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 +4  visit this page (nbme16#41)
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The solid red bits are of interest here: We're looking at blasto yeast buds (yeast at 37C). Always compare to RBC:

Blasto = RBC size

Coccidio > RBC

Histo < RBC

"history < of blasting (rbc) < coc(c)k" dont @ me

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 +0  visit this page (nbme16#26)
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Heres how to think this question through:

The key word here is "supplement." Of the 7 lipid-lowering agents (FA2020, p.320), 2 of those are non-pharmacologic agents: Niacin and Fish oil. By process of elimination, we were to arrive at the mechanism for VitaminB3, a "supplement"

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chaosawaits  The key word is "most appropriate vitamin" leaving you with only niacin +

 +1  visit this page (nbme16#6)
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L strain was the only strain where A correlated with - viral growth and B correlated with + viral growth.

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l0ud_minority  I hate these questions +

 +0  visit this page (nbme16#21)
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this question is a fancy way of asking about wound healing. phase 1) cleaning, 2) organize, 3) strengthen. FA2020 p.216

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 +1  visit this page (nbme15#43)
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abd mass + hypervascular + young pt = Wilms Tumor

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lovebug  FA2019 P588 +
aashkad  FA2020 p606 +

 +0  visit this page (nbme15#16)
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"best heard in interscapular region" boom. coarc

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 +0  visit this page (nbme15#26)
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proteolytic enzymes from microglial cells liquefy the brain. coagulative necrosis: infarction in every other organ except brain

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 +2  visit this page (nbme22#6)
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So do you ignore the distraction about his mother and consider which of the organisms can lead to nodule formation on the vocal cord?

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neovanilla  yep _(ใƒ„)_/ยฏ +2
agraham416  this might be a stretch, but considering that the mom was using cocaine during pregnancy may mean she's kind of wild, so I wouldn't be surprised if HPV was involved. that was my reasoning. +

 +0  visit this page (nbme22#8)
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Ataxia due to vitamin deficiency can only be caused by Thiamine or Vitamin E deficiency.

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 +5  visit this page (nbme22#17)
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Pott's Fracture: forced eversion of the footโž deltoid ligt avulses medial malleolus โž fibular fracture higher than tib fx

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impostersyndromel1000  as an aspiring MSK radiologist im really upset I missed this. Thanks for explanation. +

 +3  visit this page (nbme22#20)
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the Fibularis Brevis is the only pure foot eversion muscle listed here. Everting his foot would exacerbate his injury and cause him more pain at the fracture

imo contraction of any of these muscles would be painful in this scenario

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weirdmed51  Due to its poor mechanical leverage, fibularis tertius can produce only two weak movements: Foot dorsiflexion around the talocrural (ankle) joint, with the help of extensor digitorum longus and tibialis anterior muscles. Foot eversion at the subtalar joint with the aid of fibularis longus and fibularis brevis muscles. +2

 +3  visit this page (nbme22#23)
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  • enzyme deficiencys = AR

  • homozygous presence of CYP..."

QED: homozygous + AR = 25%

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 +1  visit this page (nbme23#32)
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I took the simplistic approach: I chose the opposite of whatever the kidney usually does and then lack of neg PTH feedback

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 +3  visit this page (nbme23#22)
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rheumatic hrt dz = mitral stenosis = pulmonary edema (bilateral crackles) = dyspnea

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 +12  visit this page (nbme23#47)
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found this super useful book on amazon about Budd-Chiari (check out the sick cover)

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llamastep1  Thank you for that +
focus  hahahahaha. DEAD. +
anjum  I endorse clicking that link +2
azibird  Hahahahahahaha, that's a must click. Someone please buy it and let me know. +
chediakhigashi  hahahaha +
aakb  I don't know what I was expecting... +
jaramaiha  The hussle is real :D +

 +0  visit this page (nbme24#1)
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pretty good summary

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drdoom  welcome, O great physician of the skull and oral cavity. we revere your intricate understandings of the face, jaw, maxilla and all their tiny and hidden foramina. teach us your ways. +8

 +0  visit this page (nbme24#16)
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Follow the Calcium and work backwards. โ†“Ca means โ†“ Phosphate resorption in the PCT (which pulls Ca with it)

25-hydrovitD normal b/c its unrelated to PTH.

