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 +7  (nbme24#39)

Falling on outstretched hand: scaphoid is most common one to be fractured, lunate is most common to be dislocated. Lunate dislocation can cause acute carpal tunnel syndrome.

Think of the mnemonic "Straight Line To Pinky, Here Comes The Thumb" for the bones of the palm, drawing a football shape starting below the thumb MCP joint adjacent to the radius, then moving to your medial wrist, and then back to the thumb.

Scaphoid, lunate, triquetrum, pisiform, hamate, capitate, trapezoid, trapezium. The lunate looks like it's posteriorly dislocated here.

sympathetikey  Yep. I didn't even look at the X-ray.
dr.xx  loonies love lunate
wes79  she landed on her "right hand", but the X-ray is showing a left hand??
wes79  i legit have no idea whats going on in that xray lol
nbme4unme  X-ray confused the hell out of me, I was going to put lunate based on Q stem but ended up putting Pisiform because it looks like that's what's messed up in the photo? Should have ignored the picture haha.
nwinkelmann  for @dr.xx, love your mnemonic. I added to it, or at least found an explanation on why it works. "loonies love lunate" and "loonies" are "dislocated" from reality.
doctorevil  She Looks Too Pretty, Try To Catch Her is a mnemonic that works for me.
niboonsh  Some Lovers Try Positions That They Cant Handle

 +9  (nbme24#30)

This is the most common cause of painless bloody discharge from the nipple in a woman of reproductive age. It is a benign tumor and there are no characteristic radiologic/mammographic changes.

 +14  (nbme24#4)

I think the reason you need to inject gonadotropins in this case is because you need FSH and LH to produce sperm. FSH stimulates the sertoli cells, which line the seminiferous tubules and help the spermatogonia produce spermatocytes. Testosterone is a product of Leydig cells when they're stimulated by LH, so injecting testosterone would bypass that step but it wouldn't really help with spermatogenesis. However, injecting GnRH also doesn't doesn't really help because you need that pulsatile GnRH at night to make LH and FSH whereas long-acting GnRH analogs actually decrease LH and FSH production.

m-ice  Adding on to the answer above. I was stuck between the gonadotropin injections and clomiphene. But, clomiphene acts to increase activity of GnRH which then exerts its effects on the pituitary. The man in this question had his pituitary removed because of an adenoma. So, he needs the FSH and LH directly.
mousie  agree! Removal of the pituitary would case a deficit in Gonadotropins (LH, FSH) and therefore nothing to simulate the testes to make sperm... replacing the T with a patch would not stimulate the testes to make sperm and if his axis was intact (although its not) this would further down regulate the production of sperm. I eliminated Clomiphene because if he dosent have T to induce negative influence on the hypothalamus he will have increased GnRH and further increasing it with Clomiphene would not correct the deficit in Gonadotropins.
neonem  Oh duh... that makes much more sense. Thanks! P.s. I thought clomiphene was more of a fertility drug for women, since it blocks negative feedback of estrogen on the hypothalamus/pituitary. But in men the system is under feedback due to testosterone, not estrogen.

 +10  (nbme24#15)

the body responds to blood loss by hematopoiesis. This occurs by upregulating transferrin (an iron transporter in the blood), erythropoietin production (a hormone made exclusively in the renal peritubular interstitial cells), and heme synthesis. First step of heme synthesis was actually alluded to in another question on this test: condensation of glycine and succinyl CoA into delta-aminolevulinate. This is rate-limiting step of heme synthesis.

wowo  FA2019 p417

 +5  (nbme24#5)

The patient has low cortisol, which causes body wasting. The patient is hyperpigmented since low cortisol increases ACTH secretion from the pituitary, but this shares a common precursor protein with melanocyte-stimulating hormone (MSH), so that's often a sign of either adrenal failure or an ACTH-secreting tumor. Put together, the high ACTH but low cortisol happening over a period of 6 months means that the adrenal must be getting hit by something -- only option here was autoimmune adrenalitis. Waterhouse-Friderichsen syndrome also causes adrenal insufficiency but this happens acutely, in the timeframe of hours-days.

