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Welcome to azibird’s page.
Contributor score: 92


Comments ...

 +0  (free120#35)

How can we differentiate RSV from the common cold? Is it the bilateral, diffuse wheezes and expiratory rhonchi? Along with the intercostal retractions, signifying significant respiratory problems?

nbmeanswersownersucks  I was initially thinking it was rhinovirus too but in retrospect I think the wheezes etc make RSV more likely +

 +0  (free120#9)

I read this question as analyzing immunoglobulins in the bone marrow vs out circulating peripherally. I now realize this is wrong, and they are just analyzing the DNA of different cell population, like a hepatocyte for example, not immunoglobulins present in the liver.

With this cleared up, I can see how V(D)J recombination could make the original DNA section shorter. But how could V(D)J recombination possibly make the DNA section longer? There are bands on the gel that are higher molecular weight in the bone marrow. Recombination only shortens the DNA, someone please correct me.

Also why is there no band in the bone marrow that is the same size as peripheral bands? Surely the HSCs have not undergone recombination, where is their DNA???

azibird  Here is the figure from Kaplan Immunology. See how recombination only makes the sequence shorter? https://imgur.com/a/fI2jHfu Kaplan also says: "While heavy chain gene segments are undergoing recombination, the enzyme terminal deoxyribonucleotidyl transferase (Tdt) randomly inserts bases (without a template on the complementary strand) at the junctions of V, D, and J segments (N-nucleotide addition). The random addition of the nucleo- tide generates junctional diversity." However, this would not account for the equal stepwise lengthening of DNA, which is clearly from these recombinable units. +

 +0  (free120#34)

This patient has a mixed hyperbilirubinemia. How could Gilbert syndrome, cause direct bilirubin to increase? The syndrome is caused by mildly decreased UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake. So there's absolutely no way it could increase direct bilirubin! I thought this must mean that there was an obstruction or extravascular hemolysis.


 +5  (nbme18#16)

The IMA comes off the aorta between the renal arteries and bifurcation. The IMA supplies the hindgut, which spans the distal 1/3 of transverse colon to upper portion of anal canal. Compromise of the IMA would lead to decreased blood supply to these structures, of which "Descending colon" is the only answer choice.


 +1  (nbme18#30)

Follow-up vs support group?

The only thing that saved me was the ancient Step 1 adage: "Never refer!"

Especially when the answer to another question in the same exam was "Encourage the patient to participate in a support group for persons with her condition"

I mean REALLY! The only difference is that they used the word "encourage" instead of refer. Exact same answer.


 +1  (nbme18#20)

Endothelin (ET)-1, a potent vasoconstrictor peptide from vascular endothelial cells, is also synthesized and secreted by cardiomyocytes and induces hypertrophy of cardiomyocytes through activating phospholipase C, protein kinase C, extracellular signal-regulated kinase (ERK) 1 and ERK2, and upregulation of c-Fos and c-Jun.

https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000112596.06954.00?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed

motherhen  is this super out of left field or am I supposed to know this +
ab721  @motherhen I don't know if this is correct, but I personally tried to reason this one out. If hypertrophy is occurring, more sarcomeres are added which means more beta-myosin. Hypertrophy also means the cell is doing more work, so a transcription factor is likely to be upregulated. From there, the only option with both of those increased had endothelin increased as well, though unclear why that's necessarily increased. +

 +1  (nbme18#32)

This really sounds like it's describing Alport syndrome, but Alport syndrome is X-linked DOMINANT! What is going on here? Is this a mistake? How to explain calling it X-linked RECESSIVE?

Alport Syndrome Mutation in type IV collagen -> thinning and splitting of glomerular basement membrane. Most commonly X-linked dominant. Eye problems (eg, retinopathy, anterior lenticonus), glomerulonephritis, sensorineural deafness; “can’t see, can’t pee, can’t hear a bee.” EM—“basket-weave” appearance due to irregular thickening of GBM

cneal46  lolll apparently 15% of cases are inherited x-recessive. I just ignored the inheritance part and answered based on the functions of all those proteins +

 +5  (nbme18#37)

Costanzo Physiology 6th E p456

Regulation of Vitamin D Synthesis Whether the renal cells produce 1,25- dihydroxycholecalciferol (the active metabolite) or 24,25-dihydroxycholecalciferol (the inactive metabolite) depends on the “status” of Ca2+ in the body. When Ca2+ is sufficient, with an adequate dietary intake of Ca2+ and normal or increased plasma Ca2+ concentration, the inactive metabolite is preferentially synthesized because there is no need for more Ca2+. When Ca2+ is insufficient, with a low dietary intake of Ca2+ and decreased plasma Ca2+ concentration, the active metabolite is preferentially synthesized to ensure that additional Ca2+ will be absorbed from the gastrointestinal tract.


 +0  (nbme18#28)

Can someone explain the physical findings?

"Cardiac examination shows a grade 2/6 pansystolic murmur heard best at the lower left sternal border, which increaes on inspiration. The point of maximal impulse is palpated in the sub-xiphoid area S1 and S2 sounds are distant"

I don't understand how any of these would correspond to cor pulmonale.

drdoom  Backfilling of blood from the lungs into the R ventricle is stretching out the R side (dilation) and also remodeling the heart via hypertrophy (the heart has to pack on mass to eject the ever greater amount of blood piling up from lungs). Dilation of the R ventricle “pulls apart” the leaves of the tricuspid valve=``lower left sternal border``; when the heart is in systole, the tricuspid valves don’t make good contact and blood rushes from high pressure compartment (RV) to the low pressure (RA) == ``pansystolic murmur`` +
drdoom  The tricuspid murmur gets worse with inspiration because when you ask someone to take a good, deep breath, the diaphragm (a very strong muscle, indeed) pulls the entire thoracic cage down and out (expansion) — including the heart! Because the heart “gets pulled from all directions”, the tricuspid leaflets make even less contact == bigger hole == more pronounced murmur during systole. +2
drdoom  The point of maximal impulse (the heart apex) is way below the xiphoid because this guy’s heart is so big from the years of dilation and hypertrophy — that’s also why the S2 sounds are distant: the great vessels (and their valves) are buried even deeper than usual, so you can’t hear them snapping shut (aortic & pulmonic valves; S2=“dub”). +
cancelstep  Similar to what's been said, but here's how I answered: Agree that a pancystolic murmur at LL Sternal Border is tricuspid regurgitation, increases with inspiration because increased right ventricle preload would increase amount of regurgitation. PMI in sub-xiphoid area means that the strongest contraction is happening sub-xiphoid which has to be due to right ventricular hypertrophy (left ventricular hypertrophy would push PMI towards axilla). Diffuse, scattered wheezes bilaterally are probably indicative of COPD from history of smoking which would cause a secondary pulmonary hypertension due to hypoxemia and vasoconstriction in the lungs (primary is idiopathic, most commonly occurs in younger/middle-aged females). So this explains why you have RVH. Pulmonary edema would be crackles on lung auscultation and would point to Left HF, but not the case here. Also, BP 150/80 in a 68-year old without any medication is definitely high, but not causing AS. Peripheral/liver edema = RHF +

