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Comments ...

 +2  (nbme18#7)

monoclonal IgG kappa (light chain) spike on electrophoresis, lytic bone lesions in the spine, cardiomegaly all point to multiple myeloma. Causes a primary amyloidosis that can deposit in multiple tissues, like the heart in this patient.

underd0g  Why can't the answer be plasma cell infiltration? +1
notyasupreme  @underd0g I put that too, but I think if you look at the histo picture, it literally shows all the eosinophilic looking bullshit from amyloidosis, and it was specifically asking the cardiac symptoms. The cause of MM is plasma cell, but the cause of the cardiac is the primary amyloid deposition = restricitive cardiomyopathy +
trishasingh  In multiple myeloma there is overproduction of immunoglobulin light chain that causes majority of the symptoms, like bence jones proteins in the urine and infiltration of organs like the kidneys and the heart. It causes diastolic dysfunction of the heart. Other infiltrative diseases, like haemochromatosis and sarcoidosis also cause diastolic dysfunction of the heart. +

 +4  (nbme18#4)

After the addition of furosemide, her BUN/Cr ratio went up to 38 and Fraction Excretion of Na < 1%. Both of those hint a prerenal azotemia. Which also makes sense since she has congestive heart failure which would decrease blood flow to the kidney and then taking a strong diuretic would lower her blood volume even more.

lokotriene  FA2020 p601 +
lokotriene  UW:15207 Deals with this same concept and has a great explanation about the pathophys. +

 +3  (nbme16#43)

The patient can only achieve erections via direct stimulation aka touch. The pudendal nerve provides somatic innervation and thus sensation to the penis as well as the perineum. A purely sensory stimulated erection involves a reflex arc between the pudendal afferent nerves and efferent sacral parasympathetic nerves (aka pelvic splanchnic nerves).





Subcomments ...

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tdlnieav sointca rtfneiree wthi eht rosnibtaop oit)rdo?sna(b of rloaoCipfxn.ci

redvelvet  divalent cations interfere with the absorption of tetracyclines, not fluoroquinolones. anti-acids interfere with the absorption of fluoroquinolones. (like in this q, it's ca carbonate) +2  
keyseph  According to SketchyPharm, divalent cations also interfere with the absorption of fluoroquinolones +8  
nbmeanswersownersucks  Calcium carbonate is an antacid but it has Calcium in it....which is a divalent cation +2  


submitted by beastaran1(1),

Believe this one is tubulointerstitial fibrosis of the kidney:

medullary cystic disease is characterized by autosomal dominant inheritance pattern progressive and slow impairment in renal function that ultimately results in end-stage renal disease no or minimal proteinuria with a bland urine sediment medullary cysts on renal ultrasound in most cases medullary cysts are not present can see shrunken kidneys on ultrasound

makepoopinggreatagain  Tubular atrophy (hint: dilated ureter/calyx in image) ↓ Posterior urethral valves is the 1 cause of bladder obstruction in males ...Diagnosed by hydronephrosis and thick walled bladder +  
nbmeanswersownersucks  this can't be posterior urethral valve because then both kidneys would be effected. +8  
j44n  I agree its the medullary cystic kindey disease-> FA19-592 talks about it +  


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  


submitted by jorgejeje(5),
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sI a saec fo longnctiea gnlo Q,T tereh rea owt npiplicar csaues; noW-oraRadm d(tonan)im dna lreeJlv adn -NlneLsegaeni odesnm,yr het encosd eno derleta to esnafsde r(ie)ee.svcs I'st otpraitmn ot eemrberm hte apnoiilhetrs of teh GKE adn the celcy fo itoacn taioepltn fo eht rcdacia lcuesm clel seeubca eht TQ si dolerterac twhi eht rptnioeoazalri A(FSE ,III) larimsi ihwt eth arhthrnisiam,tyc hte seno atth ffatec mapsituso alnhscne AFS(E )III rae ermo edtrale htiw strletioana ni TQ and vaueirntlcr .asrimyhthra

nbmeanswersownersucks  **phase lol +1  


submitted by masn8cc(2),

Can someone explain how they r/o aortic stenosis? because that could enlarge the LA and give the same sx of hoarseness etc. And the murmur also fits with AS