sajaqua1  The combination of low blood pressure (from lack of mineralocorticoids) and low glucocorticoids (cortisol) indicate adrenal failure. Hyperpigmented skin is a sign of elevated ACTH, indicating that this is a failure of the adrenal gland and not the pituitary. In the industrialized western world, autoimmune destruction of adrenal glands is the leading cause of primary adrenal failure (disseminated tuberculoid destruction of the adrenal glands is significant outside of industrialized nations). It also fits the time line better than Waterhouse-Friederichsen syndrome, which is sudden in onset and associated with hemorraging. Metastases to the adrenal glands *might* be a possibility, but autoimmune destruction is simply likelier.
mamorumyheart  Chronic Addisons disease. Pretty straightforward here. Decreased gland function -> decreased Cortisol, decreased Aldosterone -> hypotension (with hyponatremic volume contraction) Hyperpigmentation from increased ACTH (from POMC) making MSH. (FA) Due to adrenal atrophy or destruction by disease (autoimmune destruction most common in the Western world; TB most common in the developing world).
ac3  I picked autoimmune adrenalitis but was tempted to pick Waterhouse syndrome because of the low BP (hemorrhaging). But I believe Waterhouse-Fried. syndrome is more likely associated with Neisseria infection

 +6  (nbme24#3)

Just had to know that NRTIs (specifically the nucleosides) cause lactic acidosis

brethren_md  Also NRTIs are hepatotoxic, cause the increased liver enzymes seen in the patient.
sherry  Actually, NNRTIs are more well-known for hepatotoxicity. But I guess NRTIs is the next best option for this one.

 +5  (nbme24#43)

Histoplasma can act like TB and cause cavitary lesions and calcified nodules with fibrotic scarring. In general, fungi are combatted by lymphocytes and macrophages, not eosinophils or neutrophils.

 +13  (nbme24#26)

General theme of pathology: hypoxia impairs oxidative phosphorylation --> less ATP --> less Na-K pump activity so sodium builds up in the cell, causing swelling. This is the first step. Then you'd get the calcium buildup in the cell and eventual anaerobic glycolysis, causing lactic acid production and lowered pH... but this happens later and isn't the direct cause of cellular swelling, which is what the question is after.

aneurysmclip  can we have a moment of appreciation for Dr Sattar
makinallkindzofgainz  blessed be His name

haliburton  ^^^ THIS ONE SHOWS DUCT ^^^

 +9  (nbme24#44)

I think the idea here is that if you take someone off a PPI, if there's no neoplasm or any problem with gastrin production then you should see it go down from baseline due to more negative feedback of gastric acidity. If not, you probably have a neoplasm that's just making tons of gastrin, such as in the case of Zollinger-Ellison syndrome.

gonyyong  I thought it was that if you are taking a PPI, you will see elevated gastrin regardless of it you have a gastrinoma. Thus to confirm diagnosis, you make them stop taking it, then re-measure gastrin → if it's still high, you have confirmed. If it's normal, it's something else

 +8  (nbme24#45)

Cerebellopontine angle mass = Vestibular schwannoma (AKA acoustic neuroma). Derived from Schwann cells, which are of neural crest origin.

yotsubato  Ugh. Of course they dont put schwann cells as a choice. So I pick oligodendrocytes like a dumbass
madojo  Schwann cells = PNS Oligodendrocytes = CNS
suckitnbme  NBME loves their neural crest cells

 +10  (nbme24#9)

I think metastasis was the best option here because there are multiple malignant neoplasms... primary cancers tend to start as a single mass in the tissue of origin. In the lung, metastases are more common than primary neoplasms.

dbg  I seriously could not figure out whether those white opacities were actual lesions or reflections from the actual picture (flash light) ... mind went all the way maybe this is the shiny pleura so they're going after mesothelioma. smh
dbg  shiny pleura with tiiiiny granulations if you look closely. but obviously was far off
et-tu-bromocriptine  "Multiple cannonball lesions" is indicative of a metastatic cancer. I think if they were leaning towards a mesothelioma, they'd show the border/edge of the lung ensheathed by a malignant neoplasm (see image): https://library.med.utah.edu/WebPath/jpeg1/LUNG081.jpg
bullshitusmle  guys something I learned from NBMEs is that if there is a clinical vignette dont even look at the images they give you ,they are all useless and time-consuming
goaiable  The way i narrowed it down was that the patient had signs of weight loss since three months whereas her cough developed recently (3 weeks). If the cancer arose in the lung then I think the cough or other pulmonary symptoms should emerge earlier.
almondbreeze  FA2019 pg 669 in the lung, metastasis (usually multiple lesions) are more common the primary neoplasms. most often from breast, colon, prostate, and bladder ca.

