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Recent comments (see more)

... madojo made a comment (step2ck_form6)
 +0  submitted by madojo(205)

Huntington Disease is a neurological disorder characterized by a classic triad of choreiform movement (in this case the bilateral writhing motions of the upper extremities), dementia/depression, and behavioural changes (aliens).

... madojo made a comment (step2ck_form6)
 +0  submitted by madojo(205)

Per UW, evaluation of fetal demise includes fetal autopsy, gross and microscopic examination of placenta, membranes, cord, and karyotype and genetic analysis. Evaluation of fetal demise on moms side includes kleihauer betke test for fetomaternal hemmorhage, antiphospholipid antibodies and coag studies.

... empem28 made a comment (nbme21)
 +0  submitted by empem28(1)

Nobody has answered this question through the lens of a learning objective quite yet so here's my 2 cents: Km is INCREASED bc this patient has an enzyme with an overall LOWER affinity (can be corrected to normal after an increase in substrate) which is characteristic of COMPETITIVE inhibition, which is why the line of the pt. is one of competitive inhibition on a LB plot

... epiglotitties made a comment (nbme20)
 +0  submitted by epiglotitties(27)

This isn't the scenario in this question, but I was wondering what would happen if you had told the parents the diagnosis and they didn't want their child to know?

... bubblegum21 made a comment (nbme24)
 +0  submitted by bubblegum21(1)

Alcohol withdrawal - - > increased catecholamines - - > increased insulin (via B2) - - > cellular uptake of K+ - - > hypokalemia

... drdoom made a comment (nbme25)
 +0  submitted by drdoom(1165)

This question might be tricky because the mutation of interest here is inherited from the dad side (paternal) but affects the mitochondria.

That is, the mutation is not a mutation of the mitochondrial DNA.

In their explanation, the NBME says, “Mitochondrial diseases are strictly inherited through the mother” but that is incorrect; it would be more correct for them to have said: Mitochondrial DNA mutations are strictly inherited through the mother.

In other words, the stem does not describe a "mitochondrial disease" in the way the NBME defines it.

Yes, mitochondria are affected but the mutation is in nuclear DNA that govern the maintenance of "healthy mitochondria". The mutation affects the function and operation of mitochondria but the mutation itself is in the nuclear DNA (which control something about the "quality" of mitochondria but what exactly is not yet understood).

This explains why dad and dad's brother show the same “proximal muscle weakness of the lower extremities”.

drdoom  Clarifying further: The disease of interest is better described as a "non-mitochondrial DNA–derived" mitochondrial myopathy. It's a mouthful, I know. Yes, mitochondria are affected but the mutation is in somatic (nuclear) genes that govern the maintenance/operation/function of "healthy mitochondria". This is why it is being inherited through the dad and yet manifests in mitochondrial dysfunction. +
... yogurt-dimple made a comment (nbme25)
 +0  submitted by yogurt-dimple(2)

Am I crazy, or does the question stem imply that this was inherited paternally?

raspberry-muffin  In this question sounds like inherited paternally , but this muscle biopsy confirmed Mitochondrial inheritance. Muscle biopsy: Immunohistochemistry typically shows ragged red fibers, which are caused by sub-sarcolemmal and inter-myofibrillar accumulation of defective mitochondria in muscles (mitochondria stain red). Probably Mother has the same condition too. +
yogurt-dimple  Gotcha. Yeah, the red ragged fibers tipped me off to mitochondrial myopathy, but because the stem implied paternal inheritance, I figured there was just another disease I had forgotten about that presents with them. +
drdoom  @raspberry-muffin I'm not convinced. It is highly unlikely the NBME would write this question and expect you to "assume" mom has condition without making any mention of mom. Plus, it is simply highly improbable that myopathy is present in both mom and dad lineage. That seems off to me. +
drdoom  @yogurt-dimple, I think this a key line in the explanation: “However, there are additional mutations that affect mitochondrial RNA translation, trafficking and incorporation of respiratory protein complexes, and maintenance of the inner mitochondrial membrane that can also lead to mitochondrial myopathy.” +
drdoom  Yes, they say, "Mitochondrial diseases are strictly inherited through the mother" but this is not a mitochondrial disease — this is a "non-mitochondrial–derived" mitochondrial myopathy; yes, mitochondria are affected but the mutation is in somatic (nuclear) genes that govern the maintenance of "healthy mitochondria". This is because the mutation affects the function/operation of mitochondria but the mutation itself is in the nuclear DNA (which control something about the "quality" of mitochondria but what exactly is not yet known). +
... shelbinator94 made a comment (nbme18)
 +0  submitted by shelbinator94(1)

Why couldn't this be branching enzyme impairment? They both cause cardiac symptoms (according to Amboss at least)

... merpaperple made a comment (step2ck_form8)
 +0  submitted by merpaperple(32)

