NBME Answers : chj7's page

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submitted by motherhen(69), visit this page

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Kartagener syndrome, an autosomal recessive ciliary disorder. Presents with triad of chronic sinusitis, bronchiectasis and situs inversus.

Since the brother is known to be phenotypically normal, he can either be AA, Aa or Aa. Thus, there is a 2/3 chance is a carrier.

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stefanmil Can you explain how is this Kartagener? It didn't come to my mind at all :/ thanks +

kcd0321 I thought it was Cystic fibrosis: chronic cough with "thick" green sputum, cramps in the abdomen (malabsorption issues because of pancreatic insufficiency maybe), and then the frequent respiratory infections. Its also AR so the same principle of AA, Aa, or Aa, so he has a 2/3 chance of being a carrier. +8

srmtn isn't Aa or aA the same in terms of heterozygosity? I thought about that and put 1/2 :/ +

chj7 @srmtn They represent two different events: getting the "bad" allele from the mom OR the dad. Thus, they individually contribute to the risk of being a carrier. +

submitted by azibird(279), visit this page

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Follow-up vs support group?

The only thing that saved me was the ancient Step 1 adage: "Never refer!"

Especially when the answer to another question in the same exam was "Encourage the patient to participate in a support group for persons with her condition"

I mean REALLY! The only difference is that they used the word "encourage" instead of refer. Exact same answer.

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cbreland Note to self: Never refer, even when that seems like the better answer +

chj7 Take this with a grain of salt but I felt like a treatment plan with goals should be tailored to the patient and would require a physician to assess performance/make modifications. A support group could provide mental support when facing a disease but seems not individually-targeted enough for trying to get a patient to stick to a dietary/exercise treatment plan. I have to admit I did really self-doubt when I saw the 2 questions on the test. +

submitted by acerj(13), visit this page

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Catalytic efficiency is defined as K_cat/K_M.

If you know what that is (I did not), then this problem is a simple division.

See here for more info (stop at the first line of the article for your own sanity): https://en.wikipedia.org/wiki/Specificity_constant

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aakb This problem may not solved just by knowing the above equation, if you're like me and get confused when you see lots of numbers and letters together. You need to use Kcat/Km to find the catalytic efficiency for both E487 and K487. Doing this, you'll see both A and B are true. Catalytic efficiency for K487 is 9.5/5600 = 0.002, which is decreased (A) and for e487 you get 180/37 = 4, making B true. Now how do you pick between A and B? The patient has disulfram-like reactions whenever he consumes alcohol since his acetylaldehyde dehydrogenase is slower (decreased catalytic efficiency), seen w/ K487, which the patient actually has if the question is read closely. So if you knew he had k487 from reading the confusing question stem it would have been easy to pick between A and B but if you're like me and can't seem to make those connections quickly, knowing something about ethanol metabolism helps. +2

tekkenman101 The fastest way to answer this question is realizing the patient has the oriental variant, so all options regarding E can be excluded. Then you can see that the Km of the K-variant is much larger than the E-one. Larger Km = decreased binding = decreased turnover/catalytic efficiency. 30 seconds tops. +8

chj7 Not wanting people to get confused here. Km does reflect binding (higher Km means you need more substrate to reach same Vmax--> decreased binding). However, turnover number (the number of times each enzyme site converts substrate to product per unit time) is reflected by Kcat, NOT Km. One way to determine catalytic efficiency is Kcat/Km, which is also termed the specificity constant. You CANNOT answer this question by only looking at Km. +4

submitted by azibird(279), visit this page

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A laminectomy removes the lamina and spinous process. The lamina is the posterior bridging segment (D). The lateral bridging segment is the pedicle (B).