 +1  (nbme18#6)

What is going on here? The mother is not the patient, why are we exploring this further when the son is completely normal? I get it that we would say this if the patient were concerned, but he's not and he's normal so why don't we just tell her that everything is normal? Exploring further will probably make the patient feel worse.

drdoom  Another way to read the stem is like this: “Assume you will make a statement that assures mom that boy is fine. What other statement do you want to make?” Since we’re *already* assuring mom, the best next thing is to ask an open-ended question. There’s a reason for this. As a physician, you really don’t want to say more than what you are (1) sure of or (2) obliged to. “Accept him as he is” = judgy. “He’s not going to get any taller” = you don’t know this for sure. +

 +0  (nbme18#1)

FA2020 p491 Neural tube defects Neuropores fail to fuse (4th week)

The 4th week falls in the range of 3 to 8, but such a wide range threw me off and I picked 0 to 2 anyway.

overa  the first 2 weeks are "all or none". so usually if the fetus is exposed to teratogens here, it will either terminate the pregnancy or the baby will be unaffected. +

 +0  (nbme18#31)

Nocardia is the only non-tuberculoid bacteria listed in FA that leads to caseous necrosis.

FA2020 p209


 +1  (nbme18#28)

Agranulocytosis (rare side effect of PTU) commonly presents with acute pharyngitis.

"Symptoms of anti thyroid drug-induced agranulocytosis do not differ from those of other causes of agranulocytosis. High fever and sore throat are the most frequent signs. Acute pharyngitis and other infections in the oral cavity are the most common clinical diagnoses at presentation." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5318340/

"The most common presentations were fever (92%) and sore throat (85%). Initial clinical diagnoses were acute pharyngitis (46%), acute tonsillitis (38%), pneumonia (15%) and urinary tract infection (8%)." https://www.ncbi.nlm.nih.gov/pubmed/10627862

The word ulcerating threw me off and I started thinking about noninfectious causes of inflammation. Agranulocytosis leads to infection, keep it simple.


 +4  (nbme18#1)

This is the most poorly drawn cell diagram. I see zero ribosomes, so I figured F was the smooth endoplasmic reticulum. However, now I can see that the curved organelle is the golgi apparatus and F must represent the whole endoplasmic reticulum.

I believe plasma membrane proteins are synthesized in the rough endoplasmic reticulum.

FA2020 p46 Rough endoplasmic reticulum Site of synthesis of secretory (exported) proteins and of N-linked oligosaccharide addition to lysosomal and other proteins.

Free ribosomes—unattached to any membrane; site of synthesis of cytosolic, peroxisomal, and mitochondrial proteins.

Smooth endoplasmic reticulum Site of steroid synthesis and detoxification of drugs and poisons. Lacks surface ribosomes. Location of glucose-6-phosphatase (last step of glycogenolysis).

nbmeanswersownersucks  I was under the impression that translation of transmembrane proteins begins with ribosomes in the cytoplasm that then translocate to the rough ER once the signal sequence is reached by the ribosome? i.e. technically translation begins in the cytoplasm but finishes in the rough ER. Am I wrong about that? +3
nbmeanswersownersucks  It was UWORLD 6544 about insulin translation. They state that the translation is initiated in the cytoplasm then relocates to the RER (d/t the signal sequence) and is finished there. So is there a difference in translation steps for proteins that are excreted like insulin and transmembrane proteins? +2
nsinghey  Same, I am not sure about this. My best guess is that since insulin is not a functional protein, it is not synthesized in the RER (even though it it excreted from the cell). Actual proteins are made in the RER +2

 +1  (nbme18#15)

A laminectomy removes the lamina and spinous process. The lamina is the posterior bridging segment (D). The lateral bridging segment is the pedicle (B).

However, I don't understand how you could access the herniated disc from this angle, the spinal cord would be in the way! Can someone explain?

https://www.mayoclinic.org/tests-procedures/laminectomy/about/pac-20394533

scrambledeggs  Take a look at the section labeled Laminotomy and Discectomy. https://eorthopod.com/lumbar-discectomy/ +2

 +14  (nbme24#25)

Who else came here after getting triggered by this answer?


 +0  (nbme24#13)

Why are there lots of RBCs but few RBC casts? That made me think about a post tubule process.

boostcap23  Any amount of RBC casts is an abnormality and indicates tubular pathology. Normally should have none. Just like how even a single neutrophil in CSF is abnormal. +1

 +1  (nbme24#37)

Can anyone address the 3rd percentile head circumference? Does that qualify as microcephaly? Microcephaly plus Brazil had me sold on Zika, so I convinced myself that kissing could transmit it because I know it can transmit sexually.

I probably should have rethought it after not finding mosquito as a choice, and the classic Toxoplasmosis triad is there, but what's with the microcephaly?

UW ID: 15034 for those curious about Zika Classic findings are microcephaly, arthrogryposis (contractures), seizures, hypertonia, ocular abnormalities, cortical thinning, ventriculomegaly, and subcortical calcifications.

mamabara  No answers as to why, but I also had the same line of thinking thanks to the Uworld question too... my best guess is that Toxo is the better answer based on the choices given? Even though the presentation (especially immigrating from Brazil) really made me think Zika +

 +2  (nbme23#48)

Who else got this just because it said "all-night dance party?" Applied my knowledge of raves and nothing else.


 +5  (nbme23#44)

What is the educational objective of this question? To see if we know that radiation doesn't stick? Not that cool.


 +2  (nbme23#42)

Why is there a decreased FVC? There is a mass pressing on her trachea, how could that possible affect lung volume? If we give her enough time, why couldn't she take in a full breath?


 +1  (nbme23#5)

Would rickets present in a newborn? This article describing a case series says "There are few other published cases of congenital rickets caused by maternal VDD." So maybe rickets usually presents later in life. Mayo Clinic says it's usually after "an extreme and prolonged vitamin D deficiency."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2795674/ https://www.mayoclinic.org/diseases-conditions/rickets/symptoms-causes/syc-20351943

rongloz  This was exactly my reasoning of choosing Osteogenesis versus Rickets +

 +0  (nbme22#25)

Histamine decreases arteriolar resistance, but I guess not capillary resistance.

