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Comments ...

 +1  (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 +2
kevin  The key demographic for RSV is infants (<2yo), so based on age alone RSV is what they're going for imo. +4
lpp06  Signs of respiratory distress = bronchiolitis over rhinovirus +1

 +1  (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. +

 +1  (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.


 +6  (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.


 +5  (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.

cbreland  Note to self: Never refer, even when that seems like the better answer +

 +4  (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 +10
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. +5
motherhen  genius +1
yerpderp  Loud S2 made me think of pulmonary hypertension which would have an incr endothelin +1
geekymle  that loud s2 was from systemic hypertension. +
utap2001  systemic hypertension -> induce LV hypertrophy -> induce pulmonary hypertension -> endothelin increase, plus loud S2 and S4 gallop +

 +2  (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 +1
doublethinker  According to the rare diseases government website, it's OFTEN X-linked recessive: "Alport syndrome can be inherited in three different ways. About 80 percent of cases are caused by mutations in the COL4A5 gene and are inherited in an X-linked recessive pattern." Question def threw me off tho, because I was continuously thinking it's X-linked dominant... https://rarediseases.info.nih.gov/diseases/5785/alport-syndrome +

 +12  (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.

cbreland  Constanzo is the best resource, change my mind +

 +1  (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. +3
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 +3

 +2  (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. +4
cbreland  I had it down between the correct answer and "your son is average". Picked the wrong one. As stated by @drdoom, the stem says you have already reassured that everything is fine. It would be a good time to get extra info from mom instead of say the same thing over again. Really the question gave us the answer (I still picked wrong, but we'll do better on test day!) +1

 +1  (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. +3

 -5  (nbme18#31)

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

FA2020 p209


 +2  (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.


 +7  (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? +4
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
kevster123  I just put F cause it said transmembrane domains and I know the rough ER got a lot of balls on it that translate it through and to translate through the balls you're passing through membranes. +
drdoom  @nbmeanswersownersucks @nsinghey et al. There is extensive discussion of this on an NBME 24 thread. This link will take you to the comments (just don't scroll up to spoil the answer for yourself!): https://nbmeanswers.com/exam/nbme24/939#1379 +
drdoom  also, this thread from NBME 21 discusses cell transport more generally (same warnings apply! don't scroll up!): https://nbmeanswers.com/exam/nbme21/742#257 +
brise  The question is saying where is it initially produced? It is produced in the RER, therefore F. Not asking where it's production starts- asking where is it produced etc. +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/ +5
coby219  "Intervertebral disc (nucleus pulposus) herniates posterolaterally through annulus fibrosus (outer ring) into central canal due to thin posterior longitudinal ligament and thicker anterior longitudinal ligament along midline of vertebral bodies. Nerve affected is usually below the level of herniation." - first aid 19 p455 +3

 +35  (nbme24#25)

Who else came here after getting triggered by this answer?

yousif11  This question did not age well +9

 +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

 +3  (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 +
larryd  I thought this was Zika too and put kissing. According to the CDC website, congenital Zika is more likely to present with focal pigmentary mottling and chorioretinal atrophy (vs the chorioretinits seen in the newborn in the question).https://www.cdc.gov/pregnancy/zika/testing-follow-up/zika-syndrome-birth-defects.html +

 +9  (nbme23#48)

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


 +6  (nbme23#44)

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

koko  That you may face such questions as a doctor..so ,you need to update your knowledge on such things maybe +
koko  That you may face such questions as a doctor..so ,you need to update your knowledge on such things maybe +

 +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.


 +7  (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.


