nbmeanswers.com will be going offline for ~hour for some updates! we’ll be right back! --the webmaster (2:17am) ❤️
Welcome to d_holles's page.
Contributor score: 29
School:


Comments ...

 +0  (nbme23#49)

Pt has ASA intolerance asthma, which means NSAID is contraindicated. Pick colchicine.


 +0  (nbme23#23)

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


 +0  (nbme23#10)

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

yex  There is a Q on UWorld about rotator cuff tendinitis #380186 w/ a similar presentation... I kind of remembered about that, but honestly I do not know how I got it right.

 +1  (nbme22#24)

This is a Pathoma Ch3 Q (p28).

Tumor invasion and spread

  1. Epithelial tumor cells are attached to one another by E-cadherin (cellular adhesion molecule). Downregulation of E-cadherin → dissociation of attached cells.
  2. Cells attach to laminin and destroy basement membrane via collagenase.
  3. Cells attach to fibronectin in the ECM and spread locally.
  4. Entrance into vascular or lymphatic spaces allows for metastasis.

https://imgur.com/a/FD16HiB


 +0  (nbme22#22)

I was never taught what t-test vs Chi-squared was. Going off of the FA table didn't help. This video below explained the concept really well.

https://www.youtube.com/watch?v=Tda29m0SKYE

For the Q refer to @mc1's comment.


 +0  (nbme22#31)

Can portal HTN contribute to hepatic encephalopathy?


 +0  (nbme22#44)

Damn I feel like NBME fucking loves scabies or some shit.


 +0  (nbme22#14)

Goljan mentioned this (not sure what lecture -- might have been the endo one).


 +0  (nbme22#50)

This video explains the pediatric neurocutaneous disorders well.

https://www.youtube.com/watch?v=Lom7tnK8HCk

Basically the key here is hypopigmented macules. NF1 has cafe au liate spots (hyperpigmented macules) while TSC has ash leaf spots (hypopigmented macules). This is a decode the buzzword style question. I felt like I didn't really understand these orders until I watched the above video.


 +1  (nbme22#35)

This is a good picture of an experiment showing this:

https://www.nature.com/articles/1210296/figures/1

Oncogene volume 26, pages 2212–2219 (2007)


 +1  (nbme22#11)

I got this one via process of elimination. Not sure how you are supposed to remember all that shit.


 +0  (nbme22#5)

This question confused me bc I thought loperamide could not cross the BBB and therefore could not cause respiratory depression (mu-opioid agonism at the brainstem results in CNS/respiratory depression, 1). But @dr.xx is correct in noting that ↓ RR and CNS depression in the Pt should call for an mu-opioid antagonist rather than bethanchol (cholinomimetic) to treat constipation.

  1. https://anesthesiology.pubs.asahq.org/article.aspx?articleid=2675905
nwinkelmann  http://medresearch.in/index.php/IJPR/article/view/782/1271 This explains a case in an infant. "Respiratory depression and coma after overdosage have been shown to be reversible by injection of naloxone [6]. Owing to its structural similarity to opioid, loperamide toxicity can be reversed by using Nalaxone which is a specific opioid antagonist acts competitively at opioid receptors. Naloxone hydrochloride is usually given intravenously for a rapid onset of action which occurs within 2 minutes."
yb_26  FA 2019: "Loperamide has poor CNS penetration" - so it still penetrates => can cause respiratory depression
whoissaad  Also maybe because the blood brain barrier in a baby is not developed as well as in an adult.

 +2  (nbme22#15)

Goljan stresses the Boards giving the leukemia questions away based on the age given in the question stems.

ALL = 0-14

AML = 15-39; 40-59

CLL = 60+

CML = 40-59

https://forums.studentdoctor.net/threads/goljan-on-leukemias.303605/

impostersyndromel1000  thanks for the reminder, often overlooked are the simple demographic hints. helps you make an educated guess
hyperfukus  also a key thing to remember in general is a person who undergoes chemo is a big demographic hint to later developing AML regardless of the clues :) and yes the AGE!!!

