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Comments ...

 +2  (nbme18#22)

I feel like whenever there is a physician as the patient in the question stem, you should just start thinking substance abuse disorders. Not the first time I've seen this.


 +3  (nbme18#21)

2 lytic lesions sounds like a metastatic origin

The most common locations for bone metastasis: Prostate, Breast > Kidney, Thyroid, Lung

Lead (PB) K e T t L e

lokotriene  FA2020 p223 +

 +3  (nbme18#45)

Parasite Hints in FA: Microcytic anemia - Necator or Ancylostoma

The boy has been running around barefoot (entrance site for laravae). These hookworms suck blood from the intestines leading to iron deficiency anemia.


 +4  (nbme17#0)

Haemophilus ducreyi (chancroid) - deep, purulent, painful ulcers with suppurative lymphadenitis (no mention in stem), grayish necrotic base

HSV - multiple, shallow, painful ulcers with erythematous base

NSFW (obviously) link to example of chancroid with gray necrotic base

bingcentipede  If you also look at the lesions, they like the "dew drops on a rose" appearance. Multiple vesicles that hurt when burst +3

 +0  (nbme17#41)

Most everything is a combination of genetics and environment. This is the only answer that acknowledges that even if the role is minor.


 +5  (nbme17#33)

My reasoning for this question:

  • In both situations, you see a cyclical increase in pain before receiving the injection. This could be seen if the effect was wearing off; however, if you notice, there is a decrease in pain before the injection is even given. I believe this implies that something inherent about the injection is providing pain relief.
  • Furthermore, both curves follow the same path with an eventual decrease in pain, regardless of intervention.
  • Maybe an additional point - I am not questioning their pain, but fibromyalgia typically shows no abnormal lab results in addition to typically coexisting with some form of mental pathology. I don't think placebo being demonstrated is far off.
j44n  I agree that was my though process, except i didnt notice the decrease before the injection, good eye! also the other answers didnt really apply regression toward the mean is the phenomenon that arises if a random variable is extreme on its first or first few measurements but closer to the mean or average on further measurements and there was no way for us to know about confounding or their selection procedures so from that we couldn't really know about the types of errors they made +1

 +0  (nbme19#43)

Vinblastine interferes with tubulin function, thus disrupting the migration, phagocytosis, degranulation, and cytoskeleton of neutrophils





Subcomments ...

submitted by lae(22),
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hrcconi ihoinscrbt ssueac qaumouss tpasmeiala of eth ttidfraepdsosieu mranuolc elihpeiutm ni het ibrohnc nad locebnrosih

---- heste alnmoruc hiueiptelm lymalnro tectruoinb to eht yaimuccilor rcelacaen adn ngkmsoi sloa asgemda shti aecealrc,n os nca egt het lecu fomr ttha oot

donttrustmyanswers  Pseudostratified columnar epithelium is only present in the bronchi. The bronchioles have simple ciliated columnar epithelium. +4  
flapjacks  ^you CAN trust this answer. Confirmed in FA +1  
abcdefbhiximab  Chronic bronchitis is due to hypertrophy and hyperplasia of mucus-secreting glands in BRONCHI where there is pseudostratified columnar epithelium. All of the other answers point to the alveolar sacs. And centriacinar emphysema only affects the respiratory bronchioles anyway while sparing distal alveoli. pg 674 FA 2020 +4  
step7777  It also has to do with the Reid index, which is increased due to mucus gland tissue undergoing hyperplasia and hypertrophy in the Bronchi that is producing excess mucus. Columnar epithelium is usually glandular. pg. 660 FA 2019 +  


submitted by cassdawg(1179),

Here is a great image showing the timeline for the different pubertal changes in males and females. Tanner stages are found in FA2020 p673.

In females, the earliest detectable sign of pubertal change is breast bud development which only slightly precedes pubic hair development. In males, testicular enlargement is the first detectable sign.

flapjacks  You share excellent charts. Thank you! +2  
eleezi  **Page 637 FA2020. Thanks for the info! +  


submitted by tinyhorse(7),

Frankly pretty floored that anybody thought that this question contained enough information for someone to confidently answer it.