 +3  (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 × 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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PCP is a o-tityvhidanecpes adn csosievaitid ncatseetih thta lyganerle acts as a roednw btu nca sloa aucse bceniirled ogasgsnrei oplduec whti ipan ivsnisttieyin eh(t seapmurn ru.gd) ieractlV yusastnmg is a olncomym mntinoeed yhiplacs mxea gnd.nfii

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/ +  
schep  I spent so much time on this question. I also ruled out cocaine, methamphetamine and PCP because (I thought) his vitals didn't match. Then I was forced to convince myself that someone on oxy or a benzo would suddenly get violent... +  


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PCP is a aoysiphnvectetid- dna ssedtcivaoii caiseethtn atth legeayrnl tsac as a ronwde utb anc slao ecsau lbnreedici sggasrione cpluedo ihwt aipn tsvieysniiint h(et npamseru u)drg. lrVcaite nsmstyagu is a coylmmno imdeentno isaclpyh eamx fd.iingn

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/ +  
schep  I spent so much time on this question. I also ruled out cocaine, methamphetamine and PCP because (I thought) his vitals didn't match. Then I was forced to convince myself that someone on oxy or a benzo would suddenly get violent... +  


submitted by b1ackcoffee(45),

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(45),

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/ +3  
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." +13  
mangomango  Hypertensive heart disease causes concentric LVH - impaired diastolic function, preserved ejection fraction +1  


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/ +3  
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." +13  
mangomango  Hypertensive heart disease causes concentric LVH - impaired diastolic function, preserved ejection fraction +1  


submitted by azibird(180),

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(373),
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varunmehru  in the question stem, they are asking about a constant region. VDJ rearrangement is for the variable. It doesn't make sense :( +3  
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. +7  
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. +3  


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. +4  
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 +3  
cbreland  Can't believe this was that simple... +4  


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(49),
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rtTiainnsospo of het vaAn eegn romf tno-ieacsytmicnnrvas ontceEroucsc si ohw it esnsftrar ta.icssneer hTye ues ansosprstno hchwi ear cdloeta on mapdliss. If ouy have dalpsmi os,sl oyu nowt' vaeh nssrpaoto,ns dan etseainrsc lliw .ecsdaree

azibird  Why can't this be a point mutation? +6  
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(373),
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/g.n/w.onudb7s4l:ewhb1i6mih/.c.m4pp7wt4ntv/ no cmmo esussi in ypte 1 dna teyp 2 iatiscbed

azibird  That article does not once mention the word diarrhea. +2  


submitted by m-ice(340),
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trecniViisn si a echuceoeatitrhmp gdru ttah bslsitaiez losbmiutceru dan etsnrpev hmte mrfo sbiaenmgl.sdsi eTh lelc ni eth ertiupc si kcsut in apshna,ea htiw uulrotiscebm cdhatate to tsi roh,esocosmm nalube to lplu ehtm rtpaa bcueeas ti nantco samdssbeeil its om.screbutuil

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. +14  
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(1553),
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hsTi is htriee a tprohiceyrp rsca or kiloed. oBth sraei ude to -renspeeosxvoir of TF.abt-Ge

charcot_bouchard  i think its a foreign body granuloma +11  
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(90),
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Make a tepnunt rqaseu whit a sscro of B B+ dna B 0B; B+ entsrrspee 50% cnfiuotn wleih B0 nsrsetrpee %0 nl(u)l ftui.nnco So in tihs c,sea hte unadbhs oldwu haev a B B0 getenoyp elhiw the wief sha a B B+ .npeyotge

sroCs fo teshe wto wlli lsrtue in hte fnogilwlo gstee;pnyo BB, B0,B BB,+ 0B+B BB = %001 itc,nuonf BB+ = %75 tnioufn,c BB0 = 50% i,ufotnnc +0BB = 52% cntfoinu

So eth rawnse ilwl eb 1 in 4 hvea a %52 fntincou evnig hte ypotsng.ee

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. +2  
hemehero  Is there a way to know that B+B0 will = 25% function. I was stuck between 25% function and 10% function, but couldn't figure out how to reason between the two of them. +  
neil_simmons  The question says the mother has a mutation known to cause 50% decrease in beta-globin gene function of one allele. So if one allele is working at 50% (B+) and the other allele is working at 0% (B0), then that would mean that particular set of alleles would function at 25%. +  


submitted by whoissaad(82),
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tyeArr of uudcts rfendsee si a cnbhra fo ofnriei evlisac ry.trae oS ywh is B ?gwrno