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 +6  visit this page (nbme24#23)
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duct through the bucc. (you can feel it with your tongue)

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 +1  visit this page (nbme24#44)
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To me: this seemed more straightforward. You'd want to follow up and check Gastrin levels on a patient who previously had 4x normal.

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thotcandy  He could have 4x the normal because of current PPI use. the point was that you'd get him off, wait for it to normalize, then check again to see if it's due to neoplasm or PPIs +1




Subcomments ...

submitted by specialist_jello(31), visit this page
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I get HOT T Bone STEAK IL 1 for fever

but 90% neutrophils, why cant it be LTB4 neutrophil chemotaxis?

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dentist  i picked LTB4 i guess the question itself is "which causes the patient's fever and leukocytosis" LTB4 wouldn't be a direct cause of fever. dumb question +1


submitted by cassdawg(1781), visit this page
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Orchiectomy will remove the testosterone stimulus prostatic cancer cells are dependent upon for growth and division. With removal of this stimulus, the cells will undergo apoptosis (scattered shrunken cells are apoptotic bodies).

The other answers are unlikely:

  • Corpora amylacea are small hyaline masses in the prostate gland of unknown significance. It would not be a change from normal to find these.
  • Edema is unlikely as this is more characteristic of diseases like prostatitis where inflammatory cytokines cause leaky blood vessels. Orchiectomy would not cause prostatic inflammation.
  • There is no stimulus for hypertrophy and rather with orchiectomy you are removing a growth stimulus.
  • Necrosis of the blood vessel walls is not likely because the blood vessels are not affected by the loss of the androgens, rather the actual prostatic cells are.
  • Widespread necrosis is also not likely as this is not the mechanism of death after testosterone removal (death will occur by apoptosis rather than necrosis) and widespread necrosis is more characteristic of infarct or something that causes massive sudden tissue death.
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dentist  so the MI detail is extraneous +1
fanderina  yeah i thought the answer was necrosis because of the MI +
chaosawaits  I also only chose necrosis because of the MI +
coco  this question ask which of the following microscopic changes in the prostate resulting from the ORCHIECTOMY is most likely present? +1


submitted by cassdawg(1781), visit this page
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Cimetidine is one of the cytochrome p450 inhibitors which would allow increase of the concentration of diazepam to toxic levels by inhibiting its elimination. (https://en.wikipedia.org/wiki/Diazepam)

SICKFACES.COM when I Am Really drinking Grapefruit Juice (FA2020 p252)

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drdoom  sickfaces.com is down again .. +4
zalzale96  I low key expected a porn site to open when I click that link :p +13
feochromocytoma  Also a reminder that alcohol can be both an inducer AND inhibitor of the P450 - - - Chronic alcohol is an inducer of P450 Acute alcohol is an inhibitor of P450 +3
dentist  Famotidine- also a H2 blocker, but not cyp450 inh +1


submitted by utap2001(27), visit this page
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  • Fur is a TRANSCRIPTION FACTOR that acts as a REPRESSOR to control the gene expression.

  • if INCREASE IRON CONCENTRATION--> INCREASE Fur DNA binding = INCREASE the REPRESSOR function and the opposite action w/ [LOW IRON].

  • Fur helps in the BACTERIAL VIRULENCE FACTORS control.

