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Welcome to dickassโ€™s page.
Contributor score: 127


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 +0  visit this page (nbme20#42)
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Patient has acutely decompensated heart failure, most likely due to an MI 5 days ago. Orthopnea-dyspnea-edema would mean he likely also has jugular venous distention and hepatic congestion.

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 +3  visit this page (nbme20#33)
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Got this one wrong because of those 2 unaffected children. Here's the explanation from FA pg 59:

Mitochondrial inheritance - Transmitted only through the mother. All offspring of affected females may show signs of disease.

Variable expression in a population or even within a family due to heteroplasmy.

Heteroplasmy basically means that multiple mitochondria are transmitted to each offspring. Their ratio may change at each generation, and cause more severe or less severe disease, even within the same family.

Those unaffected dudes lucked out.

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dickass  That'll teach me not to skim FA, you really gotta look up the words you don't know. +1
chandlerbas  heteroplasmy is a fancy way of saying variable expressivity just specific to mitochondrial diseases i do declare +

 +2  visit this page (nbme20#19)
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SIADH: + Excessive free water retention + Euvolemic hyponatremia with continued urinary Na excretion + Urine osmolality > serum osmolality

Body responds to water retention with DECREASED aldosterone and INCREASED ANP and BNP

Water retention => Less aldosterone => Less ENAC channels => Less sodium reuptake => Loss of sodium in urine

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 +8  visit this page (nbme20#24)
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...migrant workers ...has not received routine medical care ==> she was not screened for hypothyroidism

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lovebug  Wow good point! :D +1

 +2  visit this page (nbme20#38)
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Yeah, so, turns out this is not Nephrogenic DI due to lithium use, you don't give lithium to treat schizophrenia.

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mbourne  If it was Nephrogenic DI, you would have essentially have the effects of too LITTLE ADH. This patient shows severe hyponatremia, essentially the effects of too much water in the serum. This could be from SIADH or polydipsia, and the question stem and answer choices leave us with Psychogenic Polydipsia as the correct response. +1
rockodude  I was thinking about carbamazepine causing SIADH but that is an anti-epileptic not antipsychotic and also as someone said above, the urine would have high osmolarity due to water reuptake at the collecting duct. just fyi +

 +2  visit this page (nbme20#32)
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Nonmaleficence: โ€œDo no harm.โ€

Even if the patient wants to die, I guess.

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champagnesupernova3  FA says you cant assist suicide but you can prescribe pain medication which they can conveniently overdose on +1
dickass  "Physicians may, however, prescribe medically appropriate analgesics even if they shorten the patient's life." (wink, wink) It's vague, but I guess the main point is to let the patient have relief, side effects no longer important. I still don't think you can just give the patient a bottle of benzos though. +1
raga7  FA 2018 PG 260 +1
misterdoctor69  FA 2020 p. 268 +

 +5  visit this page (nbme20#31)
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Paclitaxel hyperstabilizes polymerized microtubules (made up of alpha- and beta- tubulin)

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md_caffeiner  And clinical use is in breast and ovarian CA (FA19 433) +2
len49  TAXes stabilize society. +1
alimd  Tarzan: taxanes (e.g. paclitaxel, docetaxel, cabazitaxel. SKETCHY +1

 +6  visit this page (nbme20#41)
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FA pg 567:

Congenital solitary functioning kidney: Condition of being born with only one functioning kidney. Majority asymptomatic with compensatory hypertrophy of contralateral kidney, ...

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dermgirl  FA 2020 Pg 579 +2

 +8  visit this page (nbme20#9)
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Remember kids, GFR corresponds with Salt (mineralocorticoids), Sugar (glucocorticoids), and Sex (androgens).

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misterdoctor69  Thanks @dickass, not sure why you got downvoted :( +

 +7  visit this page (nbme20#37)
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FA pg 70:

Vit E deficiency:

Neurologic presentation may appear similar to vitamin B12 deficiency, but without megaloblastic anemia, hypersegmented neutrophils, or ย serum methylmalonic acid levels.