 +3  (nbme21#23)

20% albumin is HYPERtonic and causes drawing of fluid out of the interstitum and into the blood.

"Albumin (Human) 20% is indicated in the emergency treatment of hypovolemia with or without shock. Its effectiveness in reversing hypovolemia depends largely upon its ability to draw interstitial fluid into the circulation. It is most effective in patients who are well hydrated. When blood volume deficit is the result of hemorrhage, compatible red blood cells or whole blood should be administered as quickly as possible."

https://www.drugs.com/pro/albumin-human-20.html


 +2  (nbme21#20)

this is a classic description of persistent Mullerian duct syndrome

wikipedia.org/Mullerian_duct_syndrome

due to lack of MIF (mutation in the gene that makes MIF) → persistence of the Mullerian duct → uterus and fallopian tube present in a XY male w/ testes (typically cryptorchid).


 +0  (nbme21#5)

Here's an excellent image from AMBOSS if people are having difficulty visualizing this: https://imgur.com/a/VmhQRWm


 +1  (nbme21#2)

Also, I think what is key is to realize that injuring CN X ('intraoperative CN X injury') does not lead to diaphragm paralysis, only phrenic nerve injury would do that.

amboss.com/us/CN+X+injury

Furthermore, the other options ('idiosyncratic rxn to sevoflurane' and 'ryanodine receptor defect') are for malignant hyperthermia, NOT unable to breath spontaneously.





Subcomments ...

The effects of excess thyroid hormone: attempted compensatory TSH suppression, increase in both T4 and free T4, and normal TBG. Note that the question doesn’t even hinge on TBG and is also unlikely to on the real thing.

d_holles  When do we care about TBG? +  
zpatel  @d_holles in pregnancy. +  


Splitting is an immature defense mechanism often employed by patients with borderline personality disorder. When splitting, a person fails to see others as capable of having both positive and negative qualities; at any given time, it’s all or nothing.

d_holles  Got this one wrong -- thought it was acting out. +1  


Stroke characterized by left hemiparesis and right CN12 palsy. Crossed findings mean a brainstem lesion. Right (ipsilateral) tongue, left-sided (contralateral) weakness means the exiting right hypoglossal nerve has been affected (within the right medulla). C is the pyramid where the corticospinal tract runs to control muscles (prior to the decussation). This is known as the medial medullary syndrome or Dejerine syndrome.

d_holles  It seems to me that the brain stem problems can all be answered using the Rule of 4s rather than memorizing the actual brain stem histology. +1  


Air and fluid = hydropneumothorax. If that fluid is blood (s/p stabbing), it’s a hemopneumothorax. Lack of mediastinal shift indicates that it’s not under tension.

d_holles  @benwhite_dotcom how can it not be under tension if air is entering the pleural cavity? +1  
nwinkelmann  Because the stab wound isn't functioning like a flap, meaning the air can escape. The reason a tension pneumothorax occurs is because the wound acts as a flap, where on inspiration it is open and air enters, but on expiration is closes and traps the air. +1  


submitted by wired-in(22),

Maintenance dose formula is (CssCltau)/F where Css is steady-state target plasma conc. of drug, Cl is clearance, tau is dosage interval & F is bioavailability.

Neither dosage interval nor bioavailability is given, so ignoring those & plugging in the numbers (careful to convert units to mg/kg/day): (12 ug/mL * 1 mg/1000 ug) * (0.09 L/hr/kg * 1000 mL/1 L * 24 hr/1 day) = 25.92 mg/kg/day

...which isn't any of the answer choices listed. They must have rounded 0.09 L/hr/kg to 0.1 L/hr/kg, and doing so gives exactly 28.8 mg/kg/day (choice C)

lispectedwumbologist  That's so infuriating I stared at this question for 20 minutes thinking I did something wrong +14  
hyoid  ^^^^^ +2  
seagull  lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that. +2  
praderwilli  Big mad +3  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +3  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +4  
bigjimbo  JOKES +  
cr  in ur maths, why did u put 24h/1day and not 1day/24h? if the given Cl was 0.09L/hr/kg. I know it just is a math question, but i´d appreciate if someone could explain it. +  
d_holles  LMAO games NBME plays +  
hyperfukus  magic math!!!!! how TF r we supposed to know when they round and when they don't like wtf im so pissed someone please tell me step isn't like this...with such precise decimal answers and a calculator fxn you would assume they wanted an actual answer! +  