ΔP = Q × R

In the arteriole, resistance decreases, so flow increases. In the capillary, resistance has not decreased, so the increased flow they receive translates to increased pressure and filtration.


 +3  (nbme22#44)

In what century is this question taking place?? Dicoumarol was replaced by warfarin in the mid-1950s! It's on the FDA's list of discontinued drug products!

From wikipedia: "Identified in 1940, dicoumarol became the prototype of the 4-hydroxycoumarin anticoagulant drug class. Dicoumarol itself, for a short time, was employed as a medicinal anticoagulant drug, but since the mid-1950s has been replaced by its simpler derivative warfarin, and other 4-hydroxycoumarin drugs."

Did the grandpa have some leftover dicoumarol in the cabinet from his DVT in the summer of 1949?? This question is absolutely ridiculous.

https://en.wikipedia.org/wiki/Dicoumarol https://pubchem.ncbi.nlm.nih.gov/compound/Dicumarol#section=Uses


 +1  (nbme22#1)

Here is a part of the UWorld table about cervical radiculopathies. And yes they did say that C7 is the most frequently involved. I think the answer is that C6 would involve the biceps, C8 would involve the fingers, and pronation is median nerve. So it has to be C7.

https://imgur.com/a/GvmCUj1


 +0  (nbme21#40)

What if you know it's CNIII and remember CN's III, IV, V1, V2, and VI all run through the cavernous sinus, but don't remember which is which in the picture?

CN's IV and VI only control one muscle each and are therefore very small in diameter. V1 and V2 serve a lot of functions and are therefore large. III is intermediate.

Also they are organized in an ascending manner - III above IV above V1 above V2, and VI to the side.


 +0  (nbme21#35)

I don't feel like any of these comments have fully addressed why the patient currently has increased resting CO and NOT decreased SV. Here is how a friend of mine explained it:

MAP (at resting HR) = 2/3 DBP + 1/3 SBP = 77 mmHg in this patient, which is lower than normal (93 mmHg if you use 120/80). So MAP is decreased and the kidneys/other organs aren't getting the perfusion they need, leading to RAAS activation and SOB/edema. MAP = CO Ă— TPR, so this could be due to low CO relative to TPR (what we usually expect) or low TPR relative to CO. This patient's large AV fistula has dropped her TPR very low, which means her CO must have been very high for the past 15 years to compensate (high output heart failure. She has only 5 days of symptoms, which means she is early on in her HF. Since she had such a high CO to begin with, her drop in SV this early on would still leave here with an INCREASED SV compared to a normal patient. Unless her pulse is super high, her heart must be pumping a massive stroke volume to maintain a normal systolic blood pressure with such a low TPR (MAP = SV x HR x TPR). Eventually, her SV may decrease to be below normal, but not so early on.

For completeness: Not decreased arterial O2 sat because blood is flowing from artery to vein, not the other way around. Not decreased mixed venous O2 sat because arterial blood is flooding the subclavian vein right before mixed O2 sat would be measured. Not increased SVR because of the large AV fistula.


 +6  (nbme21#24)

FA2020 p72

Ethanol metabolism increases NADH/ NAD+ ratio in liver, causing:

Hepatosteatosis— Increased conversion of DHAP to glycerol-3-P; acetyl-CoA diverges into fatty acid synthesis, which combines with glycerol-3-P to synthesize triglycerides

Increased NADH/NAD+ ratio inhibits TCA cycle -> acetyl-CoA used in lipogenesis (-> hepatosteatosis).





Subcomments ...

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PPC is a osytncd-itpaiehev adn eiviocdsaist ehiasetnct atht ngleleary acst as a nrweod btu cna salo saeuc bdnilieerc oagissengr lcupoed itwh pani tnstiisyvenii eht( runmsaep dur.g) artVielc tguymnsas is a oylmconm enmdneoti pcahyils eaxm nf.ngidi

azibird  FA specifically mentions hypertension and tachycardia, so I ruled it out immediately. But you're right, it's a hallucinogen, I thought it was a stimulant. +1  
azibird  "PCP (10mg/kg, s.c.) causes hypertension that is associated with decrease or tendency to decrease the levels of epinephrine and norpinephrine in the hypothalamus and the brainstem regions." https://www.sciencedirect.com/science/article/abs/pii/0006899384901847 "Over 50% of adult patients present with the classic toxidrome of PCP intoxication: violent behavior, nystagmus, tachycardia, hypertension, anesthesia, and analgesia." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2859735/ +  


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CPP is a icpihsatnedto-eyv dna dstoaeciisiv nieetctsah taht gnaleleyr cast sa a wneodr ubt cna oasl cueas idrnecible ionssgareg oueldcp ithw pian sitisnyiinvte (eth pnumasre gr)u.d tVcareil antgysums si a oloymnmc mndtieone spcaihly axem gdnfnii.

azibird  FA specifically mentions hypertension and tachycardia, so I ruled it out immediately. But you're right, it's a hallucinogen, I thought it was a stimulant. +1  
azibird  "PCP (10mg/kg, s.c.) causes hypertension that is associated with decrease or tendency to decrease the levels of epinephrine and norpinephrine in the hypothalamus and the brainstem regions." https://www.sciencedirect.com/science/article/abs/pii/0006899384901847 "Over 50% of adult patients present with the classic toxidrome of PCP intoxication: violent behavior, nystagmus, tachycardia, hypertension, anesthesia, and analgesia." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2859735/ +  


submitted by b1ackcoffee(27),

Calcium is low while PTH is high. It’s primary hyperparathyroidism (not secondary). Ans is branch of IJV.

b1ackcoffee  I got that it must be some vein, I just didn’t know the tributaries. Oh well, anatomy fucks me again! +  
azibird  I believe this would be more likely called a type of pseudohypoparathyroidism. Akin to PTH resistance, the PTH just can't get out to do its thing. Good catch though, I didn't even get what was happening here. +  
azibird  From wikipedia: "Each parathyroid vein drains into the superior, middle and inferior thyroid veins. The superior and middle thyroid veins drain into the internal jugular vein, and the inferior thyroid vein drains into the brachiocephalic vein." https://en.wikipedia.org/wiki/Parathyroid_gland +  


submitted by b1ackcoffee(27),

Calcium is low while PTH is high. It’s primary hyperparathyroidism (not secondary). Ans is branch of IJV.

