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Comments ...

 +0  (nbme23#22)

Old dudette have Aortic stenosis. Atrial contraction become essential for this patient. so AS + AFIb is dangerous because this reduces the LV preload significantly and this patient develops HF. So AFib in AS patient need to correct immediately


 +0  (nbme23#28)

A case of Fanconi syndrome. If it was isolated Type 2 RTA option B would be the answer.


 +0  (nbme23#1)

After everything its jjust an epidem ques. Below 55 vs Above 55 years

ls3076  can you elaborate please?

 +0  (nbme23#44)

This patient has a orbital blowout fracture. see the tear drop sign.


 +0  (nbme24#49)

Apparently theres role of sympathetic system in psychogenic erection and its comes from T11-L2. So if patient have transaction at L5 they lose reflex erection but still retain psychogenic one.

ABove T9 transaction cause loss of psychogenic erection

charcot_bouchard  Below L5* (Not at)

 +1  (nbme20#23)

pKa is pH at which any drug is at its 50% ionized state.

Now we are alk urine i.e inc pH. when pH>pKa it will have two diff path for acidic drug & basic drug.

Acidic drug will inc its elimination (inc ionized form), basic drug will be more absorbed. so we need to know the drug is basic /acidic.

Now if u alk urine its elimination inc. so it have to be acidic. or u can know its a sodi salt of drug with CNS property i.e most like Phenobarbital (Weak acid)

so if pKa of drug is 6---at pH 7 we will start eliminating

but if pKa is 0 we need to raise pH of urine at 11 to start eliminating.at that point prev drug (pKa=6) would be totally out of system.

thats why A is the right ans (pKa = 6)

charcot_bouchard  Correction : Not 0. i means if pKa is 10
charcot_bouchard  2nd update : cont to learn school grade chem. if pKa > 7 it is base. and if pKa is < 7 it is acid. Since we established the drug have to be a weak acid pKa cant be more than 7.
dbg  thanks, but Pka and PH are not at all the same thing

 +1  (nbme20#6)

Narcolepsy has one of the following 3 chraracter - 1. Cataplexy 2. dec orexin in csf 3. REM latency <15 min

its ass with (not dx criteria( Hypnagogin/pompic hallcination. Sleep paralysis

charcot_bouchard  oh dx criteria must also include excessive daytime slepeiness for 3 time per week over 3 month

 +0  (nbme24#18)

I get why its lateral but dont all cranial nerve except 4 arise Ventrally? WTF they add this Dorso before lateral?


 +0  (nbme24#11)

Allodynia is central pain sensitization. Triggering of pain by a non painful stimuli. Also seen in Fibromyalgia. [vs Hyperalgesia : Inc response to painful stimuli]

Its a positive (i.e Actively feeling, not lack of feeling) symptpms. so B & C is not the answer. D isnt answer either. as vanilloid receptor (TRPV1) is also afferent nociceptive transmission (modulated by capsaicin). Activation is soon followed by desensitization.

A - IDK. if problem was in DRG there would be lot more symptoms.





Subcomments ...

submitted by dr.xx(34),

right. he absolutely must remain in the waiting area so that he is at hand to attack his wife whenever her exam ends. go NBME!

meningitis  I guess it was all about not offering battering information in order to not make matters worse since he will figure out that the wife told on him.. Also, its a HUGE STRETCH but the only reason I thought he should stay in the waiting room was just in case the wife died they could detain him and call the police for questioning. +2  
temmy  Also, he should stay there because his wife did not grant him the permission to see him. Patients requests trumps. +  
nephcard  Doctor should not believe what wife told her. There may be some other reason for injury so batttering information should not be provided. But her wish of not letting her husband in should be fulfilled +  
charcot_bouchard  No. In real life patient lies. In Board ques they always tell the truth. Unless they make it very obvious. in fact its a board ques rule. So u believe her untill proven otherwise. +  
drdoom  The prevailing rule of American medicine and law is individual autonomy. No other person is granted “default access” or privilege to another person’s body—that includes the physician! The physician must receive consent from a (conscious) “person” before they become “a patient”. In the same way, the person (the patient) must give consent before anyone else is permitted to be involved in her care, spouses included! +  


submitted by aladar50(15),

The important thing for most of the ethics questions are to look for the answer where you are being the nicest/most professional while respecting the patient’s autonomy, beneficence, non-maleficence, etc. Most of the choices here were either accusatory or basically being mean to the patient. The correct choice is to help the patient but also motivate them to continue physical therapy and to only use the permit as little as necessary. A similar question (which I think was on NBME 23 -- they are kind of blending together) was the one where the patient had test results that indicated he had cancer but the resident said not to (voluntarily) tell him until the oncologist came in later that day, and the patient asked you about the results. You don’t want to the lie to the patient and say you don’t know or that he doesn’t have cancer, but you also don’t want to be insubordinate to the resident’s (reasonable) request.

drdoom  @aladar Your response is good but it’s actually mistaken: You *never* lie to patients. Period. In medicine, it’s our inclination not to be insubordinate to a “superior” (even if the request sounds reasonable -- “let’s not inform the patient until the oncologist comes”) but *your* relationship with *your* patient takes precedence over your relationship with a colleague or a supervisor. So, when a patient asks you a question directly, (1) you must not lie and (2) for the purposes of Step 1, you mustn’t avoid providing an answer to the question (either by deferring to someone else or by “pulling a politician” [providing a response which does not address the original question]). +  
drdoom  As an addendum, legally speaking, you have a contractual relationship with your patient, *not with another employee of the hospital* or even another “well-respected” colleague. This is why, from a legal as well as moral standpoint, your relationship with someone for whom you provide medical care takes precedence over “collegial relationships” (i.e., relationships with colleagues, other providers, or employers). +  
imnotarobotbut  @drdoom, it's not about lying to the patient but it would be wrong for an inexperienced medical student to give the patient their cancer diagnosis, or for a doctor to give a cancer diagnosis if they feel that the patient should be seen by oncology. In fact, the correct answer that the question that was referred to by aladar50 says that you do NOT give the patient their cancer diagnosis even if they asked you directly about it. +  
charcot_bouchard  Dont give it to him. DOnt lie to him that yyou dont know. Tell him let me get the resident rn so we can discuss together Best of both world +  


submitted by seagull(350),

This patient is tripping balls. Better do a drug screen which seems obvious.

sympathetikey  When the answer is so obvious that you pick a stupid answer instead of it. DOH +3  
jooceman739  Funny thing I noticed is "he is alert and cooperative. He appears to be in pain" So he was so high that he was alert and cooperative during the basal ganglia hemorrhage +2  
yotsubato  @sympathetikey That fucking guy who drinks 2 six packs a day with liver failure got me like that. +  
yogi  probably the "drug" have to be a stimulant or a hallucinogen which causes HTN & Tachycardia. +2  
charcot_bouchard  Lol. I got the right answer but took long time +  
goodkarmaonly  The patient's B.P. and pulse are raised + Bilateral dilated pupils = Most likely use of a stimulant Thats how I reasoned it anyways +  


submitted by seagull(350),

This is a panic attack. Hyperventilation drops pCO2 leading to a respiratory alkalosis. po2 is relatively unaffected (don't ask me how?)

sympathetikey  Yeah haha I had the same conundrum. +  
sajaqua1  If she's breathing deep as she breathes fast, then oxygen is still reaching the alveoli , so arterial pO2 would not be effected. +3  
imnotarobotbut  lmao i'm so freaking dumb i thought she was having alcohol withdrawals because it was relieved by alcohol +  
soph  Maybe Po2 is unaffected bc its perfusion (blood) limited not difusion limited (under normal circumstances). +  
charcot_bouchard  PErioral tingling- due to transient hypocalcemia induced by resp alkalosis. +  


submitted by sajaqua1(169),

Gynecomastia, spider angiomata, and hypogonadism (as well as palmar erythema) are all signs of excess estrogen. The liver in patients with hepatic disease is impaired and so cannot clear estrogen sufficiently. Six 12 oz beers daily (72 oz, or half a gallon) is too much, and is destroying his liver.