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dickass  and VitB12 neurologic symptoms are described on pg 518 +

 +1  visit this page (nbme20#1)
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Testicles have significant aromatase activity. This enzymatic activity is regulated by LH (and of course bHCG)

https://www.ncbi.nlm.nih.gov/pubmed/9267128

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 +3  visit this page (nbme20#4)
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It can't be the Facial nerve, physical examination was normal. Someone would probably notice the face symptoms.

I went with Glossopharyngeal, but that wasn't it.

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garima  I thought the same for olfactory, he would have realize he can't smell... :O +4

 +4  visit this page (nbme20#35)
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I spent like 5 minutes trying to figure out what kind of trick question this was. They're just trying to get you to figure out 'oh look the spleen is YUGE!'

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Subcomments ...

submitted by dickass(127), visit this page
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Nonmaleficence: โ€œDo no harm.โ€

Even if the patient wants to die, I guess.

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champagnesupernova3  FA says you cant assist suicide but you can prescribe pain medication which they can conveniently overdose on +1
dickass  "Physicians may, however, prescribe medically appropriate analgesics even if they shorten the patient's life." (wink, wink) It's vague, but I guess the main point is to let the patient have relief, side effects no longer important. I still don't think you can just give the patient a bottle of benzos though. +1
raga7  FA 2018 PG 260 +1
misterdoctor69  FA 2020 p. 268 +


submitted by hayayah(1212), visit this page
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Frontotemporal dementia (formerly known as Pick disease): Early changes in personality and behavior (behavioral variant), or aphasia (primary progressive aphasia). May have associated movement disorders (eg, parkinsonism).

While this presents very similiarly to Hungtington's, you can differentiate it because in this stem it says "atrophy of the frontal lobes bilaterally" whereas Huntington's has atrophy of caudate and putamen with ex vacuo ventriculomegaly.

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dickass  and the patient has no chorea +6
chj7  Also, in frontotemporal dementia, due to disease of the "cortex", memory/speech/behavioural changes occur early on. (In Pathoma at the beginning of the dementia lecture, he emphasizes distinguishing between disorders of the cortex vs. disorders of the striatum (ie. Huntington's & Parkinson's) as clinical presentations are easily separated.) +1


submitted by hayayah(1212), visit this page
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Patient has a craniopharyngioma. Most common childhood supratentorial tumor. Derived from remnants of Rathke pouch (oral ectoderm). Calcification is common. Cholesterol crystals found in โ€œmotor oilโ€-like fluid within tumor.

A cystic suprasellar mass with calcifications and enhancement of the wall or solid portions in a child or adolescent is almost always a craniopharyngioma.

May be confused with pituitary adenoma (both cause bitemporal hemianopia).

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dickass  Cholesterol crystals in motor oil +
passfail  I also just thoughtL: failure to secrete GH = tumor affecting anterior pituitary hormone --> anterior pituitary is derived from Rathke's pouch +
ally123  "Due to the proximity of the tumor to the hormone-producing cells of the hypothalamus and the pituitary gland, there is significant endocrine dysfunction in most children and adolescents presenting with craniopharyngioma...Among the hormone deficiencies, growth hormone deficiency is the most common and is seen in approximately 75% of children with craniopharyngioma." Source: http://campus.neurochirurgie.fr/Programme_Enseignement/_art1030/endocrinManifest.pdf +


submitted by dickass(127), visit this page
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Got this one wrong because of those 2 unaffected children. Here's the explanation from FA pg 59:

Mitochondrial inheritance - Transmitted only through the mother. All offspring of affected females may show signs of disease.

Variable expression in a population or even within a family due to heteroplasmy.

Heteroplasmy basically means that multiple mitochondria are transmitted to each offspring. Their ratio may change at each generation, and cause more severe or less severe disease, even within the same family.

Those unaffected dudes lucked out.