Both histoplasmosis and blastomycosis are associated with living in Ohio and can cause pulmonary disease. Histoplasmosis is more associated with hilar lymphadenopathy and can cause cavitations (recall from Sketchy that it can resemble Tb) - another association to note with Histo is hepatosplenomegaly. Blastomycosis is uniquely associated with extra-pulmonary involvement in the bone, prostate, and skin

... athenathefirst made a comment (free120)
 +0  submitted by athenathefirst(9)

I got this right because I thought of the cavernous sinus which has CN 3, CN4, CN V1 & V2. Out of all of all the options V2 is the only one that controls upper lip. For option C, pupillary reflex is controlled by CN 2 and 3, and if there is a fracture to the orbital floor the closest to the sinuses to be injured is CN5 (V2). Idk I could be wrong but if you guys agree let me know pls.

athenathefirst  Page 530 FA 2019 (Cavernous Sinus) +
... drdoom made a comment (free120)
 +2  submitted by drdoom(1165)

Mom and her daughter have the same sequence of FBN1. What is special is that compared to a “normal” (wild-type) FBN1, mom and daughter have one little tiny mutation in their sequence: a single nucleotide (A,T,G,C) that is different than most other folks.

(Interestingly, this nucleotide difference does not alter the amino acid encoded by this part of the gene; that makes Choice D (change the folding of the protein) and Choice E (truncated protein) very unlikely.)

Back to our question. Even though mom and daughter have the same mutation, mom shows no signs of Marfan syndrome; this eliminates Choice A (disease-causing mutation in the patient and her mother).

You might think this is an example of variable expressivity (not an option but a good guess), and it might be.

In the stem they say:

The same nucleotide change is found in 15 of 200 individuals without Marfan syndrome.

Interesting! This means that in a “normal” sample of people (who have no signs of Marfan), 15 out of 200 still have this mutation.

(They don't say anything about how many Marfan people have the mutation but we don't need that information to answer the question.)

When a gene can be found in multiple “versions”, we call the gene polymorphic (literally, many-shapes or many-forms).

So the best response is Choice B (polymorphism).

... notpennysboat made a comment (nbme18)
 +0  submitted by notpennysboat(2)

The graft is placed below the renal arteries and above the aortic bifurcation, which contains the IMA. IMA supplies the hindgut (distal 1/3 of transverse colon to to upper portion of the rectum).

FA 2019 pg. 357

... xxmixmastersuperionxx made a comment (nbme22)
 +0  submitted by xxmixmastersuperionxx(1)

So are we just not going to talk about how an NBME question writer just sketched this real quick and put it on a question

... dennydrash made a comment (nbme23)
 +0  submitted by dennydrash(1)

I always remember locus caeruleus as Marcus Aurelius (if anyone has seen the movie Gladiator) its about action and being hopped on up Nor epi would recommend

... dennydrash made a comment (nbme23)
 +0  submitted by dennydrash(1)

My two Leishmania questions were literally back to back lol

... syloruspincter made a comment (nbme21)
 +0  submitted by syloruspincter(1)

I don't believe this question is addressing hereditary angioedema (which is definitely a manifestation of C1-INH deficiency), but rather just overactive complement (since its inhibitor is deficient). Remember that byproducts of the complement cascade include C3a, C4a, and C5a, which are all anaphylatoxins. "Episodes of cutaneous urticaria and occasional episodes of laryngospasm" describes an allergic reaction that can be mediated by the anaphylatoxins produced in the cascade. The other answer choices would lead to decreased complement activity and therefore release of fewer anaphylatoxins.

... kms123 made a comment (free120)
 +0  submitted by kms123(2)

can someone explain why it's not degranulation of eosinophils?

fhegedus  Eosinophils (FA 2020 page 408) are involved in type I hypersensitivity reactions (asthma, allergy, analphylaxis), parasitic infections and other pathologies. They are not involved in edema formation. I hope this helps! :) +
fhegedus  Also, the patient in the question got a laceration, which probably led to a bacterial infection; so neutrophils would be predominant, not eosinophils. +
... kms123 made a comment (nbme22)
 +1  submitted by kms123(2)

How would we rule out antithrombin deficiency?

... pygmymarmoset made a comment (nbme24)
 +0  submitted by pygmymarmoset(1)

So I thought about the "tombstone" picture on p.207 of Pathoma where the desmosomes are defective. The cells in the basal layer stay attached to the basement membrane, but the cells above get disconnected. So that made me think of breaking the connection between cells in the basal layer and cells above the basal layer (suprabasal).