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?! +  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +1  
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +  


submitted by sympathetikey(252),

Per FA (pg. 636): Concerning breast cancer...

"Amplification/overexpression of estrogen/ progesterone receptors or c-erbB2 (HER2, an EGF receptor) is common; ER ⊝, PR ⊝, and HER2/neu ⊝ form more aggressive."

sympathetikey  FA 2019 +  
meningitis  Why others not it: Anticipation: Trinucleotide repeats; CAG (Huntington), CTG (Myotonic dyst), GAA (ataxia telangiectasia), CGG(Fragile X) Chromosomal rearrangement: Many but can think of Trisomy 21, BCR-Abl, etc Imprinting: Prader willi, angelman Loss of heterozygosity: loss of a single parent's contribution to part of its genome. A common occurrence in cancer, it often indicates the presence of tumor suppressor gene in the lost region. +  
kai  trinucleotide repeats are not associated with breast cancer Neither are chromosomal rearrangements BRCA1,2 tumor supressor genes are associated with breast cancer, which is why I chose E, but I guess I should have bought the new First Aid.......... +  
charcot_bouchard  GAA is Freidrich Ataxia +  


submitted by seagull(350),

Did anyone think that influenza was right? I understand that Herpes-Z can cause pneumonia but why is this answer better over influenza?

jrod77  I believe it's the vesicular rash that gives it away. I thought it was influenza too, but i re-read the questions and I realized they included a rash which disqualifies influenza. +1  
charcot_bouchard  Also h/o of immunsupression, disseminated VZV. Influenza itself doesnt cause severe disease. secondary PNA does. which u will see in elderly. usually +  


submitted by cbrodo(12),

The posterior columns (Fasciculus cuneatus/Fasciculus gracilis) carry information to the brain regarding proprioception, vibration, discriminative touch and pressure. Physical exam findings suggest a lesion here (the spinothalamic tract carries pinprick/pain and temperature, and these were normal). Since the patient has abnormal findings in the lower extremities, and normal findings in the upper extremities, the answer is Fasciculus gracilis. This is because information from body areas below the level of T6 is carried by gracilis and information from body areas above the level of T6 is carried by cuneatus.

kai  kick Goals (gracilis) with your feet Cook and eat (cuneatus) with your hands +2  
temmy  i remember gracilis is for legs by saying i have graciously long legs and they are inside while arms can spread out to remember their orientation on the spinal cord +  
jess123  I remember it as gracilis = grass so feet haha +  
link981  Just to add found on page 492 on FA 2018. +  
charcot_bouchard  Hey Temmy, I can spread my legs too :) +  
maxillarythirdmolar  I can't feel GRACIE's ~fine touch~ as she ~vibrates~ my balls. +  


submitted by temmy(21),

What of if the cancer is a urothelial cancer in the bladder due to radiation therapy. would it not cause similar signs

charcot_bouchard  Chance of bilateral ureteral ca is very rare. Also preincipal r/f for transitional cell ca is Smoking not radiation +  


submitted by sajaqua1(169),

The single most important thing about this gross pathology is that the disease is multinodular. This indicates metastases from distant sites.

Liver abscesses are usualy singular, filled with creamy yellow pus, and may show a fibrous capsule. Cirrhosis often shows a yellow color due to fatty change as well as regenerative nodules, which are not present here. A focal nodular hyperplasia is a singular tumor of the liver, and this is multinodular. Hepatitis B is a little harder to distinguish because from what I can tell it can be multinodular in some cases, but this liver also shows none of the sclerosis from chronic inflammation that would likely accompany Hep B. Finally, we see no dark discoloration to indicate infarction.

monkd  It doesn't explain the sudden death, but I suppose they aren't asking for that! +  
charcot_bouchard  I hate this type of ques. Here it is. Tell me what it is? +  


submitted by colonelred_(43),

Attributable risk = incidence in exposed – incidence in unexposed

= 30/1,000 (smokers) - 30/3,000 (nonsmokers)
= 0.03 - 0.01
= 0.02 (so the attributable risk is about 2%)

Applying it to a population of 10,000:

= 0.02 * 10,000
= 200

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking +  
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer. +  
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers? +  


submitted by colonelred_(43),

Attributable risk = incidence in exposed – incidence in unexposed

= 30/1,000 (smokers) - 30/3,000 (nonsmokers)
= 0.03 - 0.01
= 0.02 (so the attributable risk is about 2%)

Applying it to a population of 10,000:

= 0.02 * 10,000
= 200

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking +  
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer. +  
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers? +  


submitted by viz28(0),

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? +  


submitted by sympathetikey(252),

Mad at myself for changing my answer.

Faulty logic made me wonder if hitting your head would caused increased ICP so, like a cushing ulcer, you would get increased Vagus nerve activity and maybe bradycardia + hypotension. But I guess the RAAS system would have counteracted that and caused vasoconstriction over 24 hours, so Hypovolemic shock is definitely the best choice.

Always should go with the obvious answer :)

seagull  I had the idea that this was a neurogenic shock and increasing intracranial pressure could affect the vagus too. I think the question really wants us to go that direction. +1  
uslme123  The Cushing reflex leads to bradycardia! +  
purdude  Wait I'm confused. I thought hypovolemic shock leads to an increased SVR? +1  
littletreetrunk  apparently, there's a thing called sympathetic escape that can happen after a while (i.e. he's been out for 24 hours): Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion. +  
littletreetrunk  also also if he hit his head he could have loss of sympathetic outflow from a hypoxic medulla which could lead to vasodilation, which further reduces arterial pressure, but this was a hard one for me lol. I also put increased ICP wah. +  
catch-22  Any lack of sympathetic outflow/increased vagal outflow should reduce HR, not increase it. Further, you would expect brainstem signs if there was hypoxia to the brainstem. For example, if you had damage to the solitary nucleus, you wouldn't be able to regulate your HR in response to reduced BP. Since this patient has reduced BP and increased HR, this indicates that the primary disturbance is likely the reduced BP. He's also been in a desert for 24+ hours so. +  
charcot_bouchard  In a patient who develops hypotension following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive cardiogenic shock have been ruled out! Plus Absent Bradycardia rules it out +  


submitted by yex(4),

Hmmm. Well my mind has blown off because what hit my mind was dehydration since he was in the desert. As soon as my mind started to wander about all of the other options that could make sense... I just clicked and moved!

charcot_bouchard  Smart boi +  


submitted by d_holles(29),

Even tho FA and SketchyMicro doesn't mention it, both Anaplasma and Ehrlichosis are carried by Robin of Ixodes.

