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 +3  (nbme18#14)

Most problems with cell division occur in anaphase of Meiosis I.

realfakedreams  @hayayah - made an account just to say thank you. I appreciate that you exist.
bswsu  @realfakedreams, I created an account just to upvote your comment.

 +4  (nbme23#39)

Femfibrozil is a fibrate, used for lowering TG levels.

mousie  I also chose Gemfibrozil too because its the best TG lowering drug listed but I can see where there might be some red flags for this drug in the way they asked the question... 40 year old obese woman with some upper abdominal pain ..... HELLO GALL STONES which is a common adverse outcome of Fibrates.
uslme123  Well I didn't wanna give a fat, forty, female, that smokes a fibrate. So a statin, for me, was the best next option.
whoissaad  Used same reasoning to choose statins. Fibrates are the main drug of choice for hypertriglyceridemia but given her symptoms, statins made more sense. Why do they do this to us...
roaaaj  what a tricky question! there are multiple factors should be taken in consideration.. she has triglyceridemia which put her in risk of pancreatitis, and most importantly atherosclerotic disease, and all of that would outweigh the risk of giving her gallstone.
paulkarr  Yeah I had statins selected initially because "statins are always the answer" but when I saw them stating first line "recently diagnosed with hyper TG" I figured this follow-up was purely to address that. So Fibrate is the best move.

 +29  (nbme23#43)

Coloboma is an eye abnormality that occurs before birth. They're missing pieces of tissue in structures that form the eye.

  • Colobomas affecting the iris, which result in a "keyhole" appearance of the pupil, generally do not lead to vision loss.

  • Colobomas involving the retina result in vision loss in specific parts of the visual field.

  • Large retinal colobomas or those affecting the optic nerve can cause low vision, which means vision loss that cannot be completely corrected with glasses or contact lenses.

mousie  thanks for this explanation!
macrohphage95  can any one explain to me why not lens ?
krewfoo99  @macrophage95 Lens are an interal part of the refractive power of the eye. Without the lens the image would not be formed on the retina, thus leading to visual loss
qfever  Do anyone know why not choroid?
adong  @qfever, no choroid would also be more detrimental to vision since it supplies blood to the retina
irgunner  That random zanki card with colobomas associated with a failure of the choroid fissure to close messed me up
mnemonicsfordayz  Seems like the key to this question is in what is omitted from the question stem: there is no mention of vision loss. If we assume there is no vision loss, then we can eliminate things associated with visual acuity (weird to think of in 2 week old but whatever): C, D, E, F. Also, by @hayayah 's reasoning, we eliminate E & F. If you reconsider the "asymmetric left pupil" then the only likely answer between A & B is B, Iris because the iris' central opening forms the pupil. I mistakenly put A because I was thinking of the choroid fissure and I read the question incorrectly - but it's a poorly worded question IMO.

 +18  (nbme23#11)

He has fecal incontinence so his external sphincter is damaged, which is innervated by the pudendal n. (S2-S4). The pelvic splanchnic nerves, which mediate the erection process, are also S2-S4.

thomasburton  Why could this not be dysuria?
lilyo  I think that you are thinking about urinary incontinence. If we damage the pudendal nerve S2-S4, you can exhibit urinary and fecal incontinence since this nerve innervates both the urethral and the external anal sphincters. However since the pelvic splanchnic nerves also have roots that originate in S2-S4 a patient with pudendal nerve damage will also have impotence since these control the erection reflex. He wouldn't have dysuria which is painful urination. Most likely caused by a urethral infection or a blockade of the urinary tract. He would have urinary incontinence. I hope this helps.
alexxxx30  dysuria is painful urination...if it said urinary incontinence then you'd be right. But decreased innervation wouldn't cause pain (that would mores be associated with UTI)
peqmd  Another approach is fecal incontinence => parasympathetic nerve dysfunction => no boner
dul071  ahhhhh fucked up with terminology again thinking dysuria was urinary incontinence

 +7  (nbme23#39)

Carbonic anhydrase inhibitors (eg, acetazolamide) and loop diuretics (eg, furosemide) are thought to exert their effect on ICP by reducing cerebrospinal fluid (CSF) production at the choroid plexus.

Google says mechanism is unknown LOL.

usmleuser007  Just FYI: Mannitol can also be used to reduce ICP by drawing free water out of CNS Howeveer, it can cause hypernatremia, pulmonary edema, and expansion of ECV can exacerbate heart failure

 +14  (nbme22#15)

This is a patient case of postpartum thyroiditis. Can arise up to a year after delivery and has lymphocytic infiltrate.

almondbreeze  FA 2019 pg 338
waterloo  Although history seems to point towards that, she has an enlarged thyroid, and in postpartum thyroiditis, thyroid usually normal in size (from FA). regardless either would have lymphocytes infiltrating.

 +8  (nbme22#16)

Pregnancy + Hx of thrombosis --> think antiphospholipid syndrome

The PT and PTT are prolonged d/t interference from the antibodies to phospholipids. Thrombin time normal.

Had to find research articles about it so take it from here and don't waste your time...

monoloco  yeah, i’ve never heard of antiphospholipids increasing PT time ...
goldenwakosu  Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis)
johnthurtjr  I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies.
link981  No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it
yb_26  UWorld mentioned "prolong aPTT (and sometimes PT)" in APS
oslerweberrendu  @yb_26 Can u please tell the QID because the one I have seen it says, "Although patients often have prolonged ptt (because the antiphospholipid interferes with ptt test), pt is normal." QID: 1298

 +5  (nbme22#22)

Growth hormone releasing hormone acts via G-coupled receptors. G coupled receptors need GTP to become activated and GTPase to become inactivated.

No GTP-ase --> chronically active growth hormone releasing hormone receptor --> constant activation of adenylyl cyclase / cAMP pathway and release of growth hormone.

mcl  This figure is useful https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png
mcl  [link](https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png)
meningitis  How did you knkow it was GHRH and not GH perse?
meningitis  nevermind; I just read down below. Thank you

 +6  (nbme22#46)

X in the image is the small intestine. Its characteristic feathery appearance after a barium meal is due to permanent circular folds and villi. The villi give the small intestine a great mucosal surface area.

nwinkelmann  Yes. The appearance of the mucosal folds depends upon the diameter of the bowel, and when they fold they appear feathery. Mucosal folds are largest and most numerous in the jejunum and tend to disappear in the lower part of the ileum.

 +14  (nbme21#11)

HELLP syndrome: Hemolysis Elevated Liver enzymes Low Platelets.

A manifestation of severe preeclampsia. Blood smear shows schistocytes. Can lead to DIC and hepatic subcapsular hematomas Ž rupture Ž severe hypotension.

mambaforstep  FA 2019 pg 629
qball  One thing I find odd with this question is HELLP is a manifestation of severe preeclampsia but she has had an otherwise unremarkable pregnancy. Shouldn't she have hypertension/edema in regards to her pregnancy beforehand?
demihesmisome  Pre-eclampsia, if not severe, can be entirely asymptomatic.

 +13  (nbme21#22)

Cysteine-cysteine chemokine receptor 5 (CCR5) is a protein found on the surface of CD4 cells.

yotsubato  Note, this is NOT in FA
sbryant6  It is in UWorld.
almondbreeze  it's in FA2019 pg.110
almondbreeze  but missing the full name for CCR5
demihesmisome  CXCR4 is also a chemokine receptor.

 -4  (nbme21#28)

Mixed venous oxygen saturation (SvO2) is measured in the pulmonary artery. SvO2 samples the true mixed venous blood leaving the right heart. Measurement of mixed venous oxygen saturation (SvO2) from the pulmonary artery has been advocated as an indirect index of tissue oxygenation.

In cardiogenic shock you have decreased CO --> decreased O2 delivery --> decreased SvO2.

 +4  (nbme21#8)

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
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.
kimcharito  it said broad based gait and nystagmus
lilmonkey  She is/was an alcoholic and appears pretty much homeless, just not drunk at this moment.
fatboyslim  @ dr janitor. The question says "physical exam shows a broad-based gait and nystagmus."
suckitnbme  NBME questions also stereotype the shit out of their patients

 +17  (nbme21#27)

The thyroid is supplied with arterial blood from the superior thyroid artery, a branch of the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk.

