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Comments ...

 +4  (nbme24#32)

Histamine increases microvascular permeability, i.e. Fluid + Proteins, this increases pressure in the interstitium > lymph flow increases

 +4  (nbme24#31)

POMC is a prohormone peptide chain.

It is translated and later enzymes cut this peptide in the subpeptides.

Transcription is wrong (i had this too...) b/c its not the mRNA that makes different peptide hormones. Moreover, what I see now is, that posttranscriptional modification is more or less splicing... so post-translat. modification. next time we make it correct ;-)

medguru2295  This is a perfect explanation. I never knew it was the protein modified (I initially though alternate splicing too)
nerdstewiegriffin  Is this an example of polycistronic mRNA?

 +1  (nbme23#33)

in ß Thalassemia there is HbA2 increase and HbA decreases, even in ß+ , normal electrophoresis rules this out. same for A)-C)

 +3  (nbme23#50)

all those non maths guys here, dont skip these questions, try to arrange the units, here you´d easily find out that you just have to multiply! Give it a try :-)

charcot_bouchard  This was like Filtered Load ques of Renal. Where u multiply icoming fluid (GFR) with the desired substances conc (Px) so FIltered load of A is GFR x Pa Same here. Myocardial O2 supply is Blood flow x Conc of O2 in that blood flow
powerhouseofthecell  For us non math folk, how do you compare the mL/min to mLO2/mL to get mLO2/min? Sorry. Do you just find out that when you have the units beside each other, cross multiplying them gives you the correct one? I need to know this trick. I can't find this on google.

 +2  (nbme23#28)

just know where the big stuff / important stuff is resorbed, it is the PCT. No need to know RTAs here...

 +1  (nbme22#26)

one important aspect not mentioned: the " long " 1 year "benign" history of the symptoms... not likely for malginant lymphomas, astros or metastasis to stay that calm

of course in addition to all other mentioned here "not brain infiltrating etc."

 +0  (nbme21#35)

cns problem, anemia (hypo) and kidney problem.

Finally only lead can cause all of it

 +4  (nbme21#42)

Gonadotrophs are the FSH/LH producing pituitary cells. No ovaries, no hormones, no feedback inhibition.

Subcomments ...

submitted by lsmarshall(267),

"Parasternal heave (lift) occurs during right ventricular hypertrophy (i.e. enlargement) or very rarely severe left atrial enlargement." RV hypertrophy can be seen so easily because the RV is at the anterior surface of the chest.

In this patient blood from LA to LV decreases in saturation, so it is going somehwere. From the O2 sat. we can deduce there is probably a VSD (increased RV pressure would cause RVH and parasternal heave). Furthermor, the vignette is likely describing tetralogy of fallot (caused by anterosuperior displacement of the infundibular septum). In Tet spells, RV outflow is too obstructed and patient gets cyanosis and R>L shunting Squats increase SVR, decreasing R>L shunting, putting more blood through pulmonary circuit and relieving cyanosis.

seagull  i'm pretty sure your a prof and not a student. +7  
nor16  nevertheless, we are greatful for explanation! +  
niboonsh  I remember seeing a question describe parasternal lift in the context of pulm htn. still got this wrong tho fml +  

submitted by jus2234(12),

The graph shows a decrease in compliance of the lungs. Of the options, diffuse pulmonary fibrosis is the only choice that is an example of a restrictive lung disease which would decrease compliance

nor16  asthma = emphysema = chronic bronchitits, obstructive. leaves 2 out of 5... +1  
usmile1  Common causes of decreased lung compliance are pulmonary fibrosis, pneumonia and pulmonary edema. So yes pneumonia could possibly cause the decreased compliance shown, but the vignette says the patient has "9 month history of progressive SOB." That couldn't reasonably be pneumonia, leaving diffuse pulmonary fibrosis as the best answer. +1  

Pathoma says there are 3 things that differentiate leukemoid from CML: + Leukocyte alkaline phosphatase (only in leukemoid) + Basophils (only in CML) + t(9;22) translocation (only in CML)

nor16  yeah but pathoma doesnt help here... +1  
thotcandy  Yeah but LAP is normally 20-100 so a 100-250 U/L is still + which would indicate Leukemoid reaction, no? That's why I didn't pick it, Because I figured 250 u/l was just some random number and it didn't make sense. a -LAP would be in the normal range, 20-100 which would THEN indicate CML. +  

submitted by sajaqua1(347),

A and J represent the gracile fasciculus, while B and I represent the cuneate fasciculus. Together they make up the dorsal column-medial lemniscal tract, responsible for pinpoint perception, proprioception, vibration, and pressure. Input is ipsilateral.