bulgaine  FA 2019 does mention it P 149 +  
charcot_bouchard  Ehrlichia - Lone star tick +  


submitted by docred123(3),

Hi guys can someone please elaborate on these findings. I understand she has lung cancer that's impeding her trachea. But how is this representative of an obstructive disorder? Aren't lung cancers restrictive if anything? Thanks

nlkrueger  I agree that it's confusing but I looked at it as a physical *obstruction* since it's impinging on the airway.... but yeah idk this is weird +  
ferrero  Doesn't the trachea have cartilage rings so it wouldn't collapse which makes it seem less like a typical obstructive disorder? I'm really not sure why FVC would change because I don't see how total lung capacity or residual volume would change because those are static conditions where there is no airflow at all. I understand FEV1, peak expiratory flow, peak inspiratory flow etc. +  
mousie  Agree this is a really tough Q but I also think I really over thought it... I eliminated all with a normal Ratio bc something obstructing would obviously produce an obstructive pattern although I don't know why FVC would be decreased. I wasn't sure about both peak expiratory and inspiration flow being decreased can someone help me with this or tell me I'm totally overthinking again.. are they both decreased simply bc theres an obstruction ..? +1  
mimi21  Yea I got confused on this question. But I guess they wanted us to look at it as a obstructive disease . If this were the case all of those function tests would dec. ( See FA ) +  
gh889  Because the obstruction is above the alveolar regions there is a decrease in air flow, not lung volumes, which would make this an obstructive pathology. +2  
charcot_bouchard  FVC here dec same way it dec in Obstructive lung disease. Read the concept of Equal pressure point of BnB. There he says in bronchitis we have onstructive pattern because inflammed airways gen more resistance. so EPP comes early. I guess here due to tracheal narrowing pressure inc downstream. which collapses smaller airway. result in air trapping. +  


submitted by .ooo. (9),

I personally thought of this questions thinking of it in these terms.. Since the patient has a mass in the trachea peak expiratory and inspiratory flow will be interrupted, and would therefore be decreased. FVC1 would also have to decrease by this. This eliminated all the other choices.

charcot_bouchard  Are you Me? +  


Why is it 99% and not 95%? It asked for onset of disease at less than 9 years of age. I'm clearly missing something here

cbrodo  @fulminant_life because the mean age is 3.8 with a standard deviation of 1.8. An age of onset of 9 years is nearly 3 standard deviations above the mean. Therefore, since we know +/- 2 SD covers 95% of the bell curve, it must be higher than that. The only option higher than 95% is 99%. +5  
charcot_bouchard  Yes 9.2 was the upper limit for 99% CI. I picked 95 first because i thought 2.5% would be out of this range. But changed ans because it should be less than 2.5% because 9.2 is so close to 9. Also they are asking CLOSEST to which of the following? +  


submitted by link981(23),

However weird, you have to respect the patient's beliefs as long as they aren't putting the newborn at harm. In these types of questions you have to build patient-physician relationships because the patient might become offended if you disregard their beliefs. So while the newborn most likely has gas and not "the evil eye", choice E is the least "offending" answer that suggests treatment.

charcot_bouchard  Exactly. If she was cracking the egg on Baby's head u stop her lol (i am cracking up on my own jokes) +  


submitted by sympathetikey(252),

Keys were the:

-Glucosuria

-Phosphaturia

-Amino aciduria

Those should be re-absorbed by the PCT, so if they're not, Type 2 RTA.

lamhtu  To be even clearer, this sounds like **Fanconi syndrome, which has lead to Type II RTA** +3  
yb_26  To be even clearer: Wilson disease => Fanconi syndrome => type II (proximal) RTA +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  


submitted by sympathetikey(252),

Keys were the:

-Glucosuria

-Phosphaturia

-Amino aciduria

Those should be re-absorbed by the PCT, so if they're not, Type 2 RTA.

lamhtu  To be even clearer, this sounds like **Fanconi syndrome, which has lead to Type II RTA** +3  
yb_26  To be even clearer: Wilson disease => Fanconi syndrome => type II (proximal) RTA +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  
charcot_bouchard  To be even clearer, you all have been pretty clear +  


Skin provides insulation and prevents heat loss. This patient's body will compensate for increased rate of heat loss by increasing metabolic rate.

davidw  This is directly from Goljan I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to Chapter 5). • Loss of protein from the plasma loss may result in generalized pitting edema. II) Infection of the wound site and sepsis may occur. (a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients. (b) Other pathogens include methicillin-resistant S. aureus and Candida species. (3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18). (4) Hypermetabolic syndrome may occur if >40% of the body surface is burned. +1  
yex  Can someone explain why is it not increased ECF? +  
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning +1  
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :) +  
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess. +  
yex  Increased ECF, bc I was thinking about the edema formation.... :-/ +  


The most important hints to the question are as follows, with #2 being the most specific:

1) patient reports pain with overhead motion and reports recurrent overhead motion during work. Overhead motion can damage the supraspinatus muscle due to impingement by the acromion.

2) Pain is worst with internal rotation of the shoulder - this is consistent with the findings of the empty-can test, which indicates a supraspinatus injury.

mousie  I was thinking along the lines of overhead motion - damage to the subacromial bursa which is between the acromion and the supraspinatus ... also its the most commonly injured rotator cuff m. so could have guessed this one right +  
sympathetikey  Thanks for the explanation. I was scratching my head as to why this is correct, since supraspinatus only does 15 degrees of abduction, but you make a lot of sense. +1  
charcot_bouchard  IDK WTF i picked Trapezius +2  
ls3076  why would injury to supraspinatus cause weakness with internal rotation though? +  


submitted by nor16(3),

all those non maths guys here, dont skip these questions, try to arrange the units, here you´d easily find out that you just have to multiply! Give it a try :-)

charcot_bouchard  This was like Filtered Load ques of Renal. Where u multiply icoming fluid (GFR) with the desired substances conc (Px) so FIltered load of A is GFR x Pa Same here. Myocardial O2 supply is Blood flow x Conc of O2 in that blood flow +  


submitted by guillo12(12),

Fick principle: CO= Rate of O2 consumption/arterivenous O2 concentration

CO means cardiac output or Flow of blood

charcot_bouchard  This wasnt Fick +  


submitted by sajaqua1(169),

Wouldn't total AV nodal ablation destroy to autorhythmicity of the pacemaker? That would mean that below the AV node the rhythm would be provided by a ventricular foci, and those usually create wide QRS complexes.

haliburton  that was my reasoning as well. guess not. +  
yotsubato  Shitty NBME grammar strikes again. +  
charcot_bouchard  No. No guys. Bundle of his located below AV node and it can generate impulse. it calls junction escape rhythm and narrow complex. Below this is purkinje, bundle branch & ventricular muscle. those are wide complex +  


Apparently theres role of sympathetic system in psychogenic erection and its comes from T11-L2. So if patient have transaction at L5 they lose reflex erection but still retain psychogenic one.

ABove T9 transaction cause loss of psychogenic erection

charcot_bouchard  Below L5* (Not at) +  


pKa is pH at which any drug is at its 50% ionized state.

Now we are alk urine i.e inc pH. when pH>pKa it will have two diff path for acidic drug & basic drug.

Acidic drug will inc its elimination (inc ionized form), basic drug will be more absorbed. so we need to know the drug is basic /acidic.

