The maneuver described is known as Finkelstein's test, which is meant to be specific for DeQuervain tenosynovitis.

Remember the tip that you can use clindamycin for anaerobes above the diaphragm, and metronidazole for below.

From UpToDate: For patients with SCLC, systemic chemotherapy is an important component of treatment, because SCLC is disseminated at presentation in almost all patients. For those with limited-stage disease, thoracic radiation therapy is used in combination with chemotherapy. Prophylactic cranial irradiation is often used to decrease the incidence of brain metastases and prolong survival. Prophylactic cranial irradiation and thoracic radiation may also be beneficial in those with a complete or partial response to initial systemic chemotherapy.

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).

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.

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

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

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”.

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

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.