However, I don't understand how you could access the herniated disc from this angle, the spinal cord would be in the way! Can someone explain?

https://www.mayoclinic.org/tests-procedures/laminectomy/about/pac-20394533

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scrambledeggs Take a look at the section labeled Laminotomy and Discectomy. https://eorthopod.com/lumbar-discectomy/ +7

coby219 "Intervertebral disc (nucleus pulposus) herniates posterolaterally through annulus fibrosus (outer ring) into central canal due to thin posterior longitudinal ligament and thicker anterior longitudinal ligament along midline of vertebral bodies. Nerve affected is usually below the level of herniation." - first aid 19 p455 +5

chj7 Adding to coby219, after knowing herniation most commonly occurs posterolaterally, we would most likely choose between B and D. The only reasonable choice from a surgical perspective would be D b/c we would most likely be entering the patient's vertebrae from the back (thus, B would be harder to access). +1

freemanpeng Question stem said" laminectomy". I just ingored it and kept struggling between lamina(D) and pedicle(B)...... So, it's not about neurosurgery; it's just basic anatomy! +1

submitted by azibird(279), visit this page

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This is the most poorly drawn cell diagram. I see zero ribosomes, so I figured F was the smooth endoplasmic reticulum. However, now I can see that the curved organelle is the golgi apparatus and F must represent the whole endoplasmic reticulum.

I believe plasma membrane proteins are synthesized in the rough endoplasmic reticulum.

FA2020 p46 Rough endoplasmic reticulum Site of synthesis of secretory (exported) proteins and of N-linked oligosaccharide addition to lysosomal and other proteins.

Free ribosomes—unattached to any membrane; site of synthesis of cytosolic, peroxisomal, and mitochondrial proteins.

Smooth endoplasmic reticulum Site of steroid synthesis and detoxification of drugs and poisons. Lacks surface ribosomes. Location of glucose-6-phosphatase (last step of glycogenolysis).

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nbmeanswersownersucks I was under the impression that translation of transmembrane proteins begins with ribosomes in the cytoplasm that then translocate to the rough ER once the signal sequence is reached by the ribosome? i.e. technically translation begins in the cytoplasm but finishes in the rough ER. Am I wrong about that? +5

nbmeanswersownersucks It was UWORLD 6544 about insulin translation. They state that the translation is initiated in the cytoplasm then relocates to the RER (d/t the signal sequence) and is finished there. So is there a difference in translation steps for proteins that are excreted like insulin and transmembrane proteins? +2

nsinghey Same, I am not sure about this. My best guess is that since insulin is not a functional protein, it is not synthesized in the RER (even though it it excreted from the cell). Actual proteins are made in the RER +2

kevster123 I just put F cause it said transmembrane domains and I know the rough ER got a lot of balls on it that translate it through and to translate through the balls you're passing through membranes. +

drdoom @nbmeanswersownersucks @nsinghey et al. There is extensive discussion of this on an NBME 24 thread. This link will take you to the comments (just don't scroll up to spoil the answer for yourself!): https://nbmeanswers.com/exam/nbme24/939#1379 +

drdoom also, this thread from NBME 21 discusses cell transport more generally (same warnings apply! don't scroll up!): https://nbmeanswers.com/exam/nbme21/742#257 +

brise The question is saying where is it initially produced? It is produced in the RER, therefore F. Not asking where it's production starts- asking where is it produced etc. +3

chj7 I'm not sure if this is what the question was trying to ask but technically the "polypeptide" is initially sequenced in the cytosol; once the N-terminal signal sequence is synthesized, SRP translocates ribosomes to the rER where translation continues/completes and the "protein" is folded/formed in rER. (I like UW #757's diagram on this) So if they truly mean where the precursor "protein" is initially formed, rER is correct. But honestly the above is a way too complex form of thinking that I feel would NOT help on the actual exam and most likely strays away from the learning objective of this question; more likely the question writers were trying to distinguish btw proteins translocated to the rER (membrane proteins, secretory proteins, ER/Golgi/lysosomal proteins) vs. proteins that are synthesized by free ribosomes (cytosol/nucleosol proteins, peroxisomal/ some mitochondrial proteins). +1

submitted by mousie(272), visit this page

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Read pathoma...... chapter 1 p 5 on "cell death" Liquefactive necrosis occurs in brain infarct ( proteolytic enzymes from microglial cells liquify the brain) & Abscess (proteolytic enzymes from neutrophils liquify tissue [in this case pulmonary parenchyma]) & pancreatitis (same thing)