I thought of this as squamous cell carcinoma of the lung causing increased PTHrP and hypercalcemia.

d_holles  I thought this was medullary thyroid cancer but demographically SCC works better. +  
smc213  Medullary thyroid carcinoma increases calcitonin levels leading to decreased serum Ca2+ by increasing Ca2+ renal excretion. So high levels of calcitonin secreted by the tumor may lead to hypOcalcemia. Source: Pathoma +3  


How is this the answer if there is no family history of recurrent fractures? I thought osteogenesis imperfecta was autosomal dominant?

seagull  Exactly!! it's an autosomal dominate disease! +  
emcee  Autosomal dominant diseases are variably expressive. Still, I think this was a badly written question (should have given us some family history). +  
wutuwantbruv  Also, FA says that fractures may occur during the birthing process, which is what I believe they were going for. I don't believe these findings would be seen at birth with any of the other choices. +  
d_holles  Yeah I thought I outsmarted NBME by selecting Rickets bc it said no family history ... guess I got played lol. +3  


submitted by yotsubato(207),

Was it just me, or did "age at onset in years" appear RIGHT above the number of patients, rather than the mean. Which confused me for a good 3 minutes.

fulminant_life  Definitely was the same for me. I was so confused for like 5 mins +2  
d_holles  dude i almost didn't get the question bc of this ... i thought the age of onset was the actual age of onset (36) +3  
mellowpenguins  Are you serious. NBME strikes again with shitty formatting. +  
yex  OMG!! Now I just realized that. Super confused and also thought onset of age was 36. :-/ +  


submitted by mousie(74),

Why no sweating? I mean I get Ecstasy is probably the drug of choice before an all night dance party (lol) but don't understand why there would be cold extremities and no sweating when is FA it says hyperthermia and rhabdo????

sympathetikey  FA says, "euphoria, disinhibition, hyperactivity, distorted sensory and time perception, bruxism. Lifethreatening effects include hypertension, tachycardia, hyperthermia, hyponatremia, serotonin syndrome." So I think they wanted you to see Sinus Tachy and jump for MDMA. Idk why Ketamine couldn't also potentially be correct though. +1  
amorah  I picked ketamine because it said no diaphoresis. But if you need to find a reason, I guess the half life of ketamine might rule it out. Remember from sketchy, ketamine is used for anaesthesia induction, so probably won't keep the HR and BP high for 8 hrs. In fact, its action is ~10-15 mins-ish iv. +2  
yotsubato  Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore? +  
fulminant_life  you wouldnt see tachycardia with ketamine. It causes cardiovascular depression but honestly i saw " all-night dance party" picked the mdma answer and moved on lol +2  
monkd  Ketamine acts as a sympathomimetic but oh well. NBME hasn't caught on to ketamine as a drug of recreation :) +  
usmleuser007  Why not LSD? +  
d_holles  @usmleuser007 LSD doesn't cause HTN and ↑ HR. +  
sbryant6  @fulminant_life FALSE. KETAMINE CAUSES CARDIOVASCULAR STIMULATION. +1  


The way I thought about this question was that in MM there is a TON of antibodies being made, so the VDJ segment is being broken up/selected/rearranged many times and has been shortened to 1.5kb. As for the T Cells, that region isn’t being used (since there is no clonal expansion or selection) so it’s still got the full 6kb length untouched.

d_holles  T cells still undergo VDJ recombination to form their TCRs. +  


submitted by seagull(349),

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not +  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +1  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +1  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +  
jaxx  Not a clue. This was so random. +  
wolvarien  I did not +  
ls3076  no way +  
hyperfukus  no clue +  


submitted by armymed88(13),

Hypopigmented lesions refer to Ash-leaf spots, CNS lesions likely hamartomas . TS also associated with seizures.