b1ackcoffee  I got that it must be some vein, I just didn’t know the tributaries. Oh well, anatomy fucks me again! +  
azibird  I believe this would be more likely called a type of pseudohypoparathyroidism. Akin to PTH resistance, the PTH just can't get out to do its thing. Good catch though, I didn't even get what was happening here. +  
azibird  From wikipedia: "Each parathyroid vein drains into the superior, middle and inferior thyroid veins. The superior and middle thyroid veins drain into the internal jugular vein, and the inferior thyroid vein drains into the brachiocephalic vein." https://en.wikipedia.org/wiki/Parathyroid_gland +  


Is the decrease in baroreceptor output due to the body adapting to the hypertension?

azibird  Apparently. "Baroreceptor activity is reset during sustained increases in blood pressure so that in patients with essential hypertension, baroreceptor responsiveness is maintained." "It is a universally accepted phenomenon that vascular baroreceptors reset to operate at higher pressure levels in hypertension." Okay, so they can reset to normal levels, but wouldn't this patient already have undergone their reset? Why would the receptors further decrease? I thought that eventually their LV would hypertrophy and fail, leading to decreased stroke work. https://www.ahajournals.org/doi/full/10.1161/01.HYP.0000160355.93303.72 https://pubmed.ncbi.nlm.nih.gov/3042363/ +1  
azibird  From Costanzo Physiology: "The sensitivity of the baroreceptors can be altered by disease. For example, in chronic hypertension (elevated blood pressure), the baroreceptors do not “see” the elevated blood pressure as abnormal. In such cases, the hypertension will be maintained, rather than corrected, by the baroreceptor reflex. The mechanism of this defect is either decreased sensitivity of the baroreceptors to increases in arterial pressure or an increase in the blood pressure set point of the brain stem centers." +6  
mangomango  Hypertensive heart disease causes concentric LVH - impaired diastolic function, preserved ejection fraction +  


Is the decrease in baroreceptor output due to the body adapting to the hypertension?

azibird  Apparently. "Baroreceptor activity is reset during sustained increases in blood pressure so that in patients with essential hypertension, baroreceptor responsiveness is maintained." "It is a universally accepted phenomenon that vascular baroreceptors reset to operate at higher pressure levels in hypertension." Okay, so they can reset to normal levels, but wouldn't this patient already have undergone their reset? Why would the receptors further decrease? I thought that eventually their LV would hypertrophy and fail, leading to decreased stroke work. https://www.ahajournals.org/doi/full/10.1161/01.HYP.0000160355.93303.72 https://pubmed.ncbi.nlm.nih.gov/3042363/ +1  
azibird  From Costanzo Physiology: "The sensitivity of the baroreceptors can be altered by disease. For example, in chronic hypertension (elevated blood pressure), the baroreceptors do not “see” the elevated blood pressure as abnormal. In such cases, the hypertension will be maintained, rather than corrected, by the baroreceptor reflex. The mechanism of this defect is either decreased sensitivity of the baroreceptors to increases in arterial pressure or an increase in the blood pressure set point of the brain stem centers." +6  
mangomango  Hypertensive heart disease causes concentric LVH - impaired diastolic function, preserved ejection fraction +  


submitted by azibird(92),

I read this question as analyzing immunoglobulins in the bone marrow vs out circulating peripherally. I now realize this is wrong, and they are just analyzing the DNA of different cell population, like a hepatocyte for example, not immunoglobulins present in the liver.

With this cleared up, I can see how V(D)J recombination could make the original DNA section shorter. But how could V(D)J recombination possibly make the DNA section longer? There are bands on the gel that are higher molecular weight in the bone marrow. Recombination only shortens the DNA, someone please correct me.

Also why is there no band in the bone marrow that is the same size as peripheral bands? Surely the HSCs have not undergone recombination, where is their DNA???

azibird  Here is the figure from Kaplan Immunology. See how recombination only makes the sequence shorter? https://imgur.com/a/fI2jHfu Kaplan also says: "While heavy chain gene segments are undergoing recombination, the enzyme terminal deoxyribonucleotidyl transferase (Tdt) randomly inserts bases (without a template on the complementary strand) at the junctions of V, D, and J segments (N-nucleotide addition). The random addition of the nucleo- tide generates junctional diversity." However, this would not account for the equal stepwise lengthening of DNA, which is clearly from these recombinable units. +  


submitted by sugaplum(240),
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shTi isutnoeq si isnkag tuabo VJD etreangrmeanr ihhcw sphpena in teh oneb omraw.r eTh gsnee ear lal dehocpp up buscaee the B lcle si trnigy ot ageenter a quunie tociimbnoan fro sti rtroeecp
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hetpCra 3 fo wh"o teh mmunie ssmyte wsor"k - weaesmo okbo

varunmehru  in the question stem, they are asking about a constant region. VDJ rearrangement is for the variable. It doesn't make sense :( +1  
sallz  Both the constant (heavy chains) and the light chains undergo gene rearrangement. The heavy chain undergoes V(D)J random recombinations, while the light chain undergo VJ random recombinations. So gene rearrangement could work for both regions. +5  
azibird  The constant region does not undergo recombination. That's why it's called constant. It's just right next to the variable region though, so they get expressed together as one protein. That's why the constant-labeled DNA region is variable length here. +1  


between macrophages and neutrophils; neutrohpils are more acute. here is long standing :)

azibird  Is there anything else to it? I was thinking neutrophils because they could be filled with diplococci in gonorrhea. +2  
nbmeanswersownersucks  I think if they wanted neutrophils they would've had to mention something about maybe pus or white discharge but since this is chronic and scarred, its unlikely neutrophils would be present i.e. no longer an active infection +1  


Where do you get off selling peoples comments I understand you built the platform but charging $5 a month for something that was built by users that thought it was free for everyone. You should be ashamed of yourself.

