasoning > memorizing

 +0  (nbme23#2)

Another way to look at: this question is essentially asking what is the MCC side effect of chemotherapeutic agents in general? Answer = bone marrow suppression thus affects granulocytes.

 +5  (nbme23#13)

Per pathologyonlines.com

Leukoplakia = risk factors include male gender, 40-70 years old, smoking, White patch or plaque, 5 mm or more, on oral mucous membranes that cannot be removed by scraping, not due to another disease entity such as lichen planus or candidiasis and not reversed by removal of irritants and lesion must be considered precancerous until proven otherwise. Premalignant lesion transformation would lead to invasion of the submucosa.

Micro = Varies histologically from acanthosis, hyperkeratosis, dysplasia or carcinoma in situ (associated with lymphocytes and macrophages). This article explains it much better and has pictures: https://emedicine.medscape.com/article/1840467-overview#a6. Based on this article and the pictures, I'd say the histo slide in the question is at least moderate squamous dysplasia.

Hairy Leukoplakia = White, confluent patches of fluffy (hairy) mucosa, bilateral, along lateral tongue, and associated with HIV+ patients (AIDS may appear within 2 - 3 years) but actually due to EBV infection

Histo = Hyperkeratotic oral mucosa due to piling of keratotic squamous epithelium, Cowdry type A intranuclear inclusions, Balloon cells with margination of chromatin (nuclear beading); EBV present in clear cells of spinous layer, variable koilocytosis, superimposed Candida infection, without inflammatory response.

From pictures (and this video: https://youtu.be/Shx61qKuIv8 timestamp 1:22), hairy leukoplakia has a lightly stained band of cells "ballon cells" in the stratum spinosum which is where the EBV lives. It looks much different than the histo slide shown in the question.

yb_26  great explanation, thanks for sharing!
shriya goyal  great explanation thanks
cathartic_medstu  on point

 +4  (nbme23#4)

So this question was something I really struggled with. I didn't recognize that the presentation was of MERRF as someone stated below, and I know you don't need to know that to answer the question, but it would have been helpful. My biggest frustration was the wording of the biopsy results "abnormal accumulations of mitochondria." This annoyed me because the definition of ragged red fibers (which I'm assuming was their intention) is "accumulations of abnormal mitochondria." Those are two very different statements in my mind, lol. The first, to me, just means there's too much mitochondria, but the second means there's too much AND they aren't functioning properly. It's also just the fact of remembering all of the terms for ETC at the time of reading the question (i.e. I didn't think about the fact that ETC is also called cellular respiraton or just respiration).

I also didn't really understand fully what VO2max is = "VO2 max, also known as maximal oxygen uptake, is the measurement of the maximum amount of oxygen a person can utilize during intense exercise... and is based on the premise that the more oxygen consumed during exercise, the more the body will generate adenosine triphosphate (ATP) energy in cells... VO2 max is reached when your oxygen consumption remains at a steady state despite an increase in the workload. It is at this plateau that the [muscle] moves from aerobic metabolism to anaerobic metabolism" https://www.verywellfit.com/what-is-vo2-max-3120097.

Based purely on this definition, where VO2max = essentially the time at which aerobic switches to anaerobic respiration, my interpretation of too much mitochondria vs too much and bad mitochrondria didn't matter, because even when the mitochondria are functioning properly, they reach a point and switch to anaerobic, thus if there was too much normal mitochondria, this would occur faster because there would be more overall cellular respiration occuring, meaning the body would switch to anaerobic and utilize glycolisis to lactate for energy, stop utilizing the mitochondria, and thus VO2max would decrease.

HOWEVER.... because this is a MERRF question, the order of events is a little different, despite the outcome being the same (at least that's how I understand it). So, I think the key to any mitochondrial disorder is remembering that the mutations are almost certainly going to affect an encoded protein and thus a deficiency of that protein. One article that I found said that the tRNA mutations (as in MERRF) cause: "disrupt mitochondrial protein synthesis, decreasing the activity of Complex I and to a lesser extent Complex IV... which decreases respiration and lowers proton pumping, dramatically decreasing the membrane potential and proton electrochemical potential gradient across the mitochondrial inner membrane. The proton electrochemical potential gradient is the driving force for ATP synthesis and decreasing it substantially lowers the maximal rate of ATP synthesis." https://febs.onlinelibrary.wiley.com/doi/full/10.1046/j.1432-1327.1999.00066.x

Based on my understanding of oxidative phosphorylation, O2 consumption (i.e. taking the electron from complex IV and putting it on 1/2 O2 to create H2O and H+ drives the proton gradient which drives ATP production. Thus: deficient respiratory oxidation (i.e. mtDNA mutations of the ETC enzymes) leads to lowered O2 consumption (so lowered VO2 max) which then leads to lowered ATP production, and thus defective mitochondria. Then, lowered mitochondrial function leads to decreased aerobic respiration shunting ATP production to anaerobic respiration, driven by glycolysis, and thus increasing lactate levels.

Hope this helps! This took me WAY TOO LONG to figure out, lol, but hopefully I never freaking forget it, lol.

Also, if you want any more reading, I finally found an article that actually fully explains the biochemical and pathophysiology of mitochondrial myopathies: https://academic.oup.com/brain/article/126/2/413/332457

Sorry it's so long!

djtallahassee  lol yea. I thought they were trying to say there was an abnormally large amount of mitochondria present which made me get the opposite answer :/
alexxxx30  no I so agree. The grammar was completely wrong (clearly whoever wrote the question needs to work on english). This was very frustrating to me because I recognized that it was ragged red fibers, but then the wording made me doubt my own knowledge (thinking how could the test writer mess that up?). abnormal accumulations either means too much or too little. accumulations of abnormal mito means thee mitochondria is faulty. Correct grammar is putting the adjective right next to the word it is describing. So this was definitely wrong and I share your sentiment. This really frustrated me!

 +9  (nbme23#42)

@gh889 "Because the obstruction is above the alveolar regions there is a decrease in air flow, not lung volumes, which would make this an obstructive pathology" is the most helpful explanation. If you know the most basic definition/pathophysiology of obstructive vs restrictive (which I do, just didn't in that most simplified way), then you can figure anything out. If something is impacting airway flow = obstructive, if something is impacting airway volume = restrictive. THANK YOU!

burningmoon  How about emphysema? airway volume changed but it's obstructive.
almondbreeze  i think OP meant to say that something DECREASING airway volume = restrictive
jgraham3  I think they mean if something is impacting LUNG volume (ie. expansion/compliance) = restrictive Airway disorder --> obs. / Parenchymal disorder --> res. With emphysema the airway collapses (obs.) before they are able to exhale fully thus the air is trapped

 +12  (nbme23#32)

So, for some reason, neurotransmitters is something I've ALWAYS struggled with... probably because I wasn't taught it well so never really learned it, just learned enough for whatever exam. I just found this boo through NCBI and its FANTASTIC! It's from 2001 so might be old, but it was great. You can search through the book and find the chapters. I pretty much just went through all of the neurotransmitter chapter. https://www.ncbi.nlm.nih.gov/books/NBK10799/

My main take-aways: Glutamate = major excitatory neurotransmitter. Two types of receptors: 1) metabotropic, most of which are presynaptic Gi which leads to decreased NMDA receptor activity and risk of exocitotixicity, or postsynaptic Gq receptors that lead to increase Na+, K+, and decreased glutamate causes depolarization and increased Mg++ displacement and NMDA receptor activity and risk of exocitotxicity, and 2) ionotropic channels including NMDA and AMPA/kainate channels, which all allow nonspecific cation influx, but only NMDA allows Ca++ influx (and only in a voltage dependent manner after sufficient depolarization has displaced the inhibitor Mg++ ion in the channel).

GABA and glycine = inhibitory neurotransmitters. 1) GABA-A and GABA-C = ionotropic channels that lead to eflux of Cl-, and despite this causing depolarization, the neuron still stays below resting potential. GABA-A binding site for barbiturates, steroids, GABA, and picrotoxin = inside pore of channel. GABA-A binding site of benzodiazepines = outside of pore of channel. 2) Glycine channel is a very similar Cl- eflux channel. 3) GABA-B is a metabotropic channel that activates Gi leading to decreased cAMP which activates efflux K+ channels and inhibits Ca++ influx channels leading to hyperpolarization.

Biogenic amines = catecholamines dopamine (coordination of body movement, reward, motivation, reinforcement), norepinephrine (sleep, wakefulness, attention, feeding behavior, epinephrine (lowest concentration in CNS), plus serotonin (sleep, wakefulness, depression, anxiety, nausea) and histamine (arousal, attention, allergy, tissue damage, and may influence blood brain flow). Obviously, all of this is in addition to adrenergic neurotransmission and flight, fright, and fight response.

ATP and other purines = excitatory transmission, co-released with other small-molecule neurotransmitters. Adenosine isn't classically considered a neurotransmitter because it isn't stored/released in Ca++ dependent manner, but derived from ATP before having an excitatory potential.

Acetylcholine = major neurotransmitter involved in neurotransmission via muscarin and nicotinic receptors.

Peptide neurotransmitters = commonly released as propeptide larger precursors that are cleaved by specific enzymes that were in the same neurotransmitter vesicle upon release. Five types = brain/gut peptides, opioid peptides, pituitary peptids, hypothalamic releasing hormones, and those not classified. Examples = precursor that gives rise to substance P (hippocampus, neocortex, and GIT and released from small diameter PNS C fibers that transmit pain and temperature information, powerful hypotensive, inhibited by opioid peptides), neurokinin A, neuropeptide K, and neuropeptide gamma, and opioid peptides including plant alkaloids (like morphine), synthetic opioid derivatives, and endorphins, dynorphins, and enkephalins. In general opioid peptides are depressants (i.e. analgesia mechanism), involved in complex behaviors (sexual attraction, aggressive/submissive behaviors), and implicated (though not definitive) in psychiatric disorders.

