For anyone looking for more info:
Page 147 of Pathoma
3 types of Sex cord tumors: Granulosa-theca (follicle cells), Sertoli-Leydig, and fibroma.
G-T tumor: estrogen excess
S-L tumor: androgen excess
Fibroma: benign, fibroblasts, cause meig's syndrome
I think there's something that hasn't been mentioned and people are over looking:
Patient is presenting with CRC + anemia which most commonly occurs with RIGHT sided cancer. And how does that cancer develop? Micro-satellite instability (vs left sided = obstruction and polyp-adenoma sequence).
Misat instab mostly commonly occurs in HNPCC due to mismatch repair defect.
Thus, even though there's a type in the gene, or even if you don't know the gene, there's enough info to figure out it's HNPCC.
FAP doesn't match the picture, and is a pylop-adenoma sequence cancer. Li-fraumeni is defect in p53 (which is the last stage of pylop-adenoma sequence so I assume it follows that too?).
The constipation is kinda tricky because you'd think obstruction but the big key here is ANEMIA due to CHRONIC BLEEDING.
What is there that rules out deltoid? overhead abduction is >15' so shouldn't that point more towards deltoid?
https://ars.els-cdn.com/content/image/3-s2.0-B9780123821843000106-f10-04-9780123821843.jpg
this picture will help. The US we were given is somewhere between 3rd and 4th picture.
From what I understand, the whole thing is the gestational sac, including the chorion and everything inside. From there, between the chorion and the amnion/yolk sac is the chorionic cavity.
then you have the amniotic cavity that engulfs the embryo and Yolk sac around the 3rd week. then AC expands and takes up full volume of Chorionic cavity around 9th week.
the yolk stalk is the only remaining thing by 7th week which eventually becomes the umbilical cord. which connects to the chorion/by then the placenta.
So, pt is 8 weeks pregnant, thus AC has pretty much fully expanded, and the yolk sac is tiny with a small sliver of the yolk stalk visible connecting fetus and sac.
i figured it was cocaine or amphetamines so I picked plasma free metanephrines. Why is this not correct?
According to this:
Sympathomimetics: Ephedrine, Pseudoephedrine (Sudafed), Amphetamines, Albuterol (Proventil) can cause positive results in serum metanephrines.
https://www.ncbi.nlm.nih.gov/books/NBK278970/table/pheochromocytoma.table4drug/
Ugh, I saw Low BP and thought gallstone pancreatitis w/ hemorrhage so I picked ecchymoses/Cullen's sign.
Everyone asking why not PPIs?
if you give NSAIDs which decrease PGs so you get GERD, the simplest way to fix it is to bring those PGs back, so misoprostol.
Just simply -PGs --> +PGs
TIL cytosine arabinoside is another name for cytarabine (pyrimidine analog)
So the xray was similar to this
this is a large volume gas emboli (which you would expect from a diver due to nitrogen precipitation). You can kinda see it in the xray overlapping the heart shadow/left diaphragm.
This is a giant pocket of air, basically so I just figured it would be hyper-resonant due to hyperinflation.
IPEX: FOXP3 deficiency --> Regulatory T cell dysfunc --> autoimmunity
Enteropathy(diarrhea)
Endocrinopathy
Nail dystrophy
dermatitis (eczematous)
+/- other autoimmune conditions
associated with diabetes in male infants
Page 102 in FA19
Cerebellar Vermis lesions: Truncal Ataxia (wide based/drunk sailor gaite) + Nystagmus
Cerebellar Hemisphere lesion: Intention tremor, Limb Ataxia, Loss of balance --> fall to IPSILATERAL side.
Vermis = central --> affects central body
hemispheres = lateral --> affects limbs
pg 499 of FA19
LD4 = vasoconstriction + bronchoconstriction - does it have a role in prinzmetal? I picked this thinking vasospasm due to atherosclerosis.
PGE2 = pain + fever. so i suppose because it's ischemia and not an inflammation, that's not the answer?