C and H make up the lateral corticospinal tract (also called the lateral cerebrospinal fasciculus), responsible for motor command of ipsilateral limbs.

D and G represent the lateral spinothalamic tract. It is responsible for pain and temperature conduction. The input arises in a limb (left lower extremity in this case), enters through the dorsal root (pictured between J and H), decussates and ascends at the anterior commissure (just behind E and F), and finally synapses on the second order neuron in the lateral spinothalamic tract. So the spinothalamic tract is responsible for contralateral pain and temperature sensation. Because our patient has lost sensation on the left, the lesion is in the right.

E and F are the anterior corticospinal tract. It is involved in motor control of proximal muscles, typically of the trunk.

nor16  good job +4  

submitted by sbryant6(68),

Pontine arteries are small branches of the basilar artery that can rupture in the setting of poorly controlled hypertension.

nor16  vertical gaze intact = mesencephalon intact horizontal gaze damaged = pons damaged (RPRF) Pons damaged = no access of corticobulbar tracts to motor nuclei in brain stem -> speech impaired +1  

submitted by notadoctor(106),

Celiac sprue is a malabsorption syndrome that results in steatorrhea and results in iron deficiency anemia. As far as I'm aware, none of the others result in iron deficiency anemia. (I had Bacterial overgrowth as a close second but I don't believe that's associated with iron deficiency).

yb_26  bacterial overgrowth is associated with iron deficiency, but also with Vit B12-deficiency, so I guess pts will have macrocytic anemia +1  
nor16  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/. Vit B12 is key here, moreover, no bloating (IBS and bacterial overgrowth with bloating). bacterial overgrowth is a close one! +  

Acknowledge the patient's difficulty. I hate these questions

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

submitted by meningitis(269),

Process of elimination on this one.

  • I eliminated Carbomyl phosphate, Arginine due to urea cycle.
  • I eliminated ATP because ATP alone wouldn't change F6P into glucosamine
  • NAG I got lucky and I eliminated it due to its use in ECM and collagen so I didn't think it was relevant and I kind of remembered it being in urea cycle.
dr.xx  you mean, pure luck? :) +12  
impostersyndromel1000  lol pretty sound logic here mate +1  
nor16  same here, Glutamine is a NH3 (-amin) donor, so guessing made sense +  

submitted by nwinkelmann(187),

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

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

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

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

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

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

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

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

nor16  nice job, but i dont think you need all this for these questions +2  

submitted by luckeroo(3),

why was this gemfibrozil and not niacin? I was lucky and guessed, but I thought niacin combined could also trigger myopathy?

.ooo.   Gemfibrozil is a CYP450 inhibitor causing an increase drug concentration of statin which would lead to the adverse side effect of myopathy. Not sure about niacin in combination with statin but believe this would be more likely to occur. Hope this helps! +1  
yb_26  yes, it can be seen with niacin and esetemibe as well, according to UWorld. But first choice in such questions is always fibrates. +  
nor16  number one no-go combi is statin+fibrate here +2  

submitted by mguan1993(3),

can someone explain why the answer is not adrenal gland? I feel ike if adrenal gland was the issue there would also be decreased concentrations of FSH, LH, and estrogen right?

mguan1993  ^nvm had a brain fart and go adrenal gland mixed up with anterior pituitary lmao +1  
nor16  ovaries are #1 estrogen producer no estrogen no lubricant = dyspareunia no estrogen and no fsh/lh --> there must be a "higher" problem, up there in the brain +3  
pg32  I agree that hypothalamus is the most logical answer, but if she had overactivation of the adrenal gland (cortisol secreting tumor), that could also inhibit GnRH and cause these same symptoms. +  
drzed  @pg32 the physical examination would not be normal with either a ACTH or cortisol secreting tumor. +  

submitted by niboonsh(173),

i got this question right but why couldnt it be ginko biloba?