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. +  
jurrutia  A of ductus deferens would be the direct supply, vesical artery would be indirectly (via a of ductus def) +  


submitted by usmleuser007(396),
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Arfet omes scraerhe hsit is hwy the hoetr swarsen aer roc:rnctei

aslBa toneeatiykrc a&;mp ilmnaa cudlia

  • trcerconI bc/ ilnama icudla is a moctenonp fo eht staenemb eebmrmna cihwh si fundo wnbetee het iplheutmie nad udnyenlgir ecncvointe etssiu ,(..ge pdeiermsi and dirmse of hte .sk)in
  • tI is a uhrolgy 40 noerament iwde lece-tctlunroen onez eewenbt hte pmasla eamernbm of teh balas escll adn eth tec-een(reosndl) mainal danse fo hte tbamesne eamrenb.m II()WK
  • blsaa ttekycinoare csetahat ot the amntbsee nmraebme gunis meiemdsmseooh

uaarGrln retinctakoye am;p& atmsrut mrnecou

  • atmSrut dculium arsesptea hetes wot rye.asl
  • erthe aer on msoeeosmd that tonccne tehes wto lrysae
  • Iegam fro eerfrcnee

miLnaa uailcd ;pam& iaamLn daesn -- ickcl for emgia

  • tboh rae rtpa of hte baneemst embeanmr nda ton the esiidmrep

leMocnayet pma;& blaas teecrnoitky --- icklc ofr emgai

  • aer hbto cndtcneeo to ertaohec vai E-dinsraehc
  • ti si yabblopr hte ademag to tihs nicocnonte ttha
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(54),
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fondu this puesr uufesl ookb no onamaz ouatb hrd-uiCBdia (ekcch uto eth kics o)rcev

llamastep1  Thank you for that +  
focus  hahahahaha. DEAD. +  
anjum  I endorse clicking that link +1  
azibird  Hahahahahahaha, that's a must click. Someone please buy it and let me know. +  
chediakhigashi  hahahaha +  
aakb  I don't know what I was expecting... +  


submitted by usmle11a(76),
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hTe mcdlaei uqrneestremi to tnobia a etmpir rvay by t,tesa btu ear ullyaus cfndneoi ot eiccspif esypt of stlibsaiiide or tdo.csionin eheTs sa a geanerl uler culndie het sue of ayn isestivsa ivdece shuc sa a aricewehlh, sutr,cech or e,cna as lwle as a gsisinm gel ro .otfo emSo sestta aols dncieul tariecn ,urialcsracvdoa ,inpa ro riyrroaespt oictonsi.dn tuboA lfha of SU sstate 2)6( iednlcu nsdbnlise sa a fuaingqily iiatdsybil gaelninb the roepns ot onibta a litayidbsi apignrk ripmte orf eus sa a rpegsan,se and 41 stetas lundeci a adlsibde hdan as a alyngfuiqi yi.tlaiisbd uFro tetass uedcnil edanes,fs dna otw attess Vri(ginai and eNw Yrk)o incdelu mental lsesnil or vpnedlmaeleot iaissdltbeii as nyuifqliag aletbsdiisii

oru yug uses a neca ..s.o

bwt i otg it rgnow :) eacsu i uhtthog ti is pu to hte DVM

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. +5  


submitted by hayayah(1076),
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loaCboom is na yee ryotmlinaba taht usrcco obeerf h.itrb yheTe'r gsinism ieespc of tuises in cetsruusrt ttah omrf the .eey

  • sCamboool atfcgnief eht ,isir chhiw elrsut ni a "l"eehyok epraepcana fo teh pup,li arnegylle od nto aedl to sioinv sos.l