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mumenrider4ever Also talked about under liquefactive necrosis on pg. 209 FA 2020 +3

lokotriene UW: 302 & 9989 are both great for representing/explaining this. +

tekkenman101 pancreatitis is fat saponification not liquefactive according to FA. +

chj7 @tekkenman101 Inflammation of the pancreas itself is liquefactive due to pancreatic enzymes digesting everything; inflammation of the fat surrounding the pancreas leads to fat necrosis. (Dr. Sattar distinguishes this when he talks about the different types of necrosis) +1

submitted by hayayah(1212), visit this page

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Frontotemporal dementia (formerly known as Pick disease): Early changes in personality and behavior (behavioral variant), or aphasia (primary progressive aphasia). May have associated movement disorders (eg, parkinsonism).

While this presents very similiarly to Hungtington's, you can differentiate it because in this stem it says "atrophy of the frontal lobes bilaterally" whereas Huntington's has atrophy of caudate and putamen with ex vacuo ventriculomegaly.

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dickass and the patient has no chorea +6

chj7 Also, in frontotemporal dementia, due to disease of the "cortex", memory/speech/behavioural changes occur early on. (In Pathoma at the beginning of the dementia lecture, he emphasizes distinguishing between disorders of the cortex vs. disorders of the striatum (ie. Huntington's & Parkinson's) as clinical presentations are easily separated.) +1

submitted by usmleboy(19), visit this page

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An antibody can only recognize a single epitope. Since we see the more Y added leads to less X bound, then you can reason they share the same binding sites, and Y is overpowering X.

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srmtn OMG this is the reason why! thank you!!! +

srmtn but there are antibodies that can interact with 10 epitopes...example IgM... sorry got lost again :( +

chj7 For anyone still dwelling on this, the process they talk about in the question stem is possibly polyclonal (thus the issue of multiple epitopes). +

submitted by hayayah(1212), visit this page

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Septic shock is a type of distributive shock which is marked by massive vasodilation (d/t inflammatory response) causing decreased SVR, decreased preload / PCWP, and increased CO.

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smc213 Septic shock can also present with hypothermia <36C +3

bethune Why is it not gastrointestinal bleeding? +4

beanie368 GI bleeding would present with increased SVR as a response to hypovolemia +10

mysteriousmantyping Why would this not be pulmonary embolism? +1

step1passfail Pulmonary embolism would cause a decrease in cardiac output. There is increased pressure in the high compliant RV which can bulge and compress the LV, decreasing its preload. CO=Heart rate x stroke volume and stroke volume is partially determined by preload. If the pulmonary embolism is large enough, it can also obstruct the pulmonary vessels and subsequently not have enough blood going to the LA and LV, ultimately making the cardiac output near 0. +3

chj7 Out of all the different types of shock, cardiac output is increased only in distributive shock (ie. anaphylactic, septic). +1

submitted by cassdawg(1781), visit this page

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This man has SIADH (syndrome of inappropriate antidiuretic hormone) which is likely caused by a paraneoplastic syndrome associated with small cell lung cancer (FA2020 p228)

This man presents with hyonatremia, hypochloremia, normal potassium, normal BUN and creatinine, decreased plasma osmolality, and increased urine osmolality. SIADH is characterized by urine osmolality>serum osmolality and hyponatremia (p338). This is because ADH triggers retention of water by insertion of awuaporins into the collecting tubules. The increased body water triggers decreased secretion of renin and decreased activation of the renin-angiotensin-aldosterone system. Less aldosterone leads to less retention of sodium and less excretion of potassium. This combined with dilution from retention of water leads to hyponatremia with potassium normal. BUN/creatinine are unaffected because the kidneys are undamaged.

This is NOT ectopic ACTH secretion because that would lead to Cushing's syndrome which does not have the characteristic osmolality differences and increased cortisol can mimic mineralocorticoids leading to hypernatremia.