Now if u alk urine its elimination inc. so it have to be acidic. or u can know its a sodi salt of drug with CNS property i.e most like Phenobarbital (Weak acid)

so if pKa of drug is 6---at pH 7 we will start eliminating

but if pKa is 0 we need to raise pH of urine at 11 to start eliminating.at that point prev drug (pKa=6) would be totally out of system.

thats why A is the right ans (pKa = 6)

charcot_bouchard  Correction : Not 0. i means if pKa is 10 +  
charcot_bouchard  2nd update : cont to learn school grade chem. if pKa > 7 it is base. and if pKa is < 7 it is acid. Since we established the drug have to be a weak acid pKa cant be more than 7. +  
dbg  thanks, but Pka and PH are not at all the same thing +  


submitted by strugglebus(60),

Auto dom disease are usually heterozygous (or so they want us to assume)

xxabi  How do you know is autosomal dominant? +1  
scpomp  Hereditary spherocytosis +  
fshowon  Isnt the mean corpuscular hemoglobin concentration increased in spherocytosis? Thats what through me off. +  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +1  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +  


submitted by strugglebus(60),

Auto dom disease are usually heterozygous (or so they want us to assume)

xxabi  How do you know is autosomal dominant? +1  
scpomp  Hereditary spherocytosis +  
fshowon  Isnt the mean corpuscular hemoglobin concentration increased in spherocytosis? Thats what through me off. +  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +1  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +  


pKa is pH at which any drug is at its 50% ionized state.

Now we are alk urine i.e inc pH. when pH>pKa it will have two diff path for acidic drug & basic drug.

Acidic drug will inc its elimination (inc ionized form), basic drug will be more absorbed. so we need to know the drug is basic /acidic.

Now if u alk urine its elimination inc. so it have to be acidic. or u can know its a sodi salt of drug with CNS property i.e most like Phenobarbital (Weak acid)

so if pKa of drug is 6---at pH 7 we will start eliminating

but if pKa is 0 we need to raise pH of urine at 11 to start eliminating.at that point prev drug (pKa=6) would be totally out of system.

thats why A is the right ans (pKa = 6)

charcot_bouchard  Correction : Not 0. i means if pKa is 10 +  
charcot_bouchard  2nd update : cont to learn school grade chem. if pKa > 7 it is base. and if pKa is < 7 it is acid. Since we established the drug have to be a weak acid pKa cant be more than 7. +  
dbg  thanks, but Pka and PH are not at all the same thing +  


submitted by hayayah(330),

The right and left ventricle are drained by separate parts of the foramen of monro. (Left side is drained by left monro, right side by right monro). An obstruction of the right foramen of monro will enlarge the right ventricle.

hmorela  My mnemonic for CSF flow: "Little Infants Crying For Food. Sorry, All Done." Lateral ventricle - intraventricular foramen of monro - cerebral aqueduct - forth ventricle - foramen of lusaka/magendie - subarachnoid space - arachnoid granulations - dural venous sinuses +3  
charcot_bouchard  u missed 3rd ventricle, how about " Little Igor the 3rd, Crying for..." +  


submitted by hayayah(330),

Little finger = ulnar nerve.

C8-T1 are the roots of the ulnar nerve, which is a branch of the medial cord. The ulnar nerve is not found in the carpal tunnel (the medial nerve is).

Ulnar n. damage can lead to loss of wrist flexion and adduction, flexion of medial fingers, abduction and adduction of fingers (interossei), actions of medial 2 lumbrical muscles. Loss of sensation over medial 1 1/2 fingers, including hypothenar eminence.

sugaplum  Also to add: since it is a bilateral sx it is more likely to be coming from the spinal cord then from equal compression of ulnar nerve (in guyons canal) on both sides. unless she is a cyclist +  
thefoggymist  shouldn't the other nerves of the same roots be affected? +  
thefoggymist  shouldn't the other nerves of the same roots be affected? +  
charcot_bouchard  Not really. In klumpeke paralysis ulnar nerve s/s dominates (Almost same cause) +  


submitted by hayayah(330),

Prostatitis is characterized by dysuria, frequency, urgency, low back pain. Warm, tender, enlarged prostate.

Acute bacterial prostatitis—in older men most common bacterium is E. coli.

ergogenic22  In young men it could be chlamydia but the question stem makes no mention of sexual activity, so it is e. coli +2  
charcot_bouchard  First this guy isnt older! He may incite Daddy issue but not older. At this age people tend to be more monogamous so E Coli the more likely answer. But again cont NBME 20 trend this one was pretty vague too. +  


submitted by hayayah(330),

Case of arteriolosclerosis.

Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin appearance')

  • Consequence of malignant hypertension (>180/120 w/ acute end-organ damage)
  • Results in reduced vessel caliber with end-organ ischemia
  • May lead to fibrinoid necrosis of the vessel wall with hemorrhage; classically causes acute renal failure (ARF) with a characteristic 'flea-bitten' appearance
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +3  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +6  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +2  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


submitted by hayayah(330),

Case of arteriolosclerosis.

Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin appearance')

  • Consequence of malignant hypertension (>180/120 w/ acute end-organ damage)
  • Results in reduced vessel caliber with end-organ ischemia
  • May lead to fibrinoid necrosis of the vessel wall with hemorrhage; classically causes acute renal failure (ARF) with a characteristic 'flea-bitten' appearance
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +3  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +6  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +2  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


Fibromuscular hyperplasia will cause pre renal azotemia. S. BUN/Cr is >20 in pre renal azotemia but in the question its value is indicative of intrinsic renal failure. very confusing!!

charcot_bouchard  Not really, Hypotension cause pre renal azotemia. Here long standing HTN resulting in end organ damage so intrinsic renal failure +1  
cry2mucheveryday  ugh! i just noticed there's a fairly long h/o of poorly controlled HTN which makes this question simpler now. Thanks!! +  


submitted by breis(6),

Psittacosis (sometimes called ornithosis or parrot disease or parrot fever) is an infection of the lung (pneumonia) caused by the bacterium Chlamydophila (Chlamydia) psittaci.

Signs and symptoms: fever. cough, usually without much phlegm. headache. rash. muscle aches. chest pain. shortness of breath. sore throat.

charcot_bouchard  Update on my prev comment : Yes this is psittacosis. not hypersensitivity pneumonitis. How do u know? Lymphocyte and Presence of Granuloma - response to intracellular chlamydia. Now HS can also cause loose granuloma too and the clinical picture still more look like HS You know what ......... fuck this ques +  
shemle  Here Pt. doesn't have fever! +  


submitted by strugglebus(60),

Lysine is used in elastin and collagen cross linking; it is cross linked by lysyl oxidase to make collagen fibers

charcot_bouchard  Thats my brother from UFAP mother +1  


Narcolepsy has one of the following 3 chraracter - 1. Cataplexy 2. dec orexin in csf 3. REM latency <15 min

its ass with (not dx criteria( Hypnagogin/pompic hallcination. Sleep paralysis

charcot_bouchard  oh dx criteria must also include excessive daytime slepeiness for 3 time per week over 3 month +  


submitted by hayayah(330),

The tubes are catheters put in for urine to flow into a bag. So urine output is going to increase. The patient is also hyperkalemic. Aldosterone responds to hyperkalemia by increasing K+ excretion.

Hyperkalemia will stimulate aldosterone secretion even if renin is suppressed due to his hypertension. Although Na+ will be reabsorbed, this will be transient (should resolve once the potassium levels normalized) and since his urine output will most likely return to normal, his blood pressure should also normalize.

charcot_bouchard  Postobstructive diuresis Postobstructive diuresis is a polyuric state in which copious amounts of salt and water are eliminated after the relief of a urinary tract obstruction. The incidence of POD is unclear but estimates suggest 0.5% to 52% of patients will experience POD after relief of obstruction.10 It generally occurs after relieving BOO, bilateral ureteric obstruction, or unilateral ureteric obstruction in a solitary kidney.11 Diuresis is a normal physiologic response to help eliminate excess volume and solutes accumulated during the prolonged obstruction. In most patients, the diuresis will resolve once the kidneys normalize the volume and solute status and homeostasis is achieved. Some patients will continue to eliminate salt and water even after homeostasis has been reached, referred to as pathologic POD. These patients are at risk of severe dehydration, electrolyte imbalances, hypovolemic shock, and even death if fluid and electrolyte replacement is not initiated.9 +3  


submitted by hayayah(330),

This is an example of Shingles. Herpes simplex and herpes zoster viruses cause abnormal cell division in epidermal cells, and this creates multinucleated giant cells.