fcambridge  How is Tuberous Sclerosis the most likely given that it is an AD disorder and there is no family history of "seizure disorder or major medical illnesses"? +1  
d_holles  @fcambridge variable expressivity of TSC allows for many different phenotypes. +  


submitted by pppro(5),

Patient has BPH. Give alpha one antagonist to reduce smooth muscle contraction and relieve difficulty urinating.

d_holles  lol i thought it was some kind of urinary retention problem and put H. +4  
sbryant6  How is H wrong? Oxybutinin or tolterodine treat urinary incontinence by blocking M3 muscarinic acetylcholine receptors --> urinary retention. We're just supposed to assume they are talking about BPH here because he is old? +  
jaxx  I agree. I picked "H" for that same logic. Does anyone know where we should have come to the conclusion that this was BPH? +  
forerofore  they are telling you he's having "difficulty urinating", one of the clinical criteria for BPH is reduced urinary flow rate. this is not incontinence because they are not telling you he leaks at all, just that he pees "a lot" +  


submitted by niboonsh(55),

https://www.youtube.com/watch?v=4-DuvwoH2zQ if ur lazy like me, this is a good refresher video

d_holles  Amazing video dude. Somehow never learned this in neuro lol. +1  


submitted by yo(21),

I just knew that sperm need fructose, not sure what disease process this is though. He was pretty normal so 5a reducatase doesn't present like that. I wasn't sure if there was any odd use of the other answers. here is a link. Feel free to expand.

https://www.labce.com/spg27422_question.aspx

Fructose makes up 99% of the reducing sugar present in semen. This sugar is produced in the seminal vesicles. Diminished levels of fructose have been shown to parallel androgen deficiency and the testosterone level. Following testosterone therapy, the level of fructose increases. Although the fructose test is not part of a routine semen analysis, it is useful in cases of azoospermia (absence of sperm in semen). In azoospermia secondary to the absence of vesicles or if there is an obstruction, no fructose is present. In testicular azoospermia, fructose is present. When azoospermia and low semen volume exists, the fructose test should also be done, on a postejaculate urine sample to check for retrograde ejaculation. This occurs when the ejaculate goes into the bladder instead of out the urethra. The procedure for determining the amount of fructose in semen involves heating semen in a strong acid in the presence of resorcinol. Fructose gives a red color (Selivonoff reaction) and may be read in a photometer. The normal average is 315mg/dL fructose.

sam.l  Thank you for the explanation. I'm still confused about this answer. I was in between Zinc and fructose. Zinc deficiency also presents with anosmia (pg 71 First Aid 2019). Fructose is used for the movement. His hormones are normal. +1  
d_holles  Apparently diabetes, occlusion, and inflammation can result in ↓ fructose in sperm. Mauss et al, Fert Stert 25, 1974 https://www.fertstert.org/article/S0015-0282(16)40391-2/pdf +1  
cienfuegos  Thanks all for the info, quick note on the Zinc reply above @Sam.I: anosmia = lost sense of smell. +  
sam1  Great find yo! I believe this question was alluding to cystic fibrosis and the congenital absence of the vas deferens. Here is a link to a NEJM article about it below: https://www.nejm.org/doi/full/10.1056/NEJM196807112790203 +  
burak  zinc deficiency cause hypogonadism. there is no hypogonadism, sperms are damaged? +  


the infarct occurred 16 hrs ago, from 12-24hrs after the infarct there will be Red Neurons.

tsl19  FA 2018 - p. 496: ischemia -> pyknosis within 12-24 hours. +  
d_holles  yeah the infarct occurring 16 hr ago is key. i zoomed in only on the died 1 hr later +  


submitted by hayayah(330),

Wernicke-Korsakoff syndrome. Don't have to be an alcoholic to get this, just usually is related to alcoholism / thiamine deficiency.

