NBME Answers : kai's page

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submitted by aladar50(41), visit this page

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So there’s 100 residents, and the prevalence after 2 years is =10 at the beginning, +5 in the first year, +10 second year, and -3 that healed, for a total prevalence of 22 residents or 22/100=22 percent. Thus, prevalence = above the standard. For incidence, it’s 15 new cases out of 90 residents over the 2 years (100 total residents – 10 that already had ulcers), or 15 new ulcers per 180 patient⋅years. This would be 83.3 new ulcers per 1000 patient⋅years if you extrapolated it out -- basically (1000/180) * 15 -- thus, incidence = above the standard.

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zelderonmorningstar Okay I feel like an idiot cause I thought: Above the Standard = Doing a good job keeping old people from getting ulcers. Thumbs up. Below the Standard = I wouldn’t let my worst enemy into your ulcer ridden elder abuse shack. +68

aladar50 @zelderon Ohh damn. I could totally see how one could view the answer choices that way. I think it is important to read how they are phrased - they are asking if the center is above THE standard or below THE standard. The “standard” is an arbitrary set point, and the results of the study are either above or below that cut off. Maybe if it was “above/below standards” that would work. Also, being above the standard could either be a good thing or bad thing. If say you were talking about qualifying for a competition and you have to do 50 push ups in a minute, then being above=good and below=bad. In this case, having more ulcers than the standard = bad. +4

saynomore @aladar Thank you!!! but how did you get the 15 new ulcers per 180 patient⋅years? I mean I understand the 15 part, but not the second part ... hence why I messed this up, lol :| +2

aladar50 @saysomore Because the study is looking at 100 residents over a period of 2 years. Since 10 already had the disease at the start, when looking at incidence you only include the subjects that have /the potential/ of developing the disease, so 90 patients over 2 years. This would be 90 patient⋅years per year, or a total of 180 patient⋅years over the course of the study. +7

sympathetikey @zelderonmorningstar I thought the same exact thing. Had the right logic, but then just put the backwards answer. +4

kai I wonder if they chose this wording on purpose just to fuck with us or if this was accidental. My guess is there's some evil doctor twirling his thumbs somewhere thinking you guys are below the standard. +16

symptomatology Got it wrong!messed up in understanding options, Btw, 15/90 is somewhat 16 percent and their standerd is 50/1000 5 percent!.. this is how i knew that incidance is way up! +

donttrustmyanswers Patients with an ulcer are not immune to getting new ulcers --> You should include all patients at risk. But either way, the answer is the same as long as you can read NBME speak. +

doublethinker Damn, guess my reading comprehension is not "up to the standard" of the NBME writers. Smh. +

prolific_pygophilic If you forgot that its patient years (15/180) not (15/90) you still get the right answer because they are both above 5% :). +

submitted by thomasalterman(181), visit this page

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Trihexphenidyl and Benztropine are antimuscarinics that can treat the resting tremor and rigidity of parkinsonism.

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mousie haloperidol induced Parkinson's... ? adding a anticholinergic can counter these adverse effects of the antipsychotic .. ? +3

fulminant_life @mousie yeah it balances the dopamine-cholinergic imbalance caused by the antipsychotics +

kai +So antipsychotics induce Extrapyramidal side effects which is drug induced Parkinson = low Dopamine High Ach, and you would treat this with anticholinergic (Benztropine).This is neurologic. +Antipsychotics also produce non-neurologic, systemic anti-cholinergic effects like dry mouth, sedation, hypotension etc +

an1 UW asked this too, benztropine is the drug of choice +

submitted by cbrodo(77), visit this page

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The posterior columns (Fasciculus cuneatus/Fasciculus gracilis) carry information to the brain regarding proprioception, vibration, discriminative touch and pressure. Physical exam findings suggest a lesion here (the spinothalamic tract carries pinprick/pain and temperature, and these were normal). Since the patient has abnormal findings in the lower extremities, and normal findings in the upper extremities, the answer is Fasciculus gracilis. This is because information from body areas below the level of T6 is carried by gracilis and information from body areas above the level of T6 is carried by cuneatus.

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kai kick Goals (gracilis) with your feet Cook and eat (cuneatus) with your hands +4

temmy i remember gracilis is for legs by saying i have graciously long legs and they are inside while arms can spread out to remember their orientation on the spinal cord +4

jess123 I remember it as gracilis = grass so feet haha +5

link981 Just to add found on page 492 on FA 2018. +

charcot_bouchard Hey Temmy, I can spread my legs too :) +

maxillarythirdmolar I can't feel GRACIE's ~fine touch~ as she ~vibrates~ my balls. +4

cat5280 Could someone please explain why you were able to eliminate the spinocerebellar tracts? +1

drzed Lmao I remember gracilis because of the gracilis muscle in the legs! +3

alexxxx30 cat5280...so spinocerebellar tract does 4 things to know 1. proprioception in the Romberg test 2. intention tremor if damaged 3. shin to knee test 4. dysdiadochokinesia (being able to rapidly pronate/supinate the upper extremity) yes the patient has proprioception issues, but the other symptom of vibration loss points us more to a fasciculus gracilis issue. If the patient had presented with proprioception and and intention tremor then we would think spinocerebellar +3