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dickass  That'll teach me not to skim FA, you really gotta look up the words you don't know. +1
chandlerbas  heteroplasmy is a fancy way of saying variable expressivity just specific to mitochondrial diseases i do declare +


submitted by hayayah(1212), visit this page
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Oxytocin uses IP3 signaling pathway.

GnRH, Oxytocin, ADH (V1-receptor), TRH, Histamine (H1-receptor), Angiotensin II, Gastrin.

FA mnemonic: "GOAT HAG"

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dickass  I figured "if Oxytocin can cause milk secretion and enough uterine contractions to expel a full baby, it's probably activating smooth muscle contraction through Gq coupled second messengers" +9
randi  signaling pathways in FA2019 p332 +3
realnorthomfs  FA2020 p337 +
bfinard1  Can someone smarter than me explain how the IP3 pathway involves phosphoinositide hydrolysis? +
peachespeaches  IP3=phosphoinositide +


submitted by hayayah(1212), visit this page
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This patient has small cell carcinoma. This type of cancer is associated with paraneoplastic syndromes such as: Cushing Syndrome, SIADH, or antibodies against Ca2+ channels (Lambert-Eaton) or neurons. Amplification of myc oncogenes is also common.

SIADH (Syndrome of inappropriate antidiuretic hormone secretion) is characterized by:

  • Excessive free water retention
  • Euvolemic hyponatremia with continued urinary Na+ excretion
  • Urine osmolality > serum osmolality

Body responds to water retention with aldosterone and ยANP and BNP. That is what causes the increased urinary Na+ secretion ยŽwhich leads to normalization of extracellular fluid volume ยŽand the euvolemic hyponatremia.

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hello  Why would body respond to water retention with ALDO? ALDO would increase water retention... +7
nala_ula  @hello, the body's response is to decrease Aldosterone since there is increased volume retention and subsequently increased blood pressure. This concept confused me a lot, but I ended up just viewing it as separate responses. First, the increased volume retention leads to increase ANP and BNP secretion that lead to decreased Na+ reabsorption in the tubules (page 294 in FA 2019) and second, this increased volume basically leads to increased pressure so lets also decrease aldosterone so there is no Na+ retention (since water comes with it)... I thought it was counterintuitive to secrete so much Na+ since you're already having decreased serum osmolality (decreased Na+ concentration) because of the water retention, but I'm guessing that this is just another way our body's well intentions end up making us worse XD +37
compasses  see page 344 FA2019 for SIADH. +
dickass  author pasted text straight from FA but the arrows didn't copy over, inverting the original meaning +4
medninja  The idea of increasing urine Na is getting rid of water, thats why this mechanism end increasing urine Na secretion even when there are very low serum Na levels. +
srmtn  this is a paraneoplasic SX related to small cell Ca. so increase in ADH (SIADH) makes free water retention (increase in weight) and dilutional hipoNa in serum and hiperNa+ in urine. sodium is the main factor in osmolality so since is hipoNa+ the osm will be decreased. +
skonys  I think it's as simple as SIADH -> Inc ADH secretion therefore increased free water reabsorption (Dec Serum Osmolality) and Increased Urine Na+ because there's less water (less dilute/more concentrated). Remember that ADH creates a positive Na+ and Urea gradiant in the collecting duct to facilitate their reabsorption in the medulla (thus reestablishing the gradient. Here are the criteria from https://www.ncbi.nlm.nih.gov/books/NBK507777/ The Schwartz and Bartter Clinical Criterion Serum sodium less than 135mEq/L Serum osmolality less than 275 mOsm/kg Urine sodium greater than 40 mEq/L (due to ADH-mediated free water absorption from renal collecting tubules) +1


submitted by dr_jan_itor(87), visit this page
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Can anyone answer why this one can't be F. Beta thalasemia major? I was thinking becaues of his anemia and the "european descent" which includes the mediteranian europeans. Unless NMBE writers think that european only means the ones with extra white people lol