Overall, neurotransmitters = type types: small-molecule transmitters and neuropeptides, where small-molecules transmitters are faster and mediate rapid synaptic transmission (i.e. androgen SNS fight/flight/fright quick response), where as neuropeptides (along with biologic amines and some small molecule transmitters) are slower and mediate gradual, prolonged neurotransmission.

Some pictures: http://tmedweb.tulane.edu/pharmwiki/doku.php/overview_of_cns_neurotransmitters, https://www.semanticscholar.org/paper/Targeting-GABAB-receptors-for-anti-abuse-drug-Phillips-Reed/a049643bb25c8631e0267a40182e6d310d1f31fb/figure/0, and https://www.bluelight.org/xf/threads/difference-between-gaba-a-and-gaba-b.733916/#lg=_xfUid-1-1562540128&slide=0

sweetmed  This is amazing. thank you
sweetmed  This is amazing. thank you
paulkarr  Woah...
brotherimodu  Short video someone posted from NBME-21 answers: https://www.youtube.com/watch?v=4-DuvwoH2zQ

 +0  (nbme23#9)

So, in researching this further, I figured out a way to rule the other answeres out. Per this article, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4683803/, humoral hypercalcemia of malignancy is caused by 4 mechanisms with excess PTHrP secretion being MCC. Excess PTHrP secretion occurs in "squamous cell cancers, urinary tract cancers (renal cancer and bladder cancer), breast cancer, nonHodgkin's lymphoma, and ovarian cancer account for the majority of malignancies leading to hypercalcemia via PTHrP." The other 3 causes include hypercalcemia secondary to overproduction of cacitriol, osteolytic metastases, and PTH mediated hypercalcemia (parathyroid carcinoma and ectopic production). Also, FA only mentions PTHrP in regards to SCC of lung and renal cell carcinoma.

Prostate, colon, and pancreatic cancers are more commonly adenocarcinoma, and less likely to release PTHrP, and thyroid cancer is also less likely, though I did find one article that found PTHrP released by all of these cancers so I don't know. I guess I'm just going to go with SCC of lung being MCC of PTHrP humoral hypercalcemia of malignancy, plus patient's demographics (60's male).

 +0  (nbme23#7)

I found this about raised ICP: "Presentation of raised intracranial pressure = headache, papilledema, nausea/vomiting, worse in the morning as ICP raises during the night as a consequence of recombency, a rise in PCO2 during sleep caused by respiratory depression, and probably a decrease in CSF absorption, pupillary dilation, ptosis, imapired gaze, respiratory irregularity, AMS, and changes in BP, HR, and respiratory pattern are usually late signs of raised ICP and related to brainstem distortion or ischemia."


 +2  (nbme22#4)

This article explains the pathophysiology well: https://www.ncbi.nlm.nih.gov/books/NBK431048/.

The right ventricle is primarily supplied by the RCA which also supplies the SA node and AV node (90% of hearts because they are right dominant), leading to loss of contractility of the right side, and thus fluid buildup causing elevated central venous pressure. Elevated pressures in the liver and portal system would lead to hepatomegaly and free fluid accumulation in the peritoneum.

henoch280  Hellppp. pls why is it not decreased capillary oncotic pressure?
whoissaad  @ henoch280 Because there is no change in the levels of protein in the blood.
drzed  theoretically you could develop liver failure from the increase in central venous pressure (e.g. cardiac cirrhosis) and THEN you would develop a decrease in oncotic pressure.

 +1  (nbme22#7)

So, I thought this question was super vague and not great... that being said, having gotten it wrong and not really having a good explanation for the answer, I did a little research and found this article: https://www.ahajournals.org/doi/pdf/10.1161/01.STR.30.4.715

This was the main conclusion: "The results of the present study, aimed at assessing the effects of stroke on sexual functioning, reveal a significant decline in libido, coital frequency, sexual arousal, and satisfaction with sexual life in both stroke patients and their spouses. The present results also demonstrate that disorders of sexual functions are most significantly associated with various psychosocial factors, such as patients’ general attitude toward sexuality, fear of impotence, and ability to discuss sexuality, as well as with the degree of poststroke functional disability. Moreover, sexual dysfunction was related to the presence and degree of depression, diabetes mellitus, and cardiovascular medication. The etiology or location of the stroke and the gender or marital status of the patients were not associated with changes in poststroke sexuality in patients in the present study."

Looking at the question again, I'm guessing the "fatigue and difficulting sleeping and concentrating" statement was supposed to be a clue for depression, especially since it started after his stroke. Also, no physical abnormalities suggest functioning is intact and thus nocturnal erections would be preserved normally. This is just stupid.

ls3076  appreciate this kind of effort to look up journal articles but honestly this is not really what nbme answers is for... we should be able to get the answer from process of elimination/basic science concepts and not from looking up studies as we obviously can't do this on the test

 +7  (nbme22#9)

I've never been good at converting units :( lol so had to ask my brother. He told me that:

distance × distance = distance2 = area


distance × distance × distance = distance2 × distance = distance3 = volume

Gotta love public school for never been taught that ... geesh (obviously I've done the equations and stuff, just never been told it that way/that simple before). Knowing that makes figuring out the equation much easier:

Flow rate = velocity × CSA = 20 cm/sec × 2cm2 = 40cm3/sec

To convert to L/min, just multiply:

40cm3/sec × 60 sec/min × 1L/1,000cm3 = 2400 L/1,000 min = 2.4 L/min

Hope this helped!

impostersyndromel1000  to all my public school peeps out there (and not the nice public schools in rich areas, the real public schools)... we made it!
angelaq11  Thankfully I was taught how to convert units, but let me tell you that I was SO lost on this one. It's USELESS to know how to do it if you (I, I mean I) don't know the damn formula xD. Obviously got this one wrong, but it's good to know that if it ever comes up again (and I know it won't) I already know it.

 +1  (nbme22#41)

Here's some epidemiology information about spontaneous pneumos: There are two kinds, primary spontaneous pneumos (PSP) and secondary (SSP). PSPs occur in people aged 20-30 years, with a peak incidence is in the early 20s, is rarely observed in people older than 40 years, with a male to female ratio of 6.2:1, and most frequently occurs in tall, thin men, though smoking increases risk even further. SSPs occur in patients with underlying lung conditions, such as COPD/older patients. If the patient's demographic was older and had history of lung disease, but that wasn't an option, then I think smoking would be the appropriate choice because smoking is the biggest risk factor for underlying lung conditions.

Regarding the trauma, traumatic injury pneumos most commonly occur due to motor vehicle acidents where there is injury (i.e. fracture) to chest wall, and with blast injuries. Although the question didn't specify the chest wall was void of fractures, it also didn't say fractures were present, so I think it would be safe to assume that the collision injury didn't have enough force to cause the pneumo, especially with keeping in mind the epidemilogy of primary spontaneous pneumos.

At least, this is my thought process having researched it more, now.

 +3  (nbme22#1)


Like most other causes of hyponatremia, heart failure impairs the ability to excrete ingested water by increasing antidiuretic hormone levels. When cardiac output and systemic blood pressure are reduced, "hypovolemic" hormones, such as renin (with a subsequent increase in angiotensin II formation), antidiuretic hormone (ADH), and norepinephrine, respond [1-3]. Although edematous patients with heart failure have increased plasma and extracellular fluid volumes, the body perceives volume depletion (reduced effective arterial blood volume) since the low cardiac output decreases the pressure perfusing the baroreceptors in the carotid sinus and the renal afferent arteriole. The degree of neurohumoral activation is generally related to the severity of cardiac dysfunction, as assessed by left ventricular ejection fraction or functional class [2]. The neurohumoral changes limit both sodium and water excretion in an attempt to return perfusion pressure to normal. ADH release directly enhances water reabsorption in the collecting tubules, whereas angiotensin II and norepinephrine limit distal water delivery (and thereby water excretion) by lowering the glomerular filtration rate (due to a marked reduction in renal perfusion) and by increasing proximal sodium and water reabsorption [4]. In addition, both the low cardiac output and high angiotensin II levels are potent stimuli to thirst, leading to enhanced water intake.


 +2  (nbme22#50)

I know that complete moles do not contain fetal tissue (i.e. only chorionic villus, cytotrophoblast, and syncyciotrophoblasts) and partial mole as fetal tissue, chorionic villus, cytotrophoblast, and syncyciotrophoblast. Obviously hematopoietic stem cells are fetal parts as they turn into blood cells, but what is the overall definition of fetal parts?

 -1  (nbme22#46)

I interpreted the patient to have PCOS (hirsutism, amenorrhea, ovarian mass) though the super elevated testosterone is more concerning for ncer (per this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1069067/). If the patient has PCOS, she is likely obese and at higher risk for NAFLD which can be associated with elevated alkaline phosphatase, lipid accumulation, and elevated testosterone, but not DUE to androgenic effects ("serum androgen levels were not associated with the presence of NALFD. This is indirectly confirmed with our result on phenotypes. Namely, there is no difference in NAFLD prevalence between hyperandrogenic, and non-hyperandrogenic or reproductive PCOS phenotypes. NAFLD is considered a hepatic component of metabolic syndrome with a central pathogenic role of insulin resistance that also affects the hypothalamo-pituitary-ovarian axis in subjects with PCOS... Hyperandrogenic state may be due to insulin resistance." http://bit.ly/2FWKGjy).