https://en.wikipedia.org/wiki/Ferric_uptake_regulator_family

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dentist  is getting this question correct contingent upon memorizing that fur is a transcription factor? +
pakimd  @utap2001 can you explain how you figured that fur is a repressor and not a promoter? +
pakimd  oh i just clicked on the link you posted. sorry +
utap2001  It doesn't matter if Fur is suppressor or promoter. The question stem says " Ferric uptake regulation protein (Fur) binds tightly to DNA a short distance from the 5โ€™end of the genes for these virulence factors." So it's function to modulate the transcription of DNA. +4
drdoom  @dentist, utap2001 hits the key sentence of the stem. No one has ever heard of Fur, but the description of a protein that binds tightly to DNA, and does so nearby the start of a gene (5'), is unlikely to be anything other than a transcription factor. +
drdoom  (Transcription of DNA is such a highly conserved and tightly regulated process that no protein other than a TF can willy-nilly bind to DNA in the manner described in the stem.) +
blue4415  @ pakimd Because the more Fur binding๏ผŒiron in the โ€œmedia โ€œ increases its concentration; -last sentence And itโ€™s name is โ€œferric uptake โ€œ regulator protein (which regulate the mRNA transcription ), you can imagine the mRNA product is a ferric uptake transport or like DMT-1 in human intestinal . All above , itโ€™s like a repressor , which is a transcription factor +


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DKA is a state of decreased insulin; since we know that insulin causes a shift of K+ into the cells low levels of insulin will prevent this and result in hyperkalemia. In addition, due to hyperglycemia and high ECF osmolality water will shift out of the cells into the ECF and K+ shifts out with the water which will futher increase the hyperkalemia

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dentist  I know Insulin cause shift K+ into cells due to closing of ATP-sensitive K channels (blocking K from leaving)? Does it increase K in the cells by another mechanism? +
makinallkindzofgainz  @dentist - Insulin stimulates the Na+-K+-ATPase pump, this drives K+ into the cell (Source: Amboss) +
castlblack  Another mechansim = acidosis causes hyperkalemia due to H+/K+ antiporters. H+ is high in blood so shifts into cells via this antiporter, which shifts K+ out. --potassium section of acid/base chapter in Costanzo physiology +


submitted by mattnatomy(46), visit this page
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Severe hypertension often leads to hyperplastic arteriolosclerosis (onion-skin appearance). Also see proliferation of smooth muscle cells.

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meningitis  and explains the flame hemorrhages (Goljan) caused by malignant HTN +5
taediggity  FA 2020 pg. 537 +
dentist  FA 2020 pg 301* +
ally123  The flame hemmorhages are also a good buzz word for recognizing he has hypertensive retinopathy 2e chronic, uncontrolled HTN. Pt's with hypertensive retinopathy can also present with "cotton wool spots" and "macular star". Pics on FA 2019, p. 299 +2
surfacegomd  Pathoma (2018) p. 69 +
madamestep  @ally123 I think the best buzzword for hypertensive retinopathy here is "190/135 mmHg" +


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would anyone be able to clarify what the others would be? A) Allergen mediated vasoconstriction, leading to ischemic tissue injury: Type I B) Binding of antigen to IgE on the surface of mast cells leading to mast cell degranulation: Type I C) deposition of antigen-antibody complexes within postcapillary venules, leading to activation of complement: Not sure D) Phagocytosis of antigen by neutrophils, leading to oxidant mediated tissue damage: Type III?

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sunny  i think C is type III +3
sunny  i think C is type III +1
dentist  In Type III HS, First C happens then then D happens +1


submitted by bobson150(28), visit this page
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Is the grey supposed to be a suture? If not why would this not be wound healing therefore granulation tissue?

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asapdoc  If you look at the picture you can see the epithelioid and giant cells. I only picked granuloma because I remember seeing a similar picture in Uworld. +5
dentist  granulation tissue is a part of the normal wound healing process, and happens within the first week. +
castlblack  I agree I looked at that grey blob and thought foreign body --> granuloma +


submitted by usmlehulk(7), visit this page
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can someone please explain this question. i thought the patient is actually having cleft lip and palate, but why is the correct answer addressing only the cleft lip.

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dentist  The question asks "the most likely cause of the facial finding involving the lip in this patient..." +8
snripper  lmao. gottem +4
ace9yak  cleft lip = 'processes' clef palate = 'shelves' +2
mutteringly  Don't let a dentist tell you whats up :( +1


submitted by welpdedelp(270), visit this page
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It was scabies, which is transmitted person-operon.