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dickass  European implies northern european (they even specified the patient was a person of pallor), mediterranean descent is usually implied by country of origin or by straight-out writing 'mediterranean'. +
poisonivy  The MCV is normal, thalassemias are microcytic anemias, that hint helps to rule out the thalassemias. However, I got it wrong, not sure why it cannot be a homozygous mutation in the ankyrin gene +2
adong  @poisonivy, other commenter pointed out it's autosomal dominant so best answer would be heterozygous +


submitted by jotajota94(14), visit this page
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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.
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yex  Nice! ...and we are supposed to read the stem and do all this in a minute or so? :-/ +28
charcot_bouchard  Allele frequency 1/40. so carrier freq 1/20. 80% of 1/20 is 1/25 (80/100 x 1/20) +15
dickass  Ah feck, 2pq got me +1
hello_planet  A handy shortcut for Hardy-Weinberg is that you generally can assume p ~= 1 if q if fairly low. It also tends to be easier to work in fractions if the answer choices are in fractions so you don't have to bounce back and forth between fractions and decimals. So with that, you send up with 2pq = 2 * 1 * 1/50 = 2/50 = 1/25. +9
topgunber  hate this whole scramble thing: In one line: 2 * q * 80%. This is for diseased individuals (two q alleles).I = 1/1600 = q^2 The frequency of q = 1/40 Now carriers is 2 p q. P is close to one assuming HW eqm (p+q=1). There's an additional step in this question due to the two different mutations. so 2(q) = 1/20. 80% of these carriers are deletions so multiply 1/20 * 0.8 = 1/25 +


submitted by breis(56), visit this page
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Patient has Midsystolic murmur heard at the cardiac apex. there is also a LEFT ATRIAL abnormality. Echo shows LEFT ATRIUM is enlarged.

Mid systolic... enlarged left atrium...

Best choice: Mitral Regurg

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hpsbwz  Why is it regurg instead of stenosis? +3
minhphuongpnt07  Vague question requires a lot clinical reasoning. mitral regurgitation: holosystolic murmur( this cv: midsystolic), enlarged LA, LV Mitral stenosis: diastolic murmur, enlarged LA, normal LV. only best explanation I can think of: early stage Mitral regur, that's why the murmur is not holosystolic but midsystolic and LV still adequately handle the situation +4
dickass  @hpsbwz it's regurgitation because the murmur is SYSTOLIC, when the mitral valve is not supposed to make any sound. mitral valve leaks in systole, which causes blood to back up, which causes the left atrium to work harder and eventually hypertrophy. Mitral stenosis would be a DIASTOLIC sound, which is when the left atrium normally contracts. +9
themangobandit  I'm still confused as to why mitral regurg has an enlarged left atrium. Are we supposed to think that it was mitral stenosis for a time, the high LA pressure led to hypertrophy, and then became mitral regurg? That's how it works in rheumatic fever, right? +
shapeshifter51  I agree that mitral regurgitation is a holosystolic murmur heard best heard over the apex. However, with the murmur being found in the mitral valve area of auscultation it was the only answer choice that could result in LA enlargement and normal LV. Ruled out mitral valve stenosis since it is a diastolic murmur. +1
weenathon  @themangobandit I believe mitral regurg could cause an enlarged left atrium from the increased amount of blood flooding back into the left atrium with each systole causing increased pressure on the wall. +
rockodude  why is LV size normal? doesnt cause MR cause increased preload and overload over time leading to enlarged LV? +


submitted by hayayah(1212), visit this page
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Familial adenomatous polyposis is an autosomal dominant mutation. Thousands of polyps arise starting after puberty; pancolonic; always involves rectum. Prophylactic colectomy or else 100% progress to CRC.

Autosomal dominant diseases have, on average, 50% chance of being passed down to offspring.

