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TB can spread to psoas L1-2 often, which then goes to the actual L1-L2 vertebrae itself (Potts or osteomyelitis)
I get why the TNF inhibitor would cause Tb and it literally said osteomyelitis, but the question says "gram stain is negative". Does that mean it doesn't gram stain?? I read it as it having a negative gram stain and crossed out Tb osteomyelitis as a result
Mycobacterium doesn't gram stain due to mycolic acid in it's membrane. It'll take the carbol-fuschin stain (acid fast) or grow on a lowenstein-jensen culture but not gram
Also, the nice little puppet show from sketchy for those visual learners like me.
how could i forget that puppet show?!
Physeo video explain this very clearly,
negative stranded can't be read by a translator so it needs to be transcribed into + first. Only then can it be used for protein. + is basically mRNA already.
There's only one double stranded RNA family as far as I know- Reovirus so no encephalitis
How did you know it was cryptoccocus and not something else like candidiasis?
Was stuck between cryptococcus and candida as well. I think the tip might be that Candida is in mold form at higher (body) temp.
But amphotericin b can be used for both and given that it's a serious infection you would probably just go straight for that instead of fluconazole.
Patients with T cell dysfunction (HIV) are more susceptible to cutaneous candida infections (esophagitis, etc). Patients with neutropenia (chemotherapy, post-transplant) are more susceptible to invasive candida infections (bloodstream infection, meningitis)
I totally hated this Q! I almost completely overlooked the "no tonsillar tissue", and thank God I didn't because that's the clue that made me change my answer. I had CGD (yeah, I know, S. pneumoniae not catalase +), but it said that he had muuultiple infections since birth. And I took to heart that "since birth" thing, because, isn't Bruton supposed to present with infections from around 6moa? I hope I don't screw this up next week
@angelaq11 I thought the same thing!! because it said "since birth" I thought Ok this is not Bruton :(
So factors II, VII, IX, and X are precursor proteins? GTFO
Yeah thats the easy part. But the histology is whats hard
I might be mistaken but I also thought Epstein Bar Virus was also implicated in gastric lymphomas?
Found in fish oils and are shown to lower triglyceride levels.
alpha-Linolenic ==> omaga 3
Yeah but in a chronic case this guy would produce more RBC and not be hypoxic anymore.
How do you know the gracile fasciculus is damage?!?!
which parte of the image its damage?, the pink? or black?
i still don't see where the damage is lol! FML
i finally figured it out lol that was a slow moment i hope im not this slow on step yikes!
@hyperfukus I had the same problem at first, marked it and then came back. If you remember, in the spinal cord the white matter and gray matter are "reversed" compared to the brain. That said, if the butterfly shaped region (ie, the gray matter) is colored (in this case) lilac and the rest (ie, white matter) is blackish, the only thing that is actually abnormal, is the region where the dorsal columns are, because it stains just like the normal gray matter. After that, you have to think about which fasciculus is damaged, the gracilis or the cuneatus. The gracilis is medial while the cuneatus is lateral (picture someone with glued legs and open arms). Hope this helped
Check out FA2020 pg 508
myelin= black --> color of the normal white matter
no myelin= pink --> color of the normal gray matter and the damaged area
Dorsal columns= vibration, proprioception, pressure fine touch
F. graciLis= Lower body
F. cUtaneous= Upper body
doesn't there have to be an airway obstruction (mucus, foreign object etc.) in order for this to happen? 100% O2 without any airway obstruction should not cause absorption atelectasis, right?
And Tension Pneumothorax is wrong bc PEEP would furthur exacerbate that.
@iloveallpotatoes yea i realized that now after getting it wrong :(
@bighead478, they are using a cuffed endotracheal tube and mechanically ventilating this patient which is creating an iatrogenic "obstruction" and as @haliburton mentioned, having a high FiO2 leads to over-absorption by the blood which leads to absorption atelectasis if no other gas is allowed to enter/there is no communication with atmospheric pressure during expiration. Thus, we add positive end-expiratory pressure which keeps alveoli open at the end of expiration to prevent collapse
At first, E2F flashed through my mind.
then I thought maybe EF2 is elongation factor for transcription. DUMB. :(
How is that NOT posterior to middle concha? bad question
@yotsubato - That would have been if it was the spehnoid sinus (I got it wrong too btw)
Sphenoethmoidal RECESS not sphenoethmoidal SINUS
Agreed! It's along the lines of those marathon runners who collapse questions. Nothing but water for 24 hours = getting rid of too much sodium.
are we just going to ignore the diarrhea for 3 days? what is its significance
Temmy, We aint Ignoring the Diarrhea, Actually the most likely electrolytes to get lost with it is sodium> chloride> potassium> bicarbonate... Plus the Water intoxication -> HYPONATREMIA
Because glucose is not an electrolyte, it does not conduct electricity in solution. The question is asking "Which of the following electrolyte abnormalities".