Then, as said by @btl-nyc, elevated testosterone in a female is converted to estrogen and estrone and feedback inhibits the hypothalamus leading to decreased FHS and LH levels, but FSH is inhibited more, so there is an increased LH:FSH ratio.

Finally, regarding PSA (which does occur in women, who knew? lol), the correlation between testosterone and PSA in men is still pretty week (in this study, there was only a correlation and a weak one at that, after multivariate analysis adjusting for several things https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436005/) so there is definitely not a correlation in women. However, per this study (https://www.ncbi.nlm.nih.gov/pubmed/9062481/) there may be an association between certain androgens (not testosterone) and PSA in women.

 +1  (nbme22#19)

Can someone explain how to rule out the other answer choicers?

warbyparker1  you can r/o SMA because as kidneys ascend they get stuck low in the INFERIOR MA (L3 level). So I guess there should be no problem w SMA
hello  I think friability of vascular tissue would indicate in inflammatory process (the one I can think of is strawberry cervix) -- so i think that's why you can rule out choice C.

 +0  (nbme22#1)

This is a good animation video of abnormalities of gut rotation (MUSIC IS WEIRD, lol): https://www.youtube.com/watch?v=gT85dJTT2QE and part 1 if you want to see a good animation of the normal gut rotation (also weird music, i.e. is the same, lol): https://www.youtube.com/watch?v=49awxUGZvdY

 +2  (nbme22#15)

The explanation by liverdietrying plus the explanation in the article posted below (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989649/) are the best, just need to be combined :). The differential diagnosis table 1 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989649/table/OM-10-0041-SLTB1/?report=objectonly) specifically identifies the condition in this question as postpartum thyroiditis.

Ultimately, if you know that hypothyroidism has a transient hyperthyroidism phase (due to autoimmune destruction of the cells which already had preformed TH and so it was released upon destruction) before hypothyroidism (nonfunctioning cells so can't take up iodine) and that hypothyroidism is a lymphocytic infiltrating thyroiditis, you will know the answer. I had a hard time understanding this at first because we evaluate/diagnose based on the presence of anti-TPO Ab, but the underlying pathogenesis of the thyroid destruction is cell-mediated (type IV hypersensitivity) not Ab mediated (type II hpyersensitivity) like graves. Hashimoto's = lymphocytic infiltration wiht germinal centers (which can transform to B cell lymphoma) with hurthle cells (pinker cytoplasm cells).

 +4  (nbme22#47)

Hyperacute = minutes to hours, host preformed Ab against graft endothelial cell Ag = compliment activation, endothelial damage, inflammation (within the tissue, NOT interstitium), clotting cascade, ischemic necrosis and thrombosis. https://tpis.upmc.com/tpislibrary/kidney/KHAcuRej.html

Acute = weeks to months = graft Ag activates host CD4 and CD8 T cells leading to parenchymal cell damage, interstitial lymphocytic infiltration, and endotheliaitis. https://tpis.upmc.com/tpislibrary/kidney/KARejMod.html

Chronic = months to years, chronic DTH (type IV hypersensitivity) reaction in vessel wall leading to intimal smooth muscle cell proliferation and vessle occlusion, with biopsy showing narrowed vascular lumen and extensive smooth muscle.

GVHD = graft cells (most typically bone marrow transplants) recognize host cells as self/foreign and lead to destruction of host tissue leading to rash, jaundice, diarrhea, and GI hemorrhage (this occurs because most bone marrow transplant patients have undergone full radiation which attacks the rapidly providing cells most (i.e. skin, GI mucosa, hair, hepatocytes) so graft destruction of host cells in those areas leads to symptoms).


 +1  (nbme22#39)

I found this when trying to understand why increased NO caused headaches: Nitrates/nitrites are a very common headache and migraine food triggers (WebMD) and raise nitric oxide levels. High levels of nitric oxide are associated with migraine (Study). Headaches and migraines are also very common in medications that boost nitric oxide, such a viagra (study), but it is unclear why this happens. The original hypothesis was that nitric oxide increases blood vessel size and triggers a migraine, but the viagra study and others disproved this. Newer studies on nitric oxide shows that it increases the peptide (CGRP) that is considered responsible for triggering migraines (Study) after increases in inflammation. Because nitric oxide is associated neurogenic inflammation diseases, it's likely that headaches and migraines from nitric oxide are a warning sign of this inflammation (Study).

The research is basically stating that nitrates raise nitric oxide levels and high nitric oxide levels increase inflammation and headaches and migraines. However, the exact reason why this happens is unknown.


taediggity  Goljan and FA mentioned this as Monday Disease for people who worked in industries that heavily used nitrates, where they would build tolerance during the week and then get a headache when they went back to work on Monday

 +1  (nbme22#9)

This link has a labeled electron microscope image of cardiac myocytes like the question next to a cartoon image, so it's really helpful. There is also a good description. Scroll all the way down to the last figure.


 +3  (nbme22#36)

FA 2019 page 264: A process (not just a document/signature) that requires: Disclosure: discussion of pertinent information (using medical interpreter, if needed), Understanding: ability to comprehend, Capacity: ability to reason a nd make one's, own decisions (distinc t from competence, a legal determination), Voluntariness: freedom from coercion and manipulation.

Patients must have an intelligent understanding of their diagnosis and the risks/benefits of proposed treatment and alternative options, including no treatment.

 +5  (nbme22#35)

I HATED this picture, just like everyone else, lol, so I did some more digging. Everyone below is correct, that the presentation is suggesting an infectious process. UTIs can cause acute pyelonephritis, and if chronic, progresses to chronic. Pyelonephritis is a tubulointerstitial disease. I found this information regarding it, and in the last part, it describes the gross pathology of chronic pyelonephritis. From my interpretation, it sounds like what the picture is showing, but I wasn't able to find a better/just as good one online yet, so I don't know for sure.

Acute Tubulointerstitial Nephritis: Acute inflammation of tubules and interstitium can cause ARF, and if the inflammatory process persists this can evolve into chronic tubulointerstitial nephritis and chronic interstitial fibrosis and tubular atrophy with risk of progression to end-stage kidney disease. Two major categories of acute tubulointerstitial nephritis are acute pyelonephritis and acute hypersensitivity tubulointerstitial nephritis.

Acute pyelonephritis: Caused by bacterial infection most commonly E. coli infection. Hypersensitivity tubulointerstitial nephritis: Caused by an allergic response, for example, to a drug or other substances that are ingested, such as herbal remedies.

By far the most common route of infection in acute pyelonephritis is an ascending infection in the urinary tract, for example, derived from a bacterial bladder infection. Acute pyelonephritis = extensive influx of PMNs within the interstitium, tubules (tubulitis), and lumens of tubules (WBC casts) (http://bit.ly/2JiPyBD).

With persistence or recurrence of acute pyelonephritis, the disease process evolves into chronic pyelonephritis, which usually is accompanied by marked erosion of the papillary tip resulting in dilation of the adjacent calyx (caliectasis).

The most characteristic pathologic features of chronic pyelonephritis are the gross changes in the kidney with broad-based scars in the parenchyma overlying areas of cortical and medullary atrophy with adjacent caliectasis. Also, the presentation suggests hydronephrosis, and from my research, hydronephrosis, when chronic/sever, can contribute to the marked loss of cortex and scars/fibrosis of the medulla (https://webpath.med.utah.edu/RENAHTML/RENAL007.html) and caliectasis (which I think is present on this picture). This is the closest picture with description I could find that matches the stem presentation (i.e. hydroureter and hydronephrosis, suggesting vesicoureteral reflux leading to infection from "a long standing obstruction (probably congenital)" so likely from a child) https://webpath.med.utah.edu/RENAHTML/RENAL008.html.

Also, to mention on the other comments expressing frustration that the same picture was used for tumors and tubular atrophy, from what I read, that gross pathology, is the general appearance of hydroureter due to obstructive uropathy (i.e. tubular atrophy, fibrosis/scarring, caliectasis/calyx dilation, and thin cortical rim due to atrophy. Pathologyonline.com says that the caliectasis is exaggerated in less severe cases/partial obstruction since GFR is not suppressed https://www.pathologyoutlines.com/topic/kidneyobstructive.html).

Hope this helps everyone! It sure helped me, but took WAY too long to understand, lol.

nor16  nice job, but i dont think you need all this for these questions

 +0  (nbme22#1)

Per Wikipedia: The triceps reflex, a deep tendon reflex, is a reflex as it elicits involuntary contraction of the triceps brachii muscle. It is initiated by the Cervical (of the neck region) spinal nerve 7 nerve root (the small segment of the nerve that emerges from the spinal cord). The reflex is tested as part of the neurological examination to assess the sensory and motor pathways within the C7 and C8 spinal nerves.

Also, from a different website: The triceps reflex is mediated by the C6 and C7 nerve roots, predominantly by C7. https://informatics.med.nyu.edu/modules/pub/neurosurgery/reflexes.html.

 +5  (nbme21#2)

In case anyone is a dense as I am and just didn't understand/remember what exactly expiratory flow is = FEV1. In restrictive conditions, FEV1 is normal or increased due to decreased FVC. Interstitial fibrosis = increased airway parenchyma scaffold around the airways, which is what provides radial traction. The greater the radial traction, the lower the collapsing force, and so expiratory flow is increased.

champagnesupernova3  FEV1 is increased due to greater recoil of the lung tissue. FEV1/FVC is increased bc of that and bc of decrease in FVC

 +0  (nbme21#45)

So I looked into this further too because I pretty much know nothing about the make up of semen. From the research I found, as as stated below by yo, fructose is the most important constituent of semen in terms or sperm function. Below is information I found to address the other answer choices.