blueberriesyum  People are going to move to a different platform now that this isn't free anymore. +1  
azibird  Oh shit, is that what's happening? Someone explain. I was wondering why there are so many questions missing, is that related? +  
thisshouldbefree  @azibird i dont think the missing questions is related to that as i dont think ppl would delete them +1  
drdoom  @thisshouldbefree after you pass a certain score threshold, you can add missing questions via a form on the main exam pages +  
pelparente  Yah it sucks that they are charging now, but I'm assuming they have to pay hosting fees for the website. It is basically going to cost you at most 10 bucks for your dedicated period, which isn't terrible, and good on them if they make a bit of money for having this idea. That's capitalism. I would love for it to be free, but please don't delete your comments if you posted something... I still need to study and these answers don't seem to be aggregated anywhere else. @not_greedy_like_you make another website that is free then get this content on there and create competition so they have to go back to free in order to have anyone on here if you feel so strongly. +  


submitted by match95(36),
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ninotTsaorpsi of eht vAna gene ormf nsnia-ttavnsoicymerc roncEetosucc si woh it ansetfrsr rieesnsat.c heyT use snoropssatn iwchh era aldtcoe no lpdsmis.a If you heva siapldm ,slos uyo nto'w vhae oatnnrs,sosp dan sencirseat llwi .dceesaer

azibird  Why can't this be a point mutation? +3  
freenbme23  I don't think that this implies that it can't be point mutation, but rather plasmid loss is more likely. Also, the point mutation Would have to ultimately lead to the plasmid loss. +  


submitted by sugaplum(240),
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1.w/iw4.hdcspl/ie..vhmt74/6pnn:4wb7ob/guntm om mocn usssei ni ytep 1 and epyt 2 cbaiesdit

azibird  That article does not once mention the word diarrhea. +1  


submitted by m-ice(286),
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ictennirisV is a acutmheeopetrchi urgd that tlazebsiis silctburomue and pstreevn hemt form aesgbinls.msid Teh lcel ni eth pceritu is ktusc ni eahsapan, hiwt ubotcmilurse ahaetcdt to tis erss,ooohmcm enubla ot lupl hmte aaptr esuaceb ti cotnna ilbsaeedmss ist .oictsbuuerml

vshummy  So I get that by process of elimination cyclophosphamide, cyclosporine, doxorubicin, and 5-fluorouracil are not related to microtubules but vincristine in First Aid 2019 says it prevents microtubule formation, doesn’t stabilize it because the one that stabilizes microtubules is paclitaxel. +  
vshummy  Okay, I realize now- the picture is stuck in metaphase, not anaphase. Both paclitaxel and vincristine stop the cell in metaphase but by two different mechanisms. Vincristine prevents mitotic *spindle* formation while paclitaxel prevents mitotic spindle *breakdown*. Mitotic spindle is needed to pull the chromosomes apart before anaphase begins. +13  
azibird  No, I think you were right to begin with. Without spindle formation the cell should be stuck in prophase (vincristine). Without breakdown it should be stuck in metaphase (paclitaxel). Metaphase is shown here with spindle fully formed, so it should be paclitaxel. +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  


submitted by seagull(1165),
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shiT si itreeh a hpyocrrteip scra or kedilo. ohtB aiesr edu to ponrevixoesrse- fo a-Fb.tGeT

charcot_bouchard  i think its a foreign body granuloma +9  
curbstep  If it is then would Tumor Necrosis Factor be valid answer as TNF-a is involved in granuloma formation? +  
azibird  Because it specifically asks which subsgtance THAT PROMOTES FIBROBLAST MIGRATION AND PROLIFRERATION. I believe both TGF-b and TNF-a would be involved, but only TGF-b has this effect of fibroblasts. +1  


submitted by brethren_md(81),
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Meka a tpuentn quresa htiw a rcsos of B B+ and B B0; B+ snetresper 50% fotcunin wlehi B0 eterseprns %0 )llu(n foitcu.nn oS ni hsti sea,c hte suabdhn udwol aveh a B 0B enpgoeyt ilweh eht ewfi hsa a B +B eg.onepyt

sCors fo etshe tow wlli lruest ni het gonoflwil osp;tynege B,B 0B,B B,B+ +0BB BB = 1%00 nfn,icotu BB+ = 57% ncinfu,ot B0B = %50 c,tniufno 0BB+ = %52 octuinnf

So teh wsarne illw eb 1 in 4 haev a 25% ountfnci ievng eht nsoepg.tey

tyrionwill  how about the choice of D: 1 in 4 have 50% function, which is true. shall 50% function needs transfusion? +  
tyrionwill  In FA, it defines beta thalassemia into minor (HbA2 >3.5%) and major (both HbF and HbA2 go further up), and the major needs transfusion frequently. How can we take this classification based upon quantitive way like in this question? how much percentage of function left does not need a frequent transfusion? +  
azibird  D says one in TWO, not one in FOUR. +1  


submitted by whoissaad(66),
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yArert fo cdsuut efsndere is a bnhacr of ofenrii ciaelvs areyr.t oS hwy is B wor?ng

happysingh  the question is asking about "adequate arterial supply" +  
azibird  The artery of the ductus deferens is USUALLY a branch of the SUPERIOR vesical artery, although it can branch from the inferior vesical artery in some individuals. +  


submitted by usmleuser007(333),
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etrfA oems aeserrch tish si hwy hte orhet snarsew aer eicrnort:c

aBlsa nckraeyetito am&;p amlnai aluicd

  • eotrnIrcc /bc laiamn clduai is a neopcnomt fo eth tbeenmsa rmenbmea hcwhi si dnfou enbetew eht eeiulhtpmi adn rngeluynid encietonvc isseut (.eg,. despirime nad dseimr fo eht i)sk.n
  • It is a hogluyr 04 rteanoemn idew tctcneerl-uenol nzeo bwenete eth aasmpl emaernbm fo teh salba lcles and teh nree-n)deoltsce( anmali sedna fo teh aetmbnse nme.eabmr W)(IKI
  • sbaal tnycetoreaki scaeatth ot hte msanbtee emrmbena uigns heememsmoisod

uGanarlr ynecoekittra pa&;m umasrtt ermcoun

  • tSamurt duimclu ertsaapes eehts wot s.reyal
  • rteeh are on sdmsoeome tath ntcocne thsee wot ealrsy
  • gIaem rfo erfnreeec