 +7  (nbme21#40)

Note: The abducens n. is actually the nerve most likely to be damaged by an expanding internal carotid aneurysm in the cavernous sinus but they give you specific CN3 function in this question.

hungrybox  One pupil larger than the other indicates damage to the pupillary light reflex - afferent: CN II, efferent: CN III.
cienfuegos  A little more info regarding other sxs (via UW): -cavernous carotid aneurysm: small usually asx, enlargement can cause u/l throbbing HA &/or CN deficits. VI most common thus ipsilateral lateral rectus weakness, can cause esotropia = inward eye deviation & horizontal diplopia worse when looking toward lesion -can also damage III, IV and V1/2 -can occasionally compress optic nerve or chiasm thus ipsilateral monoocular vision loss or non-specific visual acuity decrease

 +31  (nbme21#33)

the majority of carbon dioxide molecules are carried as part of the bicarbonate buffer system. In this system, carbon dioxide diffuses into the RBCs. Carbonic anhydrase (CA) within RBCs quickly converts the carbon dioxide into carbonic acid (H2CO3). Carbonic acid is an unstable intermediate molecule that immediately dissociates into bicarbonate ions (HCO3-) and hydrogen (H+) ions.

The newly synthesized bicarbonate ion is transported out of the RBC into the plasma in exchange for a chloride ion (Cl−); this is called the chloride shift. When the blood reaches the lungs, the bicarbonate ion is transported back into the RBC in exchange for the chloride ion. The H+ ion dissociates from the hemoglobin and binds to the bicarbonate ion. This produces the carbonic acid intermediate, which is converted back into carbon dioxide through the enzymatic action of CA. The carbon dioxide produced is expelled through the lungs during exhalation.

hungrybox  Amazing explanation. Thank you!!
namira  in case anyone wants to visualize things... https://o.quizlet.com/V6hf-2fgWeaWYu1u23fryQ.png
ergogenic22  CO2 is carried in the blood is bound to hemoglobin, known as carbaminohemoglobin (HbCO2) (5%), dissolved CO2 (5%), bicarb is 90%
pg32  Nice explanation, but can anyone clarify how we know from the question that we are measuring HCO3 rather than dissolved CO2?
qball  @pg32 This question is asking about what accounts for the LARGER amount of co2 and the HCO3 buffer is about 85% of this transport and dissolved C02 is about 5-7%. https://courses.lumenlearning.com/wm-biology2/chapter/transport-of-carbon-dioxide-in-the-blood/
teepot123  fa 19 pg 656

 +2  (nbme21#46)

Most human cancers are d/t a loss of function of TP53 gene.

 +7  (nbme21#1)

Invasive cervical carcinoma is associated with hydronephrosis and renal failure d/t CA spreading through uterine wall and into the bladder.

 -1  (nbme21#28)

Although half these hormones can actually also be secreted from the duodenum, the duodenum is associated the most with CCK release.

didelphus  Gastrin, intrinsic factor, and pepsin are secreted by the stomach. VIP is synthesized in neurons, so CCK (from I cells of duodenum) would be most directly affected by a duodenectomy.
teepot123  fa 19 pg 365

 +18  (nbme21#23)

Lymph flow rate is usually low. It is influenced primarily by the rate of lymph formation. For example, if blood capillary pressure is increased by arterial vasodilation or venous constriction, the flow rate of lymph increases. Also, the flow rate is affected by compression of lymphatics by contraction of neighboring musculature and by negative intrathoracic pressure (breathing).

Interstitial pressure (so pressure in the ECF, which would increase if given IV saline) and lymph flow are positively related. A small increase in interstitial volume greatly increases its pressure, promoting lymph flow that acts to restore the interstitial volume to normal.

more on this topic: https://www.ncbi.nlm.nih.gov/books/NBK53448/

linwanrun1357  Do not understand the breathing (choice C and D) breath in and out are different?
khanhluong  I don't know if it's correct or not but how I approached C & D was that they both cause vasoconstriction in the arterioles (because this is the lung where hypoxia causes vasoconstriction), which decreases hydrostatic pressure through the capillaries and eventually decreases lymph flow. Maybe I completely got this question right for wrong reason, but I felt that it works with all of the answers. For F) I was thinking that it would cause increased capillary oncotic pressure which causes more fluid to go into the capillary than into the lymph vessels... Here's a picture: http://www.lymphedemablog.com/wp-content/uploads/2011/09/Lymphatics.gif

 +3  (nbme21#24)

Hyperacute transplant rejection occurs within minutes d/t pre-existing recipient antibodies that react to donor antigen (type II hypersensitivity reaction), activate complement.

mcl  [Useful figures illustrating transplant rejection](https://www.stomponstep1.com/transplant-rejection-hyperacute-acute-chronic-graft-versus-host/)

 +0  (nbme21#14)

Cretinism (congenital hypothyroidism) is the most common cause of treatable mental disability. Causes poor brain development.

 +16  (nbme21#50)

Catheter placement:


Recall that the lung apex extends above the first rib.

hungrybox  His expression is so blissful. U can tell they're shootin up some full u-opioid agonist codeine type of shit and not some shitty partial u-opioid agonist buprenorphine type of shit or some shit like loperamide that doesn't even act on the CNS
rerdwins  even better, if you recall that the esophagus is RETROperitoneal ( its in like half the answer choices). hence, to get to it you have to go WAAYYYYY deep ( like rick and morty smuggling shit). after that, the lung option makes the most sense.
hello  Also, pulmonary artery is way too far away to be damaged by internal jugular vein catherization.
makinallkindzofgainz  @hungrybox my mans just slipped in 3 high yield facts within a joke
makinallkindzofgainz  @hayayah, I have an issue with that picture unless I'm missing something. In every other source I have, the internal jugular vein lies LATERAL to the common carotid artery. The picture you provided shows the internal jugular veins medial to the common carotid artery.
cmun777  Look at the other side... I think it must be the manipulation of turning the head to the opposite side that better exposes the jugular for catheterization purposes

 +13  (nbme21#26)

Stretch or dilation of the cervix and vagina are strong stimuli for oxytocin secretion, mediated by neural pathways called the Ferguson reflex.

Article: https://www.sciencedirect.com/topics/neuroscience/ferguson-reflex

readit  This is also why ob-gyn's will massage the uterus (which is part of the birth canal) after delivery. It's to get the body to release oxytocin and cause the uterus to contract (to prevent postpartum hemorrhage)
jennybones  Please why is estrogen not the answer, I thought estrogen would upregulate oxytocin receptors and increase oxytocin secretion?
drzed  During pregnancy, oxytocin RECEPTORS are upregulated (by estrogen) as parturition approaches, but the ferugson reflex creates a positive feedback loop where the dilation of the cervix further releases more oxytocin. The inciting event that starts this feedback loop is the dilation of the cervix leading to a direct release of oxytocin, not the presence of more oxytocin receptors.

 +3  (nbme21#16)

This pt has an ASD which is a "hole" between the LA and RA. Fixing it could damage the AV bundles.

sahusema  the atrioventricular bundle is also called the bundle of his

 +10  (nbme21#8)

Renal artery stenosis is going to decrease blood flow to the kidney. JG cells sense the decrease in perfusion pressure and secrete renin.

Renin is produced by the JG cells, JG cells are in the cortex (they are modified smooth muscle of the afferent arteriole).

 +8  (nbme21#47)

Secondary hyperparathyroidism (usually d/t chronic renal failure).

Lab findings include ↑ PTH (response to low calcium), ↓ serum calcium (renal failure), ↑ serum phosphate (renal failure), and ↑ alkaline phosphatase (PTH activating osteoBlasts).

haliburton  also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia.
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain
nala_ula  Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism.
privatejoker  Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious.
fatboyslim  @cr the question asked "the patient's BONE PAIN is most likely caused by which of the following?" Increased levels of 25-hydroxycholecalciferol might exist in that patient, but it wouldn't cause bone pain. PTH causes bone pain because of bone resorption
suckitnbme  @privatejoker ALP is included in the standard lab values
makinallkindzofgainz  @privatejoker ALP is listed under "Phosphatase (alkaline), serum" in the lab values
pg32  Why does AlkPhos increase in renal osteodystrophy? The PTH would be trying to stimulate bone resorption (increase osteoCLAST activity), not bone formation (osteoBLAST activity).
drzed  @pg32 the only way to stimulate an osteoclast in this case (e.g. via PTH) is by stimulating osteoblasts first (thru RANKL/RANK interaction), thus ALP increases.

 +2  (nbme21#44)

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.
d_holles  So you're saying that there's two crosses, making it ipsilateral? @mci

 +11  (nbme21#29)

P. 91 of FA has a quick explanation for this!

Basically once you're in a starving state there's still hepatic gluconeogenesis going on (as well as using FFA) but the gluconeogenesis is coming from peripheral tissue lactate and alanine.

 +5  (nbme21#19)

This pt has osteomalacia / rickets (since he's a kiddo). Caused by defective mineralization of osteoid (osteomalacia) or cartilaginous growth plates (rickets, only in children).

Most commonly d/t Vitamin D deficiency.

Children with rickets have pathologic bow legs (genu varum), bead-like costochondral junctions (rachitic rosary), craniotabes (soft skull).