bmalamet  You would not see a "viable pulsation above the manubrium, which you should not confuse with a "brisk carotid upstroke" associated with aortic stenosis. +2  
nbmeanswersownersucks  "brisk carotid upstroke" is the description of a normal carotid pulse. Aortic stenosis has a slowly rising/late peaking upstroke since the stenosis impedes flow out of the LV. +4  
overa  AS affects the LV first. it isn't until later in the disease progression that there will be a significant enough enlargement of the LA to cause impingement of the LA. By the time the problem was that bad there would also be pulmonary findings of backed-up pressure (in my not so expert opinion). +  
305charlie94  Can anyone explain why the trachea is deviated in an aortic aneurysm? Made me think of a pneumothorax here +1  
baja_blast  ^It's basically mass effect. Aortic aneurism takes up space in the thorax, displacing the trachea to the right. Take a look at this CXR: https://radiopaedia.org/cases/thoracic-aortic-aneurysm-3?lang=us +3  


submitted by azibird(158),

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. +  


submitted by chadgas(1),

Did anyone have any difficulty deciding between C and E? I knew it was a Vitamin D deficiency, but doesn't calcitriol feedback to decrease PTH production?

nbmeanswersownersucks  I think it is because the question stem asks about the deficiency that "DIRECTLY" affects a process. Vitamin D directly affects calcium reabsorption whereas it is the rise in Calcium (caused by Vitamin D) that then negatively regulates PTH production (so Vitamin D indirectly regulates PTH). The "directly" wording has gotten the best of me more than a few times so now I've become hyper-aware of that wording. +3  
nbmeanssux  Also, I just realized it asks about "vitamin deficiency" and calcium is technically a mineral :/ +  


submitted by pelparente(16),

If it ain't broke don't fix it. The patient is showing improvement and there are no signs of developing drug resistance or unwanted side effects, so maintain the patient on her current therapy.

Typical antiretroviral HIV therapy regime is:

3 NRTIs OR 2 NRTIs AND 1 NNRTI OR 1 Protease inhibitor OR 1 Integrase inhibitor

In this case the patient is on 2 NRTIs (emtricitabine, tenofovir) and an NNRTI (efavirenz)

nbmeanswersownersucks  and here comes my dumbass that read the lower CD4 count as his newer labs (instead of old) and was trying to figure out why his drug combo wasn't working.... +11  


submitted by azibird(158),

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. +  


submitted by aoa05(21),

Weakness with decreased muscle bulk implies problems that include the lower motor neuron system. Decreased DTRs implies a disrupted reflex loop but the absence of sensory loss implies that it is on the motor side of the reflex loop. Of the available choices, B is the best fit. "A" is arguably true because a strictly motor polyneuropathy (such as in lead poisoning) could account for the findings, but a 3-month course could hardly be called "acute."

itsalwayslupus  I was able to deduce the right answer, but what is the specific reason against "demyelination of the corticospinal pathways"? just out of curiousity +1  
lsp1992  I believe it's because damage to the corticospinal tract would be considered UMN damage, while degeneration of motorneurons is LMN damage. LMN damage causes decreased reflexes. UMN disease would cause hyperreflexia....I think. That's how I reasoned through it at least +11  
nbmeanswersownersucks  I also think you can rule out peripheral neuropathy because typically that includes both motor and sensory +2  
saqeer  yes but is not Achilles an S1 reflex (sacral cord) ? how does the degeneration in lumbar cord affects it ? i rule it out first thing because of this :S +  
meryen13  i think she just had a dics herniation. there can be problem with temperature and sensation in some case but those are usually very severe herniations. not sure tho... but it can on your differentials. +  
djeffs1  I assumed that "motoneurons of the lumbar chord" means upper and not peripheral +  


submitted by medninja(15),

MEN 1--> Pituitary tumors, pancreatic endocrine tumors (zollinger ellison or gastrinoma) and parathyroid adenomas.

nbmeanswersownersucks  the question hints at a possible parathyroid adenoma with her history of 2 episodes of renal calculi. +3  
feochromocytoma  Yup, also as a tip for next time, if you see that a patient has some sort of pancreatic cell tumor, such as Zollinger in this case, look for other MEN 1 associated findings. +  


submitted by bingcentipede(209),

IgG antibodies can cross the placenta, leading to thyroid enlargement. This can also explain the stridor and issues with respiration in the newborn. Essentially, this is causing neonatal Graves disease.