nor16  and why no therapy, i.e. cognitive training` +  
jessica_kaushal  first step is to make the patient's environment accomodating for the patient. +1  
jessica_kaushal  first step is to make the patient's environment accomodating for the patient. +  
tryntofigritout  Because this is a western medicine test. Even though it has shown great protection against AD and memory protection, this test won't allow that. I initially clicked on ginko but thought to myself... na this test doesn't accept an eastern idea. so clicked on the one I know they wanted me to say, and I got it right. ha +3  

submitted by enbeemee(9),

i get why it's flagellin, but is the specific reason that LPS is wrong is because it's just not how the vaccine is made? LPS would also elicit an immune reaction, right?

nor16  Lipid A of LPS can be sensed by CD14 of macrophages causing shock, its not a protein, so no immune reaction as in vaccination (humoral, IgG class switch via Th2 and B Cells). +2  
eclipse  actually they do use LPS as adjuvant in vaccines +1  
eclipse  actually they do use LPS as adjuvant in vaccines +1  
hyperfukus  TLRs recognize common motifs called pathogen-associated molecular pattern (PAMP) in bacteria, fungi, viruses, and other pathogens. TLR signaling in the modulation of innate immunity + adaptive immunity against pathogens, TLR agonists: CpG-DNA, flagellin, and lipid became essential candidates of effective+safe vaccine adjuvants. TLR agonists improve the efficacy of vaccine, reducing TCR-based selection thresholds and enhancing the magnitude and quality of memory T-cell response. +2  
hyperfukus  some extra info in case they ask another annoying q +3  
usmlecharserssssss  and how many of yours answered LPS ? +3  

submitted by ragacha(10),

PAGE 492 FA 2018 DAMAGE IN DORSAL COLUMN (funtion are: pressure, vibration, fine touch, proprioception) SYNAPSE 1 : N. graciLe ( Lower body, Legs) AND N. cUneatus (Upper body, arms)

nor16  Cuneatus = Cervical, write into columns CG ( fron left to right) Cuneatus, Gracilis (CG) +1  

submitted by neonem(372),

This is a case of acute gout. Monosodium urate crystals are taken up by neutrophils, leading to an acute inflammatory reaction. T-cells aren't really involved in gout (more rheumatoid arthritis).

hungrybox  Great explanation! So frustrating that I got this wrong, should have been easy. +2  
temmy  the way i thought about it was how did the neutrophils get there? the answer is via increased vascular permeability +9  
nor16  they, unfortunately, did not ask " how did neutrophils get there" but " whats the cause of the swelling " not to confuse with " what causes the swelling " +1  
divya  absolutely right temmy. that's how i thought about it too. +  

submitted by usmleuser007(220),

For RCC: (As per UWORLD)

Symmetric bilateral lower extremity pitting edema and tortuous abdominal veins are concerning for an inferior vena cava (IVC) obstruction, which, in the setting of a left-sided flank mass, suggests renal cell carcinoma (RCC) with extension into the IVC.  RCC accounts for >90% of all malignancies arising in the kidney and is highly associated with smoking.  Patients with RCC classically have a triad of flank pain, palpable mass, and hematuria, although many remain asymptomatic until the disease is advanced. RCC is a highly vascular tumor that invades the renal vein in up to 25% of cases.  IVC obstruction can occur due to intraluminal extension and thrombus formation, rather than mass effect from the tumor itself. 

The obstruction can occur acutely or gradually over time.  In chronic cases, collateral venous circulation may develop based on the site of the obstruction.  Prominent abdominal wall collateral veins, as in this patient, suggest obstruction of the upper segment of the IVC.

nor16  high blood pressure, i.e. Hypertension, risk factors for atheroscl., bruit !!! over left abdomen, secondary art. Hypertension. they always want the renal artery stenosis (like vWF in coag. disorders...) +