  • Dec. Vitamin D (normal function is to reabsorb Ca2+ and PO4)

  • Dec. serum Ca2+

  • Dec.  serum PO4

  • Inc. PTH

 +8  (nbme21#31)

With this question, I think they want you to recognize that the patient isn't having chest pain related to the heart. They emphasize several rib fractures and a pneumothorax but don't indicate any heart damage (lack of adventitious sounds = no pulmonary edema indicated or a lung issue related to heart problem).

The pericarditis is what's innervated by the phrenic n. Seeing as how his heart is fine, the fractured ribs are probably what are causing him pain via the intercostal nerves.

didelphus  Visceral pain is typically poorly localized (heart attacks are usually described as "crushing pressure" that radiates to the shoulder or neck), so this patients "sharp" right-sided pain in the setting in multiple right-sided rib fractures is likely related to the ribs. The intercostals run with the ribs and provide sensation to the chest wall.

 +1  (nbme20#29)

An adverse effect of doxycycline is photosensitivity.

rio19111  Why not Cipro?
raspushok  Which antibiotics increase photosensitivity? Several antibiotic classes commonly cause photosensitivity, including tetracyclines (doxycycline), quinolones (ciprofloxacin, norfloxacin), and sulphonamides (trimethoprim/sulfamethoxazole, sulfasalazine). The tetracycline minocycline is not generally associated with photosensitivity. WHY not damn cipro?
medninja  I think it is because Cipro is not commonly used for acne treatment

 +3  (nbme20#48)

Pt. has Familial dyslipidemias. Type I—Hyperchylomicronemia.

estefanyargueta  Lipoprotein lipase: degradation of TGs circulating in chylomicrons and VLDLs.
breis  FA 2019 pg 94

 +1  (nbme20#15)

Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, and ICP.

He wants to increase ICP (cerebral vasodilation) which he can do by decreasing the respiratory rate (hypoventilation).

 +8  (nbme20#21)

Hypersensitivity pneumonitis—mixed type III/IV hypersensitivity reaction to environmental antigen. Causes dyspnea, cough, chest tightness, headache. Often seen in farmers and those exposed to birds. Reversible in early stages if stimulus is avoided.

It's a type of restrictive lung disease.

 +4  (nbme20#32)

Glucagonoma: Tumor of pancreatic α cells Žcausing an overproduction of glucagon.

Presents with 5D’s:

  • Dermatitis(necrolytic migratory erythema)
  • Diabetes (hyperglycemia)
  • DVT
  • Declining weight
  • Depression
killme  And the sixth D: Diarrhea
ergogenic22  a) CAT1 and CAT2 are important enzymes of fatty acid beta oxidation. Glucagon upregulates this process b) glycogen formation is inhibited by glucagon, so that glucose can be used by cells c) acetyl CoA carboxylase is used for fatty acid synthesis and thus decreased by increased glucagon d) glucagon increases ketogenesis
dermgirl  Basically, they want to know what is the function of glucagon.

 +3  (nbme20#18)

Zollinger-Ellison syndrome: Gastrin-secreting tumor (gastrinoma) of pancreas or duodenum.

hello  Can you please explain how gastrin relates to the physical exam findings in the patient?
amorah  I believe the logic behind it is patient has pain and black stool, suggesting peptic ulcer with bleeding. Since pain is not relieved by antiacid and H2 blockers, it suggests ectopic source to stimulate the excessive acid. Among all, gastrin by ZE syndrome fits the most.

 +1  (nbme20#10)

She has a vitamin C deficiency. Scurvy features swollen gums, easy bruising, petechiae, perifollicular and subperiosteal hemorrhages.

 +5  (nbme20#31)

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/
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

 +10  (nbme20#7)

This is a primary central nervous system lymphoma. Most commonly associated with HIV/AIDS; pathogenesis involves EBV infection.

Considered an AIDS-defining illness. Variable presentation: confusion, memory loss, seizures. Mass lesion(s) (may be ring-enhancing in immunocompromised patient) on MRI, needs to be distinguished from toxoplasmosis via CSF analysis or other lab tests. Toxo usually has multiple ring enhancing lesions.

peridot  For those who are curious, this is on p.422 of FA2019

 +14  (nbme20#17)

Also, you shouldn't be seeing end-organ damage or increased renin / kidney response with a previously healthy patient that just developed essential HTN. The body doesn't want to increase renin when it has HTN. However, if you have stenosis, the kidneys freak out because they're not getting enough flow and think the whole body isn't either, so they activate the RAAS system. When you give them an ACE-I, the renin is still being produced by the kidney, it just isn't being converted to angiotensin-II.

To eliminate other choices:

  • He has increased renin activity so you can eliminate primary aldosteronism. That has inc. aldosterone, dec. renin.
  • No signs or sxs of Cushing's so that's eliminated.
  • 11-B-hydroxylase deficiency would sxs with the genitalia. You'd have dec. renin activity (aldosterone-like effects still present).
  • Essential HTN: explained above
sammyj98  I like you sticking up for the kidneys, thinking they're increasing Renin for the benefit of the whole body, but lets face it, the kidneys are a couple selfish dicks who want the high blood pressure all for themselves. LeftVentricularSolidarity

 +6  (nbme20#4)

A fractured cribriform plate (anterior skull trauma) can result in leaking of cerebrospinal fluid into the nose and loss of sense of smell. Smell plays a large role in the perception of taste. So, in practice, a patient may complain of loss of taste rather than of smell.

brownielove79  can it be a facial nerve??? with lateral head trauma (injury during passage through middle ear, or external auditory canal??) doubt!!!
doodimoodi  Olfaction is actually more important that tongue sensation in terms of food taste (think of how food tastes bland when you have a cold)
doodimoodi  than*
champagnesupernova3  If taste is completely lost then it's an olfactory issue. If its lost only on a part of the tongue then the nerve that provides taste to that area is suspected.
veryhungrycaterpillar  UWorld QID 12227 The sense of taste isn't lost due to CSF in the nose, but due to avulsion of olfactory rootlets.

 +6  (nbme20#47)

You have a 25% chance of inheriting the same HLA markers as your siblings.

masonkingcobra  Two siblings have a 25% chance of being genotypically HLA identical, a 50% chance of being HLA haploidentical (sharing one haplotype), and a 25% chance that they share no HLA haplotypes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628004/
alimd  It looks exactly like an Autosomal recessive mode of inheritance.

 +3  (nbme20#36)

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
dr_cruceta  because the question said irregular vacuolated cells, describing fat cells. Rhabdomyosarcoma comes from skeletal muscle.

 +2  (nbme20#49)

Beta blockers as antiarrhythmics suppress abnormal pacemakers by decreasing the slope of phase 4 --> prolonging phase 4.

chandlerbas  piano player sliding the keys to the left ---> delays diastolic depolarization --> rate control

 +1  (nbme20#12)

Pelvic splanchnic nerves are part of the parasympathetic system.

masonkingcobra  The inferior hypogastric plexus innervates internal pelvic viscera; has both sympathetic and parasympathetic components; parasympathetic contribution helps stimulate detrusor of bladder (along with pelvic splanchnic nerves), sympathetic contribution helps stimulate internal urethral sphincter

 +8  (nbme20#44)

Down Syndrome Labs:

  • inc. nuchal translucency
  • inc. hCG
  • inc. inhibin
  • decreased AFP
  • decreased PAPPA
celeste  I remember this as Down Syndrome has high HI (hCg and inhibit)
temmy  Thanks celeste. I'll remember Hi

 +0  (nbme20#44)


 +6  (nbme20#19)

It's transitional cell carcinoma, which smoking is a common risk factor for; it can involve the renal pelvis/calyces. The histo image shows the papillary nature of the tumor (however it can also be flat or nodular according to Pathoma).

Also known as urothelial carcinoma. Most common tumor of urinary tract system (can occur in renal calyces, renal pelvis, ureters, and bladder). Can be suggested by painless hematuria (no casts).

usmlecrasher  i'm sorry guys it's bladder cancer blocking urine flow => reflux ureteral widening => reflux nephropathy.
hello_planet  FA 2019 pg 588

 +9  (nbme20#13)

Diagnosis of Syph: Visualized by immunofluorescence or dark-field microscopy; serology is important – two types of antibodies:

  • Ab binds to cardiolipin: an antigen found in mammalian mitochondrial membranes and in treponemes; a cheap source of antigen is cow heart, which is used in screening tests; very sensitive in primary, except early, and secondary syphilis – titer may decline in tertiary and with treatment; but not specific – must confirm with FTA-ABS.
  • Examples include Venereal Disease Research Lab (VDRL), Rapid plasma Reagin (RPR), Automated Reagin Test (ART), or Recombinant Antigen Test (ICE)

  • Specific tests for treponemal antibody are more expensive; earliest antibodies bind to spirochetes: these tests are more specific and positive earlier; usually remain positive for life, but positive n patients with other treponemal diseases and may be positive in Mono, RF, Lupus, Leprosy, Lime, and Drug users.