A Tzank smear showing multinucleated giant cells is characteristic of Varicella Zoster Virus infections. (HSV will have similar findings).

ergogenic22  other identifying terms for herpes: Single dermatome (does not cross the midline), painful (burning and itching),and lesions in multiple stages. +1  
redvelvet  and why neutrophile infiltration, is it a thing? or just a distracting thing? +  
charcot_bouchard  Neutrophil comes into party always first. but it was distracting for me too. +  


submitted by hayayah(330),

Neoplasia is new tissue growth that is unregulated, irreversible, and monoclonal.

Clonality can be determined by glucose-6-phosphate dehydrogenase (G6PD) enzyme isoforms. G6PD is X-linked.

*For more information check out Ch. 3 Neoplasia in Pathoma

hello  This is great, thank you. +2  
breis  Pathoma ch. 3 pg 23 "Basic Principles" +1  
charcot_bouchard  Shoutout to Imam Satter! Without him this question wasnt possible for me to answer in 10 sec. +2  


submitted by hayayah(330),

This man is showing sxs of an MI.

Initial phase of myocardial infarction leads to subendocardial necrosis involving < 50% of the myocardial thickness (subendocardial infarction); EKG shows ST-segment depression.

Continued or severe ischemia (>20 minutes) leads to transmural necrosis involving most of the myocardial wall (transmural infarction); EKG shows ST-segment elevation.

charcot_bouchard  May i know where do u read this +  


submitted by strugglebus(60),

Bronchophony= pneumonia Expiratory stridor= tracheobronchial obstruction (mass/foreign body) Inspiratory stridor = laryngeal obstruction Succussion splash= test for pyloric stenosis

When there is a fractured rib it will cause a trauma pnemothorax which can cause air to escape and become trapped under the skin leading to crepitus.

charcot_bouchard  Actually when a fractured rib puncture lung then it cause sc emphysema. +  


This is LITERALLY the same photo they used to describe the 4-year-old boy with diffuse cortical necrosis from NBME 18. Can someone explain what's going on here

lancestephenson  *Tubular atrophy, not cortical necrosis lol +  
charcot_bouchard  Can u fuckers talk about spoilers +  


submitted by kentuckyfan(13),

Since the pain is radicular, a disc herniation is most likely.

charcot_bouchard  Why it cant be a lumbar vertebra fracture +  
whoissaad  @charcot The patient is young and doesn't have any risk factors for weak bones. Also, disc herniation is a common problem in the young. The disc gets fibrosed and stiff in the elderly so they have less chance for disc herniation. So basically age was the key to answering this question. +  


submitted by hayayah(330),

Benign tumors are usually well-differentiated and well-demarcated, with low mitotic activity, no metastases, and no necrosis.

Malignant tumors (cancers) may show poor differentiation, erratic growth, local invasion, metastasis, and apoptosis. High mitotic activity.

Fat tumors:

  • Lipoma: benign, low mitotic activity
  • Liposarcoma: malignant, increased mitotic activity
whossayin  why can't it be a rhabdomyosarcoma? +  
charcot_bouchard  Because of histology and gross appearance... very graphic description of fat cell tumor there +1  


submitted by youssefa(6),

From Faid 2019 new figure: IGF-1 mainly functions as an anabolic hormone on muscles and bones (pretty much like insulin-> decreases serum glucose). GH acts separately by promoting insulin resistance (increasing serum glucose). Therefore, IGF-1 is not the answer. If GH was among the answers it would have got really confusing.

charcot_bouchard  Can anyone take a little time to curse on that daughter? +1  
dbg  Sure, charcot. Just wished on her to get a couple of charcots (the triad, your aneuryms, marie tooth, etc). +  


submitted by step420(17),

This is mullerian agenesis. Normal ovaries but absent uterus.

endochondral   why not androgen insensitivity? +  
shaeking  I was wondering the same thing because doesn't androgen insensitivity also have normal female secondary characteristics. Was it the levels of hormones because she doesn't have abnormally high testosterone? +  
swb  Androgen insensitivity has the same presentation and symptoms. What's the clue that it is mullerian agenesis instead ? +  
sugaplum  Testosterone would be high if it was androgen insensitivity FA 2019 Pg 625 +2  
charcot_bouchard  Testo would be high in AIS. in AIS pubic hair, axillary hair doesnt devlop because of androgen insensitivity. both have normal breast dev and primary amenorrhea +  


submitted by yotsubato(207),

"physicians should always encourage healthy minor-guardian communication."

Also you're going to do some serious things to cure this girl's disease, leading up to amputation. You cant hide that from her.

djjix  Non sense ... you can hide the amputation from her +3  
charcot_bouchard  Just show her one leg twice. +  


Salivary secretion 1. At low flow = High concentration of potassium; low concentrations of sodium, bicarb, & chloride 2. at high flow = low concentration of potassium; high concentrations of sodium, bicarb, & chloride

sherry  That's exactly what I was thinking when I was taking the test. But I was sidetracked by same HCO3 level. Can somebody explain this part to me?? +  
charcot_bouchard  Because salivary duct removes Na & Cl while secrete K & Hco3 in lumen. In low flow rate HCO3 & K inc because duct is doing its thing for more time. At high flow rate K slightly dec (as cant be secrted as much) but HCO3 stays almost same. the reason is high flow indicates higher metabolism & higher bicarb production. +  
cienfuegos  Regarding the bicarb (via BRS Physiology, which explains flow rate as coming down to "contact time" where slow flow allows more reabsorption of NaCl): The only ion that does not “fit” this contact time explanation is HCO3−; HCO3− secretion is selectively stimulated when saliva secretion is stimulated. +1  


submitted by celeste(26),

Sounds like a hypertrophic scar. "Hypertrophic scars contain primarily type III collagen oriented parallel to the epidermal surface with abundant nodules containing myofibroblasts, large extracellular collagen filaments and plentiful acidic mucopolysaccharides." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022978/

johnthurtjr  I think it may actually be a keloid, not a hypertrophic scar, as it expands beyond the borders of the original incision. +2  
thepacksurvives  I believe this is a keloid; a hypertrophic scar does not extend past the borders of it's original incision, while a keloid does. regardless, the answer to this question is the same :) +  
breis  First AID pg 219 Scar formation: Hypertrophic vs. Keloid +  
charcot_bouchard  They give granulation tissue is a option which is type 3 collagen. so if it was hypertrophic scar it would be ap problem since its only excessive growth of Type 3. while keloid is excessive growth of both 1 and 3 +  


submitted by xxabi(78),

Swelling of the cell (e.g., hydropic degeneration): tissue ischemia → decreased ATP production → decreased Na+/K+ ATPase and Ca2+pump activity → diffusion of Na+ and water into the cell → cellular swelling

endochondral1  can someone explain how to cross out the other choices> +1  
endochondral1  what is hydropic degneration and where do i learn about it? why is it not the loss of plasma membrane integrity? +  
shaeking  Endochondral1, I had the same question. I tried figuring it out and this is what I came up with. The CHF and congestion of the lungs is reducing the amount of oxygen getting to the renal cells. With hypoxia there is decreased aerobic resp in mitochondria with decreased ATP. Without ATPase Na builds up and water follows. As far as the loss of membrane integrity. I think it would cause cellular destruction not just hydropic changes. This is my best guess. +1  
charcot_bouchard  Membrane damage is irreversible stage of cellular injury. if membrane is damaged cell is dying & it will shrink. or totally destroyed by inflammation. they are specifically asking hydropic changes ie cellular swelling. which is the 1st sign of reversible cell injury due to failure of Na/K pump +  


according to uworld hypersensitivity pneumonitis is due to dust and that was also an option....