From UpToDate: "Neonatal Graves disease refers to the hyperthyroidism that is seen in a small percentage of infants born to mothers with Graves disease. Although neonatal Graves disease is usually self-limited, it can be severe, even life-threatening, and have deleterious effects on neural development"

nbmeanswersownersucks  Was anyone else thrown off because the neck mass was asymmetric and graves usually causes diffuse enlargement of the thyroid? +4  


submitted by cassdawg(930),

This is metastatic renal cell carcinoma (FA2020 p605) for the following reasons:

  • Polycythemia - this is the primary clue, as it is associated with ectopic EPO (erythropoitin) secretion in paraneoplastic syndromes (FA2020 p228), which can be caused by pheochromocytoma, renal cell carcinoma, heptocellular carcinoma, hemangioblastoma and leiomyoma. Of these, only liver and kidney would be a choice given and hepatocellular carcinoma is incorrect because he did not have any associated finding of jaundice, hepatomegaly, ascites, or anorexia (FA2020 p392). Plus, the liver does not commonly metastasize to brain whereas kidney does (FA2020 p223)
  • Hypercalcemia - this is likely indicative of PTHrP secretion, and renal cell carcinoma is one of the cancers that can do this. However, this is fairly nonspecific as there are many cancers that can secrete PTHrP.
  • Heamaturia - suggestive of kidney/urinary tract involvement
  • Negative for carcinoembryonic antigen - this is a nonspecific marker mainly for colon and pancreatic cancers (FA2020 p226)
hungrybox  WOW. Amazing explanation. Great work!! +  
nbmeanswersownersucks  Additionally the histo looks like the Clear cell type of RCC. The large white/clear spaces with "chicken-wire" vessels and stroma between them. +3  


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

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


submitted by cassdawg(930),

This is mesenteric artery stenosis causing postpranidal intestinal ischemia/angina. I definitely did not know this answering the question and I personally got to the answer by attempting to logically think through the symptoms:

  • Weight loss and abdominal pain in general pointed to intestinal ischemia of some sort and since most absorption of nutrients happens in the jejunum, ischemia there would cause weight loss. Jejunum is supplied by SMA
  • Bruit to me meant a larger vessel was blocked since to be able to hear it it has to be a pretty large vessel, SMA is one of the larger arteries listed
  • No liver symptoms (i.e. jaundice) so eliminated hepatic artery

If anyone has a better explanation please offer it.

deathcap4qt  great explanation for not knowing the answer! You're right in that it has to do with a vessel of a larger size. Generally Celia, SMA or IMA. pt hx of atherosclerosis should be a big hint. FA 2019 pg 380. +2  
nbmeanswersownersucks  SMA is the MOST COMMON vessel involved in ischemic bowel disease. +1  
baja_blast  I reasoned this out by remembering that the Abdominal Aorta was the most common place for atherosclerosis and picking the only option that branches off immediately from there. Not sure if that's what they were going for but it got me to the right answer. +1  
topgunber  i think thats a great explanation ^, namely because its possible obstruction at the other vessels may not cause symptoms due to collateral circulation. SMA on the other hand, if stenosed, would have a number of regions with ischemia- not to mention its involved in a watershed area. +  


submitted by cassdawg(930),

This is anesthesia being given via lumbar puncture. [FA2020 p507]

The needle will pass through the supraspinous ligament, intraspinous ligament, and ligamentum flavum before entering the epidural space.

The anterior longitudinal ligament is on the anterior side of the spinal cord. The costotransverse would not be punctured. Image of the anterior longitudinal and costotransverse spinal ligaments here.

The denticulate ligament is what holds the pia mater to the dura mater. Since this is likely epidural anesthesia it would not be punctured.