Zinc deficiency (in serum), per FA, has been implicated in delayed wound healing, suppressed immunity, male hypogonadism, decreased adult hiar (axillary, facial, pubic), dysgeusia, anosmia, acromdermatitis enteropathica (defect in intestinal zinc absorption), and may predispose to alcoholic cirrhosis. FA didn't specify the levels in the semen, but per the below article, seminal zinc content was found to have nor correlation to sperm/semen activity/level/etc. I don't know if we're supposed to know that, but now I do, lol. https://www.ncbi.nlm.nih.gov/pubmed/3570537.

As hungrybox mentioned, selenlium is only mentioned once in FA as a treatment for tinea, so I looked into it further. Selenium is a content of semen, but levels vary so much that it serves no prognostic clincal relevance to infertility, per this article: https://www.ncbi.nlm.nih.gov/pubmed/3235210.

To rule out all of the answers (because I didn't really know anything about the quality fo semen), I found this "By t-statistics, there was no significant difference in the semen Na concentration among the different groups (7 groups total based on sperm count), indicating the insignificant role of Na in sperm motility.". https://www.ncbi.nlm.nih.gov/pubmed/721152.

Finally, I don't think the 5-alpha reductase enzyme is actually in semen, but I could be wrong. Either way, it wouldn't be abnormally elevated or low if the testosterone levels are normal.

 +6  (nbme21#45)

So I looked into this further too because I pretty much know nothing about the make up of semen. From the research I found, as as stated below by yo, fructose is the most important constituent of semen in terms or sperm function. Below is information I found to address the other answer choices.

Zinc deficiency (in serum), per FA, has been implicated in delayed wound healing, suppressed immunity, male hypogonadism, decreased adult hiar (axillary, facial, pubic), dysgeusia, anosmia, acromdermatitis enteropathica (defect in intestinal zinc absorption), and may predispose to alcoholic cirrhosis. FA didn't specify the levels in the semen, but per the below article, seminal zinc content was found to have nor correlation to sperm/semen activity/level/etc. I don't know if we're supposed to know that, but now I do, lol. https://www.ncbi.nlm.nih.gov/pubmed/3570537.

As hungrybox mentioned, selenlium is only mentioned once in FA as a treatment for tinea, so I looked into it further. Selenium is a content of semen, but levels vary so much that it serves no prognostic clincal relevance to infertility, per this article: https://www.ncbi.nlm.nih.gov/pubmed/3235210.

To rule out all of the answers (because I didn't really know anything about the quality fo semen), I found this "By t-statistics, there was no significant difference in the semen Na concentration among the different groups (7 groups total based on sperm count), indicating the insignificant role of Na in sperm motility.". https://www.ncbi.nlm.nih.gov/pubmed/721152.

Finally, I don't think the 5-alpha reductase enzyme is actually in semen, but I could be wrong. Either way, it wouldn't be abnormally elevated or low if the testosterone levels are normal.

bartolomoose  as per goljan, selenium is involved in glutathione peroxidase
chandlerbas  selenium has a role in glutathione peroxidase. excess selenium = garlic breath, hair loss, and nail changes, might see peripheral neuropathy. deficiency (pt on TPN) = dilated cardiomyopathy
chandlerbas  also zinc aids in sperm motility https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773819/ thats why i chose zinc but whateverrr im over it

 +0  (nbme21#41)

If you struggle with Biochem and haven't heard of Moof Universitry, I would highly recommend checking it out. The below information I got from this video: https://courses.moofuniversity.com/courses/take/medical-biochemistry-for-usmle-step-1-exam/lessons/4363869-porphyrias-porphyria-cutanea-tarda-pct and it's great.

Porphryia cutanea tarda = AD mutation of uroporphyrinogen decarboxylase, this is the MCC of porphyria, and it presents in 40s-50s.

Main symptom of photosensitivity leading to skin lesions/blisters/bullae due to skin porphyrinogens being oxidized by light to prophryins that damage the skin, and other skin findings of hypertrichosis/hyperpigmentation.

A key feature is possible liver problems due to associated precipitating factors. MCC precipitating factors = excessive EtOH and OCPs because of CYP450 inducers reducing serum heme levels to be utilized in the new CYP450 enzymes, thus stimulating ALA synthase due to decreased heme inhibition. Other precipitating factors include viral hepatitis, especially hepatitis C, and excess iron as in hemochromatosis. These can lead to elevated AST and ALT levels.

Another sign is dark "port-wine" colored urine which pink fluoresces under Wood light. Absent symptoms = abdominal pain and CNS problems because ALA and PBG do not accumulate. Accumulated products = uroporphyrin III, uroporphyrinogen III, uroporphyrin I, and uroporphyrinogen I.

Treatment = sun exposure avoidance, removal of precipitating factors, phlebotomy, chloroquine (which can bind and lead to excretion of accumulations). Prognosis = excellent.

 +6  (nbme21#47)

Pedigree = XLD (not all generations affected = X-linked, affects males and females similarly = dominant).

Affected fathers = 100% transmission to daughters, 0% transmission to sons.
Affected mothers = 50% to daughters, 50% transmission to sons. Both parents affected = 100% transmission to daughters (due to father's X chromosome), 50% transmission to sons (due to mother's X chromosome). Both parents affected each transmitting both to daughter (homozygous daughter) = 50% and more severe.

If condition is uniformly fatal to males in utero, then the 50% affected based on transmision (as above) will die in utero, and the 50% not affected will have live births. This means, risk of female being affected = 50% and risk of live-born males being affected = 0%.

divakhan  I believe its not XLD, had it been there would still be 25% chance of males to be normal according to the Punnett square. (FA 2020 Page 59.
divakhan  ^ 50% chance of being normal.. which is NOT in the answer, it said 0% chance in males!
divakhan  Plus you'd see disease in EVERY generation if it was Dominant. For it to be XLD, the father I,1 would have transmitted it to his daughter. Instead the parents are carrier in Gen I. so its XLR disease (II, 3 being a homozygous XLR female)
plzhelp123  This is X-linked dominant (think Rett syndrome), if it were x-linked recessive, a female would need to have 2 affected x chromosomes to be symptomatic, which would mean her father would HAVE to be symptomatic as he has only one X chromosome, which is impossible as he would have perished in-utero. The reason the answer is 0 in males is because the question asks specifically about live-born males. If it had asked what is the risk of the fetus being affected then it would be 50% in males (but that 50% would not survive to birth)

 +0  (nbme20#7)

Does anyone know the significance of monocyte motility?

 +10  (nbme20#28)

This explains it really well with a picture: https://www.med.illinois.edu/m2/pathology/PathAtlasf/Atlas01.html.

Hydropic change = one of the early signs of cellular degeneration in response to injury that results in accumulation of water in the cell. Hypoxia/ischemia leads to decease in aerobic respiration in the mitochondria and decreased ATP production due to failure of the Na+/K+ ATPase leading to Na+ and water diffusion into the cell. Individual tubule cells appear swollen and "empty" with almost occluded lumen, glomerulus is hypercellular.

dickass  it's basically from pathoma chapter 1: cellular injury causes swelling
md_caffeiner  @dickass you why arent you on every q stem?
mangotango  do you mean "causing failure of the Na+/K+ ATPase" instead of "due to failure of Na+/K+ ATPase..." ? The low ATP is due to dec aerobic respiration, I believe.

Subcomments ...

Air and fluid = hydropneumothorax. If that fluid is blood (s/p stabbing), it’s a hemopneumothorax. Lack of mediastinal shift indicates that it’s not under tension.

d_holles  @benwhite_dotcom how can it not be under tension if air is entering the pleural cavity? +1  
nwinkelmann  Because the stab wound isn't functioning like a flap, meaning the air can escape. The reason a tension pneumothorax occurs is because the wound acts as a flap, where on inspiration it is open and air enters, but on expiration is closes and traps the air. +5  
groovygrinch  Also if there was tension, there would be a mediastinal shift. +2  
t123  Also the gastric bubble is elevated, actually suggesting lower pressure. Mediastinum shifts require more pressure, but the gastric bubble confirms it. +  
myoclonictonicbionic  I was overthinking and thought they're implying that the stomach bubble is the air-food level that was seen on the Xray. +  

submitted by radshopeful(14),

The classic side effect of anthracyclines is dilated cardiomyopathy. This question could have gotten tricky if you thought the pulmonary symptoms were due to the drug which could have led you to bleomycin (causes pulmonary fibrosis) but these pulmonary symptoms were most likely a result of dilated cardiomyopathy leading to HF and pulmonary edema.

nwinkelmann  What is the clue that this is not pulmonary fibrosis? How do I decide between Doxorubicin and Bleomycin? +  
ilikecheese  Also both bleomycin and methotrexate cause pulmonary fibrosis, so that helped me rule both those out and focus on the HF instead of the pulmonary symptoms +4  
adisdiadochokinetic  The S3 gallop and enlarged heart together are very strong evidence for heart failure. It's much more likely for heart failure to cause interstitial edema than for pulmonary fibrosis to directly cause heart failure. +5  

submitted by colonelred_(79),

Looked it up and found that because you’re in a supine position for a long time you’re going to have increased venous return which leads to increased CO. This negatively feedsback on RAAS, leading to decreased aldosterone. As a result, you’re going to have increased diuresis which leads to decreased blood and plasma volume.

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +3  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +6  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +2  
yotsubato  You gotta be preggers to compress your IVC +4  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +2  
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +1  
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +  
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +  

submitted by neonem(451),

Falling on outstretched hand: scaphoid is most common one to be fractured, lunate is most common to be dislocated. Lunate dislocation can cause acute carpal tunnel syndrome.

Think of the mnemonic "Straight Line To Pinky, Here Comes The Thumb" for the bones of the palm, drawing a football shape starting below the thumb MCP joint adjacent to the radius, then moving to your medial wrist, and then back to the thumb.