amarousis  so it's definitely dust but the specific type of dust was the most important in this question. the fact that they mentioned the birds is important. the dusty books would cause it but the bird dust is more important -.- +  
charcot_bouchard  Hypersensitivity Pneumonitis - Organic dust (like moldy hay) Pneumocniosis - Inorganic dust none help here though because both will present with same restrictive lung disease picture. i think since dust in library arent neither organic or inorganic and also u dont see many librarians with lung disease but bird ownership is specifically mentioned as cause of HP disease. +  


submitted by jotajota94(10),

Use the Hardy-Weinberg equation

  1. Take the square root of 1/1600, and that will give you the frequency of the recessive allele = 1/40.
  2. Calculate the frequency of the dominant allele with p+q=1, which is p= 0.975.
  3. They are telling you to calculate the frequency of the disease carriers, which is with the equation 2pq.
  4. They want only the disease carriers in which deletion is present. To calculate this, use the q value (1/40) and multiply by 80% in this should give you 0.02.
  5. Finally, calculate for 2Pq 2 (0.975)(0.02)= 0.04 = 1/25.
yex  Nice! ...and we are supposed to read the stem and do all this in a minute or so? :-/ +1  
charcot_bouchard  Allele frequency 1/40. so carrier freq 1/20. 80% of 1/20 is 1/25 (80/100 x 1/20) +2  


submitted by hayayah(330),

Heparin-induced thrombocytopenia (HIT) is the development of IgG antibodies against heparin bound platelet factor 4 (PF4). Antibody-heparin-PF4 complex activates platelets Ž thrombosis and thrombocytopenia. Highest risk with unfractionated heparin.

drw  could you also help to understand: 1) could anti-heparin-PF4 complex be also called anti-PLT antibody? 2) PLT reduction is due to both PLT thrombosis consumption and elimination in the spleen, then why hypersplenism is not correct? +  
charcot_bouchard  hypersplenism means bigger spleen eating everything. thats not the case here. here spleen is normal. autoimmune cause +  


submitted by step420(17),

Other kidney Hypertrophies due to increased stress --> not hyperplasia bc not cancerous

masonkingcobra  Above answer is incorrect because hyperplasia can be either physiological or pathological. Prolonged hyperplasia can set the seed for cancerous growth however. Robbins: Stated another way, in pure hypertrophy there are no new cells, just bigger cells containing increased amounts of structural proteins and organelles. Hyperplasia is an adaptive response in cells capable of replication, whereas hypertrophy occurs when cells have a limited capacity to divide. Hypertrophy and hyperplasia also can occur together, and obviously both result in an enlarged (hypertrophic) organ. +3  
johnthurtjr  FTR Pathoma Ch 1 Dr. Sattar mentions hyperplasia is generally the pathway to cancer, with some exceptions like the prostate and BPH. +1  
sympathetikey  Tubular hypertrophy is the natural compensation post renal transplant. Just one of those things you have to know, unfortunately. +1  
charcot_bouchard  Isnt Kidney a labile a tissue & thus should undergo both. This ques is dipshit +  


submitted by hayayah(330),

Add on to the other comment: SICKFACES.COM (when I Am drinking Grapefruit juice) is the mnemonic for remembering the CYP450 Inhibitors:

  • S odium valproate
  • I soniazid
  • C imetidine
  • K etoconazole
  • F luconazole
  • A cute alcohol abuse
  • C hloramphenicol
  • E rythromycin/clarithromycin
  • S ulfonamides
  • C iprofloxacin
  • O meprazole
  • M etronidazole

  • A miodarone

  • Grapefruit juice
charcot_bouchard  Its not a cytochrome question. IK because i go t it wrong +  


submitted by hayayah(330),

Definition of adjustment disorder:

Emotional symptoms (eg, anxiety, depression) that occur within 3 months of an identifiable psychosocial stressor (eg, divorce, illness) lasting < 6 months once the stressor has ended.

If symptoms persist > 6 months after stressor ends, it is GAD.

hello  Yep, and I think what we are supposed to take from this Q is: The only info. we have for this patient is that he ended chemo 2 months ago and has been calling the doctor a lot -- this is supposed to mean he has been calling a lot since ending chemo 2 months ago. His frequent calls starting after ending chemo and within 3 months of the stressor fits with the above-stated definition of "adjustment disorder" with anxiety. I stressor in this case could possibly be either the actual illness or the ending of chemo/treatment. It probably does not matter much in this case. +  
charcot_bouchard  I think doing uw done me wrong here. Adjustment disorder isnt diagnosed when symptom match another disorder --- it was like never a right answer. But ofc its right answer in nbme +1  
maxillarythirdmolar  Just to add to that, the tingling in his fingers may seem like a distraction/it probably is. Likely has some relation to his Chemo. +  


submitted by strugglebus(60),

OK, so if I remember correctly this is the one that shows the inheritance pattern. mitochondrial is also passed by the mother; however, it can have variable expressivity and incomplete penetrance, which is why some members were not affected.

hyoscyamine  Also, question said there was a deficiency in NADH dehydrogenase activity which is another fancy way of saying complex I in the mitochondria. +4  
yotsubato  That unaffected male really threw me off... : ( +3  
charcot_bouchard  It was pure MELAS description. the unaffected male threw me off +1  


submitted by hayayah(330),

Iron overdose is a cause of a high anion gap metabolic acidosis.

meningitis  I found this to add a little bit more explanation as to how it causes the acidosis if anyone needs it. 1. Mitochondrial toxicity - decreases aerobic respiration and shunts to lactic acid production 2. Cardio toxicity (Secondary to Mitochondrial toxicity) leads to cardiogenic shock (hypoperfusion), which causes lactic acidosis 3. Hepatotoxicity - Decreases lactate metabolism, causing lactic acidosis 4. When in trivalent form (Fe+3), it can react with 3 molecules of H2O --> FeOH3 + 3H+ This will then deplete Bicarb buffering system resulting in non-gap acidosis. Source: https://forums.studentdoctor.net/threads/iron-poisoning-anion-gap-or-non-anion-gap-acidosis.958285/ +6  
sympathetikey  None of the other choices were even metabolic acidosis. They threw us a bone with this one. +  
imnotarobotbut  Don't changes in bicarb take a few days? How did his bicarb drop down to 8 in 12 hours? +  
charcot_bouchard  its met acidsis. not compensation +1  


submitted by neonem(227),

Since this patient is a non-smoker, it is less to be small cell carcinoma, squamous cell carcinoma, or large cell carcinoma of the lung. Besides small cell carcinoma being from neuroendocrine origin, the one major lung cancer described by nests of well-differentiated, "regular" cells is a carcinoid tumor. Additionally, rosettes are histological features of carcinoid tumors (fun fact: rosettes also in neuroblastomas/ependymomas (in CNS), retinoblastomas, granulosa cell tumors (ovarian cancer))

mousie  When ever I hear Rosettes I always think NE tumors .... and I agree non smoking kind of RO small cell, squamous cell, or lg cell +2  
charcot_bouchard  I thought it was Hamartoma & pick chondrocyte! Can lung even have hamartoma? Pardon me it was the laast ques of whole nbme +  


submitted by sattanki(27),

Muscle pain + periorbital edema is a classic presentation for trichonella spiralis. Best diagnosis for this is a muscle biopsy, as the wormy likes to hangout within the muscles.

sympathetikey  That's what you get for killing polar bears. +9  
dr.xx  That's what you get for not cooking them well. +  
charcot_bouchard  Theres nothing called "well cooked polar bear meat" +  


Why is it not ovarian follicle cells? I thought the female analog of Sertoli and Leydig is theca/granulosa cells.