 +13  (nbme24#4)

This is acute hemolytic transfusion reaction, a type II hypersensitivity where pre-formed IgM antibodies bind to incompatible ABO antigens on donor RBCs, which causes intravascular hemolysis. Rh incompatibility, like colonelred_ said, comes more into play with Rh-compatibility of pregnancy and it is due to IgG antibodies, which more often cause extravascular hemolysis since splenic macrophages have those Fc-gamma-R receptors to bind whatever IgG has caught. Extravascular doesn't cause that hypotension, fever, flank pain associated with hemoglobinuria since the macrophages hold on to the degraded RBCs and convert it to biliverdin, which can safely be excreted by the liver.

mousie  Could you help me with understanding why this isn't a Type I HSR? I understand that ABO incompatibility is Type II HSR but I don't know how to tell the difference between a patient who is IgA deficient and having a Type I Reaction to an infusion vs ABO incompatibility ....
sympathetikey  @mousie - https://imgur.com/QH5rCEX Basically, think of Type 1 HS like a normal allergic reaction (itchy, wheezing, etc.). Whereas, with ABO incompatibility you get the question's presentation.
medpsychosis  When it comes to Acute hemolytic transfusion reactions, they are Type II hypersensitivity and divided into Intravascular (ABO) and Extravascular (host Ab against foreign antigen on donor RBC). The differentiating factor between them is simple. Intravascular (ABO) will present with hemoglobinuria alongside all the other common symptoms (fever,hypotension, tachypnea etc.) Extravascular hemolysis will stand out with Jaundice as one of the presenting symptoms. Hope this helps!

 -1  (nbme24#38)

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

charcot_bouchard  Can be congenital mild Tricuspid stenosis also. it also exaggerate during preg
noplanb  Wouldn't Tricuspid stenosis be a systolic murmur?
noplanb  I mean diastolic*
centeno  I think that a murmur of grade 2/6 is a clue for flow murmur. Maybe any pathologic cause of murmur would be exaggerated in pregnancy (due to increased blood volume)

 +12  (nbme24#19)

Internal anal sphincter is composed more of smooth muscle and is under parasympathetic/sympathetic control, while external anal sphincter is skeletal muscle and controlled by pudendal nerve. All of the other muscles listed are skeletal muscle of the pelvic floor and are more likely to be involved in Kegel exercises.

 +8  (nbme24#15)

Lack of CD18 (LFA-1 integrin) on phagocytes is the cause of leukocyte adhesion deficiency type 1 (LAD1). Since phagocytes like neutrophils and macrophages can't get out of the bloodstream, they are stuck in the blood, hence the leukocytosis with WBC count > 10,000. Since the leukocytes are stuck in the blood, they can't mount an effective immune response against bacteria.

sunshinesweetheart  also for completeness, LFA-1 is an integrin that binds ICAM, so LAD1 results from a defect in tight binding

 +14  (nbme24#40)

This patient isn't hypoventilating, they're HYPERventilating, hence the PCO2 < 40 mm Hg.

Let's walk it backwards: They are hyperventilating to compensate for the metabolic acidosis caused by widespread hypoxia. Hyperventilating allows you to blow off more CO2.

Why are they hypoxic? The person is hypoxic due to inflammation and acute respiratory distress syndrome from the pneumonia. All the cytokines from the inflammatory cells cause increased pulmonary capillary leakage, which blocks up the alveolar membrane so that O2 can't get through to the blood.