The posterior longitudinal ligament is on the posterior portion of the vertebral body but is anterior to the spinal cord, and thus would not be punctured.

nbmeanswersownersucks  also to add to this, the costotransverse ligaments are only present in the thorax because they run between the rib and the transverse process. Epidurals occur in the lumbar region...and if you have ribs in the lumbar region you've got a big problem on your hands +  


submitted by andro(169),

Fatty Acid degradation
-Occurs in mitochondria or peroxisomes

First step - uptake of the fatty acids by the cell and addition of CoA to them

Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)

Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )

An Acyl CoA dehydrogenase catalyzes the initial step .
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation

The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )

notyasupreme  It's actually funny because the question stem makes it seem like it's an MCAD deficiency (presence of dicarboxylic acid) and all the symptoms, but then treat it with MCAD. Whatever, I got it right but it just felt like a weird question to me. +2  
nbmeanswersownersucks  yeah I was confused too but I also think the negative serum carnitine is supposed to help r/o MCAD deficiency since that usually has elevated serum carnitine. +  
baja_blast  If Carnitine was an option here, how could we differentiate this from primary carnitine deficiency? Would it have been possible? +5  
melanoma  the presence of dicarboxylic aciduria is more related to mcad/lcad deficiency. the patient receives medium chain tryglicerides because he has the enzyme to metabolize it. +2  
melanoma  but no for the long chain +  
topgunber  just a few things, sure it sounds like mcad but lcad would present similarly, except in MCAD, giving medium chain triglycerides would worsen symptoms as compared with LCAD. + Similarly when fatty acids cant undergo Beta oxidation they undergo omega oxidation- which is why there is increased dicarboxlic acids (i.e. dont just jump for MCAD when you see dicarboxilic acids). Last of all it would be difficult to differentiate but if the patient were deficient in carnitine the treatment with MCADs would not show improvement because carnitine is required to shuttle the fatty acid into the MTs. +1  
topgunber  'a 'weird question' because my school never asked it' +1  


I was thinking it could be 22q11 microdeletion because that also would have abnormal organs (heart, thymus, parathyroids) and abnormal face. So, I'm just wondering how you're supposed to definitely know it was Trisomy 21. I had the original answer too, damnit!

nbmeanswersownersucks  I think it's more because a spontaneous microdeletion would not really explain the previous lost pregnancies whereas an unbalanced translocation in the mom could. And I think it could be any of the big trisomies (13, 18, 21) but 21 is most common. +3  
m0niagui  so, it is the mother that has Down's Sd? +  
jj375  No, the mother doesnt have down syndrome. As far as I know, the mother has a BALANCED translocation - for example (totally made the chromosome # up) she may have a piece of chrom 11 and chrom 4 swap places. However they are balanced since they are both there, no genetic material is missing os she looks healthy and is fine. BUT when her eggs are made, some eggs may get the chrom 11 (+ piece of chrom 4) and then her regular copy of chrom 4...Now that baby also gets a chromosome 4 from the dad. The baby will end up with 3 copies of part of chrom 4 but 1 part of chrom 11! So the kid is unbalanced and may die in utero (spontaneous abortions). I hope that was clear Here is a photo that may help: https://accessmedicine.mhmedical.com/data/books/hoff2/hoff2_c006f005.png +  


submitted by aoa05(21),

First, the boy had ophathalmoplegia (eye muscle problem) and hypotonia (muscle weakness), indicating that he had muscle related problems. Second, all the problems appeared to come from his mother’s side and the symptoms from different individuals of the family appeared to be very heterogeneous and diverse. All these strongly suggest heteroplasmy, a mitochondrial genetic disease, which is known to show varying degrees of expressivity owing to heterogeneity in genetic mutations in mitochondria. All the mitochondria of one person are inherited from mother’s side (from fertilized eggs) and are different from nuclear chromosome inheritance mechanism. Heteroplasmy is caused by the fact that in each human cells, there are several hundreds mitochondria. In different mitochondria, they may contain different genetic mutations. During genetic transmission, different mitochondria may end up in different eggs / fertilized eggs, leading to mitochondrial genetic disease in the offspring with varying degrees of expressivity owing to heteroplasmy