The question has you assume that both parents are heterozygotes at the locus. Why? I assume I'm missing some esoteric fact about P450 allele frequencies.

flapjacks  I got lucky guessing the same % chance that siblings share HLA markers +2  
baja_blast  I agree with OP seriously no idea how anyone could have gotten this right without totally guessing it. Am I missing something here?? +2  
snow_6  Personally I got this question wrong, partially due to me panicking in this question. Looked through it later and understood the following: - the pt. is homozygous i.e. AA; meaning each parent is heterozygous for the allele - if her sister is to have the same alleles, she is also homozygous i.e. AA - do the punnet square for Aa (mom) and Aa (dad) to get a homozygous allele of AA for only 25% of the time - based on the assumption that parents are heterozygous because question doesn't state any other extra information Only if i could've thought like this during the actual exam +  
sschulz2013  However, if one parent is homozygous and the other is heterozygous, then it works out that the sister will have the same allele 50% of the time, not 25%. So still not sure about the above answer. Don't think assuming the parents are both heterozygotes is something we should have to do. There is probably more to it than just that. +1  
j44n  the probability for being the same gene as a sibling thats homozygous is always 25% this has been on just about every practice NBME +  


submitted by cassdawg(1179),

Hormone sensitive lipase (HSL) is the enzyme which degrades triglycerides stored within adipocytes (FA2020 p93). Thus, it makes sense that it is activated in times of fasting and suppressed in the fed state.

Insulin would inhibit HSL, as insulin is a fed state enzyme secreted by the pancreas and would want to trigger storage of triglycerides.

In contrast glucagon is secreted in response to hypoglycemia by the pancreas and will trigger fasted state activation. In terms of the fed/fast state I always think of glucagon and epinephrine kind of like a superhero and their side kick, because they usually work together in the fasting state on similar targets to ensure the body has enough energy (this helps me remember that epinephrine and glucagon are fasting state hormones). Here though is epinephrine's big action away from glucagon, where glucagon has minimal effect and epinephrine has the big action of activating HSL! Glucagon has a minor role and other catecholamines and ACTH can also serve to activate HSL as well.

Another example of the synergistic work of glucagon and epinephrine is in glycogen breakdown (FA2020 p85). Both will trigger cAMP increase and protein kinase A activation which will phosphorylate glycogen phosphporylase and activate it (FAST PHOSPHORYLATE! Hormone sensitive lipase is actually phsophorylated to activate it as well).

FUN FACT: Hormone sensitive lipase actually got its name because it was sensitive to epinephrine!

flapjacks  In Type 1 DM, the glucagon response to hypoglycemia is not functional and these individuals are reliant on the epinephrine-stimulated hepatic glycogenolysis. I recall this by remembering you can administer glucagon to these patients if they're having a hypoglycemic episode. They can respond to it, but they aren't releasing it. +1  
passplease  How did you eliminate thyroxine? As it also plays a role in lipolysis. I was thrown off my the low blood pressure and therefore did not select epinephrine. Why would they still have a low blood pressure? +  
jackie_chan  ^ they have low blood pressure because DKA causes a lot of dehydration (vomiting, diuresis due to osmotically active glucose in urine) so low BP Thyroxine I eliminated because remember that thyroxine is unique in that it functions similar to a steroid hormone and acts in the nucleus to upregulate expression of many genes. I figured hormone-sensitive lipase needs to be activated, not stimulated to upregulate expression, so I thought about EPI and beta-3 stimulation. fuckPeter +  
schep  I figured since he has low BP/dehydrated, his body would try to maintain cardiac output by increasing sympathetic tone (releasing epinephrine). In hypovolemic shock, systemic vascular resistance is up because of this compensation. +  
j44n  also thyroxine works like a steroid hormone meaning it takes a while to cause its effect +  
flvent2120  That'd be cool if it were called "epinephrine sensitive lipase" +  


submitted by cassdawg(1179),

This is feedback inhibition of the RAAS (renin-angiotensin-aldosterone system) axis. Increased aldosterone will feedback and inhibit renin secretion of the kidney. (FA2020 p588)

flapjacks  Increased serum sodium concentration is not specific enough to support the diagnosis +7  
cheesetouch  Fa2018 p332: Hyperaldosteronism - primary hyperaldosteronism seen with adrenal adenoma (Conn syndrome). High aldosterone, low renin. Causes resistant hypertension. +3  
mark0polo  Serum sodium concentration wouldn't actually change because of the aldosterone escape mechanism in primary hyperaldosteronism +8  
i_hate_it_here  <- +1  


submitted by cassdawg(1179),

This is likely poison ivy, which is a Type IV (delayed) hypersensitivity mediated by T-cells. [FA2020 p112]

Notes to point to poison ivy: itchy linear vesicles (as the leaf touched), camping trip, on the extremities which would likely be exposed

Delayed type hypersensitivity helpful hint: the rash did not appear until a few days after he had returned from camping (5 days ago camping, 2 day history of rash)

flapjacks  Just some additional information since this has come up for me before: Poison ivy rash is caused by an allergic reaction to an oily resin called urushiol (Rhus dermatitis) +2  


submitted by cassdawg(1179),

She has Mycoplasma pneumoniae which causes walking (atypical, interstitial) pneumonia and increase in cold agglutinins (IgM)

FA2020 p150

If you are a sketchy person (which I am not), I am pretty sure Mycoplasma is depicted in the cold, or as a guy on skis in drug ones, which can help you remember cold agglutinins. Also Mycoplasma -> IgM (the letter M).