  • blmoooCas nonivlgvi eth anrtei rlstue ni ovinsi lsso in efiscpci arstp fo het vusali lf.die

  • raeLg tanierl boomlsoac or eoths nciftagfe the oticp never nca ueacs owl niisv,o hwhci nsmae ovinis slos ahtt antonc eb cemyteollp errdoccte whti gaslses or otnacct en.elss

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 +11  
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. +3  
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! +2  


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 caem hree jtus to drea eht scntoemm

JM at eht ivemo eshttare tegnai cooprnp meme

azibird  Same! +  


submitted by sajaqua1(532),
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HCM I infnoctu is ngatrlei ot cencar snsuerpoips. HCM I yipadlss golunnesdeyo sihynsedzet psnoriet and ptsrnsee meth ot +DC8 T lecl.s Teh rulafie ot dalpisy CMH ,I ro MHC I splayid of -lnseofn n(ad by snetnexoi arcuonec)s trpieons streirgg a lurcelal ienmmu prs,eones lagndie to dncsueoitrt fo teh ell.c

eTh moeatropse is esud for teh tardoeagnid of wrno otu, n,ctsenees or afedlommr is.teornp sA nrceac ,vdeesopl rmoe ouamnttsi elda to sndereica rnogw nsepirt.o nOly by sisnepexro of the eeasmo,prto ro ist snrrvs,pxeoioe-e cna eshet ttnamu pronsite be gedrdead fast hnegou to tno be lypsaided yb CHM I nad ldea to hte ecll genbi idlle.k zomteBrbio ksocbl teh sme,troapeo os eth tunmta prontsei era ldieapdsy no eht a,srcufe loinwalg the ummine tsemys to zeiroecng nda klli ichlpoltgaao cl.lse

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/ +26  
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) +4  
azibird  But CD8+ and NK cells kill via perforin! Why is this answer wrong? Is it because it's not the primary effect? +2  
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(532),
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etorPisor crod reomdnsy ocsurc eud to aionctrfin of eth peristoor fahl of the pnsail cd,ro ofrm osnciuclo of hte rripostoe apnsli rea.yrt urO aettpin spersent hiwt deaeesdrc osiastnne to cnirpikp bwelo eht elvel fo eht eenks sa elwl as glikwan whit a awbi-dsede atig, leklyi tciginanid loss fo ppno.ptiircooer eTh napteit si lsao imnaec whti hpenrysd-mtgeee rpslet.uhoni

steemyeHrpgnde rstpiuenloh rae ycpltlayi ecusda by an nilbiytai to kema uonghe ,DAN dseacu yb a aclk of eresacyns ssurecpror dna isvitman nnldgicui 9B ()ltfoea and B12 n)cbaoi(l.am If teh npeitta si etalfo de,fteiinc we ese teeldvae mihsyetooecn iecfeyin.dc If teh ntaetip is B12 ent,cfeidi ew ese edealetv latymlmenihoc daci nad etesicoyhmon el.vles mhiyepenomaoisrcetyH acn cesniera iosms.rhbto bThmossroi in the osteirpro alpisn raryte can aecsu sieoptrro dcor om.erdnys In ,ndiiadot ckal fo vaiimnt 2B1 rispami nylmie mfirtoano dan asled to atueSucb edbnComi aeonnegtri,De hwchi feasctf hte Soihcanamlpti rtcta g(atnciconu rof cdeesrade npicrkip oe,ntn)ssai pcirnCaooslti Tr,tca nda lrsaoD CiMluodane-ml meciLsuns artTc nuccn(agiot orf eth redcude trionrop.piceop