  • The most widely used is Fluorescent Treponemal Antibody- Absorption (FTA-ABS) or Treponema pallidum microhemagglutination (MHA-TP)

 +14  (nbme20#17)

This is reactive polycythemia vera, which is due to high altitude or lung disease. SaO2 is low, and EPO is increased.

Another way to approach the question is looking at the blood smear. It's pretty normal (no megakaryocytes, no increased number of platelets, no rods, nothing blue, etc). A blood smear from a COPD patient will be normal. Just an increased number of RBCs due to the increased EPO leading to increased Hgb.

mbourne  You shouldn't call it reactive polycythemia "vera", as polycythemia vera is a seperate disease with entirely different etiology. This is Reactive Polycythemia, or as another poster said, appropriate absolute polycythemia secondary to chronic hypoxia.

 +7  (nbme20#30)

He's not eating enough.

One of cortisol's functions is to increase gluconeogenesis, lipolysis, and proteolysis.

ankirin  Why wouldn't it be T3? Thyroid hormones also ↑blood sugar and break down lipids
waterloo  @ankirin his symptoms aren't really specific for T3. They don't mention tremors, exopthalmos etc. I think just in physiologic terms, you can bet cortisol is more increased. It's not a great question though imo

 +4  (nbme20#25)

This is a presentation of mitochondrial myopathy. They often present with myopathy, lactic acidosis, and CNS disease. 2° to failure in oxidative phosphorylation. Muscle biopsy often shows “ragged red fibers”.

There is variable expression in a population or even within a family due to heteroplasmy in mitochondrial inheritance.

 +5  (nbme20#18)

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
mbourne  @hayayah, Although this is a bit outside of the realm of Step 1, I want to clarify a point. Early MI does not typically lead to ST-depression. Early MI will typically present with hyperacute T-waves with straightening of the ST segment, and then evolve towards more familiar "STEMI" morphology. Great image representation of MI EKG changes: https://4.bp.blogspot.com/-_UbS4PvbTZE/Wr0M27TZhUI/AAAAAAAABB0/-M8FSuvTKeEGkx-7HrEd45Fl0phb2-T8gCLcBGAs/s1600/Progression%2Bof%2BACO%2Bfinal_diagram.png ST depression from subendocardial ischemia can occur with supply/demand mismatch --> ISCHEMIA, but not Myocardial INFARCTION.

 +6  (nbme20#37)

Defective homologous recombination is seen in breast/ovarian cancers with the BRCA1 gene mutation.

johnthurtjr  Ashkenazi Jews have a higher risk of inheriting the BRCA1 and BRCA 2 gene mutations, just another tip!
lebron james  BRCA1/BRACA2 are involved in the repair of DNA double stranded breaks
samsam3711  Other answers: DNA Mismatch Repair: Lynch Syndrome (MLH1, MSH2) DNA Nucleotide Excision Repair: Xeroderma Pigmentosa

 +4  (nbme20#18)

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.

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.
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"

 +23  (nbme20#32)

A big thing here too is noticing that the ALP is decreased. Osteoblast activity is measured by bone ALP. I think that was the main focus here and not that you necessarily need to know the CBFA1 gene mutation.

sympathetikey  Exactly. That's the only way I got to the answer.
pakimd  isnt increased alk phos consistent with increased osteoblastic activity?
champagnesupernova3  A defect with chondrocytes would cause an short limbs like in achondroplasia so those are ruled out
pg32  Exactly. Can also be helpful if you remember that the clavicles are formed by intramembranous ossification rather than endochondral; that allows you to rule out the chondroblast/cyte answer choices.

 +7  (nbme20#29)

Most important cause of viral myocarditis is Coxsackie (picornavirus).

 +3  (nbme20#3)

Most restriction enzymes bind palindromes.

So both 5'CCGG or 3'GGCC would have been acceptable in this scenario.

meningitis  Yes, correct. The 5'GGCC option could cause some confusion.
guillo12  I really don't understand the question nor the answer. Can someone explain it for dummies like me?
whossayin  yes please.. I'm with guillo12 on this
sugaplum  @guillo12 @whossayin questions says you've created a new cut site, 1. look at the region on the sick vs healthy. The C to G is the change 2. Write out the sick "CCGG" from 5'3'- you could write out the whole thing, but the answer only has 4 letters, so being lazy here 3. write under it, its complement, the dna base pair. So "GGCC" 4. remember both strands are going in opposite directions when you write them out on top of each other. 5. So the bottom strand actually reads 5' CCGG 3' so that is the answer I hope that clears it up
shirafune  To add to the palindrome part, many restriction endonucleases actually function as dimers. Each individual subunit usually has a nickase, so to create a double-stranded break in DNA, they must bind a palindrome so that each enzymatic domain creates a single-stranded break (thus a double-stranded break).
alimd  Why do we start from CCGG? Why not CGGG or TACC?
alimd  Why do we start from CCGG? Why not CGGG or TACC?

 +4  (nbme20#22)

In eukaryotic cells, two major pathways—the ubiquitin-proteasome pathway and lysosomal proteolysis—mediate protein degradation.

The major pathway of selective protein degradation in eukaryotic cells uses ubiquitin as a marker that targets cytosolic and nuclear proteins for rapid proteolysis.

The other major pathway of protein degradation in eukaryotic cells involves the uptake of proteins by lysosomes and digestion by proteases.

missi199  Could I ask why it is not Lysosomal protease
smc213  "Certain viruses have evolved to recruit the cellular E3 ligases to induce the degradation of cellular proteins that might have harmful effects on the viral life cycle. For instance, the protein E6 of Human papillomavirus (HPV) recruits the cellular E3 ubiquitin ligase E6-AP to induce ubiquitination and degradation of p53, thereby allowing viral replication." from: https://www.mdpi.com/1999-4915/9/11/322/htm
smc213  USMLE Kaplan: A majority of cellular proteins are degraded via the ubiquitin proteasome pathway, including many proteins that play a role in maintaining cellular homeostasis. These include proteins that regulate the cell cycle, apoptosis, etc.

 +1  (nbme20#34)

Pt has diabetes inspidus.

If urine concentrates with administration of ADH analog, the kidneys are responsive and the problem is with ADH production in the hypothalamus or release in the post. pituitary.

hello_planet  FA 2019 pg. 344

 +4  (nbme20#24)

Patient has chronic diarrhea leading to metabolic acidosis. Respiratory compensation will lead to decreased CO2 (respiratory alkalosis via hyperventilation).

usmleuser007  Aldo would increase b/c protons are anti-transported with potassium --> leads to hyperkalemia --> aldo activation ADH will also increase b/e of volume loss

 +3  (nbme20#40)

Squamous cell carcinoma characteristics: cavitation, hypercalcemia, associated with smoking.

Small cell may actually produce antibodies against presynaptic Ca channels.

smc213  Increased PTHrP seen in squamous cell lung cancer leads to increased Ca2+ levels

 +4  (nbme20#45)

Absolute risk: the difference in risk (not the proportion) attributable to the intervention as compared to a control.

(.12) - (.04) = .08

ARR = 8%

nwinkelmann  This isn't actually correct. Absolute risk is actually just the incidence, or the same as event rate. Absolute risk reduction = the difference in risk (not the proportion) attributable to the intervention as compared to the control, and thus ARR = incidence unexposed - incidence exposed x 100%. In this example, the incidence of exposed is the incidence in the new treatment group, and incidence unexposed is incidence in standard treatment group.

 +5  (nbme20#29)

Septic shock is a type of distributive shock which is marked by massive vasodilation (d/t inflammatory response) causing decreased SVR, decreased preload / PCWP, and increased CO.

smc213  Septic shock can also present with hypothermia <36C
bethune  Why is it not gastrointestinal bleeding?
beanie368  GI bleeding would present with increased SVR as a response to hypovolemia
mysteriousmantyping  Why would this not be pulmonary embolism?
step1passfail  Pulmonary embolism would cause a decrease in cardiac output. There is increased pressure in the high compliant RV which can bulge and compress the LV, decreasing its preload. CO=Heart rate x stroke volume and stroke volume is partially determined by preload. If the pulmonary embolism is large enough, it can also obstruct the pulmonary vessels and subsequently not have enough blood going to the LA and LV, ultimately making the cardiac output near 0.