Also (for immuno nerds or rationalizers), IgM is the first antibody to be produced so it would make sense that you would have IgM this early in the infection which can cause cold agglutination (she has only been sick for a few days). IgG causes warm agglutination, which is typically seen in more chronic processes like SLE and CLL (FA2020 p423). No idea if that is the actual mechanism but it is how I keep them straight in my mind and makes sense.

flapjacks  As a "sketchy person" and not a "rationalizer", I can confirm the Mycoplasma has red blood cell "pucks" agglutinized with IgM snowflakes +21  
j44n  Just to add, she has interstitial infiltrates so its an atypical pneumonia, no other kind of atypical pneumonia would cause them to have agglutination. I'm not a rationalizer I'm a massive over thinker +1  
sexymexican888  Yeah, im a sketchy person too! Side note, for autoimmune hemolytic anemia I remember it this way: IgM -> Me Cold, go INSIDE (cold agglutination, intravascular hemolysis) IgG -> Go outside its HOT (warm agglutination, extravascular hemolysis) +1  


submitted by covid_19(4),

Aplastic anemia: anemia, leukopenia, thrombocytopenia

CML, i.e. leukemias: anemia, ↓ mature WBC, ↓ plt, peripheral blood smear shows mature & maturing granulocytes (FA 2020, p. 432)

β-thalassemia major: microcytic, hypochromic anemia with target cells and anisopoikilocytosis, skeletal deformities, etc. (FA 2020, p. 418)

Cobalamin deficiency: d/t malabsorption, pancreatic insufficiency, gastrectomy, or insufficient intake, neurological Sx

Personally, I got this wrong, because to me, the RBCs in that smear looked both larger and more irregularly shaped, so in hindsight, I really should've honed in more on the HPI, i.e. the patient really has anemia and no other relevant PMx.

flapjacks  I believe Goljan mentions that the #1 cause of anemia in older adults is GI bleeds +3  
flapjacks  (colon cancer) +1  
mark0polo  Also, B-thalassemia major would present in childhood, not in a 75 year old man +2  
sexymexican888  ALSO, #1 cause of Iron deficiency anemia in a older person -> colon cancer. HOWEVER, remember golijan ALSO SAID "GUYSSSS YOU THINK RBCs JUST TURN MICROCYTIC OVERNIGHT?! LIKE YOU HAVE IRON DEFICIENCY ANEMIA AND THEYRE ALL LIKE CHEERLEADERS AND GO 1,2,3 ->MICROCYTIC?! NO!! ITS NORMOCYTIC FIRST THEN MICROCYTIC EVENTUALLY" It was hilarious lol but yeah they dont really say how long he's been weak and had fatigue so its probably pretty recent, it takes a few days for the IDA to turn microcytic +  
sexymexican888  Also an adult male (not elderly) with IDA -> peptic ulcer disease +  
sexymexican888  ALSO IDA can be due to blood loss or dietary lack. Remember iron is VERY tightly regulated in the body and there's no real official way to get rid of it except bleeding (menstruation in females & sloughed of cells in the intestine that had ferritin stored) thats why male patients with hemochromatosis get HCC and all these horrible manifestations in their 40s cause getting rid of iron is actually hard unless you're underconsuming it or bleeding +  


submitted by covid_19(4),

Aplastic anemia: anemia, leukopenia, thrombocytopenia

CML, i.e. leukemias: anemia, ↓ mature WBC, ↓ plt, peripheral blood smear shows mature & maturing granulocytes (FA 2020, p. 432)

β-thalassemia major: microcytic, hypochromic anemia with target cells and anisopoikilocytosis, skeletal deformities, etc. (FA 2020, p. 418)

Cobalamin deficiency: d/t malabsorption, pancreatic insufficiency, gastrectomy, or insufficient intake, neurological Sx