Scaphoid, lunate, triquetrum, pisiform, hamate, capitate, trapezoid, trapezium. The lunate looks like it's posteriorly dislocated here.

sympathetikey  Yep. I didn't even look at the X-ray. +4  
dr.xx  loonies love lunate +2  
wes79  she landed on her "right hand", but the X-ray is showing a left hand?? +  
wes79  i legit have no idea whats going on in that xray lol +5  
nbme4unme  X-ray confused the hell out of me, I was going to put lunate based on Q stem but ended up putting Pisiform because it looks like that's what's messed up in the photo? Should have ignored the picture haha. +  
nwinkelmann  for @dr.xx, love your mnemonic. I added to it, or at least found an explanation on why it works. "loonies love lunate" and "loonies" are "dislocated" from reality. +3  
doctorevil  She Looks Too Pretty, Try To Catch Her is a mnemonic that works for me. +  
niboonsh  Some Lovers Try Positions That They Cant Handle +4  

submitted by cocoxaurus(48),

BUT why is the serum potassium normal?

I was able to narrow it down to RTA, because none of the other answer choices made much sense, but the potassium had me second guessing myself. Can someone explain that lab finding? Thanks!

subclaviansteele  My take is that hes not super acidotic and the K is at the low end. +  
nwinkelmann  see the comment by @zbird, which explains that the urine anion gap is important (which I took to interpret as more important than the serum K+ level, lol, because the normal K threw me off too). +  

submitted by sattanki(50),

There are two mechanisms of regulating renal blood flow, the myogenic mechanism and tubulo-glomerular feedback. This question asks purely about the myogenic mechanism, which is where the afferent arteriole controls blood flow based purely off blood pressure entering the kidney, which is why decreased afferent arteriolar resistance is the best answer (the arteriole is dilating in response to the decreased blood flow in attempt to maintain normal blood flow to the kidney).

nwinkelmann  Man... I took this WAY TOO FAR, lol. I totally didn't recognize the clue of GFR and RPF as staying the same to tell me it was talking about normal, physiologic autoregulation. Silly mistake! +1  

Ugh... got tripped up with "Refer both patient and her parents to a dietician"

Over thinking...I thought the source of their arguments were at meal times especially...so maybe they can find a good solution with a dietician.

OCCAMs RAZOR THIS SHIT. keep it simple stupid. The answer fits the best after re reading it.

nwinkelmann  SAME.... ugh! +  
johnson  Also - you're almost NEVER referring/passing on a patient with the USMLE. +6  
bmd12  They are at meal times, which is why she's having difficulty following the prescribed diet bc her parents are arguing during that time so its difficult for her to correctly execute it when theyre constantly bickering, and bc she's only 13 so she cant effectively manage her diet without the help of her parents. And since the diet has been working with the patient prior to all the bickering, you can assume the diet is not the root cause. +  

submitted by mousie(135),

looking back at this Q I notice that the patient also has hypertension ...could that have been a clue to include the SMA bc its so close to the renal arteries (Renal a stenosis)?

nwinkelmann  I didn't know how to approach this either, but now this is my thought process: Patient has pain after eating. If it's not due to an ulcer (which is the only thing I could come up with because I didn't know what else it was talking about), why would eating cause pain? Well... eating causes increased GIT activity which means increased blood flow. As you pointed out, the patient has HTN and CAD, indicating likely extensive atherosclerosis. This is important because why would eating leading to increased blood flow cause pain, when usually it doesn't? Well... atherosclerosis in the heart leads to stable angina. This presentation sounds like a "stable angina" of the abdomen. +  

submitted by sajaqua1(389),

The marrow shows precursors to erythrocytes, as well as megakaryocytes. This is to show you that the issue isn't underproduction, which means that we are losing RBC and platelets somewhere ie destruction. That rules out D and E. There is nothing to indicate tha the child has disseminated tuberculosis (B). At this point we are left with A or C. A would indicate Disseminated Intravascular Coagulation (DIC) or something similar, which would result in low platelets and RBC but we would also see abnormal RBC like schistocytes ("helmet" cells). We are explicitly told that the erythrocytes are normochromic and normocytic. However, immune destruction of platelets explains it all- the destruction of platelets leads to some hemorrhaging and so a drop in RBC, and ITP classically arises after a recent upper respiratory tract viral infection.

meningitis  Just in case anyone is wondering like I did, the low platelet count explains thethose multinucleated cells. They are Megakaryocytes in Bone Marrow Biopsy. +9  
nwinkelmann  Also, don't forget that autoimmune thrombocytopenia purpura has 2 demographics: young kids, which generally resolves spontaneously fairly quickly, and then young adult females which is a true autoimmune condition that doesn't resolve. Patient's age + thrombocytopenia + essentially normal rest of heme pannel = autoimmune thrombocytopenia purprua in child. +4  
abhishek021196  That is exactly how I approached this question. Normal heme panel and a decreased Platelet count in a young boy after an infection just made me intuitively select ITP. +  

submitted by welpdedelp(154),

2/3 1/25 1/4

He has a 2/3 chance of being heterozygous (not 2/4 b/c we know he for sure doesn't have CF)

1/25 chance in the population

1/4 chance of a heterozygous couple having a child with CF

welpdedelp  ok, so it messed up the formatting 0.66667 x 1/25 x 0.25 +  
nwinkelmann  ugh... I ALWAYS forget about changing the carrier status to 2/3. Chance of affected individual = chance of father passing allele * chance of mother passing allele = 2/31/21/25*1/2 = 2/300 = 1/150. +  
zpatel  2/3(chance of heterozygous) * 1/25(meet carrier) * 1/2(chance of male to transfer affected gen) * 1/2(female to transfer affected gen) = 1/150 +1  

submitted by wonderboyg(8),

this patient's uterus was increased in size compared to a 12 week uterus. she had grape like structures and no fetus. this would indicate a hydatidiform mole. this patient also had no fetal parts so it would be a complete mole.

according to pathoma, a hydatidiform mole is an "abnormal conception characterized by swollen and edematous villi with proliferation of trophoblasts"

also in a complete mole, most villi are hydropic and trophoblasts will proliferate diffusely around these hydronic villi.

the sheetlike masses of syncytiotrophoblasts would indicate a choriocarcinoma.

nwinkelmann  Also, ball like masses of proliferating decidua, I think, means ectopic decidua, which can be seen in endometriosis, deciduocervicitis, and in the lymph nodes. Markedly dilated fetal blood vessels can be seen in rare complication of placentomegaly which could potentially lead to IUGR but could also result in a normal neonate. +4  
yb_26  @nwinkelmann no, ball-like masses of proliferating decidua are seen in endometrial papillary syncytial change +1  

submitted by sajaqua1(389),

Critical points for this question: 5 year old boy, immunosuppressed because of chemotherapy, 2 day history of fever, cough, shortness of breath, febrile (101.8 F), respirations 46/min, with cyanosis and generalized vesicular rash. Extensive nodular infiltration.

Of the options listed only measles and VZV give a rash. A rash from measles usually starts rostrally and descends caudally, and is flat and erythematous. By contrast, VZV (chickenpox) presents with generalized rash that quickly transitions from macular to papular then to vesicular.

sympathetikey  Good call. +3  
imnotarobotbut  Also, VZV causes pneumonia (what this patient probably had) and encephalopathy in the immunocompromised. +5  
nwinkelmann  What threw me off was that it didn't mention the synchronicity of the rash. I stupidly took failure to mention to mean that the rash was synchronous, which doesn't fit VZV because chickenpox rash is characterized as a dyssynchronous rash (i.e. all stages of the macule to papule to vesicle to ulceration are seen at the same time). MUST REMEMBER: don't add information not given! +1  
jboud86  If anyone wants to refresh info on Vaicella-Zoster virus, page 165 in FA 2019. +1  

The thing is, the spinothalamic tract crosses 2 vertebral levels up and then decussates at the anterior white commissure to get from the right to the left, so how do I know which vertebral level I'd be working on this guy?

chris07  I think the assumption here is that we are dealing with the cord section at the level of the problem. The picture is incredibly misleading. You have to orient yourself. The dorsal columns F, E, A, B are facing the patient's posterior. Once you properly orient it in 3D space, you know that what's labeled "right" is actually the patient's left, and what's labeled "left" is his right side. Super confusing. +2  
sne  The input arises in a limb/part of body at the level of lesion, enters through the dorsal root (pictured between A and B), decussates and ascends at the anterior commissure, and finally synapses on the second order neuron in the lateral spinothalamic tract. So the spinothalamic tract is responsible for contralateral pain and temperature sensation. So AT THE LEVEL technically would be in the dorsal column +5  
nwinkelmann  also, @chris07, I think you're wrong about the labels being wrong on the image. Becuase the spinothalamic tract = contralateral pain and temperature, and the patient's pain is on the right side, you would want to target the left spinothalamic tract for pain relief, i.e. the area labeled H. The area labeled D would be the right spinothalamic, purely because that is how the image is labeled. If you assume the label is different, you will get it wrong. +8  
kpjk  @sne I don't think entering from the dorsal root would be between A and B. It would be part of the gray matter so, lateral to B and F +  

submitted by nlkrueger(27),

.... would we really take the word of a friend who definitely can't be confirmed? I feel like this is misleading

lispectedwumbologist  All the other answer choices make you come across as an asshole. Easy way to ace ethics questions is to just not be an asshole +6  
seagull  I would be a bigger asshole when the family came I'n after I pulled the plug...opps...but the friend said +13  
dr.xx  The patient has no wife, children, or close relatives... +3  
nwinkelmann  @lispectedwumbologist this is going to be my technique, because I've gotten a couple of these wrong, but I completely agree with everyone else's sentiments of suspicion of going off what a friend said without any confirmation about state of advance directives, etc. It's really dumb. +3  
paulkarr  With these questions; you have to take what NBME says at face value. If it says no family, he really does have no family. This friend is also claiming that the 78 y/o said this about himself, so we know it's the patients wishes rather than someone else's wishes for him. (A son saying he can't let go of his father yet despite the patient's DNR type of situation). +  
suckitnbme  I think the point here isn't that we would take the patient off the ventilator because the friend said so. The answer is saying "Thank you for your input, we will take that into consideration." It's completely non-committal. +4  

submitted by dr.xx(100),

Treatment of acute gouty arthritis Several drugs are effective for terminating the acute gouty attack. Colchicine, nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids are standard approaches. Adrenocorticotropic hormone (ACTH) is also very effective, but has become increasingly scarce or too expensive to be a practical alternative in the US. Regardless of the particular agent chosen, the sooner these drugs are started, the more rapid the response. If a patient cannot take NSAIDs or colchicine, the choice is among oral, intra-articular or parenteral glucocorticoids. Local application of ice packs may help control pain. In some cases, analgesics, including opioids, may be added.