d_holles  Yeah the negative EtOH screen threw me off +1  
dr_jan_itor  Why cant it be early alzheimers and hippocampus? She could easily have been a former prominent physician and member of city council. Am i supposed to assume that simply because shes disheveled and poor hygeine that she must be an alcoholic homeless person? It also mentions no symptoms of nystagmus, ataxia, etc. +1  
kimcharito  it said broad based gait and nystagmus +1  


submitted by lamhtu(25),

Needing "higher concentrations" of the B6 for enzyme activity is another way of saying Km is higher since more is required for 1/2 vmax activity. Increased Km values result in 1/Km being smaller (closer to 0 on the x-axis), which is demonstrated in answer choice B.

A "normal" enzyme activity in the presence of higher B6 concentrations means that Vmax is not changing, but Km is.

d_holles  In other words, Normal enzyme activity = Vmax Adding more B6 to a mutated enzyme will improve it back to normal (Vmax stays constant, so Km will decreased due to ↑ affinity of the enzyme). +  
wolvarien  why the answer is no C ? +  


submitted by assoplasty(34),

I think the concept they’re testing is the increased TBG levels in pregnancy, and not just hyperthyroidism in general.

When screening for hypo/hyperthyroidism, TSH levels are ALWAYS preferentially checked because they are more sensitive to minute differences in T3/T4. Often times TSH levels can demonstrate a change even when T3/T4 levels are in the subclinical range. The only exception to this would be in pregnancy (and I guess maybe liver failure? I doubt they would ask this though). High estrogen levels prevents the liver from breaking down TBG, leading to increased TBG levels in the serum. This binds to free T4, decreasing the amount of available free T4. As a compensatory mechanism, TSH levels are transiently increased and the RATE of T4 production is increased to replenish baseline free T4 levels. However the TOTAL amount of T4 is increased.

The question is asking how to confirm hyperthyroidism in a pregnant woman --> you need to check FREE T4 levels (because they should be normal due to compensatory response). You cannot check TSH (usually elevated in pregnancy to compensate for increased TBG), and you cannot check total T4 levels (will be increased). You got the answer right either way but I think this is a different reasoning worth considering, because they can ask this concept in other contexts of hyper-estrogenism, and if they listed “TSH” as an answer choice that would be incorrect.

hungrybox  Extremely thorough answer holy shit thank u so much I hope you ACE Step 1 +3  
arkmoses  great answer assoplasty, I remember goljan talking about this in his endo lecture (dudes a flippin legend holy shit) but it kinda flew over my head! thanks for the break down! +2  
whoissaad  you mean total amount of T4 is "not changed"? 2nd para last sentence. +  
ratadecalle  @whoissaad, in a normal pregnancy total T4 is increased, but the free T4 will be normal and rest of T4 bound to TBG. If patient is hyperthyroid, total T4 would still be increased but the free T4 would now be increased as well. +  
maxillarythirdmolar  To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down. +  


submitted by niboonsh(55),

The obliques do the opposite action of their name. Inferior oblique moves the eye UP and OUT (extortion, elevation, ABduction). Since the question says that there is a fracture involving the orbital floor, that automatically rules out D (medial rectus and inferior oblique), leaving the only logical answer to be the inferior rectus and inferior oblique. https://www.youtube.com/watch?v=lWKkHWWDIEI

aishu007  hi, but inferior oblique moves up and in and not out +  
d_holles  https://www.youtube.com/watch?v=3J2UZiLVZKA In case ppl need a refresher +  


submitted by hayayah(330),

lower quadrantanopia: parietal lesion

vs upper quadrantanopia = temporal lesion

mcl  also, to differentiate whether it is the left or right parietal lobe, recall that stimuli from the left visual field hits the nasal side of the left retina and the temporal side of the right retina, then goes to the right side of the brain. [This figure](https://operativeneurosurgery.com/lib/exe/fetch.php?w=600&tok=856a37&media=optictract.jpg) is helpful. +1  
d_holles  So you're saying that there's two crosses, making it ipsilateral? @mci +  


submitted by neonem(227),

This is a postpartum mood disturbance, a pretty common disorder that has to have an onset within 4 weeks of delivery to be termed as such. Postpartum blues is the most mild, with a 50-85% incidence rate (per FA 2018), usually resolves within 10 days and treatment is only supportive but need to follow-up to assess for possible postpartum depression. Postpartum depression = 10-15% rate, characterized by depressed affect, anxiety, poor concentration for greater than 2 weeks and needs to be treated w/ CBT + SSRI. I think the question is getting at screening for this and a potentially more problematic complication, postpartum psychosis.