Limana ulcdai pa;&m nmiaLa senda -- lccik rof iaegm

  • tboh rea trap of eth beesntam nebermma and nto eth eisirdepm

coetenayMl ;a&pm alsab trocteyeikn --- lkcic ofr eigam

  • are htob ccodnntee ot eerhoatc vai -cainsedrhE
  • ti si byrolpba eth amdgea ot ihst cnitennooc htta
azibird  The stratum lucidum is only present in the thick skin of the palms, soles, and digits. So the stratum granulosum and corneum do touch in most of the body. I guess they just aren't connected by desmosomes. https://opentextbc.ca/anatomyandphysiology/chapter/5-1-layers-of-the-skin/ +  
peridot  Wow if I'm understanding this correct, lamina lucida (basement membrane) is not the same as stratum lucidum (between stratum corneum and stratum granulosum). That def confused me about this question bc I simultaneously was like wait isn't this in the basement membrane but also recalled the picture in FA with all the layers. Thanks so much for the super detailed explanation of all the answer choices! +1  


submitted by dentist(46),
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ofndu iths rseup uuslfe oobk on monaza uaotb iaCuhrdB-di ckche( otu het sikc )vocer

llamastep1  Thank you for that +  
focus  hahahahaha. DEAD. +  
anjum  I endorse clicking that link +  
azibird  Hahahahahahaha, that's a must click. Someone please buy it and let me know. +  
chediakhigashi  hahahaha +  


submitted by usmle11a(70),
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eTh ledcaim mrqutneersei ot aniotb a rmepti vyar yb aetts, tub era uyualls indcenof ot iecicfps epyts fo iesiaidbtils ro d.oitoincsn Tehse sa a eelgnar eulr lciedun teh eus fo yan iatvsssei ecdeiv husc as a hl,cihrewae erhcucs,t or en,ac as llwe as a miissgn gel or .ftoo meoS staset laso ecildun neacrit arvuca,orcsldai pina, or ersrrtyoipa .ooctinnids bAtou half fo SU seastt 62() ieunlcd ilbdnnses sa a aiilugqfyn litybsdiai albnineg het nersop to abnoti a iliytsidba gkpirna rmtpie ofr use as a npgrsse,ea dna 41 seatst ildneuc a sbeidlda dnah as a ilniqgfayu yilibsd.ait oFur staets enilcdu ,dansseef nad tow eastst iiniVrag( dna New rYo)k nleicdu mtanel inellss ro odeevnletplma iidilebssati sa lgaqfuiiyn iliaisidtebs

ruo uyg esus a enca s...o

btw i ogt it gworn ): acues i huhtogt it si pu ot teh VDM

usmle11a  also it is the dr who decides the eligibility then sends it to the DMV disability --> Dr --> DMV +4  
peridot  I'm not sure if I'm being here or if the test question changed, but I don't see anywhere in the stem that says that the patient uses a cane? I even ctrl+F the word "cane" lol. I picked referring to PM&R specialist for full assessment cause I figured that another pattern is to always gather more info, but I guess that's not the case here T_T +4  
azibird  It does NOT say he uses a cane. +2  
sonofarathorn  I can also confirm that there was no cane involved. I repeat, NO CANE. +2  


submitted by hayayah(994),
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aboolCmo is an eey rylbmaanoit ttah occrus eorbfe .ibrht eTer'hy sismign cieeps fo uietss in rssttuercu thta from het y.ee

  • mlsCaoobo fcgnfieta eht i,isr ihchw eultsr in a kh""eyloe arpeapeanc fo het u,iplp rglenlaey do ont alde to oviins ls.so

  • oCblosaom viignonlv eth eiatnr ltruse ni viinso slso ni ipsicfec sptra fo teh aivusl fid.le

  • eLgar ntrilae alcomoosb or ohets tanegfifc eth oiptc vnree anc scuea olw nv,iosi whhci nsmea iisnov loss ahtt tnoanc eb pcolemlyet cctedeorr twhi ssgsela or ctonatc sels.en

mousie  thanks for this explanation! +  
macrohphage95  can any one explain to me why not lens ? +  
krewfoo99  @macrophage95 Lens are an interal part of the refractive power of the eye. Without the lens the image would not be formed on the retina, thus leading to visual loss +4  
qfever  Do anyone know why not choroid? +1  
adong  @qfever, no choroid would also be more detrimental to vision since it supplies blood to the retina +2  
irgunner  That random zanki card with colobomas associated with a failure of the choroid fissure to close messed me up +7  
mnemonicsfordayz  Seems like the key to this question is in what is omitted from the question stem: there is no mention of vision loss. If we assume there is no vision loss, then we can eliminate things associated with visual acuity (weird to think of in 2 week old but whatever): C, D, E, F. Also, by @hayayah 's reasoning, we eliminate E & F. If you reconsider the "asymmetric left pupil" then the only likely answer between A & B is B, Iris because the iris' central opening forms the pupil. I mistakenly put A because I was thinking of the choroid fissure and I read the question incorrectly - but it's a poorly worded question IMO. +  
mamed  Key here is that it doesn't affect vision- the only thing would be the iris. All others are used in vision. Don't have to know what a coloboma actually is. +1  
azibird  The extra section of that Zanki card specifically says that a coloboma "can be seen in the iris, retina, choroid, or optic disc." Don't you dare talk trash about Zanki! +1  


Why can this not be MEN 1? And the increased serum calcium be a result of increased PTH release from parathyroid?

azibird  None of the answers are parathyroid. +1  


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I emca rehe utjs ot dare eth ctonesmm

JM ta teh vieom thatsere anetgi oopnrcp emme

azibird  Same! +  


submitted by sajaqua1(471),
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CHM I icnntfuo is leairtgn to enrcac ssepsn.poiur HMC I lpsdyias ldsyogoenneu ezyeitsnhds irentpso adn rtpensse etmh to 8+CD T .secll ehT eaurifl ot yapsidl CHM ,I or MHC I sidlpya fo nsnefo-l n(da by sxnoetine )unccserao ositenrp iersgtgr a lellruac mmunei prns,seeo inaldge to codetrituns of hte elc.l

eTh orptemoaes si deus fro het rnoadediagt fo rnow u,to ,nectenses or fmdarleom e.pnortis As neracc dople,esv more osmtuntia ldae ot nsieredca norwg np.rosiet nyOl by snpixsoere fo eth tse,ropmoea ro its xier,veosrp-eson nca hsete ntmuat rtiponse eb edgedadr sfta ouhneg ot not eb ypsdilade yb HMC I dna leda ot the llce niebg ll.dkei tBomerzibo clbosk teh rtoae,mpseo so eht mutatn nrpesito aer ysdlipdae on the ,ruesfac onlagiwl teh enumim esytms ot oingceezr dan klli ctplogaiaohl .llcse

catch-22  Another way to approach it is to think about MHC class I processing. Basically, if you inhibit the proteasome, peptides will not be generated and nothing is available to be loaded onto MHC I (remember MHC I has to be loaded before it's transported to the cell surface). Cells that don't express MHC I get killed by the natural killers. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2214736/ +21  
kai  "In conclusion, we have demonstrated that the proteasome inhibitor bortezomib down-regulates class I and enhances the sensitivity of myeloma to NK cell–mediated lysis" from the conclusion of the NIH paper +5  
maddy1994  another mechanism is by blocking proteosome u even decrease degration of proapoptotic proteins...so it enchances apoptosis(from uworld) +3  
azibird  But CD8+ and NK cells kill via perforin! Why is this answer wrong? Is it because it's not the primary effect? +1  
testready  "The proteasome is the major source of proteolytic activity involved in the generation of peptides for presentation by major histocompatibility complex class I molecules. We report the new observation that bortezomib down-regulates HLA class I on MM cells, resulting in increased NK cell–mediated lysis." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2214736/ +  


