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 +0  (nbme24#39)

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.


 +1  (nbme24#26)

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

  • Precocious puberty (prepub)
  • reproductive age: menorrhagia, metrorhagia
  • Postmeno: endometrial hyperplasia/uterine bleeding
  • minimal risk of metastasis

S-L tumor: androgen excess

  • hirsutism
  • virilization
  • reinke crystals
  • tubules and leydig cells between tubes

Fibroma: benign, fibroblasts, cause meig's syndrome

  • pleural effusion
  • ascites
  • resolves with removal of tumor

 +0  (nbme24#47)

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.


 +1  (nbme23#17)

What is there that rules out deltoid? overhead abduction is >15' so shouldn't that point more towards deltoid?

baja_blast  Deltoid only does abduction from 15 to 90 degrees. So not overhead.
donttrustmyanswers  With that logic, supraspinatus only does abduction form 0-15

 +0  (nbme23#1)

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.


 +0  (nbme23#19)

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/

drzed  Because a toxicology screen would both answer your question (e.g. that it could be amphetamine abuse) and would also pick up any other drugs that the patient might have been using. So even though the pre-test probability is high for amphetamine use, lets say it was something else, well then the tox screen would pick that up as well. Or lets say that it was simultaneous use of two drugs, same scenario.

 +0  (nbme23#48)

Ugh, I saw Low BP and thought gallstone pancreatitis w/ hemorrhage so I picked ecchymoses/Cullen's sign.


 +5  (nbme23#33)

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

hungrybox  This is the best explanation IMO Also makes me feel like an absolute idiot

 +1  (nbme23#29)

TIL cytosine arabinoside is another name for cytarabine (pyrimidine analog)


 +0  (nbme23#21)

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.


 +1  (nbme23#19)

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


 +1  (nbme23#43)

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


 -1  (nbme23#1)

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.





Subcomments ...

submitted by staghorn(0),

too real rn...

thotcandy  right? nbme predicting the future +  


submitted by dentist(18),

To me: this seemed more straightforward. You'd want to follow up and check Gastrin levels on a patient who previously had 4x normal.

thotcandy  He could have 4x the normal because of current PPI use. the point was that you'd get him off, wait for it to normalize, then check again to see if it's due to neoplasm or PPIs +  


submitted by cr(1),

Which type of cell we r going to find in blisters?, neutrophils?

thotcandy  acute inflammation so i assume neutrophils to be replaced by macrophages -> granulation tissue -> fibrosis/scar formation +  


submitted by gonyyong(53),

The kid has gynecomastia due to puberty (excess testosterone → 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?

osler_weber_rendu  How does telling an "embarrassed kid" that he will have big tits for 12-18 months help?! +6  
howdywhat  my exact thought, telling him that it will last for somewhere around a year and a half doesnt seem so reassuring +1  
suckitnbme  I thought it was reassuring in that the kid is being told this isn't permanent as well as that this isn't something serious. It's important to inform him about the prognosis. +2  
thotcandy  "don't worry your gynecomastia isn't permanent, but the mental scars from the bullying you will receive in HS definitely will be :) good luck!" +  


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) – 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

thotcandy  classic eisenmenger syndrome +  


submitted by diabetes(11),

RBC casts===> glomerulonephritis the only option there.

thotcandy  I saw BUN/cr > 20 and instantly though prerenal --> ischemic pap necrosis due to analgesics. Are nephritic syndromes just excluded from that whole thing? FA says BUN and Cr are increased for nephritic syndromes but does the ratio just not matter? +  


submitted by usmile1(33),

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.

medguru2295  This was my precise login. I wound up getting it by elimination. But, didn't like that answer as its uncommon in small children and the child seemingly had no risk factors. +  
thotcandy  @medguru2295 FA says it's most commonly seen in children and it's selflimited vs adults is rare and can lead to renal insuff +  


submitted by fahmed14(18),

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.

