welcome redditors!to snoo-finity ... and beyond!
Welcome to masonkingcobra's page.
Contributor score: 85
School:


Comments ...

 +0  (familymed1#33)

No one ever does this assay it seems:

UpToDate: However, serologic tests require validation at the local level, which is impractical in routine practice. In addition, concerns over its accuracy have limited its use.

The urea breath test is first line



charcot_bouchard  When i faced this ques i did some Kegel. Felt something in my pee pee but not in my b*e. I exclude all option because they are bigger muscle of pelvic floor except EUS & IAS. And also remeber Kegel can be used as a treatment of prem. ejaculation not premature defication.

 +2  (nbme23#33)

http://sickle.bwh.harvard.edu/thal_inheritance.html

Easy pictures to understand


 +5  (nbme23#39)

In addition to the previous explanation:

She is iron deficient and celiac affects the proximal duodenum. "I Fucked Brittany" = Iron, Folate, B12 for Duodenum, Jejunum and Ileum

krewfoo99  Great analogy lol. But just a correction, First Aid states that Celiac Disease affects distal duodenum and proximal jejunum. But you are right, it would still cause iron deficiency anemia as it affects the duodenum.

 +0  (nbme23#28)

Personally my issue with this question is that I though B12 causes demyelination in both the LCST and the DCML (SCD) but they are testing the mechanism here really with the whole methylamonic acid bit and the impaired myelin synthesis

If you're curious

https://www.nature.com/articles/scsandc20166


 +0  (nbme21#5)

Link

necrotizingfasciitis  Going off of the comments people have posted above & kinda bringing things together: PDA flows from aorta to pulmonary arteries, which reverses after birth. This means de-oxygenated blood flow from the pulmonary arteries to the aorta & less volume being sent to the LF side of the heart. This results in a decreased afterload because there is less blood flowing from the lungs to re-fill the LF ventricle, & the heart is still pumping with the same force as before, so the same volume of blood is leaving, but less in entering the LF side of the heart. From here, you use CO = SV x HR SV = preload - afterload (which is decreased due to the PDA) This results in SV being larger than normal, so when you plug that into CO = SV x HR you get a higher number for cardiac output.
didelphus  The ductus arteriosus flows from PA --> aorta in utero to bypass the lungs, which have extremely high resistance to flow. This reverses after birth due to a drop in PGE2 (which was supplied by the placenta) and increase in left-sided systemic resistance. So a PDA typically flows aorta --> PA (assuming there are no other defects).

 +0  (nbme20#8)

Robbin's: The two most important causes of aortic aneurysms are atherosclerosis and hypertension. Atherosclerosis is the more dominant factor in abdominal aortic aneurysms, while hypertension is associated with ascending aortic aneurysms.





 +2  (nbme20#38)

In psychogenic polydipsia, serum sodium is low, and after water deprivation test, urine osmolality is increased. Urine osmolality does not increase with vasopressin injection

In nephrogenic diabetes insipidus, serum sodium is high and there is no change/mild increase in urine osmolality after water deprivation

yotsubato  This patient does not undergo a water deprivation test
niboonsh  Compulsive water drinking or psychogenic polydipsia is now increasingly seen in psychiatric populations. Effects of increased water intake can lead to hyponatremia causing symptoms of nausea, vomiting, seizures, delirium and can even be life threatening if not recognized and managed early. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5579464/
missi19998  Just wondering why it in not resistance to ADH action of vasopressin
amarousis  because he would be hypernatremic with no ADH. can't resorb any water
minhphuongpnt07  low osm/urine, low os/plasma => psychogenic polydipsia
benitezmena  In this question the pt had a normal urine osm (80) a low urine osm would be <50mosmol/kg.