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Help your fellow humans! (see more)

epiglotitties asks (nbme20):
This isn't the scenario in this question, but I was wondering what would happen if you had told the parents the diagnosis and they didn't want their child to know? help answer!
yogurt-dimple asks (nbme25):
Am I crazy, or does the question stem imply that this was inherited paternally? help answer!
raspberry-muffin  In this question sounds like inherited paternally , but this muscle biopsy confirmed Mitochondrial inheritance. Muscle biopsy: Immunohistochemistry typically shows ragged red fibers, which are caused by sub-sarcolemmal and inter-myofibrillar accumulation of defective mitochondria in muscles (mitochondria stain red). Probably Mother has the same condition too. +
yogurt-dimple  Gotcha. Yeah, the red ragged fibers tipped me off to mitochondrial myopathy, but because the stem implied paternal inheritance, I figured there was just another disease I had forgotten about that presents with them. +
drdoom  @raspberry-muffin I'm not convinced. It is highly unlikely the NBME would write this question and expect you to "assume" mom has condition without making any mention of mom. Plus, it is simply highly improbable that myopathy is present in both mom and dad lineage. That seems off to me. +
drdoom  @yogurt-dimple, I think this a key line in the explanation: “However, there are additional mutations that affect mitochondrial RNA translation, trafficking and incorporation of respiratory protein complexes, and maintenance of the inner mitochondrial membrane that can also lead to mitochondrial myopathy.” +
drdoom  Yes, they say, "Mitochondrial diseases are strictly inherited through the mother" but this is not a mitochondrial disease — this is a "non-mitochondrial–derived" mitochondrial myopathy; yes, mitochondria are affected but the mutation is in somatic (nuclear) genes that govern the maintenance of "healthy mitochondria". This is because the mutation affects the function/operation of mitochondria but the mutation itself is in the nuclear DNA (which control something about the "quality" of mitochondria but what exactly is not yet known). +
shelbinator94 asks (nbme18):
Why couldn't this be branching enzyme impairment? They both cause cardiac symptoms (according to Amboss at least) help answer!
kms123 asks (free120):
can someone explain why it's not degranulation of eosinophils? help answer!
fhegedus  Eosinophils (FA 2020 page 408) are involved in type I hypersensitivity reactions (asthma, allergy, analphylaxis), parasitic infections and other pathologies. They are not involved in edema formation. I hope this helps! :) +
fhegedus  Also, the patient in the question got a laceration, which probably led to a bacterial infection; so neutrophils would be predominant, not eosinophils. +
kms123 asks (nbme22):
How would we rule out antithrombin deficiency? help answer!
sd22  PT, PRT, and TT normal in antithrombin deficiency. FA ‘20 pg. 428 +
sd22  PTT* lol autocorrect clearly hasn’t been studying +
calvin_and_hobbes asks (nbme21):
This Q stem was confusing to me because I thought pain>>itch for shingles. Any thoughts? help answer!
calvin_and_hobbes asks (nbme21):
"In addition to slightly decreased platelet count..." — why are plts slightly low in EBV infection/mono? help answer!
empem28 asks (nbme22):
totally buy the answer of K+ being increased, but can somebody explain why her extreme dehydration (decreased skin turgor, excess urine output) wouldn't lead to an increase in serum [Na+]? help answer!
sd22 asks (nbme21):
Can anyone help explain what the other options would entail? help answer!
marcspoop asks (nbme20):
Anyone else jump to phenylephrine as a drug that would clear the sinus congestion and also happens to cause constipation? Just me... cool help answer!
ekraymer asks (nbme22):
Was it wrong to see blood tinged sputum, and automatically assume its cancer? since none of the others would have caused blood tinged sputum? help answer!
calvin_and_hobbes asks (nbme20):
Due to its pink staining, I thought B was smooth muscle surrounding the corpus cavernosum. But I suppose that the cells composing the CC are contractile by themselves? And my assumption would make the penis a giant muscle — which it most certainly is not... help answer!
calvin_and_hobbes asks (nbme20):
Why is the T normal in this patient? I would have predicted underlying infection — ie, fever — before even "early" septic shock. I selected septic shock purely for the intractable low SVR despite fluids but want to understand more about the absence of fever... Thanks! help answer!
drdoom  Elderly (and immunocompromised, generally) do not mount robust fever responses to bacteria and other microorganisms; in elderly, this probably has to do with “declines” of the innate immune system (your macrophages, dendritic cells, monocytes, &c., just don't function as well as they used to). In other words, if you (1) wiped out someone's immune system and then (2) injected bacteria into their bloodstream, you wouldn't observe any fever either. The presence of a “typical” (normal) fever in an elderly or immunocompromised patient can be a super concerning sign: they might have a raging infection on the inside. +