youssefa  If more transudates are leaking into the interstitium wont this dilute the interstitial proteins and cause a decrease in oncotic pressure and increase in interstitial hydrostatic pressure? +4  
titanesxvi  @youssefa I think because it is an exudate from increased permeability of venules, the oncotic pressure in the interstitium is not going to decrease +2  
thotcandy  @youssefa transudate is like pulmonary edema due to CHF, no proteins, just fluid congestion and leaking out. That would decrease interstitial oncotic pressure because it has very little protein. Exudate due to inflammation/histamine has a high amount of protein (due to inc permeability) so the IOP doesn't change. +  


submitted by medstudied(2),

Can someone explain why the correct answer for the question here is conjugation but can’t be transposition?

catacholamine16  Transposition is when a segment of DNA (in this case, coding for resistance) jumps onto a plasmid within the same bacterial cell. That plasmid might then transfer to another nearby bacterial cell via conjugation. Transposition is happening WITHIN the bacterium. Conjugation is how that resistance gene gets transferred. +5  
lsmarshall  Also, E. coli is the classic example of a bug tat uses conjugation. ^but explanation above is correct^ +2  
seagull  I think he might have did what I did. I got Transformation mixed up with transposition. FML +2  
luciana  I still can't understand why it can't be transduction. Is it just because of bacterial types? +  
thotcandy  @luciana Yes, I believe so. You have to remember which bacteria have a conjugation pilus - E. coli is the most popular one because of its F sex factor (remember the F+ x F0 thing in FA?) +  


submitted by step420(26),

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.

thotcandy  ugh, I saw Ca2+ and stopped thinking. +2  
paperbackwriter  @thotcandy Same here :( +  


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.

myoclonictonicbionic  Thats the reason I put MBL, because the question mentioned that it got worse when she went to the beach so I was thinking some sort of contact with bacteria may have exacerbated her immune system. +  
thotcandy  @myoclonictonicbionic i think that's just the typical SLE photosensitive malar/butterfly rash +  


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.

kateinwonderland  At the end of the fourth week, the yolk sac presents the appearance of a small pear-shaped opening (traditionally called the umbilical vesicle), into the digestive tube by a long narrow tube, the vitelline duct. (Wiki) +3  
tallerthanmymom  But why does it look completely detached from the fetus? I eliminated yolk sac first because of this +  
makinallkindzofgainz  If you look reeeeeeeally closely, you'll see some signal between the yolk sac and the baby. Although you can't see the entire connection, they are connected. +1  
thotcandy  Pt is roughly 8 weeks pregnant so and typically by 9th week, Amniotic cavity has expended to fill entire volume of Gestational sac. So the entire black part around the fetus is GS/AC. +1  


submitted by yotsubato(520),

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.

qball  Nystatin does treat vaginal candidiasis but is TOPICAL. +  
thotcandy  Nystatin is NOT for esophageal candidiasis, Swish and spit, not swallow. +1  
staghorn  Me - picks Metronidazole -_- +  
alexxxx30  @thotcandy...actually you can swish and swallow nystatin for esophageal infections (per Sketchy micro candida sketch) +  
turtlepenlight  I have seen that on the wards so I hope it works! +  


submitted by brise(22),

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?

purdude  You can cross out Distal RTA because the urine pH is 5. In Distal RTA, urine pH becomes greater than 5.5 because a-IC cells can't secrete H+ +  
thotcandy  pH > 5.5 is only true for Type I RTA. Type 2 RTA is proximal so that wouldn't be considered anyways. Type 4, however, urine pH would be < 5.5 and can be caused by NSAIDs, so how do we eliminate that? +  
thotcandy  pH > 5.5 is only true for Type I RTA. Type 2 RTA is proximal so that wouldn't be considered anyways. Type 4, however, urine pH would be < 5.5 and can be caused by NSAIDs, so how do we eliminate that? +  


submitted by brise(22),

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?

purdude  You can cross out Distal RTA because the urine pH is 5. In Distal RTA, urine pH becomes greater than 5.5 because a-IC cells can't secrete H+ +  
thotcandy  pH > 5.5 is only true for Type I RTA. Type 2 RTA is proximal so that wouldn't be considered anyways. Type 4, however, urine pH would be < 5.5 and can be caused by NSAIDs, so how do we eliminate that? +  
thotcandy  pH > 5.5 is only true for Type I RTA. Type 2 RTA is proximal so that wouldn't be considered anyways. Type 4, however, urine pH would be < 5.5 and can be caused by NSAIDs, so how do we eliminate that? +  


submitted by d_holles(79),

Lesson learned -- the NBME doesn't play tricks. If it looks right, it is right.