)A toiArern rdoc os-mynedr sslo fo omotr odn,mmca as lewl sa airlleabt lsso of eath and ,pnia hte ptenait ash not tosl rootm ,confitnu os ti aconnt be s.tih B) natelrC docr mesrondy- tesnpsre sa a nonmiitcboa fo morot dna oynrses ss,ol saluyul thiw reddabl ynnsfcod.iut iThs petitan sode otn ydspial rootm ssol ro rleddba dtu.sifynnco C) reocmidH -rnmesody losA laldec SeBrnqduar-ow, tish si lcpmoete ynjriu ot heietr het left or tgihr deis of teh ainlsp ocrd. tI ersepnts tiwh rotmo fiucoynnstd dan eflxer uyoisncftnd pieatraillysl at het lvlee of teh eoi;nsl lsos of epurp otrom mnmaocd owelb eth iselno lyliapeslirta sispta(c p)ssai;re slos of adslro rmualrcicneo-d inontssea latyliialpres ta dan bloew het nseilo; dna osls of pain nad mtrpraeeute ssotenina atlytealrcrlaon 2 ot 3 bveeratr ebowl het lionse. E) Sgteyaenmr eyomdr-sn a getolcinna friealu ot lpdveeo aptr of het isnpla .crod hTe new ntsoe fo osmpytms at 28 yasre old ksame shit an nileylku i,ngdso.asi

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(293),
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So hsti neiuqsot asw hogmtnsie I arelly lgurdsget iwth. I i'ntdd ogeerznic taht eht tineptoanser aws fo RREMF sa emsoeno sdeatt belwo, nad I oknw uoy tdn'o need ot kown hatt ot swnrae hte etus,oqin but it wdulo eahv bene eup.hllf yM ebsiggt afusrittnro aws hte grodwni fo the opsiyb rstleus "boarnlam suacinuaotcml fo t"nohricaoidm. sThi dyeanon me besceau eth tonifidein fo rdgega edr fsrbie ihc(wh I'm mgunisas wsa iehtr etn)noitin si utcmoa"liusanc fo aloabrmn rnatomidh.coi" Thsoe ear tow vyer effnteidr sntmtaeets in ym indm, llo. The sftr,i to e,m jstu anems te'hesr too much di,trohoiamnc utb eht edcosn anesm heetr's too mhuc DNA ethy ner'ta foiuctngnni lpp.oryre t'Is slao jtsu eth tcfa of emgmbierren lal fo eth srmet fro ECT ta teh etmi fo iearngd teh ueoqsnit (i..e I dintd' ktihn otaub the ftca htta TCE si losa ldlcae uaclellr sernrpiota ro just pas.ietrinor)

I laso id'tdn arlyel trndsuedna llfuy hatw xVmaO2 is = O2V" xm,a aslo ownkn sa xmlaaim exyngo utpea,k si eht neeatursmme fo teh axmumim tnuamo of nyexog a onesrp anc etulizi ignudr isenent eies.rx.e.c nda si bsade no hte ersimep tath hte ermo eyoxgn dmsuecno nurdig eseirx,ce teh roem teh doyb ilwl rnateege idoennsea epihhoattspr T)(PA geryne ni .se..lcl VO2 xma si ehardce nhew uyor gyneox otonpnusmic sanreim at a sdatye atest tpeseid na secniaer in hte .wlarkdoo It si at shit taelpua ttah eth mls][ceu sveom ofmr cberioa amsbotmiel ot acaibeonr smbtoilme"a vm2tw/re1ti.lmcw3tothsp09-h.f/io:way/w2e0v--w-xsa7l.

eadsB yeplur on stih enitdo,ifin where aOx2mV = sniaelslyet hte mtei at iwhhc obecari sseiwcht to ioecbarna iptns,reirao my rapnnerotietit fo oto umhc rothimocidan vs too uchm and bda rrdtimnihoaoc ddn'ti tm,rate eubcase vnee enwh the noamiohrtdci rea nnguctinofi yopr,prel thye rhcea a toinp adn wsithc to abarn,oeci thsu fi heetr aws too uhmc anrmol aionhmtc,odir tshi duolw urocc tfrsae aebucse erhet dlwuo be rome allvoer elrclalu sirnoatripe gruconic, nemigan eht bdoy uowdl ctwsih ot ceaornabi dna iiluzte glyoiscisl to atleatc ofr g,reeyn spto ilniiutzg het hn,iitcdoramo dna tuhs mxa2VO owdul .eedsarec