Why do they have metabolic acidosis in the first place? No oxygen --> no electron transport chain and no TCA --> lactic acidosis.

diabetes  no pneumonia it is UTI
makinallkindzofgainz  The infection from the UTI spread to her lungs
makinallkindzofgainz  this is essentially urosepsis, one of the leading causes of sepsis
cmun777  UTI -> Sepsis -> ARDS (exudative pathophysiology d/t increased pulmonary vasc permeability)
peqmd  urosepsis
snripper  lmao I read it as upper respiratory tract infections, too.

 +18  (nbme24#29)

Per Pathoma: early inherited cases of Alzheimer's dementia are associated with mutations in presenilin-1/presenilin-2, as well as Down's syndrome. Down's would be due to an extra chromosome 21, which carries the gene for amyloid precursor protein (APP). Extra APP is converted to A-beta amyloid and this forms extracellular neuritic plaques, a prominent feature of Alzehimer's.

Important to not confuse Amyloid A protein (one of the answer choices) with Amyloid precursor protein. Deposition of AA amyloid is more associated with chronic inflammatory states, malignancy, and Familial Mediterranean Fever. Beta-2 microglobulin is another amyloid association: dialysis-associated (deposits in joints)

 +3  (nbme24#47)

This patient case sounds like he has iron deficiency anemia (anemia, low hematocrit, microcytic) from a GI bleed. To get this question right, you had to remember that the two major inherited GI cancer syndromes are FAP (due to mutation in APC gene, which is a tumor suppressor gene) and Lynch syndrome AKA hereditary non-polyposis colorectal carcinoma (HNPCC), caused by a mutation in a number DNA mismatch repair genes, of with MHS2 is a more common one.

The mechanisms of their carcinoma development are different; in FAP, tumors arise from a normal --> adenoma --> carcinoma sequence while in HNPCC, tumors arise from what's known as a microsatellite instability pathway, leading to spontaneous formation of a carcinoma (not preceded by a benign lesion like an adenoma)... You didn't need to know this to get this question right, but definitely good to know.

medpsychosis  To make it even simpler, if you narrowed it down to FAP vs HNPCC and looked at the image provided in the question, you'd see it's less likely to be FAP due to absence of numerous polyps which would be expected. So HNPCC would be your best choice!
yb_26  I always get Li-Fraumeni and Lynch syndromes confused :/

 +13  (nbme24#34)

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

mousie  When ever I hear Rosettes I always think NE tumors .... and I agree non smoking kind of RO small cell, squamous cell, or lg cell
charcot_bouchard  I thought it was Hamartoma & pick chondrocyte! Can lung even have hamartoma? Pardon me it was the laast ques of whole nbme
drmomo  @charcot_bouchard i thought the same. uworld gave a question on coin lesion in the lungs as classically hamartoma

 +6  (nbme24#5)

Apparently trichinella lies around in muscle of all of the random exotic animals that most people wouldn't normally eat... things like bear, wild boars/pork (like in Sketchy Micro), big cats, foxes, dogs, horses, seals, walruses. In case you needed another reason to not hunt and consume these animals?

 +9  (nbme24#11)

this patient has symptomatic aortic stenosis. This can be identified by the ventricular hypertrophy (to compensate for increased functional afterload from non-compliant aortic valve), midsystolic murmur and the location at the normal aortic area.

Per UpToDate on Clinical manifestations of Aortic Stenosis:

"Dizziness and syncope — Syncope occurs as a presenting symptom in approximately 10 percent of patients with symptomatic severe AS (or approximately 3 percent of all patients with severe AS) [3]. There are several proposed explanations for exertional dizziness (presyncope) or syncope in patients with AS, both of which reflect decreased cerebral perfusion. Exercise-induced vasodilation in the presence of an obstruction with fixed cardiac output can result in hypotension."