drdoom  ^from the article: “Absent or blunted fever response in the elderly. There is ample evidence that a blunted fever response to a serious bacterial, viral, or fungal infection suggests a poorer prognosis than does a robust fever response [13]. In addition, there is a substantial body of data, mostly from animal models, that fever—through its effects on immune function—may be an important host defense mechanism [14]. Roughly 20%–30% of elderly persons with serious bacterial or viral infections will present with a blunted or entirely absent fever response [2,3,15].” +
iwannabedonewiththis asks (nbme21):
just as a general question, would there be low levels of 1 25-(OH)2 ? help answer!
sd22  Yes, kidney has 1-alpha hydroxylase which converts 25-HCC to 1,25-HCC. CKD -> low 1-a-OHase activity -> low 1,25-HCC +
peachespeaches asks (nbme21):
I agree that Serum K decrease is the better answer, but wouldn't Urine K also decrease once blood sugar goes down with insulin treatment (i.e. osmotic diuresis would lessen)? help answer!
freemanpeng asks (nbme24):
No one talks about AR? That's much more unlikely in this case than XR help answer!
epiglotitties asks (nbme18):
I understand that feedback inhibition isn't working and is why ACTH is undetectable/low (and why there is no change after dexamethasone), but wouldn't cortisol levels increase after dexamethasone? Or does dexamethasone not count as cortisol when quantifying serum levels? pls help help answer!
misseili  This patient has Cushing Syndrome and as you stated their feedback inhibition is hampered. Low-dose dexamethasone causes a decrease in cortisol in normal individuals but not in those with Cushing Syndrome, only high dose dexamethasone causes a decrease in cortisol with Cushing Syndrome. Add'l info: In ectopic ACTH (ie Small cell lung cancer) high dose dexamethasone leads to no change in cortisol. Pathoma 2020 Pg 171 +2
freemanpeng asks (free120):
The key is when her legs up, Bp normal and symptoms free. In contast, When standing up(running), low Bp and syncope. And Low volume is surly the MMC. It's just so weird. "retrospective posture change"?? help answer!
madamestep asks (nbme24):
Anyone else get this right because they get them so often from absolutely uncontrolled stress? help answer!
bfinard1 asks (nbme20):
Can someone explain why cardiac output is high in septic shock? help answer!
drdoom  Bacteria and bacterial components (like LPS) in circulation trigger massive release of cytokines (Interleukin-1, Interleukin-6 and TNFa), resulting vasodilation. Heart rate increases to maintain decent BP. +1
bfinard1  Is stroke volume not affected by that massive vasodilation? I would think if venous system is vasodilated then you'd have reduced EDV from reduced blood flow to heart +
zedora  Both of you are correct. In septic shock there is a massive vasodilation. In order to compensate for the reduced blood pressure, there is an increased heart rate. Now, keeping this in mind, what is the CO formula? CO = HR x SV Right? Lets say under normal conditions HR is 60 & Stroke volume is 50. Your cardiac output = 60 x 50 = 3000. Now in septic shock, your heart rate is massivly increased but your stroke volume is decreased minimally. So lets plug in the numbers. Lets say, under septic shock, HR = 150 & stroke volume is now 30. The cardiac output is now gonna be = 150 x 30 = 4500, hence your CO is increased. In Septic Shock, the heart rate is massively increased compared to the amount of SV decreased. +
drdoom  @bfinard1 By vasodilation, I almost exclusively mean arterial vasodilation. When it comes to CV, I always work backward from “first principles”, and in my view the first principle of the CV system is, “Maintain pressures to maintain good flow.” All other accommodations of the CV system (changes in inotropy[strength], chronotropy[time], vasoconstriction and vasodilation) are in *service* to maintaining flows. Without good flows, you get the thing human tissues like the least: not lack of oxygen but accumulation of CO2 (and the acidity that goes with it). +
drdoom  So, all that was a long-winded way of saying that Cardiac Output will remain high when the body is producing higher-than-desired levels of CO2 (when organs and the immune system have gone into overdrive to respond to a threat or to address decompensation in some other part of the system); the plummeting of Cardiac Output heralds the beginning of the end. It signifies that the stresses being imposed on the body exceed the capabilities of the system. +
duckhunter324 asks (nbme18):
What would a rupture of the fallopian tube look like then? Compared to normal spillage.. help answer!
epiglotitties  I was wondering the same thing +
sunnyside asks (nbme20):
Can anyone justify why they did not describe an increased MCHC? FA 2019 says spherocytosis has high MCHC, and they did not even have it on the upper end of normal. help answer!
peterngo1994 asks (nbme22):
The thing that threw me of was the 74% neutrophil count. Does anyone have an explanation for this? help answer!
drdoom  Neutrophil count is different than neutrophil percentage (%). Percentages can be influenced by changes in volume, e.g., if the patient is dehydrated, percentage by volume can be skewed. +
madamestep asks (nbme23):
Remember that medullary carcinoma of the thyroid is medullary. So it's between the follicles. What's between the follicles in the thyroid? C cells that secrete calcitonin. help answer!

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