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sympathetikey  I would say this is Lynch Syndrome (APC is usually thousands of polyps) but lynch syndrome would generally have a family history of other cancers as well, so you might be right. Either way, both autosomal dominant so win win. +3
smc213  uptodate states: Classic FAP is characterized by the presence of 100 or more adenomatous colorectal polyps +
dickass  @sympathetikey Lynch Syndrome is literally called "Hereditary NON-POLYPOSIS colorectal cancer" +14
fatboyslim  I think this actually is Lynch syndrome. Lynch syndrome can also develop colonic polyps but not nearly as bad as FAP. FAP has so many polyps you can't even see the normal mucosa. If you Google Lynch colonoscopy you can see that they develop a few polyps. +
rockodude  I forgot it was AD inheritance but regardless at the time I was confused because APC is a tumor suppressor so it needs two hits. I guess AD inheritance and then you need another hit to develop CRC kind of like familial retinoblastoma or li fraumeni syndrome +


submitted by dickass(127), visit this page
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FA pg 70:

Vit E deficiency:

Neurologic presentation may appear similar to vitamin B12 deficiency, but without megaloblastic anemia, hypersegmented neutrophils, or ย serum methylmalonic acid levels.

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dickass  and VitB12 neurologic symptoms are described on pg 518 +


submitted by nwinkelmann(366), visit this page
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This explains it really well with a picture: https://www.med.illinois.edu/m2/pathology/PathAtlasf/Atlas01.html.

Hydropic change = one of the early signs of cellular degeneration in response to injury that results in accumulation of water in the cell. Hypoxia/ischemia leads to decease in aerobic respiration in the mitochondria and decreased ATP production due to failure of the Na+/K+ ATPase leading to Na+ and water diffusion into the cell. Individual tubule cells appear swollen and "empty" with almost occluded lumen, glomerulus is hypercellular.

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dickass  it's basically from pathoma chapter 1: cellular injury causes swelling +7
md_caffeiner  @dickass you why arent you on every q stem? +2
mangotango  do you mean "causing failure of the Na+/K+ ATPase" instead of "due to failure of Na+/K+ ATPase..." ? The low ATP is due to dec aerobic respiration, I believe. +2
fatboyslim  @Mangotango yes exactly. Na/K ATPase stops working due to the lack of ATP. I think nwinkelmann mixed it up +1


submitted by step420(32), visit this page
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B-HCG and LH,FSH,TSH share same alpha subunit, so HCG can activate those receptors if its in high enough quantity. Activating LH receptor will lead to more Testosterone from the Leydig cells. More testosterone can lead to more estrogen formation via aromatase.

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dickass  bHCG directly increases testicular aromatase activity, it's not because of the increased amount of testosterone. +6
vulcania  And for those who were wondering (cause I was), Sertoli cells have aromatase (FA 2019 p. 614) +10
godby  It's a slightly different question, on the stem, what's the purpose of the hCG to him, for infertility or increased sexual demand ? Just curious. +


submitted by medbitch94(56), visit this page
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WHY she has a huge ass liver too? I don't understand how you can choose big spleen over big liver or visa versa

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dickass  I like big spleens and I can not lie~ +7


submitted by step420(32), visit this page
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This is mullerian agenesis. Normal ovaries but absent uterus.

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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? +3
swb  Androgen insensitivity has the same presentation and symptoms. What's the clue that it is mullerian agenesis instead ? +27
sugaplum  Testosterone would be high if it was androgen insensitivity FA 2019 Pg 625 +22
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 +2
dickass  This is not androgen insensitivity because she has perfectly normal Estradiol, which means she has perfectly normal ovaries. She also has regular female levels of testosterone. +5
rockodude  thank you @dickass +1
j44n  Also AIS has paradoxically large boobs-> tanner stage 5 and thats not mentioned anywhere +
fatboyslim  Androgen insensitivity syndrome will have high testosterone because the testosterone receptor isn't functional, therefore the body is like what the heck and starts dumping more testosterone trying to make them a male but it doesn't work unfortunately +


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