guillo12  What does "fixed cardiac output" signify?
usmleuser007  "fixed cardiac output" might mean that with the stenosis (ie. narrowed aortic valve) there is a limited or rather reduced cardiac output. Exercise would not increase cardiac output because the stenosis is caused by a mechanical (physical) rather than a biochemical process. Therefore, At any given moment the heart can not increase its output no matter how forcefully it contracts.
fallot4logy  why not option A?arterial compression ?
sunshinesweetheart  @fallot4logy LVH does not lead to coronary artery compression. only reallyyyy rarely will pulmonary artery dilation cause coronary artery compression. plus that would cause angina but probably wouldnt decrease cerebral bloodflow to syncope. her murmur + LVH point us toward aortic stenosis which does cause those --> fixed CO
drpatinoire  @fallot4logy LVH can cause coronary artery compression, but typically leading to coronary ischemia after exercise (i.e. stable angina in this patient). The question is asking what leads to her syncope. Syncope actually means her brain is lacking blood supply abruptly.
rainlad  how do we rule out mitral valve prolapse in this case?
spow  @rainlad murmurs at the right upper sternal border are aortic in nature. Mitral murmurs are heard at left 5th intercostal at the midaxillary line.

 +7  (nbme24#36)

Anti-endomysial and anti-tissue glutaminase antibodies are pathognomonic for Celiac disease, a hypersensitivity to the gliadin antigen of wheat. It mainly manifests in the jejunum and ileum. In adults, it presents as chronic steatorrhea and bloating, while in children it does the same but also causes failure to thrive. Histologically, it is identified by crypt hyperplasia and villous flattening. If you damage your villi, you can't absorb fat through the lacteals of the small intestine --> malabsorption.

PAS-positive granules in macrophages in lamina propria = Whipple disease, an infection with Tropheryma whipplei, an intracellular gram-positive organism. This would similarly cause a malabsorptive state but is not associated with particular antibodies, and might also manifest as arthralgias, cardiac, and neurologic symptoms.

ugly_but_my_hoes_not  Damage is most prominent in the distal duodenum
ruready4this  where would you see eosinophilic infiltration of the mucosa of the small intestine?

 +8  (nbme24#34)

Sotalol is a type III antiarrhythmic (K+ channel-blocking) that also has beta-blocker activity (Type II antiarrhythmic). This explains the decreased heartrate and blood pressure (beta-1 blocking activity), with the QT prolongation - all type III AADs cause QT prolongation.

abhishek021196  Would like to add that the IA antiarrythmics = Quinidine, Disopyramide, Procainamide also prolong QT interval and can lead to tosades de Pointes and they would most likely present with Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), HF (disopyramide), thrombocytopenia. The decreased HR and BP point towards Sotalol.

 +7  (nbme24#38)

This patient has an unstable mood and a crazy relationship. She's also splitting (a defense mechanism wherein one acts like people are all-good or all-bad) as she talks about the physician and her coworkers. This characteristic is most commonly associated with borderline personality disorder. This one is in Group B ("Wild"), along with antisocial, histrionic, and narcissistic.

medskool123  i get why its borderline now (I guess I kind of always thought suicide was the biggest part of that) but can someone tell me why its not paranoid? Is it just a matter of the "better" choice? The "youre the only one i can trust" thing lead me to that.
drmomo  same here
aneurysmclip  Paranoid is where they don't trust anyone or are weary of people. because she said she trusts only the physician can be a bit confusing, but she describes her coworkers as jerks, not that "oh they're out to kill me, they're government agents watching me"

 +7  (nbme24#39)

Somatostatin is normally secreted by D cells in the pancreatic islets and GI mucosa. It basically blocks everything GI-related ("encourages somato-stasis"): decreased gastric acid & pepsinogen secretion, decreased pancreatic and small intestine fluid secretion, decreased gallbladder contraction, decreased insulin & glucagon release.

Decreasing gastrin release blocks the increase of GI motility (increased GI motility is the inherent problem of diarrhea).

The drug in the question is probably octreotide.

 +4  (nbme24#38)

This patient has major depressive disorder: loss of interest/anhedonia (need to have this or depressed mood),sleep problems, weight changes, decreased energy, thoughts of death. Meets criteria because > 2 weeks timeframe. SSRIs are first-line; paroxetine is in this category. SSRIs also help with weight gain - might be an added benefit if the patient is underweight.