Couldnt a psychogenic cause reduce libido?
"Testosterone concentration is within the reference range" and the fact that he has no difficulty masturbating = normal libido.
Low testosterone would contribute to low libido
And if he had low libido he would have difficulty masturbating
"Detection of cystine in urine: cyanide reduces cystine to cysteine → Cystine turns red and becomes detectable when it comes into contact with nitroprusside. If the test is negative, the presence of cystinuria is unlikely." - AMBOSS
I love how this cant be straight forward. All the other proteins are either subunits of desmosomes or cytoskeletal components. Because I know molecular biology that well on top of the majority of medicine....FML
@seagull: excellent comment, literally loling right now
or sobbing and threatening to hold my breath if they don't make it stop
WHY DIDN'T THEY JUST PUT HEMIDESMOSOMES THE FUCK
I think it's also because he has an infection (since he was prescribed antibiotics) boosting the immune system is more important than increasing platelet count E) or RBC count A)
Dengue is an arbovirus. The important hints are that she was traveling in endemic (tropical) and that she has **excruciating pain in the joints and muscles**. This is why dengue is aka "break-bone fever"
For anyone wanting to understand why^ the tl;dr is that prolactin gets cleaved into two toxic metabolites. Treatment is something like bromocriptine (and therefore no more breast feeding) to stop prolactin release. Lastly, you can treat with regular HF meds.
To expand, SIADH may also result in euvolemic hyponatremia. This is because, as we know, ADH increases absorption of water and therefore initially results in an increased circulating volume. However, this results in increased stretch of the atria and subsequent secretion of ANP. ANP (atrial natriuretic peptide) then results in loss of sodium and water.
Have you mixed Chlamydia in with Mycoplasma?
I mean the Q stem is not about Chlamydiae, but Chlamydiae does lack the classic PTG cell wall d/t decreased muramic acid = beta-lactam abx ineffective. FA 2018 p.148
misread the "accounts for" question as what's the reason for the atypical lymphocytes. So I answered "virus infected B lymphocytes." Anyone else misread it like that?
Shit, I misread that too and I noticed it now. Nerves get the best of us!
If the question is ask what is the atypical lymphocyte in the brain , than it should be the infected B cell, RIGHT?
why not hep B? i guess another whats the better answer ones... Just rem reading that it was more common with aids pts.. anyone have an idea about this?
Yes, I think CNS lymphoma as an AIDS defining illness wins the day.
My thought was since SHE has AIDS it is most likely from IVDA, which has a high risk of HBV that could go undiagnosed for a long time. at 32, that might not be long enough to have HBV and get HCC (but with no immune system...?)
God damn this is such BULLSHIT...
My thought process, usually wrong all the time, was that HBV (IVDU) can occur to anyone. Acute hepatitis to Chronic occurs when HBV incorporates its DNA into host and releases mutagenic proteins. This is regardless of immunosuppresion. Primary CNS Lymphoma reappears primarily when you are immunosuppressed (organ transplant, immunodeficiency, HIV/AIDS).
Hep C is far more likely to become HCC than hep B
NBME does trick now and then.. when they zig you zag. then when you think they are going to zag, they zig just to destroy yourself confidence.
The abnormal T-cells are known as Downey type II cells (Sketchy)
I was recognized EBV, then knew EBV infects Bc, and the atypical lymphocytes are Tc. Then I said CD8 are MHC1 for virii, and bingo bango, boom.
Soooooooo EBV infested B- cells is not considered atypical WTFF??
They are atypical b/c usually you do not see a super high amount of CD8+ in peripheral blood. Now there are a ton to try to stop the infected cells.
oh and primary CNS lymphoma caused by EBV has T cells NOT B cells. I just try to remember the peripheral blood has atypical lymphocytes which are CD8+ T cells, and the CNS lymphoma is the opposite, ie; B cells
^^^ THIS ONE SHOWS DUCT ^^^
If you go back and look at the image you can see that it was highly vascular which is characteristic of granulation tissue. Scar tissue formation will be closer to 1 month, plus you will see lots of fibrosis on histology.
It's a bit misleading, for me, since you do see fibrosis intermixed with the granulation tissue, but granulation tissue was a better answer.
According to FA 2017: 3-14d: Macrophages, then granulation tissue at margins.
2wk to several months: Contracted scar complete. Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus).
i'm getting pretty frustrated with NBME contradictions to FA, and FA omissions of content. this stuff is hard enough to get straight as it is.
Thats cause the NBME exam writers read FA, then make questions not fit in with FA
This fits the timeline laid out in Pathoma!