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welpdedelp  **person-person lol +9
suckitnbme  NBME loves their scabies +23
dentist  did you get scabies from "burrows" and "night itching" +1
pg32  My question is where do you get scabies originally? I knew it was transmitted person-to-person, but thought it has to originate somewhere (a pet possibly?) so I went with pets. The internet only seems to say that you get scabies from another person with scabies, so the question remains: where do people contract scabies from? +1
leaf_house  @pg32 , long quote: + "Sarcoptes scabiei mites seek the source of stimuli originating from the host when they are off the host but in close proximity to it. This behavior may facilitate their finding a host if they are dislodged from it and contaminate the host environment. Thus, direct contact with an infested host may not be required for humans and other mammals to become infected with S. scabiei. In the case of human scabies, live mites in bedding, furniture, toys, and clothing can be a source of infection. Sarcoptes scabiei var. hominis have been recovered from laundry bins in a nursing home." + from here: https://parasitesandvectors.biomedcentral.com/articles/10.1186/s13071-017-2234-1 +1
zevvyt  to summarize leafhouse: Fomites +3
surfacegomd  FA 2020 p.161 "transmission through skin-to-skin contact (most common) or via fomites" +1


submitted by alexb(53), visit this page
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Is the part with "constant studying" just supposed to support that she has a psych disorder related to perfectionism, which is why she's going to extremes to control her weight?

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rrasha2  No, the constant studying is to trick you into thinking shes abusing amphetamines.Amphetamines decrease appetite so a lot of people abuse them for weight loss. That combined with increased concentration to study all day errrday.. #onehellofadrug +1
rrasha2  forgot to mention, another side effect of amphetamines would be increased BP due to the increased catecholamines..don't forget to keep an eye out for that +1
dentist  would amphetamines influence electrolytes at all? +1


submitted by runnerman92(2), visit this page
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Increased Levels of Myeloid cells ( Erythrocytosis, thrombocythemia, and granulocytosis) plus Dizziness and Headache increase the suspicion for Polycythemia vera.

Low EPO in PV due to Negative feedback on EPO release by kidney.

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dentist  This is where the timing of everything in the question trips me up. FA say PV mechanism is increase EPO (2019, p299) +
paulkarr  Different types of Polycythemia have different effects on EPO levels. "Appropriate Absolute" and "Inappropriate Absolute" will both increase EPO levels (Inappropriate is caused by this EPO increase). Where as Polycythemia Vera has decreased EPO levels due to the negative feedback loop. FA2019 pg 425 hooks it up nicely. +5


submitted by nwinkelmann(366), visit this page
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Murmurs and maneuvers: 1st thought = how does it change with preload. All murmurs except HOCM, MVP, and atrial myxoma severity is directly proportional to change in preload (i.e. increased preload=worse murmur, etc.). Because of this, DDx can be narrowed down to HOCM, MVP, and atrial myxoma right away because the murmur worsened with decreased preload (i.e. standing up) when all but exceptions with improve.

Atrial myxoma = MCC primary cardiac tumor due to proliferation of connective tissue mesenchyme; a pedunculated mass connected via stalk to atrium septum that is suspended in the atrial blood volume and moves with the volume movement.

Presentation: triad of 1) mitral valve obstruction (i.e. malaise, symptoms of cardiac failure, syncope, etc.), 2) symptoms of embolism (i.e. facial and right arm hemiparesis in patient), and 3) constitutional symptoms (i.e. fever, weight loss, symptoms resembling connective tissue disease, because tumor releases IL-6). Others include neurologic symptoms, "pseudo-mitral valve disease" auscultatory findings (i.e. diastolic murmur), and atrial enlargement (which could compress underlying structures and cause symptoms also).

Not only does standing decrease preload, which means LA volume is lower so mass isn't as "suspended" but more mobile, standing also increases the downward gravitation force, which would contribute to the tumor moving towards the base of the atrial chamber, "plopping" on the mitral valve leaflets, and potentially extending through and causing a functional type of mitral stenosis (i.e. worsening diastolic murmur). This video explains it really well: https://www.youtube.com/watch?v=slIY64nViLg&t=161s

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dentist  Sorry, you narrowed it down to HOCM, MVP, and LA myoxma, but I only see LA myxoma as an answer choice. Wouldn't you have been able to stop right there? +3
hello  @dentist, I appreciate this full answer b/c nwinkelmann is telling those of us that were wondering "how to ddx one from the other in case we need to"? +8
hello  @dentist btw, HOCM is an answer choice (RVOT is part of HOCM) +4
thotcandy  @hello but since that's pseudo-aortic stenosis, it would present with a systolic murmur, correct? +3


submitted by mousie(272), visit this page
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help with this one please.... is this because he has hyperTG AND Cholesterol AND chylomicrons.. only LL deficiency would explain all of these findings? I chose LDL R deficiency because I guess I though it would cause all of them to increase but is this type of deficiency only associated with high LDL?