How to exclude other possibilities: In the narrative, there are genetic diseases two generations in a row in the family. Thus, it is not recessive disease. It came from his mother’s side but affected both sexes. It does not look like a penetrance issue, Additional information - MERRF syndrome (or myoclonic epilepsy with ragged red fibers) is a mitochondrial disease MERRF syndrome affects different parts of the body, particularly the muscles and nervous system. The signs and symptoms of this disorder appear at an early age, generally childhood or adolescence. The primary features displayed on a person with MERRF include myoclonus, seizures, cerebellar ataxia, myopathy, and ragged red fibers (RRF) on muscle biopsy, leading to the disease's name. Secondary features include dementia, optic atrophy, bilateral deafness, peripheral neuropathy, spasticity, or multiple lipomata. Mitochondrial disorders, including MERRFS, may present at any age

nbmeanswersownersucks  I agree with everything you said though I don't think the disease in the question is MERRF. unless I misunderstood you and you weren't saying it was MERRF but were just describing an example of a mito disease? +4  
nbmeanswersownersucks  I think it is more in line with MELAS d/t the lactic acidosis and stroke +2  
i_hate_it_here  Username checks out +  


submitted by aoa05(21),

First, the boy had ophathalmoplegia (eye muscle problem) and hypotonia (muscle weakness), indicating that he had muscle related problems. Second, all the problems appeared to come from his mother’s side and the symptoms from different individuals of the family appeared to be very heterogeneous and diverse. All these strongly suggest heteroplasmy, a mitochondrial genetic disease, which is known to show varying degrees of expressivity owing to heterogeneity in genetic mutations in mitochondria. All the mitochondria of one person are inherited from mother’s side (from fertilized eggs) and are different from nuclear chromosome inheritance mechanism. Heteroplasmy is caused by the fact that in each human cells, there are several hundreds mitochondria. In different mitochondria, they may contain different genetic mutations. During genetic transmission, different mitochondria may end up in different eggs / fertilized eggs, leading to mitochondrial genetic disease in the offspring with varying degrees of expressivity owing to heteroplasmy

How to exclude other possibilities: In the narrative, there are genetic diseases two generations in a row in the family. Thus, it is not recessive disease. It came from his mother’s side but affected both sexes. It does not look like a penetrance issue, Additional information - MERRF syndrome (or myoclonic epilepsy with ragged red fibers) is a mitochondrial disease MERRF syndrome affects different parts of the body, particularly the muscles and nervous system. The signs and symptoms of this disorder appear at an early age, generally childhood or adolescence. The primary features displayed on a person with MERRF include myoclonus, seizures, cerebellar ataxia, myopathy, and ragged red fibers (RRF) on muscle biopsy, leading to the disease's name. Secondary features include dementia, optic atrophy, bilateral deafness, peripheral neuropathy, spasticity, or multiple lipomata. Mitochondrial disorders, including MERRFS, may present at any age

nbmeanswersownersucks  I agree with everything you said though I don't think the disease in the question is MERRF. unless I misunderstood you and you weren't saying it was MERRF but were just describing an example of a mito disease? +4  
nbmeanswersownersucks  I think it is more in line with MELAS d/t the lactic acidosis and stroke +2  
i_hate_it_here  Username checks out +  


submitted by bingcentipede(209),

Since she has regular 28-day cycles, ovulation will happen on day 14. In the follicular phase before ovulation, estrogen rises to the point of the LH surge while progesterone stays low. After ovulation on day 14, progesterone rises and estrogen will gradually rise as well.

nbmeanswersownersucks  I feel like Day 6 is correct as well because estradiol levels would be elevated and progesterone decreased too. +9  
feochromocytoma  Nice username, and I agree +2  
djeffs1  @nbmeanswesownersucks thats what I chose too, but apparently the first 7 days of cycle everything is kinda uniformly low... https://womeninbalance.org/files/2012/10/HormoneCycle.jpg +  


submitted by b1ackcoffee(34),

Any good material for this and lymph node drainage in general? Is this common knowledge or low yield stuff?

cbreland  Got it with process of elimination, seems very low yield +  


submitted by azibird(158),

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. +3  
lpp06  Signs of respiratory distress = bronchiolitis over rhinovirus +1