thotcandy  but also when it looks wrong it's right, or when it looks right it's wrong, or when it looks wrong it's wrong. you never know with NBME :) +  


submitted by gh889(55),

Referring to NRTIs and NNRTIs as mainstay of treatment

Mainstay: efavirenz (NNRTI), tenofovir (NRTI), and emtricitabine (NRTI)

ususmle  I guess he is asking about integrate,,,,, where his should be integrated into host dna to get replicated .. triple therapy includes. 2drugs NRTIs and other one is integrate +  
whoissaad  @ususmle NRTIs would still inhibit DNA synthesis since they mess with the reverse transcriptase which is needed to make viral DNA. +2  
thotcandy  @ususmle HIV triple therapy is 2 NRTIs/NNRTIs + 1 protease inhibitor. Plus, if her CD4+ cunt is already 60/mm, that shit is well integrated in her CD4 cells already, right? +1  


submitted by diabetes(11),

can somebody explain how energy production by glycolysis increased, since aerobic glycolysis produce 32 net ATP,compare to 2 net ATP through anaerobic glycolysis ?

diabetes  i think the stem should be "energy production by an anaerobic glycolysis " +1  
blueberrymuffinbabey  yeah that's the bit that tripped me up too. i get that there would be increased glycolysis in general to compensate for lack of TCA function but...the fact that it says "energy production by glycolysis" is kind of misleading/confusing. +  
thotcandy  technically, glycolysis is the reaction that happens in the cytosol that generates pyruvate and 2 net ATP. after that it's TCA and Oxidative phosphorylation, which occur in the mitochondria. By definition, glycolysis is anaerobic - which is why they hammer the fact that RBC undergo glycolysis only into our heads. +  
thotcandy  technically, glycolysis is the reaction that happens in the cytosol that generates pyruvate and 2 net ATP. after that it's TCA and Oxidative phosphorylation, which occur in the mitochondria. By definition, glycolysis is anaerobic - which is why they hammer the fact that RBC undergo glycolysis only into our heads. +  
targetmle  i got it wrong because of this as i thought ATP will be decreased in anaerbic glycolysis, but proabably it was mainly 'glycolysis' is increased +  


submitted by diabetes(11),

can somebody explain how energy production by glycolysis increased, since aerobic glycolysis produce 32 net ATP,compare to 2 net ATP through anaerobic glycolysis ?

diabetes  i think the stem should be "energy production by an anaerobic glycolysis " +1  
blueberrymuffinbabey  yeah that's the bit that tripped me up too. i get that there would be increased glycolysis in general to compensate for lack of TCA function but...the fact that it says "energy production by glycolysis" is kind of misleading/confusing. +  
thotcandy  technically, glycolysis is the reaction that happens in the cytosol that generates pyruvate and 2 net ATP. after that it's TCA and Oxidative phosphorylation, which occur in the mitochondria. By definition, glycolysis is anaerobic - which is why they hammer the fact that RBC undergo glycolysis only into our heads. +  
thotcandy  technically, glycolysis is the reaction that happens in the cytosol that generates pyruvate and 2 net ATP. after that it's TCA and Oxidative phosphorylation, which occur in the mitochondria. By definition, glycolysis is anaerobic - which is why they hammer the fact that RBC undergo glycolysis only into our heads. +  
targetmle  i got it wrong because of this as i thought ATP will be decreased in anaerbic glycolysis, but proabably it was mainly 'glycolysis' is increased +  


submitted by nukie404(6),

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.