Drugs that affect serum urate concentrations (E.G., ALLOPURINOL), including antihyperuricemic agents, should not be changed, started, or stopped during an attack, as this may worsen the inflammatory response already in progress.


nwinkelmann  Love the last quote/sentence from the article! So helpful for clinical decision making! +  

submitted by mcl(453),

In case you wanna go super nerd and read about myelin, capacitance, and resistance, this guy does a good job.

nwinkelmann  This really helped me, at least the pictures did. Here's my interpretation of the pictures in not super scientific terms: capacitance is like the "capaciy" to keep ions close to the membrane. Myelin puts a barrier between the ions in the conductive environment (ECF or ICF) and the nerve membrane. The higher the capacitance, the closer the ions are to the membrane, so it's like the charge effect is "more potent" so harder to change the membrane potentia, whereas if the ions are farther from the membrane, the charge effect is "less potent" so easier to change the membrane potential and thus easier to depolarize. Thus, with myelin, there is decreased capacity of the ions to be close to the membrane, so in demyelinating conditions, the ions can be really close to the membrane, i.e. higher capacitance. +16  
sweetmed  this helped a lot! +  
roaaaj  Well explained! +  
euchromatin69  or see u world 917 same concept +  

submitted by joker4eva76(20),

This is representative of leukoplakia, a pre-cancerous lesion of squamous cells. In order for it to spread to distant sites, it must first invade through the basement membrane/submucosa. Could be confused with oral hairy leukoplakia (which also is a white patch that classically arises on the lateral tongue). However, oral hairy leukoplakia is not pre-cancerous and is often associated with EBV infections or people that are severely immunocompromised.

hpkrazydesi  How did you know that this wasnt oral hairy leukoplakia? just from the picture? +1  
nwinkelmann  To piggyback off of @hpkrazydesi, you ruled out oral hairy leukoplakia because the patient was seeing the doctor for normal health maintenance, i.e. not immunocompromised, I'm assuming. +2  
dentist  @nwinkelmann thats correct! my time to shine. +  

submitted by hayayah(883),

X in the image is the small intestine. Its characteristic feathery appearance after a barium meal is due to permanent circular folds and villi. The villi give the small intestine a great mucosal surface area.

nwinkelmann  Yes. The appearance of the mucosal folds depends upon the diameter of the bowel, and when they fold they appear feathery. Mucosal folds are largest and most numerous in the jejunum and tend to disappear in the lower part of the ileum. +  

Why is this not increased binding of DNA polymerase?

This mutation should cause cellular division ie DNA replication and cause increased binding to origin replication sequences ie TATA by DNA polymerase.

brise  It's talking about mutations on the transcription of genes that inhibit the cell division. Also RNA polymerase binds to the promoter region. +  
nwinkelmann  Also, the question specifically (though in a very wordy, convoluted way) asked what the effect of the mutation on transcription was. DNA pol is not used in transcription, it is used in replication. RNA pol is used in transcription. In terms of increased or decreased binding, argining is polar/positively charged and proline is neutral/nonpolar, so there are fewer H-bonding sites, and thus decreased binding of the RNA pol. +1  
medn00b  Could this convoluted question also mean.......... that since the gene to make p53 is messed up due to the hydrogen bonds, RNA polymerase will not be able to bind to make the mRNA ... So there will be cancer? Because P53 is a tumor suppressor... lemme know thanks guys +  

submitted by keycompany(214),

Loading Dose is the only answer that is independent of drug clearance.

nwinkelmann  I totally get this and understand it... but at the same time, couldn't loading dose differ due to renal function if patient has nephrotic syndrome so had less plasma proteins, because it would change the Vd of the drug, right? Per wiki: Volume of distribution may be increased by renal failure (due to fluid retention) and liver failure (due to altered body fluid and plasma protein binding). Conversely it may be decreased in dehydration. +  

submitted by just_1more(0),

I got that it needed to be a potassium sparing diuretic. Is there a reason it cannot be an aldosterone antagonist? I chose blocks basolateral K+ channels as these decrease the basolateral K+/Na+/ATPase because the wording of the correct answer did not make sense to me -- assuming they were going for an ENaC blocker (and that decreased luminal permeability indicates that Na+ would be remaining in the lumen, not remaining in the principal cell as I originally thought).

luckeroo  I think the reason it’s a potassium-sparing diuretic rather than an aldosterone antagonist has less to do with why the aldosterone antagonist cannot be used and more to do with the fact that a potassium-sparing diuretic would be more of a “first-line” adjunctive diuretic treatment. +1  
luckeroo  As for the answer choice, potassium sparing diuretics achieve their overall anti-aldosterone effect by competitively inhibiting aldosterone receptors on the interstitial side (decreasing the Na/K-ATPase effect of shunting Na into the blood), thereby decreasing the gradient for sodium to enter the cell from the luminal aspect, blocking ENaC. +2  
yotsubato  There is no such thing as "Basolateral K Channel" there is only basolateral Sodium Potassium Pumps which are controlled by aldosterone. FA pg 573 +9  
nwinkelmann  @yotsubato LOL.... why didn't I think of it that what?! (by the way, that LOL is for me). The only basolateral K channel is the nephron (based on the first aid picture) is in the thick ascending limb of the loop of henle. +  
hello  Spironolactone and eplerenone are potassium-sparing diurectics that inhibit the Na/K ATPase, so I'm not sure what @luckeroo is referring to. Spironolactone and aplerenone are both ALDO antagonists. Na/K ATPase is found on the basolateral membrane. None of the answer choices fit with this. Amiloride and triamterene are also potassium-sparing diuretics; their mechanism is to block ENaC channels on the luminal membrane, this is choice "B." +1  
rxfit  From Katzung Board Review: "Spironolactone and eplerenone are steroid derivatives and act as pharmacologic antagonists of aldosterone in the collecting tubules. By combining with and blocking the intracellular aldosterone receptor, these drugs reduce the expression of genes that code for the epithelial sodium ion channel (ENaC) and Na+/K+ ATPase. Amiloride and triamterene act by blocking the ENaC sodium channels (Figure 15–5). (These drugs do not block INa channels in excitable membranes.) Spironolactone and eplerenone have slow onsets and offsets of action (24–72 h). Amiloride and triamterene have durations of action of 12–24 h." So both K-sparing subtypes are technically correct. +  

submitted by seagull(840),

Why spontaneous? He's engaging in an active sport with an increased risk of Traumatic injury. So we really just assume hes not injured because the stem doesnt directly say he's injured? These questions lead to too many assumptions. (in my opinion)

nc1992  Spontaneous pneumothorax, as a condition, is significantly more likely than a traumatic pneumothorax from just about anything but a car crash (ok maybe if he was in a fight). The car crash or a stabbing is also more probable overall but there's no point in inferring something that isn't provided +1  
nwinkelmann  I picked the traumatic injury also. After reading these comments I looked into it further. Traumatic pneumos occur because of blunt or penetrating chest trauma, and I found that the MCC form of blunt trauma (>70%) is motor vehicle acidents that cause significant trauma (i.e. rib fractures) or even blast trauma. Although it didn't say there were no chest wall fractures, at the same time it didn't indicate any rib fractures, which would be most like to cause the traumatic injury pneumo in the patient's case. +1  
drdoom  The stem makes no mention of trauma. +  
hyperfukus  i guess the issue is that you have to assume what they mean by "strongest predisposing risk factor for this patient's condition" I think this is dumb bc the answer is completely different based on what you consider this patient's "CONDITION" to be? either way he has a pneumothorax so if you wan to know what caused that its prob him being active or bumping into someone but if you consider the etiology of the pneumothorax then its the bleb and that is from him being a skinny dude/smoker i went to this b/c he's also only 5/10 that's not tall in my head they could have been nicer and made him 6'1 at least...also i feel like i saw a lot of q's back in the day when i first learned this with a presentation of the person like tripping or something dumb but they already had the bleb and then got the pneumothorax +  

submitted by d_holles(104),

This question confused me bc I thought loperamide could not cross the BBB and therefore could not cause respiratory depression (mu-opioid agonism at the brainstem results in CNS/respiratory depression, 1). But @dr.xx is correct in noting that ↓ RR and CNS depression in the Pt should call for an mu-opioid antagonist rather than bethanchol (cholinomimetic) to treat constipation.