 +2  (nbme20#2)

Allopurinol inhibits xanthine oxidase. It is used for chronic gout as well as prevention of tumor-lysis associated urate nephropathy.

betcher  I got confused because the question stem she was on an extensive chemotherapy regimen and got scared away from Xanthine Oxidase because of its potentially for interaction with 6MP/Azathioprene, but I guess since neither of those were directly stated in the question stem I should have gone with Xanthine Oxidase inhibitor to prevent tumor lysis as stated above

 +9  (nbme20#40)

The only time you transfuse a Jehovah's Witness patient is when the patient is a minor (<18 years old).

medstudent65  I get why the answer is not to proceed but simply stating at admissions you dont want blood products means nothing without proper paperwork being signed.
md_caffeiner  @medstudent65 From what I recall paperwork is needed for example: if the pt is unconscious and wife says that he is Jehovah's Witness.

 +13  (nbme20#20)

Sensitivity tests are used for screening. Specificity tests are used for confirmation after positive screenings.

Sensitivity tests are used for seeing how many people truly have the disease. Specificity tests are for those who do not have the disease.

A highly sensitive test, when negative, rules OUT disease. A highly specific test, when positive, rules IN disease. So, a test with with low sensitivity cannot rule out a disease. A test with low specificity can't rule in disease.

The doctor and patient want to screen for colon cancer and rule it out. The doctor would want a test with high sensitivity to be able to do that. He knows that testing her stool for blood will not rule out the possibility of colon CA.

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in
usmlecrasher  can anyone pls explain why it is not << potential false- positive results >> ???
almondbreeze  correct me if I'm wrong, but 'high FP (choice C)=low specificity (choice B)'. Whereas high specificity is required to rule in dz
almondbreeze  picked positive predictive value myself. can anyone explain why not PPV?
williamfreakingosler  The principle @hayayah is talking about (a negative test being relied upon to reliably rule out) is negative predictive value ("NPV"). I don't see why "uncertain NPV" isn't the correct answer, particularly because NPV is predicated on the disease having the same base rate in the person(s) being tested as in the population that was characterized for the test statistic. Given that the patient has a strong family history of colon cancer, the NPV of FOBT is uncertain. Said another way, the sensitivity of a test does not change with the population, but the NPV does. The whole reason the doctor is denying FOBT is because of bayesian thinking (a priori information related to family history), and from my point of view bayesian logic is more relevant to PPV/NPV than to sensitivity, hence my confusion over why NPV isn't the right answer.
ibestalkinyo  I thought negative predictive value for the same reasoning

 +6  (nbme20#46)

By age 75, the thymus is little more than fatty tissue. Fortunately, the thymus produces all of your T cells by the time you reach puberty. They are long-lived and that's why you can lose your thymus without impairment of your immune system.

sweetmed  Memory T cells live for six months or less in healthy humans (Westera et al., 2013), whereas naive T cells can live for up to nine years
whossayin  so the bone marrow does not take the role of the thymus?
dr_jan_itor  @sweetmed, does that mean that if someone loses their thymus, they would develop imunodeficiencies appx 9 years later as the naive T cells have died off?
hpsbwz  @dr_jan_itor no, because once all of the thymocytes become T-lymphocytes, they are stored in lymphoid organs until they're needed. this is why removal of the thymus in MG does not cause any immune system deficiency.
peridot  @dr_jan_itor From wiki: "Thymic involution results in a decreased output of naïve T lymphocytes – mature T cells that are tolerant to self antigens, responsive to foreign antigens, but have not yet been stimulated by a foreign substance. In adults, naïve T-cells are hypothesized to be primarily maintained through homeostatic proliferation, or cell division of existing naïve T cells. Though homeostatic proliferation helps sustain TCR even with minimal to nearly absent thymic activity, it does not increase the receptor diversity."

 +5  (nbme20#22)

GnRH agonists like Leuprolide are effective for patients with breast CA because if given in a continuous fashion, they downregulate the GnRH receptor in the pituitary and ultimately decrease FSH and LH.

md_caffeiner  Quick question: FA19 691 says Leuprolide ClINICAl USE is Uterine fibroids, endometriosis, precocious puberty, prostate cancer, infertility... I guess all except infetility(pulsatile?) are used as continuous?
usmlecrasher  GnRH is synthesized and released in pulsatile fashion , so if you give in pulsatile way you induce GnRH effect , and if given in continuous way it will suppress synthesis, depended the desired effect you want to achieve - infertility induce GnRH with pulsatile , stop synthesis for prostate cancer , testicular cancer , hormone dependent Breast cancer give continuous

 +2  (nbme20#37)

Clinical use of K-sparing diuretics:

  • Hyperaldosteronism
  • K+ depletion
  • HF
  • hepatic ascites (spironolactone)
  • nephrogenic DI (amiloride)
  • antiandrogen
redvelvet  Patients with hepatic ascites have hyperaldosteronism; because the intravascular volume is escaped to third space(ascites). So adding spironolactone is a good choice.
champagnesupernova3  Always combine a K+ losing diuretic with a K+ sparing diuretic

 +1  (nbme20#15)

Substance P (SP) is an undecapeptide present in the CNS and the peripheral nervous system. A compound thought to be involved in the synaptic transmission of pain and other nerve impulses.

mambaforstep  also, apparently enkephalins attenuate substance p... so it would be dec her pain.

 +3  (nbme20#28)

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
benitezmena  Yes I dont understand why the called them Anti-platyelet antibodies and not specifically Anti-heparin bound to PF4 on platelets. Its just not the right antibody
benitezmena  Antiplatelet antibodies would be for ITP, but also anti-megakaryocyte antibodies would also be for ITP.

 +25  (nbme20#44)

LV stopped working, pressure backed up into pulm circuit. Pulm circuit roughly is made of 3 "parts" - the capillaries, interstitial space, and the alveoli.

In cardiogenic shock, the extra blood increases capillary hydrostatic pressure, driving fluid into the interstitial space. Compared to the alveoli, the interstitial space now has more fluid (thus more interstitial hydrostatic pressure and less oncotic pressure due to ratio of fluid to protein), and as a result of this unbalancing of forces, fluid moves into the alveoli --> pulmonary edema.

 +7  (nbme20#8)

Atrophy is decrease in tissue mass due to decrease in size (increased cytoskeleton degradation via ubiquitin-proteasome pathway and autophagy;  decreased protein synthesis) and/or number of cells (apoptosis). Causes include disuse, denervation, loss of blood supply, loss of hormonal stimulation, poor nutrition.

mambaforstep  FA 2019 pg 206

 +6  (nbme20#25)

Most common cause of gastric outlet obstruction in infants. Palpable olive-shaped mass in epigastric region, visible peristaltic waves, and nonbilious projectile vomiting at ∼2–6 weeks old.

Ultrasound shows thickened and lengthened pylorus. Treatment is surgical incision (pyloromyotomy).

katsu  FA 2019 p. 353: Most common cause of gastric outlet obstruction in infants (1:600). Palpable olive-shaped mass in epigastric region, visible peristaltic waves, and nonbilious projectile vomiting at ∼ 2–6 weeks old. More common in firstborn males; associated with exposure to macrolides. Results in hypokalemic hypochloremic metabolic alkalosis (2° to vomiting of gastric acid and subsequent volume contraction). Ultrasound shows thickened and lengthened pylorus. Treatment is surgical incision (pyloromyotomy).

 +2  (nbme20#39)

Isotretinoin is used to treat severe cystic acne. It is a teratogen. Can cause multiple severe birth defects. Contraception is mandatory. RXR is a retinoid X receptor.


 +7  (nbme20#24)

Patient has congenital hypothyroidism (cretinism). Findings: pot belly, pale, puffy-faced, umbilical hernia, macroglossia, hypotonia, poor brain development (MC cause of treatable mental retardation), large anterior fontanelles.

whossayin  how can you differentiate the symptoms of cretinism from Down syndrome?
step1soon  @whossayin Down Syndrome: upslanting palpebral fissures, atlantoaxial instability, bent little finger, congenital heart disease, displacement of the tongue, excess skin on the back of the neck, flaccid muscles, hearing loss, immune deficiency, low-set ears, mouth breathing, obesity, obstructive sleep apnea, polycythemia, seborrheic dermatitis, single line on palm, thickening of the skin of the palms and soles, thyroid disease, or vision disorder
ally123  I was confused about why the infant was jaundiced, and found this: "Hypothyroidism causes decreased rate of bilirubin conjugation, slows gut motility and impairs feeding, all contributing to jaundice." Source: http://www.pathophys.org/neonatal-hyperbilirubinemia/

 +4  (nbme20#45)

Large swollen rectal veins --> patient has external hemorrhoids. Swollen and inflamed veins in the rectum and anus that cause discomfort and bleeding. The most common cause of external hemorrhoids is repeated straining while having a bowel movement.