thisisfine   Found this difficult because FA characterizes "thoughts of harming baby or self" as postpartum psychosis - which is super rare, and doesn't fit this case. Also, CBT is first line treatment for postpartum depression - so I still like the offer to refer to a therapist as the best choice. +1  
d_holles  Same @thisisfine. +1  


submitted by haliburton(74),

this is a cervical spinal cord section. the cuneate fasciculus is intact (UE) vibration and proprioception, but the white section is the gracile fasciculus (LE) and is damaged. I think the lateral portion that is uneven is just natural/artifact.

arezpr  thorax section +3  
guillo12  How do you know the gracile fasciculus is damage?!?! +1  
cr  which parte of the image its damage?, the pink? or black? +  
usmile1  the pink park yes +1  
d_holles  If you look at https://en.wikipedia.org/wiki/Gracile_fasciculus#/media/File:Spinal_cord_tracts_-_English.svg you can see that the closer to the center = legs, while further away = arms. +1  
hyperfukus  i still don't see where the damage is lol! FML +  
hyperfukus  i finally figured it out lol that was a slow moment i hope im not this slow on step yikes! +  
angelaq11  @hyperfukus I had the same problem at first, marked it and then came back. If you remember, in the spinal cord the white matter and gray matter are "reversed" compared to the brain. That said, if the butterfly shaped region (ie, the gray matter) is colored (in this case) lilac and the rest (ie, white matter) is blackish, the only thing that is actually abnormal, is the region where the dorsal columns are, because it stains just like the normal gray matter. After that, you have to think about which fasciculus is damaged, the gracilis or the cuneatus. The gracilis is medial while the cuneatus is lateral (picture someone with glued legs and open arms). Hope this helped +  


Male internal genitalia -> Intact SRY , testes, and testosterone.

No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.

Female external genitalia -> No androgen present, which is required for male external genitalia formation.

d_holles  Not sure I understand why T is wrong, but DHT is correct. +  
d_holles  I thought about this some more -- DHT forms external genitalia while T forms 'male genital ducts'. That's why the correct answer is DHT, not T, since the PT had +ext genitalia, but -internal genitalia. I was thinking that the PT had CAIS, but that would lead to testes only w/o male genital ducts. See FA2019 p608. +  
d_holles  *I meant -ext genitalia, +int genitalia +  


Male internal genitalia -> Intact SRY , testes, and testosterone.

No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.

Female external genitalia -> No androgen present, which is required for male external genitalia formation.

d_holles  Not sure I understand why T is wrong, but DHT is correct. +  
d_holles  I thought about this some more -- DHT forms external genitalia while T forms 'male genital ducts'. That's why the correct answer is DHT, not T, since the PT had +ext genitalia, but -internal genitalia. I was thinking that the PT had CAIS, but that would lead to testes only w/o male genital ducts. See FA2019 p608. +  
d_holles  *I meant -ext genitalia, +int genitalia +  


Male internal genitalia -> Intact SRY , testes, and testosterone.

No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.

Female external genitalia -> No androgen present, which is required for male external genitalia formation.

d_holles  Not sure I understand why T is wrong, but DHT is correct. +  
d_holles  I thought about this some more -- DHT forms external genitalia while T forms 'male genital ducts'. That's why the correct answer is DHT, not T, since the PT had +ext genitalia, but -internal genitalia. I was thinking that the PT had CAIS, but that would lead to testes only w/o male genital ducts. See FA2019 p608. +  
d_holles  *I meant -ext genitalia, +int genitalia +