submitted by sajaqua1(471),
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Ptoesrori crod odnrmyse rouscc ued to ntoficnrai of the ioretrsop ahlf of hte lpsina rc,od mofr coculinos fo het iotroserp paisln erar.ty Oru tpntaie etsrnpes iwth sadeecedr sasoinent to ippircnk bwole het llvee fo eht sneke sa ewll as aiwknlg ithw a edewidbsa- agti, eilykl idinaigcnt slso of piieonorcportp. ehT ptietna is sola imcena iwth neyseemrtehgdp- n.itouhseprl

yspeeerHmdetgn pirnuhtosle ear cylptliay esuacd yb na yatiblini ot kmea ughone ,DNA edsuac by a aklc fo ceyseansr rrpscsoreu and miasitvn cudnlniig 9B (lot)eaf adn 21B .oa)a(micbln fI eth taiptne is ateolf ,nedeciitf we see ealvdtee ooeityschmne yen.fcicied If eth penttai is 21B n,ditifeec ew ese adeeltev imnalmoyeclht iacd dna cnstmeeyhoio sleve.l oeaoyimeicmsHhretnpy cna nsacerei smotbo.rsih somoiTbhrs in hte isrorepto silnap rtraye nac acseu soorpiert odcr deor.ymsn In iiddn,aot lcak of mivatni 2B1 spairim lynemi fomitaron and dlase to uStbcuae Cibmneod Dnaeteni,erog hihwc eactfsf teh mntoSiiapcahl rtatc nugan(ictco for eeescardd npicrkpi onetn)isas, Ctlcaosrinoip cartT, dna arslDo io-CnaleludMm sLiuecsnm caTtr ccnnt(oigua orf teh ureedcd oooppi.ntierrpc

)A oArntrei cdor o-nmsdery lsso fo orotm onmam,dc as lwle sa lbeartial ssol fo ahte adn npai, hte tpiante ash nto ltos roomt nnotu,fic so it aconnt eb i.hst )B netrlaC ocdr msdnreo-y rtespsne as a ibitocnoanm fo tomro nad ornsyes slso, uasyull tihw ddrlbae ynoid.uctfsn Tihs patietn sode otn lpydsia tmroo lsso ro drbdela dtycsiuon.nf C) eiodmcHr nds-eyrmo lsAo leadlc Sorr-uwe,dBnqa thsi si eoeplctm irunyj to treehi hte tfel or hgrti deis of teh nispal rc.od It srenpset itwh rtoom uysidoctfnn adn rxleef cntsoduinyf yasrleplialit at the eelvl of the sleion; lsos fo purpe otomr ncdmoma oeblw eth oesiln ellaislrptayi pssica(t ssaepri); slso fo ldsroa ncrldeo-ucirma siaeonnts llairaslpetiy ta nad lweob teh ;sienol and slso fo anpi dna retpteremua atiossenn aealrcnatlltyro 2 to 3 aertevrb bolwe teh elosni. )E Smyearentg r-mndyseo a nitcnageol afleiru ot peoedvl tapr fo teh aipsln or.dc ehT new tnoes of stsompmy ta 82 aryse old aesmk thsi an nlikylue ii,ssadgno.

yb_26  amazing, thank you! +  
aisel1787  great explanation +  
rockodude  sensation to pinprick is DCML tract. SCD affects spinocerebellar (not spinothalamic), corticospinal, and DCML. otherwise good explanation. +1  
azibird  Sensation to pinprick is not dorsal column-medial lemniscal tract, it's spinothalamic tract. So this patient has a lesion of the dorsal columns, spinothalamic tract hypersegmented neutrophils, and anemia. What the hell is going on? How is this just posterior cord syndrome? Spinothalamic is not posterior cord. +4  


submitted by nwinkelmann(265),
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oS tihs ntqisuoe swa gshnmeoti I rlyela esdglgrtu htwi. I did'tn nzgceroei ttah teh aotnesnprtei aws fo RFMRE sa enmseoo atetds bewol, nad I ownk oyu tno'd need to nkwo atth ot asernw het noieut,qs ubt ti uolwd ahev eben ephufll. yM sitbgeg nsrortuitaf was het ongwidr of the osypib suetrls abaro"nml tcsamlnociuau fo oian"dcho.mitr hsiT odnayen me bseucae het iitnefnodi fo ggdare edr ebrfsi chiwh( Im' mugissna saw tiher eintontn)i si unaclauc"mosti of amrnbalo ridnhoia.ot"mc ehsoT rae owt vrye fdenerfti esmtetnats in my n,imd llo. The t,ifsr to m,e stuj masen rtee'sh oot hucm iornctmah,iod tbu het nodsce manes eshrt'e oto hcum NAD eyth tnre'a fgucintonin .yeplporr s'tI asol just teh tcfa of mermgebnrie lla fo teh emsrt for TEC at eht tiem of daegrni hte oteuisqn i..e( I dnt'id ktinh aoutb teh tcaf taht ECT is aslo ldaelc urellcal inrepators ro sjut riepri).saotn

I lsoa idtd'n ryelal aednsutrnd ylful athw m2aVOx is = O2V" am,x oasl knnwo sa xlmiaam xngoye ,uetpak si het mmasnreetue fo eht immmuax taonmu fo xgyoen a rsoepn nca ziuitle udignr eeinstn exr.sic.ee. nad is daebs no hte rsieepm ttah eth orme yneoxg soeudmcn dnuigr eeeis,xrc het rmeo hte ybod wlli reagente iadnnseeo pasphthierto T(AP) genrye in lc..sl.e VO2 xma is ehedrca hwen uory egoynx ootipnmncsu ainmres ta a yatsde saett teidsep na nieesacr in teh ooa.wldrk tI si at iths pluaeta htta het semcu]l[ smvoe ofmr ioerbac islebtmamo to abecanior tsmiob"emal 3htyvcs7smww0v--ewl:w/.ot1ha-twm2/f0t-e./rlipxoa2i9.