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sympathetikey  First off, do yourself a favor and check this out - https://www.youtube.com/watch?v=NJYNf-Jcclo The LDL receptor is found on peripheral tissues. It recognizes B100 on LDL, IDL, and VLDL (secreted from the liver). Therefore, an issue with that would cause an increase in those, but mainly LDL. Since in this question we see that Triglycerides and Chylomicrons are elevated, that points towards a different problem. That problem is in the Lipoprotein Lipase receptor. This is the receptor that allows tissues to degrade TGs in Chylomicrons. So, if it's not working, you get increased TGs and Chylomicrons. Additionally, you get eruptive xanthomas, which are the yellow white papules the question refers to. +12
davidw  There is much easier way go to page 94 in first aid. This kid has Type 1 Hyper-Chylomicronemia which is I) Increased Chylomicrons, Increase TG and Increased Cholesterol. It can be either Lipoprotein Lipase or Apolipoprotein CII Deficiency +12
bulgaine  The video sympathetikey referred to only mentions pancreatitis in type IV but according to page 94 of FA 2019 it is also present in type I Hyper-chylomicronemia which is what the question stem is referring to with the abdominal pain, vomiting and increased amylase activity +
dentist  thats not the only difference in that video.... +
paulkarr  Pixorize has a set of videos on all the lipid disorders that made it a breeze to answer. Pixorize is basically sketchy but for biochem and other basic science subjects. +3
futurelatinadr  Pancreatitis was a huge clue for me to think of hyperchylomicronemia +1


submitted by seagull(1933), visit this page
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So, T1/2-T5/6 are the sympathetic level for the heart. The stellate ganglion are cervical sympathetic ganglion. This question seems more incorrect (or a huge leap) to me. But hey, I know people will disagree.

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dentist  you're right! heart rate is the only option under sympathetic control. +
drzed  The cervical ganglion is a fusion of the last few cervical levels and the first thoracic level, so it is plausible. +


submitted by hopsalong(32), visit this page
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I get this is a fluffy question and acknowledging the patient's reasons for missing insulin injections is the cuddliest, but I feel like this answer tows the line a bit. You don't want to say that missing doses is ok, but you also don't want to be mean to patient either. I thought this answer (A) was condoning her missing the injections, so I picked (C). In retrospect, I guess acknowledge means talk about/focus the conversation around.

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dentist  I would say: "I understand why you are missing injections, but you're going to have a BAD TIME IF YOU KEEP MISSING INJECTIONS" +4
alexxxx30  @dentist, I was searching for that answer as well, but it wasn't there so I picked C ahahaha +
123ojm  you would definitely do C as well. key word is "initial step" +
meja2  I believe that C is wrong since data suggests that teenagers tend to focus on the current situation, rather than long term, so if you want to initiate a change in behaviour its best to discuss how the behaviour affects their CURRENT situation. Option C would be to discuss long term effects. +1
fatboyslim  I think by acknowledging the patient's reasons they mean to say something like "yeah it's not always easy to remember to take ur insulin on time every day, especially when you don't immediately feel the effects of not taking the insulin" etc. In contrast to saying they are right about it. It's just about telling the patient "I hear you and I know it can be difficult". I think this concept applies to any non-compliant patient. +


submitted by mousie(272), visit this page
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Cholera = Fecal oral /Legionnaires = Legonalla pneumo = NO person to person only by inhalation of bacteria contaminated water /Lyme = tick bite /Meningiococcal = sharing respiratory and throat secretions (saliva or spit). Generally, it takes close (for example, coughing or kissing) or lengthy contact to spread these bacteria (CDC) /RMSF = tick bite