TXA2 = PLT aggregation --> thrombus --> ischemia? But i figured that would be more relevant to a stroke or a PE. But I guess TXA2 does play a role in atherosclerosis so it's the biggest contributor.
too real rn...
To me: this seemed more straightforward. You'd want to follow up and check Gastrin levels on a patient who previously had 4x normal.
Which type of cell we r going to find in blisters?, neutrophils?
The kid has gynecomastia due to puberty (excess testosterone โ estrogen) This goes away naturally (apparently in 12 to 18 months)
I think you don't have to do blood tests because he has normal sexual development for his age and there are no other signs?
Notice drop of O2 saturation from LA (95%) to LV (70%) & equal O2 saturation between LV (70%) & RV (70%) --> VSD is present
Notice the pressure of the RV (120/6) โ Normal RV pressure is 25/5 which indicates increased pressure because of the increased volume of blood coming from the LV through the VSD
Grade 4 murmur is a palpable thrill most likely due to RVH from the overloaded work
RBC casts===> glomerulonephritis the only option there.
Membranous nephropathy and minimal change disease can be easily ruled out as they are nephrotic syndromes. Tubulointerstitial nephritis (aka acute interstitial nephritis) can be ruled out as it causes WBC casts not RBC as seen in this question. Papillary necrosis - either has no casts or it might show WBC casts but not RBC because the problem is not in the glomeruli.
table of nomenclature on page 582 explains that proliferative just means hyper cellular glomeruli. Given the patients history of sore throat two weeks ago, now presenting with Nephritic Syndrome with RBC casts, proliferative glomerulonephritis is the only reasonable answer.
Histamine plays a major role in the cardinal signs of inflammation. It helps mediate vasodilation and vascular permeability (via endothelial cell contraction). These two functions are already contrary to A, B, C, and D. By increasing fluid in the interstitial space, you can reason that there will be increased lymph flow.
Can someone explain why the correct answer for the question here is conjugation but canโt be transposition?
Person has Lambert-Eaton syndrome (hx of lung cancer, and muscle activity that is better with use.
Presynaptic Ca2+ antibodies prevent the release of AcH presynaptically because the antibodies prevent the depolarization within the cell and prevents synaptic vessels of ACh from leaving.
Complement is important for removing immune complexes, so patients with complement deficiencies *(c1-c4) are more likely to develop SLE. C1q is a better answer than than MBL (D) b/c the MBL pathway is triggered by bacteria.
The rhombencephalon would be on the actual fetus so just get rid of (D). The "black hole" that the fetus is floating in is the gestational sac so get rid of (C). Now I am no ultrasound expert but I know that the amniotic cavity eventually expands to fuse with the chorion thereby eliminating the chorionic cavity (B). In terms of where the amniotic cavity is shown in this image, I am not sure, so maybe someone can help but this leaves the yolk sac which typically appears within the gestational sac around 5.5 weeks.
So for Candida we can use
Azoles (fluconazole) (inhibit CYP450 demethylation)
Amphotercin B (pore formation in fungal cell membrane)
Caspofungin (prevent crosslinking of beta glucans in cell wall)
or Nysatin for oral or esophageal cases (pore formation)
This question is saying that she is taking an ORAL drug to treat candida vaginitis.
Amphotercin is IV
Caspofungin is also IV
so we're left with azoles
Azoles inhibit synthesis of ergosterol by inhibiting CYP 450 that converts lanosterol to ergosterol.
so I was stuck on this because his BUN /creatinine ratio led me to think he had an intrinsic renal dysfunction. And a PGI2 inhibition would lead to a pre-renal azotemia, where the BUN/ creatinine ratio would be more than 20. I know that NSAIDs inhibit PGIS. But how are you supposed to cross out induction of distal tubular acidosis?
so I was stuck on this because his BUN /creatinine ratio led me to think he had an intrinsic renal dysfunction. And a PGI2 inhibition would lead to a pre-renal azotemia, where the BUN/ creatinine ratio would be more than 20. I know that NSAIDs inhibit PGIS. But how are you supposed to cross out induction of distal tubular acidosis?