 +2  (nbme20#37)

In metabolic alkalosis, potassium moves into the cells

The loss in volume through emesis triggers RAAS resulting in increased Aldosterone release and further potassium excretion

http://www.labpedia.net/test/116





Subcomments ...

submitted by m-ice(135),

The patient needs medical attention immediately, which eliminates obtaining a court order, or transferring her. A nurse does not have the same training and qualifications as a physician, so it would be inappropriate to ask them to examine the patient. Asking the hospital chaplain again could be inappropriate, and would take more time. Therefore, the best option among those given is to ask the patient if she will allow with her husband present.

sympathetikey  Garbage question. +19  
masonkingcobra  So two men is better than one apparently +5  
zoggybiscuits  GarBAGE! ? +  
bigjimbo  gárbágé +  
fulminant_life  this question is garbage. She doesnt want to be examined by a male how would the presence of her husband make any difference in that respect? +1  
dr.xx  I guess this is a garbage question because what hospital, even small and rural, does not have a female physician on staff. NBME take notice -- this is the 2010s not 1970s. https://images.app.goo.gl/xBL4cK31ta7nG4L39 +1  
medpsychosis  The question here focuses on a specific issue which is the patient's religious conservative beliefs vs. urgency of the situation. A physician is required to respect the patient's autonomy while also balancing between beneficence and non-maleficence. The answer choice where the physician asks the patient if it would be ok to perform the exam with the husband present is an attempt to respect the conservative religious belief of the patient (not being exposed or alone with another man in the absence of her husband) while also allowing the physician to provide necessary medical treatment that could be life saving for her and or the child. Again, this allows for the patient to practice autonomy as she has the right to say no. +5  
sahusema  I showed this question to my parents and they said "this is the kind of stuff you study all day?" smh +6  
sherry  I totally agree this is a garbage question. I personally think there is more garbage question on new NBME forms than the previous ones...they can argue in any way. I feel like they were just trying to make people struggle on bad options when everybody knows what they were trying to ask. +  
niboonsh  This question is a3othobillah +1  
sunshinesweetheart  this question is really not that garbage....actually easy points I was grateful for... yall are just clearly ignorant about Islam. educate yourselves, brethren, just as this exam is trying to get you to do. but yeah I agree there should be an option for female physician lol +  
drmohandes  I think this NBME24 is a waste of $60. On one hand we have these types of questions, that have 0 connection to our week-month-year-long studying. On the other hand we have "Synaptobrevin" instead of SNARE, because f*ck coming up with good questions. +  


Fibronectin is an extracellular matrix glycoprotein, while lamin is an intermediate filament that specifically provides support to the cell nucleus. Don’t confuse lamin with laminin (science hates us clearly); laminin is like fibronectin, an ECM glycoprotein and a major component of the basal lamina of basement membranes.

masonkingcobra  Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this) https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/ +3  
dr.xx  blasphemy @masonkingcobra +  


Why is it not ovarian follicle cells? I thought the female analog of Sertoli and Leydig is theca/granulosa cells.

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +3  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +2  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +2  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +2  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +11  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +6  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +3  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +4  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +1  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +1  
youssefa  Hahahahaha ya'll just bored +2  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +  
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen +  
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots +  
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
noplanb  Wait... I might actually never forget this now lol +  
drmohandes  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +1  
lilmonkey  Don't forget that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! You're welcome! +  


submitted by joker4eva76(11),

The question stem is describing a mitochondrial disease, which commonly present with lactic acidosis. There is an increase in anaerobic forms of energy production (glycolysis). The mitochondria are faulty, so they can’t use the end product of glycolysis (pyruvate) in TCA. Instead pyruvate is shunted over and is used by LDH (lactate dehydrogenase) to generate pyruvate.

Aside: Recall that LDH uses NADH and generates NAD+. Deficiency of LDH can lead to loss of regeneration of NAD+ and inhibits glycolysis.

drdoom  ... pyruvate is shunted over and is used by LDH (lactate dehydrogenase) to generate lactate*. +  
chris07  It's hinted in the answer, but I would like to clarify: max O2 consumption is decreased because O2 is consumed in the Electron Transport Chain, which occurs in the mitochondria. With the mitochondria not working, the ETC cannot work, and thus there is less demand for Oxygen. +6  
masonkingcobra  Mitochondria are the powerhouse of the cell +15  
uslme123  Apparently ragged red fibers are the result of coarse subsarcolemmal or intermyofibrillar mitochondrial accumulations.. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/mitochondrial-myopathy +  


submitted by tinydoc(63),

Type 1 Familial Dyslipidemia (pg. 94 FA 19 )

increased TG ---> pancreatitis Eruptice / pruritis Xanthomas and HSM

Can be caused by Lipoprotien lipase or Apoprotien CII deficiency

they said that LPL is fine so its APO CII

Heparin seperates LPL from Herparin Sulfate Moeity on Vasc Endothelium allowing us to test its function in the lab.