  1. https://anesthesiology.pubs.asahq.org/article.aspx?articleid=2675905
nwinkelmann  http://medresearch.in/index.php/IJPR/article/view/782/1271 This explains a case in an infant. "Respiratory depression and coma after overdosage have been shown to be reversible by injection of naloxone [6]. Owing to its structural similarity to opioid, loperamide toxicity can be reversed by using Nalaxone which is a specific opioid antagonist acts competitively at opioid receptors. Naloxone hydrochloride is usually given intravenously for a rapid onset of action which occurs within 2 minutes." +3  
yb_26  FA 2019: "Loperamide has poor CNS penetration" - so it still penetrates => can cause respiratory depression +3  
whoissaad  Also maybe because the blood brain barrier in a baby is not developed as well as in an adult. +1  

submitted by drdoom(467),

Here’s another very nice one that superimposes the pathway onto a simplified brainstem drawing (nice for the anatomical relations):


Source article:


To see even more, try google image search on “medial longitudinal fasciculus”:


endochondral1  what is A and B in this pic? i knew it was dorsal pons ipsilateral but i just didn't know what part that was on the pic? +  
nwinkelmann  A and B are the superior cerebellar peduncles.http://what-when-how.com/wp-content/uploads/2012/04/tmp15F2.jpg +  

submitted by shaydawn88(8),

I would think resolution involves the stem cells (type II pneumocytes). Is the intact basement membrane the answer because it limits spread?

aesalmon  I would also like to know if anyone can answer this question - I saw it as a Sattar "one day, one week, one month" kind of question. Its probably very simple but I still don't get it +  
bubbles  I posted a new comment explaining: basement membrane integrity is the strongest determinant of full fx recovery following pulmonary insult :) +2  
drdoom  You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the *normal* architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be *disorganized* healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.) +5  
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/ +  

submitted by drdoom(467),

You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the normal architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be disorganized healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.)

drdoom  by "restorative" i mean healing which restores the previous (and normal) tissue architecture. for that to happen, you need an intact basement membrane! +2  
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/ +  

Why wasn’t the table enough to determine prevalence in the general population?

sacredazn  For the case control question, it’s taking that principle that you can’t use case control studies to calculate relative risk and applying it to prevalence. Basically with case control studies we start by saying okay, I’m going to find 200 people with sinusitis and 400 without. Then, you go back and look at the number exposed/unexposed and calculate the odds ratio. So you can’t use case controls to calculate prevalence because it all depends on how many cases you picked in the first place. Might make more sense to think about it with a rare cancer like craniopharyngioma or something- let’s say you chose 10 cases and 10 controls and wanted to look at how many people smoked. It wouldn’t make sense to then say the prevalance of craniopharyngioma is 10/20 = 50%. +12  
dr_trazobone69  Thank you, that makes a lot of sense! So we can use relative risk (cohort studies) to calculate prevalence? +  
sacredazn  @trazobone Hmm I think the wording would be key, you could use a prospective cohort to calculate incidence, but you wouldn’t be able to find prevalence of the gen population unless you had more info. I think the concept is that really to calculate prevalence you need a proper ecologic study looking at population-level data. The way it was worded in the question was tricky though lol since when has “cannot be determined from the info given” ever been a right answer. +5  
nwinkelmann  @sacredazn thank you! this was the best explanation to use the rare disease comparison. Made everything make so much sense and hopefully I'll actually just remember it now, instead of learning the factoid and failing to recall it all the time. +1  
hyperfukus  i guess this makes sense but i don't understand why we are asked to calculate it from tables like this then? is there more info in those? +  
hello  @hyperfukus The table was given because that a 22 table is typically what you do see regarding data for case-control studies. If the 22 table wasn't include, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers. The difference in including the data-table is that 1. again, you need to report a 22 table because that is typically what you will see regarding data for a case-control study and 2. by including the 22 table, it actually tests if the test-taker realized that the data in the 2*2 table does not help at all with calculating prevalence-- because case-control studies NEVER report on prevalence. +  

submitted by niboonsh(218),

Can someone explain the difference between C. (release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes) and D. (Release of thyroid hormone from a lymphomatous thyroid gland.

drdoom  @niboonsh, ending a comment with a question mark will make it appear on the "comments seeking answers" lists +4  
nwinkelmann  A lymphomatous thyroid gland can either be due to primary thyroid lymphoma (which is almost always NHL, but is very rare) or due to Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. These, I believe, would still present with hypothyroidism, and thus would have low T4 and high TSH (opposite of this patient). +1  

submitted by someduck3(41),

Fat soluble vitamins are A,D,E,K. So both D & E could be decreased in this pt. But you have to know that Vitamin E deficiency is associated with demyelination & has been associated with posterior column demyelination. Also Vit E can be given with Alzheimer patients as it helps with free radicals..?

aesalmon  I actually thought that the posterior column findings were likely due to B12 deficiency - "subactue combined degeneration", due to malabsorption, as we see in this pt (. Turns out vitamin E can also cause symptoms which look like subacute combined degeneration: https://www.ncbi.nlm.nih.gov/pubmed/9012278, as does Copper (TIL): https://www.ncbi.nlm.nih.gov/pubmed/15249607 +3  
jooceman739  Vitamin E deficiency causes posterior column findings and hemolytic anemia :) +3  
nwinkelmann  The way I think about it is that essentially, vitamin E is an anti-oxidant. Vitamin E deficiency = LOTS of oxidation, i.e. free radicals, which are toxic to most cells in the body (particularly myelination and RBCs). That's why it can be used with Alzheimer's patients. +3  
makinallkindzofgainz  Vitamin E presents like B12 deficiency but without megaloblastic anemia +  

submitted by sacredazn(59),

The concept is a convoluted way of asking if you knew how VDJ recombination works, which is that it is actually an example of altering the DNA of the B/T lymphocyte.

Southern blot technique: So when they use a probe against some region, and outputting a size of 1.5 kb or 6 kb, this is telling you the size of the DNA fragment in each cell (doesn’t matter if they say J probe or constant region probe, they’re just saying they’re targeting some nucleotide sequence found in the Ig locus/TCR beta chain locus respectively for B/T cells).

I think the confusing part could be wondering how you know whether you’re partly through rearrangement (answer choices B thru D) or if it hasn’t occurred at all yet (correct answer). Here, the concept is that B cells undergo V(D)J rearrangement in the bone marrow, while T cells do it in the thymus, and it all happens at once. So a plasma cell in the blood like in Multiple Myeloma would have fully undergone recombination, while a T cell in the blood could either be fully educated (and have finished VDJ recombination) or immature (hasn’t started VDJ).

Since the T cell gene was 6 kb and definitely bigger than the 1.5 kb gene, the T cell hasn’t undergone recombination yet.

trichotillomaniac  very nice explanation! +7  
nwinkelmann  This was awesome! Made so much sense and hopefully I will be able to think that critically about questions in the future (because I NEVER would have come up with this on my own, hah). +4  
eacv  OMG! THANK YOU. I DIDNT KNOW ANYTHING about this!! Hope this is not testesd on real examen :p +3  
ribosome01  I would like to meet you personally and say thank you I wish I had a teacher like you +  
ajss  wow! this explanation was awesome! thanks! +  
mrglass  Also the T-cell V-D-J segments are not the same as the B-cell V-D-J segments. Therefore a B-cell J segment southern blot would look for whether the B-cell site VDJ segment in a T-cell, which would always non-rearranged. +4  
mynamejeff  Thank you! So is this because multiple myeloma produces excessive monoclonal light chain Ig? Is this the 1.5 kb gene? Whereas, T-cells that have not gone through differentiation yet and their J region includes everything (VDJ) vs. just VJ in the light chain? (FA 2020 pg 104) +  
peridot  This explanation is amazing! However, to fully understand another step of what the question is getting at, please take a look at @highyieldboardswards's and/or @mrglass' explanation as well - a very important addition!! +  

submitted by skraniotis(9),

Undialyzed renal failure leads to metabolic acidosis, and as a result bicarb gets depleted as it tries to buffer the accumulation of organic acids.

bubbles  Thanks for the explanation! Do you know why Mg would not be a potential answer? Phosphate also accumulates in those with undialyzed renal failure, so I was thinking that maybe magnesium as a divalent cation would complex with PO3 (in a mechanism similar to Ca). +  
nwinkelmann  From the little bit of research I just did (because I didn't learn anything about dialysis at my medical school), ESRD can be associated with either low or high Mg levels, so the dialysate can cause either increased or decreased Mg levels depending on the patient's serum content, therefore I don't think based on this question, would could determine if removal of dialysis would lead to elevated or decreased magnesium. The end of the first article seems to favor ESRD leading to hypermagnesemia, so if that's the case, then removal of dialysis would cause Mg to increase as well. https://www.karger.com/Article/FullText/452725 and https://www.karger.com/Article/FullText/485212 +1  
hyperfukus  why is it that we aren't learning this stuff and they r just throwing it on step there's barely a blurb in FA about ckd/eskd +1  
hyperfukus  does uremia potentially have to do with this? +  
medulla  ESRD and not getting dialysis -> he is uremic -> met acidosis -> dec bic +4  
angelaq11  @medulla this is the best and simplest explanation. I got it wrong and chose Mg, wish I had made that connection. +  

submitted by bubbles(51),

Can someone explain properly how we know that this trait follows Mendelian genetics and is autosomal recessive and furthermore how the parents were heterozygous?