Lesson learned -- the NBME doesn't play tricks. If it looks right, it is right.
Referring to NRTIs and NNRTIs as mainstay of treatment
Mainstay: efavirenz (NNRTI), tenofovir (NRTI), and emtricitabine (NRTI)
can somebody explain how energy production by glycolysis increased, since aerobic glycolysis produce 32 net ATP,compare to 2 net ATP through anaerobic glycolysis ?
can somebody explain how energy production by glycolysis increased, since aerobic glycolysis produce 32 net ATP,compare to 2 net ATP through anaerobic glycolysis ?
At first I was thinking aha! Child abuse! But I guess wormian bones are more suggestive of OI, although the no family hx part was rather bleh.
Marfanoid habitus + Mucosal neuromas + Neck mass = MEN 2B (PMM) Pheo, Medullary thyroid CA (Calcitonin secreting), mucosal neuromas
Chronic Myelogenous Leukemia vs Leukemoid Reaction has a few differentiating features:
Basophilia can be seen in Myeloproliferative diseases such as CML. However, they are not seen in Leukemoid Reactions.
Leukocyte Alkaline Phosphatase (LAP) is often elevated in Leukemoid Reactions. But it will be decreased in CML because Abnormal cells don't make the normal enzyme.
Dohle Bodies are characteristic of Leukemoid Reactions. Not seen in CML.
As vshummy pointed out FA-2019 pg 424 has all this information as well as UWorld problem...I just can't seem to find the Q.ID. Maybe someone else can tag-team in.
Pathoma says there are 3 things that differentiate leukemoid from CML: + Leukocyte alkaline phosphatase (only in leukemoid) + Basophils (only in CML) + t(9;22) translocation (only in CML)
Anyone know how to rule out small intestine on this one? I thought the omentum played a role in healing in the abdomen, but clearly I'm missing something here.
a)abduction: supraspinatus-deltoid-triceps-serratus anterior
b)adduction: subscapularis-pectoralis major-lattisimus dorsi- teres major
c)extension=horizontal abduction; post. deltoid, infraspinatus, teres minor
d)internal rotation: subscapularis
for isolated work out, d is better.
TEN REPS.
The subscapularis muscle is very important for the Internal rotation of the humerus. The internal rotation supports the upper arm during abduction and adduction.
There are some band exercises that can help you strength the Subscapularis muscle... 1. Internal Rotation - uses medial internal rotation 2. External Rotation - uses lateral external rotation 3. Front Row - You have you hand up in front of you and with your arm extended pull back the band. 4. Side Row - You're side to the band with your hand facing the hip, pull down toward your body. (ADDUCTION)
THIS IS NOT A FAIR QUESTION NBME!!!
The squamo-columnar junction situated at the external os of the cervix is one site which is highly vulnerable to metaplasia or neoplastic transformation under adverse circumstances, such as chronic infection or trauma. Usually, squamous metaplasia where squamous cells replace the columnar cells of the endocervical canal, is observed. However, in less common situations, particularly after trauma, tubal metaplasia may develop, replacing endocervical nonciliated columnar epithelial cells by โฒciliated columnarโฒ cells, similar to those seen in fallopian tubes. Tubal metaplasia is mostly seen in the upper part of the endocervical canal near the internal os, but may also be found in the endocervical glands or the lower endocervical canal. http://medind.nic.in/jbb/t08/i1/jbbt08i1p33.htm
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
To add to what everyone else has said, this slide is pretty good: https://images.slideplayer.com/32/10012453/slides/slide_2.jpg
the prompt says RPF and GFR are unchanged, thus RBF is also unchanged, to do that, the renal arteries would have to decrease their resistance.
However, as shown on page 571 of FA19, a constriction or dilation of efferent would change FF which means RPF and GFR aren't changing equally - this is ruled out by the prompt saying they're unchanged.
Leaves us with a decrease in afferent resistance.