I got it wrong too - Stupid Rote memorization recall Question.

masonkingcobra  I think you need to know that ApoCII activates LPL not necessarily know the disease +2  
yotsubato  Knowing the disease makes it easier to remember the details though +  


submitted by egghead(0),

This is one of those questions I was never going to get. It's not in FA, I don't think I've seen it in class.

hungrybox  same :( +  
masonkingcobra  My issue was the stem said no skin damage (I would think pulling out your hair damages your scalp) [Turns out it does not](http://onlinelibrary.wiley.com/doi/full/10.1111/j.1529-8019.2008.00165.x) +  
gh889  FA 2019, pg 551 +3  
meningitis  Compulsively pulling out one’s own hair. Causes significant distress and persists despite attempts to stop. Presents with areas of thinning hair or baldness on any area of the body, most commonly the scalp. Incidence highest in childhood but spans all ages. Treatment: psychotherapy is first line; medications (eg, clomipramine) may be considered. +2  
step1soon  FA 2019 pg 551 +  


submitted by mcl(230),

This image is very helpful.

seagull  http://www.siumed.edu/~dking2/erg/GI178b.htm Another histology slide with labels +1  
masonkingcobra  I like to think that the parietal cells look like "fried eggs" classically +  


Can somebody please explain why the pKa has to be 6 instead of 10?

masonkingcobra  Since an ionized form is charged (by definition), it will not easily cross a nonpolar lipid membrane. Thus, it is important to recognize the potential of the drug to ionize in order to predict its solubility and the degree to which it can be reabsorbed. The degree of ionization is determined by the drug’s pKa and the pH of its environment. Weak acids and bases are 50% ionized and 50% unionized when the surrounding pH equals the drug’s pKa. At 2 pH units above or below the pKa of the drug, nearly 100% of the drug is ionized or unionized. +3  
masonkingcobra  Basically weak acids are best excreted in alkaline urine, but weak bases are excreted more readily in acid urine. +  
masonkingcobra  In summary, because this is a weak acid at pKa 6, making the urine alkaline will result it its ionization and excretion. Ionized cant move through lipid membranes so can't get reabsorbed and is pissed out. +2  
yex  Following on masonkingcobra explanation: A pKa 4-9 can be either weak acid or base. Weak acid pKa 4-7; strong acid pKa 1-3 Weak base pKa 7-9; strong base pKa above 9 Differents pHs: stomach: 1-2 duodenum: 3-5 early jejunum: 5-7 late jejunum: 7-9 ileum: >9 urine: 4.5-8 Weak acids (pKa) gets absorbed in acidic (pH) environments and cleared in basic. Weak bases gets absorbed in basic environments and cleared in acidic. THIS DOES NOT APPLY TO STRONG BASES OR ACIDS!!!! The best explanation for this is a Biochem lecture from Pass Program and it is available on YouTube, its long but it is for sure worth it!! Look for 19 Biochemistry 1 from Pass Program on YouTube. +1  


Can somebody please explain why the pKa has to be 6 instead of 10?

masonkingcobra  Since an ionized form is charged (by definition), it will not easily cross a nonpolar lipid membrane. Thus, it is important to recognize the potential of the drug to ionize in order to predict its solubility and the degree to which it can be reabsorbed. The degree of ionization is determined by the drug’s pKa and the pH of its environment. Weak acids and bases are 50% ionized and 50% unionized when the surrounding pH equals the drug’s pKa. At 2 pH units above or below the pKa of the drug, nearly 100% of the drug is ionized or unionized. +3  
masonkingcobra  Basically weak acids are best excreted in alkaline urine, but weak bases are excreted more readily in acid urine. +  
masonkingcobra  In summary, because this is a weak acid at pKa 6, making the urine alkaline will result it its ionization and excretion. Ionized cant move through lipid membranes so can't get reabsorbed and is pissed out. +2  
yex  Following on masonkingcobra explanation: A pKa 4-9 can be either weak acid or base. Weak acid pKa 4-7; strong acid pKa 1-3 Weak base pKa 7-9; strong base pKa above 9 Differents pHs: stomach: 1-2 duodenum: 3-5 early jejunum: 5-7 late jejunum: 7-9 ileum: >9 urine: 4.5-8 Weak acids (pKa) gets absorbed in acidic (pH) environments and cleared in basic. Weak bases gets absorbed in basic environments and cleared in acidic. THIS DOES NOT APPLY TO STRONG BASES OR ACIDS!!!! The best explanation for this is a Biochem lecture from Pass Program and it is available on YouTube, its long but it is for sure worth it!! Look for 19 Biochemistry 1 from Pass Program on YouTube. +1  