I guessed a lot on this question and got lucky :(

niboonsh  Autosomal Dominant disorders usually present as defects in structural genes, where as Autosomal Recessive disorders usually present as enzyme deficiencies. P450 is an enzyme, so we are probably dealing with an autosomal recessive disorder. furthermore, the question states there was a "homozygous presence of p450.....". In autosomal recessive problemos, parents are usually heterozygous, meaning that 1/4 of their kiddos will be affected (aka homozygous), 1/2 of the kids will be carriers, and 1/4 of their kids will be unaffected. +14  
nwinkelmann  Is this how we should attack this probelm?: First clue stating endoxifen is active metabolite of Tamoxifen should make us recognize this undering first pass hepatic CYP450 metabolism? Once we know that, the fact that the metabolite is decrease suggests an enzyme defect, which is supported by patient's homozygous enzyme alleles. Then use the general rule that enzyme defects are AR whereas structural protein defects are AD inheritance patters. Once we know the pattern, think that most common transmission of AR comes from two carrier parents. So offspring alleles = 25% homozygous normal, 50% heterozygous carrier, and 25% homozygous affected, thus sister has a 25% of having the same alleles as patient (i.e. homozygous CYP450 2D6*4)? +6  
impostersyndromel1000  we had the exact same thought process, so i too am hoping this is the correct way to approach it get reasoning friend +  
ajss  thanks for this explanation, I totally forgot about AR patterns are most likely enzymes deficiencies, this kind of make the question easier if you approach it that way, thanks +  

Acknowledge the patient's difficulty. I hate these questions

nwinkelmann  Me too... also, he's had cough that's worsening for 6 months plus hemoptysis for 1 week... I didn't interpret that as "feeling healthy." The correct answer was my first choice just because it was the least "dick-ish" but to me, he didn't sound like he "felt health," so I didn't go with it. +1  
nor16  if he didnt feel healthy, why would he say something like that then... but i agree, these (especially this) question(s) are often XYZ123! +  

submitted by naughtyegg(2),

Downregulating E-cadherin is the first step cancer takes toward metastasis because low E-cadherin helps invade the basement membrane -> eventually leads to spread of cancer elsewhere. Laminin is also involved but according to pathoma, cancer will actually attach to laminin in order to destroy the basement membrane. Idk if receptor up/downregulation happens, that might be a stretch.

nwinkelmann  It makes sense that a tumor cell would increase their laminin, as opposed to decreasing, if attaching to laminin is what allows the cells to destroy the basement membrane. The more laminin, the more destruction possible. +  

submitted by rajkamal17(0),

Pretty sure I’m missing something basic here. This was SCC invading basement membrane facilitated by what? The answer is downregulation of E-cadherin but I thought that’s for metastastses (FA 18 says so too.) I ticked decreased laminin receptors (incorrect) coz laminin was found in basement membrane. At least that was my reasoning. Any help appreciated. Thanks!

naughtyegg  Downregulating E-cadherin is the first step cancer takes toward metastasis because low E-cadherin helps invade the basement membrane -> eventually leads to spread of cancer elsewhere. Laminin is also involved but according to pathoma, cancer will actually attach to laminin in order to destroy the basement membrane. Idk if receptor up/downregulation happens, that might be a stretch. +2  
nuket0wn  per medbullets, there are increased laminin and integrin receptors. Also upregulated MMPs (matrix metallo-proteinases) to breakdown the basement membrane. +1  
nwinkelmann  It makes sense that a tumor cell would increase their laminin, as opposed to decreasing, if attaching to laminin is what allows the cells to destroy the basement membrane. The more laminin, the more destruction possible. +  

submitted by airhead5(3),

Does anyone know the disease they are talking about? I was thinking lupus which makes sense with the answer, but i can’t find anything on anterior chamber of eye and choroid plexus.

liverdietrying  It's lupus, all the symptoms listed are classic especially the serositis. Anterior chamber of the eye = uveitis. Choroid plexus = cerebritis. For a great overview, check out this (free) video: https://onlinemeded.org/spa/rheumatology/lupus/acquire +4  
in_a_pass_life  I think this was reactive arthritis, not lupus. Choroid plexus not just in the brain, also in eye (can’t see, can’t pee, can’t climb a tree). Mechanism of reactive arthritis is immune complex deposition, per UWorld, which was correct answer. +4  
trichotillomaniac  The inside of the eye is divided into two chambers: the anterior chamber and the posterior chamber. Both chambers contain fluid, and when there’s inflammation in the eye, a specialist can often see inflammatory cells in the fluid. https://www.hss.edu/conditions_eye-problems-lupus.asp +  
trichotillomaniac  I agree that this is Lupus after doing some more research! +1  
nwinkelmann  I find this article describing the SLE ocular manifestations, including uveitis and cerebritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908056/ Also this talks about the lupus cerebritis (choroid plexus inflammation): https://en.wikipedia.org/wiki/Cerebritis +  
medulla  every time I read about Lupus there is something new!! +1  

submitted by the260guy(4),

But here's my problem with this question: it says that she has a 5 day history of SOB and swollen legs. So obviously the heart is failing. I picked Decreased Stroke Volume for that reason.

nwinkelmann  AV fistulas are one cause of high-output cardiac failure. This person presents with heart failure, but it is due to chronically increased resting CO. +2  
lukin4answer  @nwinkelmann yes thats right, he has failing heart. but question is asking what is the finding of this patient, I understand the cause is Fistula causing high output failure, but they didn't ask the reason of his HF, they are asking the finding. I choose decrease Stroke VOlume :/ +  

tinidazole preferred due to single dose

sweetmed  or metronidazole +  
niboonsh  what would his diagnosis be tho? +  
lostweightthxnorovirus  @niboonsh Giardia I believe. the trophozoite is pictured in the problem and has a classic "shield-like" appearance. FA 2019 pg. 155 has more information and the sketchy for it was really good! +1  
nwinkelmann  Per FA, DOC for giardia = metronidazole. MOA of metronidazole = formation of toxic free radical metabolites in the bacterial cell wall that damage DNA making it bactericidal and antiprotozoal. Metro treats = GET GAP = giardia, entamoeba, trichomonas, Gardnerella, anaerobes (below diaphragm), and H. pylori (as an alternative to amoxicillin in PCN allergy). Adverse effects = disulfiram-like reaction, HA, and metallic taste. I didn't know what Tinidazole is, and found out it is of the same drug class as Metronidazole, so makes sense why it would also be used for Giardia. For the purpose of the UMSLE 1, though, I think metronidazole would be DOC (especially because tinidazole isn't in FA). +1  
mannywillsee  This little bug has has a face, and now you can't unsee it either! +  

submitted by hungrybox(579),

Great video I used to learn this material.

  1. There are 3 major types of drugs: uppers (stimulants), downers (depressants), and hallucinogens.
  2. Heroin is an opioid. Opioids are downers.*
  3. Downers do what it sounds like. They cause "down" symptoms: sedation/decreased anxiety (and thus behavorial disinhibition), respiratory depression.
  4. Thus withdrawal will cause the opposite: hypertension/tachycardia, anxiety.
hungrybox  *other downers: alcohol, benzodiazepines, barbiturates +2  
nwinkelmann  THANK YOU! for the link to the video. this is one thing I've ALWAYS struggled with. +  
qball  I get that this is a good rule of thumb to help narrow down between alcohol and heroin, BUT is still not enough to answer this question. Some key features for depressants (downer) is alcohol (if we are talking mild withdraw) - tremors , diaphoresis and delirium (heavy withdraw) . For Heroin - Dilated pupils, yawning and lacrimation are key exam findings. +1  

submitted by hayayah(883),

Absolute risk: the difference in risk (not the proportion) attributable to the intervention as compared to a control.

(.12) - (.04) = .08

ARR = 8%

nwinkelmann  This isn't actually correct. Absolute risk is actually just the incidence, or the same as event rate. Absolute risk reduction = the difference in risk (not the proportion) attributable to the intervention as compared to the control, and thus ARR = incidence unexposed - incidence exposed x 100%. In this example, the incidence of exposed is the incidence in the new treatment group, and incidence unexposed is incidence in standard treatment group. +8  

submitted by asdfghjkl(1),

Anyone know why IGF-1 wouldn't be increased as well? GHRH is stimulated in hypoglycemic states.

nala_ula  Honestly, it's something that has confused me for a while. Why is it that GH secretion is stimulated by hypoglycemia? I mean, it's literally called growth hormone (for growth!), and hypoglycemia, which is basically a "starvation" state, will stimulate this hormone? +  
shaeking  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3529368/ This might help answer your question. I basically didn't pick IGF-1 because it would increase the uptake of glucose leading to a worsen hypoglycemic state. Didn't have a true reason otherwise. +  
temmy  IGF-1 is regulated by insulin. so it will be decreased because insulin levels are also low. +2  
nala_ula  thank you @shaeking! +  
nwinkelmann  I found this and it also explains to a more genetic/cellular level. Essentially, it says that starvation induces some factors that cause GH resistance and IGF1 suppression. +1  
nwinkelmann  Sorry forgot the link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575072/ +  

submitted by asdfghjkl(1),

Anyone know why IGF-1 wouldn't be increased as well? GHRH is stimulated in hypoglycemic states.

nala_ula  Honestly, it's something that has confused me for a while. Why is it that GH secretion is stimulated by hypoglycemia? I mean, it's literally called growth hormone (for growth!), and hypoglycemia, which is basically a "starvation" state, will stimulate this hormone? +  
shaeking  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3529368/ This might help answer your question. I basically didn't pick IGF-1 because it would increase the uptake of glucose leading to a worsen hypoglycemic state. Didn't have a true reason otherwise. +  
temmy  IGF-1 is regulated by insulin. so it will be decreased because insulin levels are also low. +2  
nala_ula  thank you @shaeking! +  
nwinkelmann  I found this and it also explains to a more genetic/cellular level. Essentially, it says that starvation induces some factors that cause GH resistance and IGF1 suppression. +1  
nwinkelmann  Sorry forgot the link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575072/ +  

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