alexxxx30 adding to my comment^ I would commit these 4 things to memory as I have gotten several questions concerning this topic (there were 2 questions on this exam where spinocerebellar tracts are involved). Memorize them and it might get you 1-2 extra points! +1

solidshake Just to clarify a point, Spinocerebellar tracts are not tested by the Romberg Test. Romberg tests conscious proprioception that is done by the dorsal columns. Spinocerebellar tracts are used for Unconscious proprioception. Look up tabes dorsalis in First Aid. One of the positive indicators is a positive romberg test, which shows that the dorsal columns have been damaged thus affecting conscious proprioception and thus impaired balanced on standing with the eyes closed +2

submitted by sajaqua1(607), visit this page

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MHC I function is integral to cancer suppression. MHC I displays endogenously synthesized proteins and presents them to CD8+ T cells. The failure to display MHC I, or MHC I display of non-self (and by extension cancerous) proteins triggers a cellular immune response, leading to destruction of the cell.

The proteasome is used for the degradation of worn out, senescent, or malformed proteins. As cancer develops, more mutations lead to increased wrong proteins. Only by expression of the proteasome, or its over-expression, can these mutant proteins be degraded fast enough to not be displayed by MHC I and lead to the cell being killed. Bortezomib blocks the proteasome, so the mutant proteins are displayed on the surface, allowing the immune system to recognize and kill pathological cells.

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catch-22 Another way to approach it is to think about MHC class I processing. Basically, if you inhibit the proteasome, peptides will not be generated and nothing is available to be loaded onto MHC I (remember MHC I has to be loaded before it's transported to the cell surface). Cells that don't express MHC I get killed by the natural killers. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2214736/ +32

kai "In conclusion, we have demonstrated that the proteasome inhibitor bortezomib down-regulates class I and enhances the sensitivity of myeloma to NK cell–mediated lysis" from the conclusion of the NIH paper +6

maddy1994 another mechanism is by blocking proteosome u even decrease degration of proapoptotic proteins...so it enchances apoptosis(from uworld) +6

azibird But CD8+ and NK cells kill via perforin! Why is this answer wrong? Is it because it's not the primary effect? +2

testready "The proteasome is the major source of proteolytic activity involved in the generation of peptides for presentation by major histocompatibility complex class I molecules. We report the new observation that bortezomib down-regulates HLA class I on MM cells, resulting in increased NK cell–mediated lysis." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2214736/ +

fatboyslim I think what OP said contradicts with what @catch-22 cited in the PubMed article. +

an1 OP said "Only by expression of the proteasome, or its over-expression, can these mutant proteins be degraded fast enough to not be displayed by MHC I". UW QID 11674 says that a protein undergoes degradation by the ubiquitin proteasome pathway, after which it goes to the ER and then is presented to the cell surface for MHC 1 response leading to apoptosis via performs and granzymes. Having a proteasome inhibitor would actually prevent the MHC response because no proteins are displayed. Also note that the question says which process will be affected, there is no mention of increase or decrease. So yes, the MHC 1/ CD8 pathways is affected, but it's actually down regulated. An absence of MHC 1 leads to NK cell mediated death. +

submitted by sympathetikey(1600), visit this page

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Per FA (pg. 636): Concerning breast cancer...

"Amplification/overexpression of estrogen/ progesterone receptors or c-erbB2 (HER2, an EGF receptor) is common; ER ⊝, PR ⊝, and HER2/neu ⊝ form more aggressive."

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sympathetikey FA 2019 +5

meningitis Why others not it: Anticipation: Trinucleotide repeats; CAG (Huntington), CTG (Myotonic dyst), GAA (ataxia telangiectasia), CGG(Fragile X) Chromosomal rearrangement: Many but can think of Trisomy 21, BCR-Abl, etc Imprinting: Prader willi, angelman Loss of heterozygosity: loss of a single parent's contribution to part of its genome. A common occurrence in cancer, it often indicates the presence of tumor suppressor gene in the lost region. +3

kai trinucleotide repeats are not associated with breast cancer Neither are chromosomal rearrangements BRCA1,2 tumor supressor genes are associated with breast cancer, which is why I chose E, but I guess I should have bought the new First Aid.......... +

charcot_bouchard GAA is Freidrich Ataxia +5

tulsigabbard So is the amplification of the receptors unrelated to BRCA 1, 2? I'm still stuck on this as Sketchy states that breast cancer falls under the "two-hit" model. +

tallerthanmymom @tulsigabbard I think one of the keys here is the question stem; " what is the most likely cause of the OVERexpression in this pts tumor cells?" --> I think that the "2-Hit" model would lead to UNDERexpression of a tumor suppression gene rather than overexpression. Whereas amplification would cause OVERexpression of the HER2/estrogen and progesterone receptors. But, I don't think that amplification would be the answer if they were asking about a triple negative cancer. +1

tallerthanmymom Also this is on page 632 of FA 2018 for those using that version +

tulsigabbard @tallerthanmymom - thank you! +

drzed I can understand why @tulsigabbard dropped out of the race--she's taking step 1 soon LOL +3