 +4  (nbme20#35)

CMV is associated with infecting organ transplant patients. CMV is transmitted via sexual contact, organ transplant, or vertically via placenta. Reactivation of CMV occurs in the immunosuppressed.

Organ transplant patients are at an increased risk of CMV pneumonia.

 +10  (nbme20#23)

In order for a drug to be cleared by the kidney, it must first be filtered in the glomeruli. Drugs with a high VD have more of the drug in the tissue that are not available to filtered by the kidney. Drugs with high protein binding won't be filtered either. So you want a drug with low Vd and low binding if you want it cleared via the kidneys and urine.

zevvyt  But a low VD corresponds to high Plasma Binding Concentration(FA 233, 2019). That's my main confusion with this question.

 +3  (nbme20#13)

Acute interstitial renal inflammation. Pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as haptens, inducing hypersensitivity (eg, diuretics, NSAIDs, penicillin derivatives, proton pump inhibitors, rifampin, quinolones, sulfonamides).

hungrybox  But how is a 2-year history acute?
jinzo  there is also " Chronic interstitial disease "
targetmle  i got it wrong because there wasnt rash, also there was proteinuria, doesnt it indicate glomerular involvement?
zevvyt  Got it wrong too cuz of that. But there can be proteinuria in nephritis, just not as much as in nephrotic syndrome. I guess that's confusing cuz this type of nephritis isn't grouped with the other nephritic conditions.

 +4  (nbme20#30)

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
charcot_bouchard  u missed 3rd ventricle, how about " Little Igor the 3rd, Crying for..."
len49  "Little Infants Try Crying For Food. Sorry All done." Added the T (try) for third
caffeinequeen  Kind of a stretch but: LIT AFF to SAD Lateral ventricles -> Interventricular foramina of Monro -> Third Ventricle -> cerebral Aqueduct of Sylvius -> Fourth ventricle -> Foramina (luschka and magendie) -> Subarachnoid space -> Arachnoid granulations (reabsorbed) -> Dural venous sinuses (drains)

 +1  (nbme20#27)

Statins can have a side effect of rhabdomyolysis.

lilyo  Statins have an increased risk of myopathy, specially when combined with other medications like Fibrates. This patient presents with muscle pain along with an elevated CK and + myoglobin test in urine. Consistent with myopathy.

 +4  (nbme20#3)

Patient has medullary carcinoma. Malignant proliferation of parafollicular "C" cells that produce calcitonin and have sheets of cells in an amyloid stroma.

xxabi  Just to add - patient likely has MEN 2A or 2B with the presence of medullary thyroid cancer and pheochromocytoma
sympathetikey  @xxabi Was going to say the same thing.
dermgirl  The patient have MEN 2B (Medullary thyroid carcinoma + Pheochromocytoma) Page 351 FA.

 +11  (nbme20#34)

Administration of Penicillin for Syphilis may lead to the Jarisch-Herxheimer reaction hours after treatment. Occurs due to lysis of spirochetes (so it can occur with Borrelia and Leptospirosis as well). The reaction is characterized by fever and chills.

The classical explanation of the Herxheimer reaction is that treatment results in the sudden death and destruction of large numbers of treponemes, with the liberation of protein products and toxins.

almondbreeze  FA pg.148

 +7  (nbme20#9)

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.

dickass  and the patient has no chorea

 -6  (nbme20#23)

Mycobacterium avium complex infections are a common opportunistic infection in patients with advanced AIDS (CD4 count <50).

realfakedreams  @hayayah you were being lazy.. smh.. Homie started anti-retroviral therapy. HIV infects CD4 T-Cells through either CCR5 or more commonly CXCR4. Because of anti-retrovirals start working, HIV isnt able to infect anymore CD4 T cells. Thus CD4 t lymphocytes levels start to rise and are able to active B cells.
myf1991  Why can't it be monocyte? macrophage eat MAC and interact with CD4

 +11  (nbme20#46)

Notice, the stem says "precorsors in the skin"

D3 (cholecalciferol) from exposure of skin (stratum basale) to sun, ingestion of fish, milk, plants.

D2 (ergocalciferol) from ingestion of plants, fungi, yeasts.

Both converted to 25-OH D3 (storage form) in liver and to the active form 1,25-(OH)2 D3 (calcitriol) in kidney.

sympathetikey  C is the 3rd letter in the alphabet. Hence, D3 = Cholecalciferol
karljeon  Thanks for the explanation. The question stem made it sound like "what future step will be decreased?" Actual question: "Decreased production of which... is most LIKELY TO OCCUR in this patient?" Maybe NBME needs a grammar Nazi working for them.
bharatpillai  question says "decreased production of which of the following precursors in skin is most likely to occur in this patient? the answer has to be 7-dehydrocholecalciferol!
bharatpillai  7 dehydrocholesterol
brbwhat  Yeah i did the same, but then realised acc to uw flowchart 7dehydrochole.. is converted to cholecalciferol in presence of uv rays. So the decreased precursor would be cholecalciferol since we already have 7 dehydrocholecalciferol not being converted by uvrays Tho the uw chart sites both ergo and chole as dietary sources.
drzed  Wouldn't 7-dehydrocholesterol build up in the skin? Since UV rays convert 7-dehydrocholesterol into cholecalciferol, if you are lacking the conversion, the reactant (7-dehydrocholesterol) should accumulate.
brbwhat  They’re asking decreased production of which of the following precursor would occur? 7 dehydrocholestrol builds up, but decreased production of cholecalciferol takes place, which is a precursor in the pathway for vitamin d formation

 +8  (nbme20#1)

NRTI's are associated with possible side effects of anemia, granulocytopenia, and myelosuppression.

sympathetikey  Especially zidovudine.
fmub  Nucleoside reverse transcriptase inhibitors (NRTIs) block reverse transcriptase (an HIV enzyme). HIV uses reverse transcriptase to convert its RNA into DNA (reverse transcription). Blocking reverse transcriptase and reverse transcription prevents HIV from replicating.

 +8  (nbme20#45)

Fanconi's is a generalized reabsorption defect in PCT causing increased excretion of amino acids, glucose, HCO3–, and PO43–, and all substances reabsorbed by the PCT.

baja_blast  FA2019 p. 581. Fanconi syndrome causes a type 2 (proximal) renal tubular acidosis

 +10  (nbme20#25)

Oxytocin uses IP3 signaling pathway.

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

FA mnemonic: "GOAT HAG"

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"

 +5  (nbme20#30)

Capitate and lunate are in the center of the palm. Capitate is not an option, so lunate is the answer.

Dislocation of lunate may cause acute carpal tunnel syndrome.

yotsubato  Lunate is the only carpal bone that is frequently dislocated. Scaphoid is frequently fractured. Hook of hamate is also frequently fractured.
redvelvet  and also point tenderness in the anatomical snuffbox may indicate a scaphoid fracture.
chandlerbas  yes lunate is the most common dislunated carpal bone ;)
almondbreeze  FA 2019 pg. 439 : dislocation of lunate may cause acute carpal tunnel syndrome

 +11  (nbme20#18)

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

 +10  (nbme20#49)

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 =/
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);
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)
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
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
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! -_-
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

 +5  (nbme20#13)

No abnormalities, only some vomiting, looks well w/ no failure to thrive. Most likely immature LES.

masonkingcobra  http://www.sedico.net/English/SedicoInformationCenter/Physicians/gerd_e.htm

 +3  (nbme20#50)

Short gastric a. branch from the splenic a.

Branches of the celiac trunk that constitute the blood supply to the stomach: common hepatic, splenic, and left gastric.

 +4  (nbme20#37)

With chronic vomiting, you lose electrolytes and a lot of acid. It triggers metabolic alkalosis which is why all the serum values are low (or on the lower end of the normal range) except for bicarbonate.

ergogenic22  decreased K+ (from increased RAAS due to volume loss) and decreased Cl- (loss of HCl from the stomach), Alkalosis from loss of HCl and thus high bicarb. For this reason high to mid range K is wrong
sbryant6  Wouldn't increased RAAS lead to increased Na+? The answer shows decreased Na+.
sbryant6  Also, remember Bulimia Nervosa is associated with hypokalemia.
sugaplum  so the range they gave for K is 3-6? so 3.2 is WNL then? or are we just operating on "it is on the lower end of normal in peds"
dbg  sodium levels in pyloric stenosis vary, nothing really classic, can be high as in this case simply due to hydration, can low in other cases if aldosterone managed to reverse that to the other extreme

 +7  (nbme20#8)

Earliest detectable secondary sexual characteristic is breast bud development in girls, testicular enlargement in boys.

pg32  How did you know this? The Tanner stages in FA simply list pubarche and breast buds developing in the same stage without stating which comes first. Thanks!
lynn  @pg32 look at the paragraph above the diagram, it says that exactly. Took me a minute too lol

 +6  (nbme20#28)


Clinical findings: thin, yellow-green, malodorous, frothy discharge and vaginal inflammation / itching.