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +8  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +5  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +  
youssefa  Hahahahaha ya'll just bored +  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +  


submitted by mousie(74),

Is 45 minutes too long to be anaphylactic and would the absence of rash (urticaria, pruritus) RO anaphylactic?

hayayah  Yes! Allergic/anaphylactic blood transfusion reaction is within minutes to 2-3 hours. (pg 114 of the 2019 FA has a list of them ordered by time) +3  
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus) +1  
seagull  The time through me off too. I though ABO mismatch since it occured around an hour. I thought TRALI would take a little longer. +4  
charcot_bouchard  Guys anaphylactic reaction to whole blood doesnt occur much except for selective IgA defi. so look out for prev history of mucosal infection. And it can have all feature of type 1 HS inclding bronchospasm. +2  
soph  I saw hypotension and though anaphylaxis........ -.- +  


submitted by neonem(227),

My best guess is that this patient has a bicuspid aortic valve and has a murmur due to increased volume overload from the pregnancy.

charcot_bouchard  Can be congenital mild Tricuspid stenosis also. it also exaggerate during preg +  
wowo  probably just a flow murmur, https://acpinternist.org/weekly/archives/2017/05/16/3.htm +1  


Why is it aphthous ulcers if there are no GI symptoms? Why can’t it be herpes zoster?

colonelred_  It’s just canker sores, they come and go. I think in herpes the gingivostomatitis really only happens when you first get infected. After that you just get recurrent cold sores. +1  
hyoid  Herpes zoster is not the same as herpes simplex virus. +4  
bigjimbo  you would see dermatome rash in zoster +1  
kateinwonderland  cf) Just in case someone wanted to know the causative organism of aphthous ulcers :The precise cause of canker sores remains unclear, though researchers suspect that a combination of factors contributes to outbreaks, even in the same person. Unlike cold sores, canker sores are not associated with herpes virus infections. +2  
charcot_bouchard  Herpes Zoster doesnt cause gingivostomatitis. Herpengina can cause vesicular lesion in mouth but happens to children in summer season by entero virus +  
drdeeznuts1  I'm wondering if this could be a mild case of Behcet syndrome without genital involvement +  
sherry  It sure can be Behcet or Pemphigus if the q provides us with more info. Canker sores just come and go for years with unclear mechanism. Also herpes zoster is shingles by VZV, not HSV1. +  


charcot_bouchard  When i faced this ques i did some Kegel. Felt something in my pee pee but not in my b*e. I exclude all option because they are bigger muscle of pelvic floor except EUS & IAS. And also remeber Kegel can be used as a treatment of prem. ejaculation not premature defication. +1  


The answer is hyporeflexia because the afferent arc of the muscle stretch reflex has to go through the dorsal rami and dorsal root ganglia. Dumb question, I know, but it’s the only answer that made sense. If you hurt the DRG, you not only lose afferent somatic sensory fibers, you also lose the sensory bodies involved in the various reflexes.

You can also get hyporeflexia from damaging the efferent neurons that innervate the muscle (like a LMN), but as you know these are in the anterior horn and ventral rami.

ankistruggles  Thanks! I agree with you. +  
brethren_md  Great explanation. +  
gonyyong  Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage +  
duat98  I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage? +1  
charcot_bouchard  Muscle atrophy wont occur because alpha motor neuron is intact. Motor control of Corticospinal tract on this is intact. so no atrophy. u can move shiti/ But remeber muscle spindle that is responsible for INITIATING stretach reflex send Ia fibre to DRG from where it synapse with Alpha motor neuron. if DRG is damage ur muscle is fine but u cant initiate strech reflex. areflexia +  


submitted by leny123(2),

General rule - Chloroquine sensitive if from Caribbean or Central America west of Panama Canal, this patient immigrated from Honduras so you can eliminate chloroquine resistance as an answer choice (in addition to the vivax/ovale info above).

charcot_bouchard  Guys along with all intelligent discussion also keep in mind he immigrated 1 year back. So it must be hypnozoites which is causing this because Murica is Malaria free. +4  


submitted by lsmarshall(181),

Urea Cycle Disorders > Isolated severe hyperammonemia (> 1000; i.e., no other severe metabolic disturbances

Ornithine transcarbamylase deficiency > (most common urea cycle dis.) orotic acidemia/aciduria, hyperammonemia

Organic Acidemias > Hyperammonemia, anion-gap acidosis, ketosis (from hypoglycemia)

Medium-chain acyl-CoA dehydrogenase deficiency > Hyperammonemia, hypoketotic hypoglycemia (seen in β-oxidation disorders, EXCEPT adrenoleukodystrophy)

Liver dysfunction > Hyperammonemia, LFTs messed up, older pt.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +3  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +  
charcot_bouchard  if it was mitochondrial disorder no one would escape +  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +1  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +  


submitted by sattanki(27),

Does anyone have any idea on this question? Thought it was ALS.

ankistruggles  I thought it was ALS too (and I think it still could be?) but my thought process was that a lower motor neuron lesion would be the more specific answer. +  
sattanki  Yeah makes sense, just threw me off cause ALS is both lower and upper motor neuron problems. Corticospinal tract would have been a better answer if they described more upper motor neuron symptoms, but as you said, they only describe lower motor neuron symptoms. Thanks! +1  
mousie  Agree I thought ALS too but eliminated Peripheral nerves and LMN because I guess I thought they were the same thing ....??? Am I way off here or could someone maybe explain how they are different? Thanks! +  
baconpies  peripheral nerves would include motor & sensory, whereas LMN would be just motor +6  
seagull  Also, a LMN damage wouldn't include both hand and LE unless it was somehow diffuse as in Guil-barre syndrome. It would likely be specific to part of a body. right??? +  
charcot_bouchard  No. if it was a peri nerve it would be limited to a particular muscle or muscles. but since its lower motor neuron it is affecting more diffusely. Like u need to take down only few Lumbo sacral neuron to get lower extremity weakness. but if it was sciatic or CFN (peri nerve) it would be specific & symptom include Sensory. +  


submitted by seagull(350),

This is either a hypertropic scar or keloid. Both arise due to over-expression of TGF-beta.

charcot_bouchard  i think its a foreign body granuloma +  


submitted by m-ice(116),

The patient has loss of pain and temperature on the right side of his face. Sensation of the face is ipsilateral, so the issue must be on the patient's right side, which we can confirm by knowing that sensation of the body is contralateral, and he has lost left sided pain and temperature of the body.

Pain and temperature sensation of the body is part of the spinothalamic tract, which always runs laterally through the brainstem. This can be confirmed by remembering that sensation to the face also runs laterally through the brainstem. So, we can confirm this is a right sided lateral brainstem issue.