1-3 wks = granulation tissue with plump fibroblasts, collagen, and blood vessels
never look at the image in the beginning. They dont want you to success. Most of the time images are made to ditract
I'm confused about the phosphate level in questions like these. Decreased calcitriol would decrease phosphate absorption while PTH decrease lowers phosphate excretion. I'm assuming that the PTH decrease has the greater effect with serum phosphate levels?
PTH = "Phosphate trashing hormone" if PTH is high Phosphate must be low - they are always opposite (unless d/t renal failure then Phosphate will be high - kidneys will be unable to get rid of phosphate)
So low Ca d/t low PTH does not effect 25 H. Vit D ... only 1,25 H Vit D (active Calcitriol)?
Clarification because I was confused: PTH stimulates kidney to produce 1,25-(OH)2 D3 (calcitriol) via 1α-hydroxylase in proximal convoluted tubule. Therefore, without parathyroid glands, low PTH, 25,D is not converted and therefore not down (normal or up). phosphate "trashed" by PTH as eloquently stated above.
Here the primary defect is high up from the parathyroid gland, there is decresed or no PTH which normally trashes phosphate but not in this case so serum PHOSPHATE INCREASES and the serum calcium is low because PTH should have prevented the urine calcium so there is calciuria and no resorption from bone-LOW CALCIUM, Vitamin-D is independent of PTH so stays NORMAL
that was my reasoning as well. guess not.
Shitty NBME grammar strikes again.
No. No guys. Bundle of his located below AV node and it can generate impulse. it calls junction escape rhythm and narrow complex. Below this is purkinje, bundle branch & ventricular muscle. those are wide complex
The atria and ventricles beat independently of each other. P waves
and QRS complexes not rhythmically associated. Atrial rate >
ventricular rate. Usually treated with pacemaker. Can be caused
by Lym3 disease
The only thing I can think of is that HIV is a (+)-sense single-stranded RNA virus that relies on an RNA dependent DNA polymerase (reverse transcriptase) to synthesize DNA.
according to [medbullets link](https://step1.medbullets.com/step1-microbiology/104196/rna-viruses_) ns ss RNA must carry RNA dependent RNA polymerase (so that is out).
also, according to medbullets there are very few ds RNA viruses, so "most likely" will be ss. Also, RNA-dependent DNA polymerase = Reverse Transcriptase. Since HIV is a ss ps RNA virus with RT, they've described an HIV cousin. not sure beyond this.
Can’t think of any retroviruses outside of HIV and HTLV and they’re both +ssRNA
If I'm reading this right, this is just a tricky dicky question. I think CO binds 200x stronger than O2. But if an O2 cycles through binding / unbinding 200 times before a CO gets kicked off, this should still clear the CO from that cell sooner or later. strange to think it is 1. essentially permanently trapped in a cell, and 2. doesn't kill you and can be treated with O2 to resolution within a few hours or a day. They must just be thinking, until that last RBC dies, you've got original CO in a circulating cell. but just a fraction (because you didn't die). not sure how that CO isn't just passed on during recycling, based on this line of thinking.
The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask weeks or in hours, who knows? smh
If that's what they're looking for why cant the NBME people just ask "How long does it take for RBCs to turn over?" Ridiculous.
also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia.
why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain
Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism.
Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious.
@cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption
@privatejoker ALP is included in the standard lab values
@privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values
Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity).
@pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases.
i think it is critical to remember that constipation is what caused the diverticulosis.
Crohn's presents with +/- bloody diarrhea, not constipation
I believe there would be no decrease in O2 saturation because oxygenated blood (high pressure) is shunted into deoxygenated circuit. As long as the lungs can keep up, this should increase venous oxygenation on average.
ty both of you for this, was wondering the same thing
O2 sat won’t change b/c you’re not adding deoxygenated blood to the arterial side. You’re just taking arterial blood and putting it into venous blood. Same reason why L->R cardiac shunts don’t decrease O2 sat (while in contrast, a R->L shunt would).
just realized: the high pressure of the arterial system keeps out low-pressure venous blood in an AV fistula (probably obvious to most ppl but it was a eureka moment for me lol)
ya you wont have decreased arterial O2 sat because oxygenation of blood is perfusion limited (FA19 --654) therefore oxygenation of the blood happens within the first .3seconds of entering the pulmonary capillary that you could even handle having more deoxygenated blood enter
But that doesn't make sense. Page 233 of First Aid 2019 edition clearly states that being plasma protein bound creates the lowest volume of distribution, because not being bound to proteins increases the chance it will reach deep into the tissues before it reaches the kidneys. Discrepancy with First Aid?
my reasoning was comparing two drugs, both with Vd of 1, the drug with the lower albumin binding would be cleared faster @kingtime. I don't think you're considering that A and B have equal Vd.