Lab findings: pH >4.5 and motile trichomonads.

 +14  (nbme20#4)

Methanol is toxic by two mechanisms:

First, methanol can be fatal due to its CNS depressant properties in the same manner as ethanol poisoning.

Second, in a process of toxication, it is metabolized to formic acid via formaldehyde in a process initiated by the enzyme alcohol dehydrogenase in the liver. Methanol is converted to formaldehyde via alcohol dehydrogenase (ADH) and formaldehyde is converted to formic acid (formate) via aldehyde dehydrogenase (ALDH).

Formate is toxic because it inhibits mitochondrial cytochrome c oxidase, causing hypoxia at the cellular level, and metabolic acidosis, among a variety of other metabolic disturbances.

sugaplum  Good pictograph comparing methanol, alcohol, and ethylene glycol. https://wikem.org/wiki/File:Toxic_alcohol_ingestion.JPG

 +15  (nbme20#38)

Patient has a craniopharyngioma. Most common childhood supratentorial tumor. Derived from remnants of Rathke pouch (oral ectoderm). Calcification is common. Cholesterol crystals found in “motor oil”-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).

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

 +15  (nbme20#7)

Acyclovir, famciclovir, valacyclovir are guanosine analogs. They undergo conversion to acyclovir monophosphate via virus encoded thymidine-kinase. Ultimately, they inhibit viral DNA polymerase by chain termination.

Mutated viral thymidine kinase can cause resistance.

len49  Foscarnet and Cidofovir on the other hand do not require phosphorylation by viral kinase, therefore should be used in strains that are shown to be resistant.

 +7  (nbme20#39)

Inguinal hernias are usually reducible, femoral hernias are not.

This is an indirect inguinal hernia. It enters internal inguinal ring lateral to inferior epigastric vessels and is superior to the inguinal ligament.

Caused by failure of processus vaginalis to close (can form hydrocele). May be noticed in infants or discovered in adulthood. Much more common in males.

yotsubato  Heres a good picture to help with the concept. https://www.google.com/url?sa=i&source=images&cd=&ved=2ahUKEwjVkIi0yN7iAhWLjqQKHbeXCTUQjRx6BAgBEAU&url=https%3A%2F%2Fwww.herniaclinic.co.nz%2Finformation%2Ftypes-of-hernias%2F&psig=AOvVaw2BzGtQLvSmUN8ymhdvETG5&ust=1560244112252834
sbryant6  Note that direct inguinal hernias typically happen in older adults. This question presents a younger baby, so it is more like to be indirect.
jawnmeechell  So a femoral hernia would be inferior to inguinal, but direct/indirect would be superior?
azharhu786  The direct and indirect hernia are both superior to the inguinal ligament but the femoral hernia is basically inferior to the inguinal ligament. The direct hernia is medial to the inferior epigastric vessels whereas, the indirect is lateral to the epigastric vessels. An indirect hernia is seen in young people whereas, direct hernia happens in adults.

 +19  (nbme20#34)

Missense mutations involve a nucleotide substitution resulting in changed amino acids. Sometimes the effects of missense mutations may be only apparent under certain environmental conditions; such missense mutations are called conditional mutations. Many missense mutations result in proteins that are still functional, at least to some degree.

Also, all the other answers would probably leave you with either a greatly altered or non-functional protein.

thefoggymist  I chose nonsense because I thought it'll make the enzyme shorter (since less bonds = more heat liable = can't work at 42 degrees) but yea, probably won't work even at 30 if it's an early nonsense.
joanmadd  A good clinically related example is HbC disease on electrophoresis. HbC disease is due to a missense mutation (glutamic acid (-) for valine (neutral)). The mutated hemoglobin is still fairly functional but when placed on gel electrophoresis the HbC migrates the least far from the negative electrode due to less negative propulsion (lack of wild type glutamic acid).

 -6  (nbme20#35)

The damage is in the L midbrain in the area affecting the corticospinal tract. Because it is in the midbrain, decussation in the pyramids (medulla) so it will show ipsilateral dysfunctional motor signs.

Photo of midbrain and important areas: shorturl.at/myHLR

masonkingcobra  Just for clarification, on the left side, you see where he had the infarction 7 years ago and the tissue is gone.
chefcurry  so is the dysfunction on the contralateral side?
praderwilli  If the decussation is in the pyramids of the medulla, shouldn't it be contralateral hemiparesis if the damage is on the right? It confuses me because of the labeling right and left at the top of the pictures.
endochondral1  that link isnt working @ hayayah....is there any good picture to look at to know where the tracts are on this section?

 +5  (nbme20#10)

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)

 +27  (nbme20#40)

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.
breis  Pathoma ch. 3 pg 23 "Basic Principles"
charcot_bouchard  Shoutout to Imam Satter! Without him this question wasnt possible for me to answer in 10 sec.

 +4  (nbme20#12)

The left upper extremity and breast are drained by the axillary lymph node. The kidney is drained by the thoracic duct. The heart has its own lymph system going on surrounding the heart.

 +0  (nbme20#14)

Of all the options, psoas major is the only one that is really associated with the lumbar vertebrae.

Q. Lumborum involves the transverse process of L1 but Psoas Major originates from L1-L5

imnotarobotbut  QL is connected to L1-L5 vertebrae as well (https://en.wikipedia.org/wiki/Quadratus_lumborum_muscle)

 +6  (nbme20#15)

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
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.

 +7  (nbme20#47)

The two most important MI complications that occur within a 2-5 day span are papillary muscle rupture and interventricular septum ruture.

Papillary muscle rupture leads to severe mitral regurgitation, heard as a systolic murmur at the apex.

dulxy071  I disagree. any sort of rupture is usually the result of the action of macrophages (to eat away dead, necrotic tissue) which come in on day 3. This was merely a word game to get the time line right. They said "TWO DAYS LATER" (keeping in mind our time line starts 16 hours after the first symptoms appeared in this stem) which actually turns out to be day 3
leaf_house  Wouldn't necrosis of the interventricular septum create a VSD, which would also produce a loud, (holo)systolic apical murmur? I don't get how we're supposed to differentiate, here.
mangotango  A VSD produces a holosytolic, harsh-sounding murmur loudest at the tricuspid area, not the mitral (apex) area -- FA, pg. 288, 289.

 +10  (nbme20#20)

Coarctation of the aorta leads to increased LV overload causing LV hypertrophy and a L axis deviation.

hungrybox  Similarly, RV overload leads to R axis deviation. Could point to PAH.

 +9  (nbme20#19)

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 ANP and BNP. That is what causes the increased urinary Na+ secretion Žwhich leads to normalization of extracellular fluid volume Žand the euvolemic hyponatremia.

hello  Why would body respond to water retention with ALDO? ALDO would increase water retention...
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
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
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.

 +4  (nbme20#36)

Rhabdomyolysis can present looking like a kidney injury (it can lead to acute tubular necrosis as well). The electrolyte findings are just like renal failure (Inc. K+, inc. PO4-, dec. Ca)

To differentiate between rhabdomyolysis and kidney injury, you check the urine to see if there are any RBCs. In rhabdomyolysis there are no free RBCs in the urine.

ergogenic22  "Crush injury" is a buzz word for rhabdo
ibestalkinyo  The mechanism by which AKI occurs after rhabdomyolysis are due to free radical formation. Other urine finding include blood on dipstick, but as hayayah said, no frank RBCs.

 +9  (nbme20#2)

The baby does not get any maternal IgM, IgA or IgE as they do not cross the placenta, so if IgM is found it may suggest the baby has encountered an infection in utero.

IgG is passed down to the baby as a means of passive immunity until the baby can form their own antibodies of different types. So if you see anything other than IgG (e.g. IgM) you know it must be d/t an infection.

hungrybox  The baby gets IgA via breast milk.
mbourne  @hungrybox, this is true. However, IgM antibodies are the first antibodies endogenously produced before class-switching occurs. So IgM antibodies in a newborn suggests infection.

 -9  (nbme20#24)

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
waterloo  both azoles and PPI inhibit cytochrome P450. So one isn't causing the other's lack of effect.