Personally, I got this wrong, because to me, the RBCs in that smear looked both larger and more irregularly shaped, so in hindsight, I really should've honed in more on the HPI, i.e. the patient really has anemia and no other relevant PMx.

flapjacks  I believe Goljan mentions that the #1 cause of anemia in older adults is GI bleeds +3  
flapjacks  (colon cancer) +1  
mark0polo  Also, B-thalassemia major would present in childhood, not in a 75 year old man +2  
sexymexican888  ALSO, #1 cause of Iron deficiency anemia in a older person -> colon cancer. HOWEVER, remember golijan ALSO SAID "GUYSSSS YOU THINK RBCs JUST TURN MICROCYTIC OVERNIGHT?! LIKE YOU HAVE IRON DEFICIENCY ANEMIA AND THEYRE ALL LIKE CHEERLEADERS AND GO 1,2,3 ->MICROCYTIC?! NO!! ITS NORMOCYTIC FIRST THEN MICROCYTIC EVENTUALLY" It was hilarious lol but yeah they dont really say how long he's been weak and had fatigue so its probably pretty recent, it takes a few days for the IDA to turn microcytic +  
sexymexican888  Also an adult male (not elderly) with IDA -> peptic ulcer disease +  
sexymexican888  ALSO IDA can be due to blood loss or dietary lack. Remember iron is VERY tightly regulated in the body and there's no real official way to get rid of it except bleeding (menstruation in females & sloughed of cells in the intestine that had ferritin stored) thats why male patients with hemochromatosis get HCC and all these horrible manifestations in their 40s cause getting rid of iron is actually hard unless you're underconsuming it or bleeding +  


submitted by cassdawg(1179),

The image shown is one of asbestosis (asbestos bodies resemble dumbbell, as seen here and found FA2020 p677). Aside from the image, he also has the major risk factor of asbestosis of working in a shipyard. Asbestosis typically affects the lower lobes of the lungs (hence the bibasilar crepitant crackles) and carries the ability to cause reticulonodular pulmonary infiltrates / fibrosis.

Similar to the pathology behind silicosis fibrosis, alveolar macrophages respond to aesbestos and release fibrogenic factors.

Alveolar macrophages phagocytize foreign materials, release cytokines and alveolar proteases.

Type I pneumocytes make up the alveolar lining, and Type II pneumocytes generate surfactant and can proliferate into Type I pneumocytes in response to alveolar damage. Kulchitsky cells are cells of origin of small cell lung cancer. Clara cells (now called club cells) are nonciliated bronchiolar exocrine cells that secrete a component of surfactant, degrade toxins, and act as reserve cells.

flapjacks  A barbell, really. +1  
cheesetouch  FA2018 P659 +8  
jer040512  eh... more like a shake weight. +2  


A 70 year old develops a progressive disinhibition syndrome with episodes of emotional outbursts, inappropriate use of language, and socially inappropriate behavior. Where is the most likely damage?

Answer: Frontal lobe disinhibition.

Bilateral amygdala (medial temporal lobe) would've been affected if it was Kluver Bucy Syndrome.

flapjacks  If you know the story of Phineas Gage, it can help +6  
helppls  How do you tell the difference from a frontal lobe issue and Kluver Bucy Syndrome? +  
nikitasr27  I would say the emotional and language part. The frontal lobe is very involved in emotions and the limbic system as well as in complex language concepts. Kluver Bucy would lack these aspects as the individual is “indifferent” to everything (no fear, no emotions) just like my ex +  
randi  Kluver-bucy is also marked by specific behaviors like hyperphagia, hyperorality, hypersexuality. Apparently can also be associated with HSV-1 encephalitis FA2019 p499. +  


submitted by ajguard26(41),
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Tee,frohre teh gamaed si ylrepu tmoro nda enyross in het etfl egl, hcwhi si no the dimlae psteac of het naftrol nad aetpialr oelbs re.elvtpsycie hTsi raea si psiupdel yb het itrnaore lebarerc r.atery

issamd1221  contralateral deficits +  
cbay0509  thank you +  
flapjacks  I think her 60 pack-year history suggests possible PAD and therefore loss of proprioception in the lower extremities, leading to an unfortunate distractor +  
an_improved_me  I don't understand why you would consider the propioceptive deficit a distractor... doesn't the DCML (which carries propioceptive information) project to the primary somatosensory cortex (via the VPL?). In this case, a lesion to the right anterior cerebral artery, which supplies both motor and sensory information to the lower limb would lead to somatosensory, propioceptive, and motor deficits. +