VHW..EE..RO eausceb this si a RFMRE nuo,etisq teh rreod fo netesv is a llitet fn,eetdirf idpeset the ouetmco ienbg eth msae t(a teasl 'tsaht woh I ndaneturds it). o,S I tkhin eth kye to yna daritmoihnloc orsierdd is rniebrgemme htta eth umniastto ear osatml ctyreainl gngio to cffeta na ddeenoc nrptieo adn suht a iyicdeencf fo hatt iernpot. enO rtaelic atht I fnudo adsi htat teh RtNA naomtitsu a(s ni MRF)ER uscea: dptr"ius ocidmlthorain ipnerot enshy,isst ecnagdiers teh yittvcia fo olmxeCp I dan to a sesler nextet xClmpeo ..IV. ihhwc ecrdsease tireapisnor dna welsor potrno uimpp,gn ytlaaicmardl aciendgser hte nbeaemrm entaioptl adn rpoont ctcemeroaielchl naoetlitp ratiegdn sarosc eth tdiohacriolmn ennir mmeaebr.n The rnotpo thmccaiereleolc ilpotntae tdranegi si teh ivnridg ecorf rfo ATP iysesnsht dan gcnedresai it lbnaslyatusit lswore het aaxlimm tear fo TAP snhsy"ties. lrr0s3l1ao/7-4ie0lyp1i.0betf1d/9l./n..26.01f2/we36.s9nh://co4myxt.ilob9.ju16i0

desaB no ym ngrdtnesdnuai fo eaivxotid ,pornohliotyhsap O2 imtosuopnnc ei.(. gaknti het torencel fomr celmpox IV nad ntgptiu ti on 21/ O2 ot aetcer O2H dna +H srvedi the oortnp ndgatire whhic rvsied TPA crotuno.pdi hsuT: encieftid ytarpresori tnoxiidao .ei(. tDmNA tnmasuito fo eht CTE e)smneyz adsle ot weerodl O2 smnpoucotni so( edrlewo VO2 xma) wchih hnet aldes ot oedrwle TAP ictn,urodpo and hstu vtieeecfd hi.drotonacmi eTn,h elrewdo irnomcohltadi fnocutni aelds ot dedseaerc eoibrac raenirsipto gnntiuhs PAT rodipuctno to bnirocaea srtaornipe,i ervnid by lysyc,igsol and hsut anniiercsg aetlcat lvlees.

eHpo sith p!lhes sTih toko me WYA TOO LNOG to fergui tou, ,oll but ufyllphoe I renve gnrkifea teogfr ,it llo.

,lsoA if uoy natw yan roem dg,aeinr I afnllyi duonf an irlteca atth lyulctaa yllfu psexilna eht ehcoiciblam and aygyosplhpooith of aochotrlindim tsayohe:pmi a/ee2tmodp/6h7ic//is3:.pt2mil5can.3cc14/obau4tr/13a2//r

yorSr ist' os lno!g

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" +3  


submitted by adong(97),
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umcCe is ieraapnnttirleo eevn thhuog tis' trap fo het gncsenida locno

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. +10  
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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morF Amssob on ePirnto tegdia:anrDo

oned"oEusgn etiospnr era dddgeear by pstraomse.oe osxoegEun tpserino rae dddeager yb seoyss"lmo

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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mroF smsobA no noiterP etraaiongD:d

E"odeognnus oenprtsi era agedrdde by s.asomtpeero nEogxuose osrnpeti era dredegda by syloosem"s

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 +