thotcandy  Literally had it on OI until I saw no family hx... Isn't it AUTOSOMAL DOMINANT? +1  


submitted by mousie(126),

Marfanoid habitus + Mucosal neuromas + Neck mass = MEN 2B (PMM) Pheo, Medullary thyroid CA (Calcitonin secreting), mucosal neuromas

thotcandy  I knew it was MEN2B but forgot medullary ca of Thyroid is parafollicular/c cells which means Calcitonin, not T3/T4 Other answers: AntiThyroglobulin: Hashimoto's (or other thyroiditis) Dexamethasone suppression test: positive/suppressed in pituitary adenoma (acth secreting), negative/unresponsive in Adrenal hyperplasia/adenoma (suppressed by high dose) or ectopic acth (unresponsive to high dose) Serum TSH test: for papillary or follicular ca, thyroid adenomas are usually cold but could also cause HyperT TSHR antibodies: graves disease, hyperT +1  


submitted by paulkarr(16),

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.

thotcandy  LAP 100-249 do not fall into the answer choice but would still be considered high value and thus +LAP to indicate leukemoid. A LAP- would be in the normal values which is 20-100, not below 250 like the answer choice indicates. +  


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)

nor16  yeah but pathoma doesnt help here... +1  
thotcandy  Yeah but LAP is normally 20-100 so a 100-250 U/L is still + which would indicate Leukemoid reaction, no? That's why I didn't pick it, Because I figured 250 u/l was just some random number and it didn't make sense. a -LAP would be in the normal range, 20-100 which would THEN indicate CML. +  


submitted by spow(5),
  • A) GABA-A receptors let Cl- in
  • B) Glycine is used in the spinal cord as an inhibitory neurotransmitter; also lets Cl- in
  • C and E) Metabotropic glutamate receptors are G-protein coupled
  • Therefore, the only thing that could let Ca2+ in is NMDA receptors
thotcandy  according to this, 5HT3 is an ion channel (mainly Na and K, but some Ca) so that was kinda effy imo +  


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.

what  Small intestine has smooth muscle in the walls which will fibrose on injury +  
youssefa  So cutting through the intestine will damage the crypts of Lieberkühn which contain stem cells that replace enterocytes/goblet cells (Faid). This lack of regenerative ability will have platelets and inflammatory cells to be recruited in order to mediate healing (which end result is fibrosis) The intestinal wall lacking crypts of Lieberkühn acts pretty much like stable cells (e.g: cardiomyocytes) which cannot be regenerated and so fibrosis ensues (e.g: Scar is always end product after MI) +1  
thotcandy  The way i thought of it was: small intestine PERFORATION repair -> the basement membrane and stem cells were definitely disrupted thus limiting regeneration ability Liver = puncture wound, not necessarily all the way through = basement membranes and stem cells are probably still intact -> regenerate without fibrosis +  


submitted by nicsar(0),

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.

thotcandy  teres major also internally rotates? It's attached to the medial lip of the humerus +1  


submitted by guillo12(31),

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!!!

arcanumm  I got this wrong too, but I think the exercise of internal rotation makes sense because it will isolate the muscle (without assistance by teres minor for adduction). +3  
tiredofstudying  The subscapularis assists in medial (internal) rotation and adduction, but the teres minor also assists in adduction, so the best choice to isolate the subscapularis would be internal (medial) rotation. Choice E +  
thotcandy  @tiredofstudying teres major also internally rotates so it wouldn't really be isolated either. I guess Tmajor isn't relevant cuz it's not a SITS muscle? Still a stupid question. +  


submitted by viz28(-1),

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 ′ciliated columnar′ 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

charcot_bouchard  But they are asking in healthy individual. I dont get why they add this ciliated part? +3  
thotcandy  @charcot_bouchard FA19 pg 612 says the only thing that's ciliated is Fallopian tubes... shit doesn't make sense yo +  


submitted by nwinkelmann(187),

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

dentist  Sorry, you narrowed it down to HOCM, MVP, and LA myoxma, but I only see LA myxoma as an answer choice. Wouldn't you have been able to stop right there? +1  
hello  @dentist, I appreciate this full answer b/c nwinkelmann is telling those of us that were wondering "how to ddx one from the other in case we need to"? +2  
hello  @dentist btw, HOCM is an answer choice (RVOT is part of HOCM) +1  
thotcandy  @hello but since that's pseudo-aortic stenosis, it would present with a systolic murmur, correct? +