Can somebody please explain why the pKa has to be 6 instead of 10?

masonkingcobra  Since an ionized form is charged (by definition), it will not easily cross a nonpolar lipid membrane. Thus, it is important to recognize the potential of the drug to ionize in order to predict its solubility and the degree to which it can be reabsorbed. The degree of ionization is determined by the drug’s pKa and the pH of its environment. Weak acids and bases are 50% ionized and 50% unionized when the surrounding pH equals the drug’s pKa. At 2 pH units above or below the pKa of the drug, nearly 100% of the drug is ionized or unionized. +3  
masonkingcobra  Basically weak acids are best excreted in alkaline urine, but weak bases are excreted more readily in acid urine. +  
masonkingcobra  In summary, because this is a weak acid at pKa 6, making the urine alkaline will result it its ionization and excretion. Ionized cant move through lipid membranes so can't get reabsorbed and is pissed out. +2  
yex  Following on masonkingcobra explanation: A pKa 4-9 can be either weak acid or base. Weak acid pKa 4-7; strong acid pKa 1-3 Weak base pKa 7-9; strong base pKa above 9 Differents pHs: stomach: 1-2 duodenum: 3-5 early jejunum: 5-7 late jejunum: 7-9 ileum: >9 urine: 4.5-8 Weak acids (pKa) gets absorbed in acidic (pH) environments and cleared in basic. Weak bases gets absorbed in basic environments and cleared in acidic. THIS DOES NOT APPLY TO STRONG BASES OR ACIDS!!!! The best explanation for this is a Biochem lecture from Pass Program and it is available on YouTube, its long but it is for sure worth it!! Look for 19 Biochemistry 1 from Pass Program on YouTube. +1  


masonkingcobra  The pathogenesis of post-transplant lymphoproliferative disorders (PTLD) in most patients relates to the outgrowth of Epstein-Barr virus (EBV)-positive B cell proliferations in the setting of chronic T cell immunosuppression. +2  


submitted by onyx(16),

A radiographically visible air-fluid level suggests a pretty large lesion (hence, “cavitary”). That's not going to become normal tissue again. Six months following resolution of symptoms you can expect healing in the form of a scar; that is, fibrosis but only in a single spot.

masonkingcobra  Robbin's: The basic mechanisms of fibrosis are the same as those of scar formation during tissue repair. However, tissue repair typically occurs after a short-lived injurious stimulus and follows an orderly sequence of steps, whereas fibrosis is induced by persistent injurious stimuli such as infections, immunologic reactions, and other types of tissue injury. The fibrosis seen in chronic diseases such as pulmonary fibrosis is often responsible for organ dysfunction and even organ failure. +1  
stevenorange  What Differentiates Normal Lung Repair and Fibrosis? Basement membrane ! https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/ +  


submitted by hayayah(447),

Pelvic splanchnic nerves are part of the parasympathetic system.

masonkingcobra  The inferior hypogastric plexus innervates internal pelvic viscera; has both sympathetic and parasympathetic components; parasympathetic contribution helps stimulate detrusor of bladder (along with pelvic splanchnic nerves), sympathetic contribution helps stimulate internal urethral sphincter +  


submitted by hayayah(447),

You have a 25% chance of inheriting the same HLA markers as your siblings.

masonkingcobra  Two siblings have a 25% chance of being genotypically HLA identical, a 50% chance of being HLA haploidentical (sharing one haplotype), and a 25% chance that they share no HLA haplotypes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628004/ +9  


submitted by hayayah(447),

The damage is in the L midbrain in the area affecting the corticospinal tract. Because it is in the midbrain, decussation in the pyramids (medulla) so it will show ipsilateral dysfunctional motor signs.