esaBd epyrul on this tonne,difii reewh aOxm2V = ayseistelln eht mtie at chwhi cebiaro csetihsw to eniraocab ,inepirsorta my reaintpirnotte of oto cmhu chntoidiarmo vs too cuhm nda bda rhinomirdacot ditdn' rt,eatm eaebsuc neev wnhe hte cariihmtdnoo are itinnonfcug yprepl,ro tyeh hrcae a ntoip and shtwic ot eo,anbaric uhts fi rheet saw too chmu rnmola ih,cioomnatdr tish woldu curoc stearf caseebu trehe wlodu eb mroe llraove llclurea iipaerrostn rccignou, agenmin eth ybod udowl shwtci to enbiaorca adn iluiezt sioycislgl ot aaelctt orf ne,ergy tpso ntiizigul teh hitocdrnm,oai dna utsh Oxa2mV dowlu er.eaedsc

EHO.E.VW..R eacbesu isht si a EMRRF su,iotneq the odrer fo vetsne is a eliltt nftdire,fe eesptdi eth ueomtco bnige het mesa t(a laets h'atts who I asnruetndd )t.i o,S I kinht eth key ot yan iidcrmthnoaol ddroiesr is mnrregbemei htta teh mstnaotui rae mstloa ayreltnci goign to cftafe na oneddec irteopn nad tush a ciceidenfy fo hatt tnrope.i eOn iltrcea htta I ndufo iads ttha eth RNAt touinasmt sa( ni MEFR)R scae:u rtdipu"s lodcniohmtiar nitpreo hsn,seisty reacdgesin teh catvtiiy fo opleCmx I dna ot a serles ttxene xmpeloC V...I ihcwh seecdsrae teporinrias adn sowlre ntoopr upmign,p raaatillymcd dcesirnage het mmrnabee ptilteaon dan pnorot teoleialrcmchce opniattel rnetiadg orascs hte ncmdalrhtiioo ninre barnemem. hTe rotpon tellcmcrecehoia tpltiaeon engadrti is het gdvniri eorfc rof APT nshsisety nad ngasdriece ti tasliultabsny rweosl eht amlamxi taer fo PAT enysthi".ss c/br/4s0/.i4jsi1pr.o/wlmeho6f2/67lo.x29i1/tt6i9dan1.y3.0yll.e-0:03.e10.9f1ulnb

asdBe no ym teniangnrusdd fo xiiadetvo htlrooh,yposipan O2 npmtunicoso .(i.e ktagin eht teolrenc frmo clmepox IV adn ptuignt it on 12/ 2O to eacetr 2OH nda H+ vrdesi het rtnopo ednaritg chhiw revids PTA ctio.urndpo :uhTs tcnfediie tiryepsrrao dniaixoto e.i(. ADNtm tnusamiot of hte ECT nm)yzsee ldeas ot wedlroe 2O nomnoiusptc o(s elrewdo V2O a)mx hiwch nthe aslde to leoedrw PAT citopdn,oru adn sthu edcifetve .rtanomidhico hTn,e lwodere ianildrctoomh conniuft salde ot eeadrcsde becaoir saeioptirrn gtshuinn TAP tdnurocpoi to rianocabe at,oresnrpii evdrni by lisysc,goly and thsu iginnacesr lceatat vleesl.

eoHp tsih p!hles shTi tkoo em AYW TOO NOGL to ueirfg u,ot lo,l btu pfolhyeul I eenrv aiefkngr tgeorf ,it l.lo

ls,Ao if oyu nwat any emor ned,riag I lifnyal fodun an rlceita ttha ayctlual fyull lixesanp het coebmiihacl dna olyspopatghyioh fo ilohindmoatcr imeoh:satpy p/c/s.d2o4c653p/2.t/3ahmml/ra1/cau3ei1iat:ire4c7t/2no/b

yroSr i'st so logn!

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 :/ +1  
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! +1  
azibird  Definitely a mitochondrial myopathy, but I actually don't think it's Myoclonic epilepsy with ragged-red fibers (MERRF). This normally entails Myoclonic jerks, Generalized seizures, Cerebellar ataxia, and Dementia (according to Amboss). Maybe it's CPEO (chronic progressive external ophthalmoplegia): progressive extraocular ophthalmoplegia with bilateral ptosis. Not sure which one would account for her poor exercise tolerance. Either way, recognizing it's mitochondrial is enough. +  


submitted by nafilnaf(1),

What does she have? My assumption was that she was getting NRTIs for HIV/AIDS which get phosphorylated by HOST thymidine kinases and the mechanism for viral resistance is mutations in reverse transcriptase

azibird  I think she has chickenpox, caused by varicella-zoster virus. From FA 2020 p 183: "Vesicular rash begins on trunk; spreads to face D and extremities with lesions of different stages" +2  


submitted by adong(84),

Cecum is intraperitoneal even though it's part of the ascending colon

azibird  How were we supposed to know this? Thanks for the clarification. I picked cecum because FA says Crohn is usually the terminal ileum and colon, so I figured cecum would be the most likely vs the descending colon. +4  
kevin  Yeah that's what I thought at first too. Figuring it was a tricky question, I went with descending colon because 1) ascending and descending are retroperitoneal, so we know the latter is for sure right, and 2) cecum has it's own name (ie it's different than the ascending colon), so it probably isn't retroperitoneal in that regard. You can remember ascending and descending are retroperitoneal by remembering the greater omentum wraps around the transverse colon and from anatomy lab that there's a mesoappendix, mesocecum, etc (peritoneal) +  


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rmoF osbsAm no eiPnrot a:groDeiantd

dus"Enognoe etsiprno aer adereddg yb .esesoprmoat xogoseunE peortisn era dreadged yb ss"smeoloy

azibird  According to UWorld question ID 11674: Referring to the presentation of viral antigens on MHC class I, it says "The ubiquitin proteasome pathway (UPP) is essential to this process because of its role in breaking down native and foreign intracellular proteins." In the AMBOSS protein degradation card it says, "endogenous proteins (those synthesized as cells)." Would viral proteins synthesized by host machinery count both foreign and endogenous? If so, then this post is correct but a bit misleading. +  
azibird  *synthesized IN cells +  


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rFom bAssom no Peiortn diaaengoD:rt

ungnodE"eos isonrpte rae rgadeded by pmo.seerstao nooExesgu nspteoir aer dadredeg by semloys"so

azibird  According to UWorld question ID 11674: Referring to the presentation of viral antigens on MHC class I, it says "The ubiquitin proteasome pathway (UPP) is essential to this process because of its role in breaking down native and foreign intracellular proteins." In the AMBOSS protein degradation card it says, "endogenous proteins (those synthesized as cells)." Would viral proteins synthesized by host machinery count both foreign and endogenous? If so, then this post is correct but a bit misleading. +  
azibird  *synthesized IN cells +