 +7  (nbme20#6)

In narcolepsy, there is a direct transition from wakefulness to REM sleep. Basically instead of going through the early stages and gradually falling into a deep sleep, you just suddenly go from being awake to being in a deep sleep.

kamilia20  FA2020 P497(Sleep physiology): Changes in narcolepsy: decrease REM latency.
baja_blast  p. 485 for us plebs still using FA 2019

 +4  (nbme20#41)

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
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.
monkey  They classify at 35 year old (<35 = Chlamydia or Neisseria and > 35 = E.coli)
mbourne  I put Pseudomonas, as that is a cause of prostatitis in older men, but it is less common than E. coli. Just keep that in mind, if E. coli wasn't an answer choice, the answer should have been Pseudomonas. If he was a younger male, then Chlamydia would have been acceptable.
brotherimodu  @mbourne I think Pseudomonas is the more common etiology for acute prostatitis in the elderly (>65ish for exams), whereas E.Coli is the more common etiology in adults 35-64yo

 +4  (nbme20#5)

Foreign body inflammatory facial skin disorder characterized by firm, hyper-pigmented papules and pustules that are painful and pruritic. Located on cheeks, jawline, and neck.

Commonly occurs as a result of shaving (“razor bumps”), primarily affects African-American males.

Images: shorturl.at/fpwY1

tyggles  A good way to remember this is that the word Barber comes from the French for beard (barbe) and these rashes will be in the distribution of a beard.

 +6  (nbme20#42)

This patient has heart failure. Normal JVP is 6-8 mmHg.

Signs of heart failure are based on cardiac pump dysfunction, Žcongestion, and low perfusion.

Symptoms: include dyspnea, orthopnea, fatigue; signs include S3 heart sound, rales, jugular venous distention (JVD), and pitting edema.

 +5  (nbme20#21)

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.
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.
dulxy071  Regardless if it can help resolve the issue, neutrophil will always be the first responder

 +5  (nbme20#44)

Renovascular disease is the most common cause of 2° HTN in adults. Can be d/t ischemia from renal stenosis or microvascular disease. Can hear renal bruits lateral to umbilicus.

Main causes of renal artery stenosis:

  • Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers.

  • Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females.

Lab values based off:

  1. Stenosis decreases blood flow to glomerulus.
  2. Juxtaglomerular apparatus (JGA) responds by secreting renin, which converts angiotensinogen to angiotensin I.
  3. Angiotensin I is converted to angiotensin II (ATII) by angiotensin converting enzyme (ACE --in lungs)
  4. ATII raises blood pressure by (1) contracting arteriolar smooth muscle, increasing total peripheral resistance and (2) promoting adrenal release of aldosterone, which increases reabsorption of sodium (where Na+ goes H2O will follow) in the distal convoluted tubule (expanding plasma volume). Can lead to hypokalemia (seen in the labs for this question)
  5. Leads to HTN with increased plasma renin and unilateral atrophy (due to low blood flow) of the affected kidney; neither feature is seen in primary hypertension
uslme123  So both causes would result in increased aldo and MR is the only way to differentiate the two?
hello  @USMLE123 I think both are causes of renal artery stenosis and that could be seen via MR angiography. It is asking what could help DIAGNOSE this patient -- and her most likely cause of the findings is fibromuscular dysplasia. So, yes, MR angiography would look different for the 2 different etiologies and thus could can be used to differentiate the two from one another. However, epidemiologically, we are looking to diagnose her with the suspected most probable cause.
yotsubato  @USLME123 I think measuring Aldosterone is an incorrect answer because you already know its increased due to low K. Knowing she has high Aldosterone wouldnt provide you evidence for a final diagnosis.

Subcomments ...

submitted by mousie(135),

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) +5  
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus) +3  
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. +6  
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. +5  
soph  I saw hypotension and though anaphylaxis........ -.- +  
usmile1  Chest Xray showed "bilateral diffuse airspace disease". This is much more indicative of TRALI than anaphylaxis which would have wheezing and possibly respiratory arrest but no actual damage to the lungs. Additionally there was no urticaria or pruritus one would expect to see with anaphylaxis. +2  

submitted by mousie(135),

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) +5  
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus) +3  
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. +6  
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. +5  
soph  I saw hypotension and though anaphylaxis........ -.- +  
usmile1  Chest Xray showed "bilateral diffuse airspace disease". This is much more indicative of TRALI than anaphylaxis which would have wheezing and possibly respiratory arrest but no actual damage to the lungs. Additionally there was no urticaria or pruritus one would expect to see with anaphylaxis. +2  

submitted by dubchak7(1),

They suggest Misoprostol to counteract NSAIDs... Why not PPIs?

hayayah  PPI's don't have many side effects! If the question didn't involve the diarrhea side effect the answer would have been to give her a PPI. +1  
tsarcoidosis  I guess one takeaway is that PPIs don't directly cause diarrhea, but they do increase the risk for C-diff, which causes diarrhea. +5  
usmleuser007  PPI side-effects: + increased risk for C. diff + Increased risk for resp infections + can cause hypomagnesia + decrease absorption of (Ca2+, Mg2+, & iron) + increased risk of osteoporotic hip fractures (d/t low serum calcium) +1  
temmy  The patient got severe gastric burning and discomfort as an effect of the drug. My logic was since the patient was taking an NSAID it had to be a COX 1 inhibitor that destroys the protective barrier of the GI mucosa due to inhibition of prostaglandin so we needed to treat with a drug that will regenerate prostaglandin and prostaglandin is a vasodilation which might be the reason for the diarrhea. +  

submitted by docred123(4),

Why is the answer to this question not Adhesivie Capsultiis...

hayayah  Adhesive capsulitis causes severe restriction of both active and passive range of movement of the glenohumeral joint in all planes (especially external rotation). +12  
catch-22  Adhesive capsulitis is aka "frozen shouder" so you can expect exactly that. The entire shoulder will be hard to move in all directions. +1  
meningitis  Since it says there is NO impingement sign, it cant be rotator cuff tendinitis correct? What other signs eliminate this option? +  

submitted by moloko270(52),


"syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli"

hayayah  Apparently, in chronic CHF you see hyponatremia. Because CHF causes a decrease in cardiac output and circulating blood volume, which in turn triggers a compensatory response aimed at preserving blood pressure. This stimulates the body to retain both water and sodium. +4  
seagull  i agree with Hayayah... the RAAS system is activated due to poor perfusion to the kidney due to decomp heart failure. +4  

submitted by sklawpirt(23),

I think the idea here is simply that one should think about where vesicles are coming from on their way to the golgi complex.

"Two steps forward and one step back." Specfically the question may be referring to a rare craniofacial disorder. an awarenesss of that disease is not necessary. What is necessary is understanding the origin from where vesicles are traficked to the Golgi apparatus.

COPI protein is needed to coat vescles from the RER to send to golgi. Thus, with a mutation in that protein, the packaged proteins that should bleb off and be sent to the golgi, instead accumulate in the RER and dilate it. Thus the answer.


hayayah  pg. 47 on FA got the good visuals! +2  
notadoctor  COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back." Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane +15  
titanesxvi  why not small lysosomes? +2  
varunmehru  and I thought large lysosomes due to lack of enzymes to degrade +  
samsam3711  The size of the lysosome is not affected by the presence or absence of protein, but its function is compromised (eg. protein is getting stuck in the RER) +  
fattyacid  I hope this helps to whomever was lost like me Null mutation: A mutation (a change) in a gene that leads to its not being transcribed into RNA and/or translated into a functional protein product. For example, a null mutation in a gene that usually encodes a specific enzyme leads to the production of a nonfunctional enzyme or no enzyme at all. +2  

submitted by _pusheen_(4),

I think this one is literally just asking what part of the kidney will be the most poorly perfused. That part would have the most renin. Also, the medulla doesn’t have JG cells so I guess that’s another reason why it couldn’t have the most renin.

sklawpirt  Exactly, it has to do with where in the kidney renin is released and requires a bit of knowledge of the artery branches that give rise to the afferent arteriole in the first place and where this branch point is located. http://anatomyforme.blogspot.com/2008/05/histology-of-kidney-lot-to-process.html Where renin production occurs in JGA cells, EPO production occurs in the renal peritubular interstitium (especially the proximal renal tubule, corext and some of the outer medulla.) Thus with the same questions stem it might ask where is concentration of EPO the highest? [And it would still be the cortex, with lower concentrations in the outer medulla, lowest concentration in the inner medulla, and none found in the papilla or renal pelvis. +8  
hayayah  Actually, the renal medulla receives significantly less blood flow than renal cortex. So the medulla is the one that's very sensitive to hypoxia and vulnerable to ischemic damage. I don't think this question is related to "what area is the most poorly perfused." It's just knowing that renal artery stenosis is going to decrease blood flow to the kidney. JG cells sense the decrease in perfusion pressure and secrete renin. Knowing that renin is produced by the JG cells and that JG cells are in the cortex should be enough to answer this question. +5  
cry2mucheveryday  I thought all the renin would collect in the pelvis where the arteries whould drain into a common vein and changed my answer to pelvis ._. +2  

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