The loss of gag reflex and paralysis of the vocal cords imply impairment of cranial nerves IX and X, both of which localize to the medulla. Therefore, the answer is right dorsolateral medulla.

duat98  You're a good man. +1  
charcot_bouchard  You must be handsome too +  


submitted by colonelred_(43),

The analysis only showed a mutation in one allele. CF is an autosomal recessive disease: the disease only manifests if there are mutations in both alleles of the CFTR gene.

If you still have 1 functional copy of the CFTR gene, you can still make the CFTR protein (the chloride channel/transporter), hence your body won’t have any issues.

This is analogous to tumor suppressor genes like Rb: so long as one of the alleles you have is functional, you can make enough of the protein to “make up” for the defective allele. If both get knocked out (Rb-/-), you lose the protection provided by the gene because now you make no protein at all.

The only thing that made sense for this question was the fact that the other allele was not included in the analysis.

charcot_bouchard  OR another allele has a diff type of mutation because CF is done by like hundreds of diff type of mutation. SO the 70 types that we screened covered one type from one parent but not another that was inherited from other parent. +4  
soph  I put D thinking there was a mutation in another protein that interacts with CFTR....thus u dont have CF but some disease with similar phenotype. Is this wrong bc its simply not the case ?? +  
nbmehelp  @charcot_bouchard I think that makes more sense if I understand what you're saying- Probably had a mutation only in 1 of 2 of the same alleles in the analysis but had another mutation in 2 of 2 alleles at a different location not included in the analysis, right? +  


submitted by xxabi(78),

Most common cause of acute prostatitis in older men is E. Coli, and then Pseudomonas.

charcot_bouchard  Grandpa is monogamous. Sexual history was just to throw u off +1  


submitted by rocmed(-3),

Desmoglein: Component of desmosomes, which connect keratinocytes in the stratum spinosum - FA 2018, p.467, Pemphigus Vulgaris

By this I can only assume that they mean that desmoglein connects keratinocytes to EACH OTHER, hence why the other options connecting keratinocytes to other structures are incorrect

charcot_bouchard  The epidermis primarily consists of keratinocytes[4] (proliferating basal and differentiated suprabasal), which comprise 90% of its cells. You are right. both are keratinocyte +  


submitted by yotsubato(207),

Cool another question taken from the list of things not in FA

charcot_bouchard  Actually it is in FA. FA 19 Page 100 - Antigen loaded onto MHC1 in RER after delivery via TAP transporter.... Remember FA is that friend who always say I told you so. +  
yotsubato  But not in this context +1  


submitted by stapes2big(3),

I’m not sure about this one but the way I thought about it was that since the confidence interval included 1, it was not significant. And thus p value must be above 0.05

tea-cats-biscuits  That makes sense! +  
asapdoc  Had the same reasoning +1  
jkan  I get that it's not significant, but why is it 0.05<p<1 and not p>1.0 +3  
jkan  nvm, it's can't be greater than 1 because then it would have a negative% confidence interval which cannot happen (Think if p>0.05 means at least 95% within confidence interval) +3  
charcot_bouchard  p=0.05 means theres 5% chance null hypothesis is true. p=1 means theres 100% chance null hypothesis is true. >1 means >100% chance which isnt possible. +1  
wowo  p is a probability, so can't be greater than 1 +3  


submitted by didelphus(14),

Any idea why hyperchloremia isn't an answer? The diarrhea would cause an normal anion gap (hyperchloremic) metabolic acidosis.

charcot_bouchard  this is the problem bet uw and nbme. in uw it would be for sure a gotcha ques. but in nbme they are usually looking for most obvious. also look what they are asking "most likely". baby would dev low Na before acidosis. Thats my 2 cents +2  
temmy  hyperchloremia will not account for the seizure that brought the patient to the hospital. seizures according to first aid is caused by hypocalcemia and hyponatremia +  
cry2mucheveryday  Children with diarrhoea who drink large amounts of water or other hypotonic fluids containing very low concentrations of salt and other solutes, or who receive intravenous infusions of 50% glucose in water, may develop hyponatraemia. This occurs because water is absorbed from the gut while the loss of salt (NaCl) continues, causing net losses of sodium in excess of water. The principal features of hyponatraemic dehydration are: there is a deficit of water and sodium, but the deficit of sodium is greater; serum sodium concentration is low (<130 mmol/l); serum osmolality is low (<275 mOsmol/l); the child is lethargic; infrequently, there are seizures. https://rehydrate.org/diarrhoea/tmsdd/2med.htm#CONSEQUENCES%20OF%20WATERY%20DIARRHOEA +  
cry2mucheveryday  Also, why is this being given formula...? May be lactase deficiency...which leads to osmotic diarrhea...leads to hyponatremia(goljan) Aren't newborns supposed to be kept on exclusive breast milk till 6 months?? +  
hello  @cry2mucheveryday Don't read too much into it. The fact that the baby is receiving formula isn't relevant to answering the Q. Btw, not everyone breast feeds. Additionally, the Q wouldn't make much sense if it said "they ran out of breastmilk"... +  
hello  @cry2mucheveryday Being on formula then the parents running out of formula is more of a clue for water intoxication. This is typically the scenario that water intoxication presents. However, I suppose if for some reason the baby was being breastfed and the parents switched to exclusively waterfeeding (and no other foods), then water intoxication would also result. +  


submitted by rerdwins(8),

best way to approach it is to ask which one has a portal circulation and a systemic circulation ( You DONT need to know the procedure to answer this question.

example: cant be superior epigastric and inferior epigastric because those are both systemic also cant be superior rectal (inferior mesenteric branch) and superior mesenteric because those are both portal system

when you narrow it down, then its a 50/50 guess.

charcot_bouchard  Not 50/50. u can rule all 4 out with this. U have described it perfectly. they are wanting a portosystemic anastomosis. Both hepatic vein and inferior phrenic vein drains into IVC. I was nt sure abt inferior phrenic but was sure abt renal and splenic. so picked that +1  


submitted by nosancuck(30),

Yo dawg we all about PVT TIM HaLL

Phenylalanine, Valine, TryptoDANK, Threonine, Isoleucine, Methionine, Histidine, Leucine Lysine

meningitis  I don't understand what the question is asking... can someone please explain it to me? Patient doesnt eat protein, shes chubby. What does methionine have to do with this? +2  
charcot_bouchard  Just basically asking which is essential amino acids. +1  
usmleuser007  Essential amino acids (something i came up with) 1. "Three HAL fans will try meth" a. Threonine = Three b. Histidine; Arginine; Lysine = HAL c. Phenylalanine = fans d. Valine; Isoleucine; Leucine = will e. Tryptophan = try f. Methionine = meth +1  
nala_ula  They're saying there is a lack of good quality protein -> slight nutritional deficiency. She may have acquired weight but it's not because of protein. So they're specifically asking what amino acid she might be missing due to her subpar diet. Since essential amino acids are those that the body cannot make itself, out off those listed, methionine is the essential amino acid. It's on page 81 of FA 2019. +6  
nala_ula  correct me if I'm wrong please :) +  
hello  For anyone confused trying to follow @usmleuser007's comment -- slightly modified Essential amino acids mnemonic "Ah, Three fans will try meth" Ah = arginine, histidine Three = Threonine Fans (phans)= Phenylalanine Vil (Will -- German accent pronouncing English word 'will') = valine, isoleucine, leucine, lysine Try = tryptophan Meth = Methionine +