Photo of midbrain and important areas: shorturl.at/myHLR

masonkingcobra  Just for clarification, on the left side, you see where he had the infarction 7 years ago and the tissue is gone. +1  
chefcurry  so is the dysfunction on the contralateral side? +  
praderwilli  If the decussation is in the pyramids of the medulla, shouldn't it be contralateral hemiparesis if the damage is on the right? It confuses me because of the labeling right and left at the top of the pictures. +  
endochondral1  that link isnt working @ hayayah....is there any good picture to look at to know where the tracts are on this section? +  


submitted by strugglebus(75),

The pons has nerves 5-8, so the trigeminal would be affected here

masonkingcobra  Thalamic pain syndrome would involve dysesthesias on the entire contralateral body so more than just the face. Also it occurs often after post-stroke. Additoinally, these dysesthesias appear weeks/months later +2  


submitted by thomas(5),

Answer is Astrocyte. Patient has glioblastoma multiforme. Although meningiomas may occur at convexities, meningiomas are benign and often asymptomatic. They may cause h/a seizures, but would be unlikely to cause death w/in 6m of onset of h/a. The size of tumor and course of illness is consistent with the course of GBM

masonkingcobra  Above is obviously incorrect because the answer is Meningeal lol. Here is a link to a good picture: http://neuropathology-web.org/chapter7/chapter7fMiscellaneous.html +4  
kernicterusthefrog  Obviously thomas is disagreeing with the presentation of the question, and I agreed with him! This absolutely sounds like GBM, with rapid onset leading to death, and the symptoms. The question stem leads you to GBM, and the gross image to meningioma (I guess). +1  
kernicterusthefrog  Furthermore, where are the meninges on the gross image form which this (meningioma) grew?! It should at least show the tissue from whence it came! +1  
nala_ula  Had the same problem, got confused since it appeared that the growth was malignant :( +  
sugaplum  FA 2019 pg 514, also agree with everyone. weird presentation. Glios are malignant death within 1 year, meningioma are often asymptomatic or have focal signs. just a gross pathology question at this point +  


submitted by hayayah(447),

LV stopped working, pressure backed up into pulm circuit. Pulm circuit roughly is made of 3 "parts" - the capillaries, interstitial space, and the alveoli.

In cardiogenic shock, the extra blood increases capillary hydrostatic pressure, driving fluid into the interstitial space. Compared to the alveoli, the interstitial space now has more fluid (thus more interstitial hydrostatic pressure and less oncotic pressure due to ratio of fluid to protein), and as a result of this unbalancing of forces, fluid moves into the alveoli --> pulmonary edema.

masonkingcobra  https://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Figure%204.1.%20Mechanisms%20of%20enhanced%20transcapillary%20filtration%20in%20response%20to%20elevations%20in%20arterial%20or%20venous%20pressure.&p=BOOKS&id=53445_fig4.1.jpg +  


submitted by step420(19),

Other kidney Hypertrophies due to increased stress --> not hyperplasia bc not cancerous

masonkingcobra  Above answer is incorrect because hyperplasia can be either physiological or pathological. Prolonged hyperplasia can set the seed for cancerous growth however. Robbins: Stated another way, in pure hypertrophy there are no new cells, just bigger cells containing increased amounts of structural proteins and organelles. Hyperplasia is an adaptive response in cells capable of replication, whereas hypertrophy occurs when cells have a limited capacity to divide. Hypertrophy and hyperplasia also can occur together, and obviously both result in an enlarged (hypertrophic) organ. +8  
johnthurtjr  FTR Pathoma Ch 1 Dr. Sattar mentions hyperplasia is generally the pathway to cancer, with some exceptions like the prostate and BPH. +2  
sympathetikey  Tubular hypertrophy is the natural compensation post renal transplant. Just one of those things you have to know, unfortunately. +1  
charcot_bouchard  Isnt Kidney a labile a tissue & thus should undergo both. This ques is dipshit +  


submitted by hayayah(447),

Case of arteriolosclerosis.

Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin appearance')

  • Consequence of malignant hypertension (>180/120 w/ acute end-organ damage)
  • Results in reduced vessel caliber with end-organ ischemia
  • May lead to fibrinoid necrosis of the vessel wall with hemorrhage; classically causes acute renal failure (ARF) with a characteristic 'flea-bitten' appearance
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +5  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +7  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +4  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


submitted by hayayah(447),

No abnormalities, only some vomiting, looks well w/ no failure to thrive. Most likely immature LES.

masonkingcobra  http://www.sedico.net/English/SedicoInformationCenter/Physicians/gerd_e.htm +1