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taylor5479 In your last point, you referred to cushing's syndrome. I could be wrong, but I was under the impression that excess ACTH also causes an increase in mineralocorticoid production, not that increased cortisol necessarily mimics mineralocorticoids. Either way, it would result in the same effect of hypernatremia. +

chj7 I think aldosterone production is mainly regulated by RAAS, while ACTH has major effects on glucocorticoid production and minor/tonic effects on aldosterone production (forgot where I saw this exactly, maybe UW?) +

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Aplastic anemia: anemia, leukopenia, thrombocytopenia

CML, i.e. leukemias: anemia, ↓ mature WBC, ↓ plt, peripheral blood smear shows mature & maturing granulocytes (FA 2020, p. 432)

β-thalassemia major: microcytic, hypochromic anemia with target cells and anisopoikilocytosis, skeletal deformities, etc. (FA 2020, p. 418)

Cobalamin deficiency: d/t malabsorption, pancreatic insufficiency, gastrectomy, or insufficient intake, neurological Sx

Personally, I got this wrong, because to me, the RBCs in that smear looked both larger and more irregularly shaped, so in hindsight, I really should've honed in more on the HPI, i.e. the patient really has anemia and no other relevant PMx.

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flapjacks I believe Goljan mentions that the #1 cause of anemia in older adults is GI bleeds +6

flapjacks (colon cancer) +2

mark0polo Also, B-thalassemia major would present in childhood, not in a 75 year old man +3

sexymexican888 ALSO, #1 cause of Iron deficiency anemia in a older person -> colon cancer. HOWEVER, remember golijan ALSO SAID "GUYSSSS YOU THINK RBCs JUST TURN MICROCYTIC OVERNIGHT?! LIKE YOU HAVE IRON DEFICIENCY ANEMIA AND THEYRE ALL LIKE CHEERLEADERS AND GO 1,2,3 ->MICROCYTIC?! NO!! ITS NORMOCYTIC FIRST THEN MICROCYTIC EVENTUALLY" It was hilarious lol but yeah they dont really say how long he's been weak and had fatigue so its probably pretty recent, it takes a few days for the IDA to turn microcytic +1

sexymexican888 Also an adult male (not elderly) with IDA -> peptic ulcer disease +1

sexymexican888 ALSO IDA can be due to blood loss or dietary lack. Remember iron is VERY tightly regulated in the body and there's no real official way to get rid of it except bleeding (menstruation in females & sloughed of cells in the intestine that had ferritin stored) thats why male patients with hemochromatosis get HCC and all these horrible manifestations in their 40s cause getting rid of iron is actually hard unless you're underconsuming it or bleeding +

chaosawaits I also thought those were some large looking microcytic RBCs +1

chj7 Side note: CML should have high platelet counts (as most chronic myeloproliferative disorders). [FA 2020 P.433] +

amy Thrombocytopenia indicates CML acceleration +

neurotic999 I got caught up between GI blood loss and B12 def. The RBCs were clearly hypochromic but they also seemed large for some reason. Also the other cell in the picture (PMN?) I assumed was a hypersegmented neutrophil and so I drifted toward B12. +1

ali_hassan guys aplastic anemia has def. of all the cells; not the case here. CML i don't need to explain. B-thalassemia would present with target cells and simply have more manifestations than just weakness and fatigue and B12 would present with some neurologic symptoms like peripheral neuropathy. while knowing GI bleed is a common cause of bleeding in the elderly population, the answer was GI blood loss (i answered it correct through ruling out the rest) +

submitted by prostar(22), visit this page

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For the sake of completeness, this is paraneoplastic cerebellar degeneration due to breast cancer- Anti - Yo antibodies. (FA2019 Pg229)

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chj7 The question stem mentioned metastatic tumor, so I assume the metastatic lesion is directly compressing the cerebellum, and the cerebellar degeneration is not necessarily due to a paraneoplastic syndrome. +