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smc213  Also, when Meningococcal meningitis is treated ... close contacts are also treated prophylactically whereas the others typically are not. There's also a subunit vaccine for n. meningitis due to high infectivity rate especially in crowded establishments. +7
dentist  So, Cholera is also p2p but Mening is more likely? +1
usmlecharserssss  in cholera people to water => water to people +
qball  Remember the fire sprinklers from Sketchy for M. Meningitis. as respiratory droplets are the easiest to transmit from person to person. +
drschmoctor  but the poop water comes from people so.... +1
llamastep1  Respiratory dropplets is easier than fecal-oral tho +2
lowyield  Can also reason that n. meningitidis is common in college students because they live in close quarters which suggests high rate of transmission even amongst immunocompetent individuals +2
peridot  I can see why fecal-oral can seem like person-to-person transmission. What helped me reason it was that in countries with lots of cases of cholera, the primary reason is lack of water sanitation. Even when you google cholera, you get pictures of people collecting dirty water and how the WHO is aiming to reduce cases of the disease by improving water sources. Therefore it's more of a systemic/environmental problem rather than the fact that one person accidentally touched another person's poopy parts and then transmitted it to their own mouth, making this less of a person-to-person thing, especially when compared to another answer choice such as Meningococcal meningitis. +
bbr  To add, think of the water in cholera as a reservoir. The bug is going to hang out there between infecting another person. In meningitis it seems we are going from 1 persons saliva to another. Without much of a reservoir inbetween. (might be using the word reservoir incorrectly). +1
weirdmed51  Rocky Mountain spotted fever: dermacenter TICK +


submitted by mousie(272), visit this page
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My understanding if BC>AC this is abnormal = conductive hearing loss = otosclerosis VS Sensoryneural hearing loss will have normal AC>BC = loss of hair cells

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dentist  VS: progressive unilateral hearing loss, doesn't affect Rinne Test, associated with NF2 and actor Mark Ruffalo Otoslcerosis is (usually....) progressive bilateral hearing loss, BC > AC. source +
tallerthanmymom  If BC > AC in BOTH ears, why does he have hearing loss in only one ear? My logic was that he probably had otosclerosis in both ears and then something extra going on in his right ear that would make it worse than the left. I still don't understand why otosclerosis is the best answer here. +5
dul071  Finally!!!! Someone who ACTUALLY explains what the fuck bone conduction even is and teaches the whole topic. Here's the link for anyone else who struggled to find someone who takes time to explain this concept https://www.youtube.com/watch?v=cZYJL9Jg-3k +4
sonofarathorn  ^ Halle-freakin-lujah +
chaosawaits  I also was very confused as to why BC > AC in both ears but he only has hearing loss in one ear. Regardless, none of the other choices explained conductive hearing loss so I chose E, but I hate questions like this because I'm right, I know what I'm talking about but I cannot have confidence in my answer which affects me in later questions. +


submitted by joker4eva76(31), visit this page
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This is representative of leukoplakia, a pre-cancerous lesion of squamous cells. In order for it to spread to distant sites, it must first invade through the basement membrane/submucosa. Could be confused with oral hairy leukoplakia (which also is a white patch that classically arises on the lateral tongue). However, oral hairy leukoplakia is not pre-cancerous and is often associated with EBV infections or people that are severely immunocompromised.

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hpkrazydesi  How did you know that this wasnt oral hairy leukoplakia? just from the picture? +3
nwinkelmann  To piggyback off of @hpkrazydesi, you ruled out oral hairy leukoplakia because the patient was seeing the doctor for normal health maintenance, i.e. not immunocompromised, I'm assuming. +2
dentist  @nwinkelmann thats correct! my time to shine. +


submitted by fallenistand(27), visit this page
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Since you see vascularity that is why it is granulation tissue. Fibrous scar would be 1 month after and you wouldn't see that much blood.

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dentist  The v-fib/death is an attempt to throw you off. The simple way of asking this question would have been: "18 days after an MI, you should see____?" +5
gubernaculum  i would use pathoma for this. it says 1-3 weeks after an MI you can see granulation tissue +2


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