The cardiac stuff might have just been a distractor, except that you probably wouldn't want to give tricyclics (i.e. amitriptyline) since they have pro-arrhythmic side effects. Patient probably has prolonged PR interval due to beta blockers.

adisdiadochokinetic  Another reason not to use TCAs (or alprazolam or haloperidol for that matter) is that the Beers criteria state to avoid the use of all of those drugs in patients over the age of 65.
t123  The cardiac stuff is not a distractor - MDD is common after an MI, and a very poor prognostic factor (reinfarction)
therealslimshady  Beers criteria also says avoid antidepressants though.

 +7  (nbme24#27)

These are gout crystals. I suppose the best way to differentiate this case from pseudogout is that the crystals are sharp & needle-shaped and not rhomboid-shaped.

sympathetikey  Yep. They tried to throw you off with the picture, but the wording in the stem says its a "photomicrograph" -- not exposed to plane polarized light, where you would see the negative birefringence.
linwanrun1357  Why is NBME so mean to us. Do those mean a lot in clinic?
suckitnbme  @linwanrun1357 I highly doubt you would be looking at your own joint fluid aspirates instead of sending it to the lab.
nnp  what those yellow white nodules signify?
peqmd  In clinic gout is typically a clinical diagnosis. If you can treat w/ NSAIDs instead of aspirate you would do that. You would aspirate if you are considering septic arthritis so you can get culture. I don't think anyone aspirate for heck of it.
lowyield  @nnp, the yellow white nodules are tophus which is a sign of chronic gout, characterized histologically by aggregates of uric acid crystals, can show up as skin nodules most commonly on external ear, olecranon bursa or achilles tendon (pg 467 FA 2020)

 +8  (nbme24#19)

This patient has pulmonary fibrosis, which causes a restrictive (not obstructive)-type disease. Since there was no occupational exposure, I'm assuming this is idiopathic pulmonary fibrosis. This causes thickened alveolar membranes, limiting gas diffusion. Therefore, eventually O2 won't be able to diffuse quickly enough into the blood across the alveolar-arterial membrane, resulting in a larger A-a difference. (I think there's normally a small A-a gradient, from 2-14 mm Hg, but when this gets too big, you get hypoxic)

yex  UW q id 7648
melanoma  uw id 1526

 +6  (nbme24#21)

NRTIs are the main HIV therapy drug that can cause bone marrow suppression (not as common with NNRTIs). This class includes zidovudine, didanosine, emtricitabine, lamivudine, stavudine, abacavir. Zidovudine is most known for this side effect.

Nelfinavir = protease inhibitor azithromycin = aminoglycoside (not really used for HIV) pentamidine = another antimicrobial, mostly used for pneumocystis I think? Lamivudine = another NRTI but less known for bone marrow suppression

adisdiadochokinetic  Azithromycin is a macrolide, not an aminoglycoside FYI, and its use in HIV is primarily as prophylaxis at very low CD4 counts for, among other things, the mycobacterium avium complex.
nbmehelp  How would we have known to choose Zidovudine over Lamivudine tho
mjmejora  @nbmehelp the sketchy with Princess Izolde (Zidovudine) eating bone marrow was my only tip off
niboonsh  you have ero bone marrow if you take idovudine
niboonsh  the z's were supposed to be bold idk what happened. you have Zero bone marrow if you take Zidovudine
t123  Zidovudine is also a very early NRTI developed. As a good rule of thumb, older drugs have worse side effects
therealslimshady  Zidovudine Zaps your bone marrow (sorry)

 +7  (nbme24#10)

Pg 491 in FA 2018 (Neurology anatomy & physiology section): 3 muscles close the jaw: Masseter, teMporalis, Medial pterygoid 1 muscle opens the jaw: Lateral pterygoid ALL are innervated by trigeminal nerve, V3 Mnemonic: M's munch (close the jaw), L's lower (loosen/relax the jaw)

sunshinesweetheart  p 495 in FA 2019

 +14  (nbme24#30)

Small cell carcinoma of the lung may produce paraneoplastic syndromes, of which ACTH and ADH are the more common subtypes. ACTH excess leads to excess stimulation on the adrenal cortex to produce cortisol, resulting Cushing's syndrome. Excess cortisol (normally a stress hormone) causes hypertension via potentiation of sympathetic stimulation on the vasculature. It can also cause hypokalemia by acting as a mineralocorticoid when in excess, saturating the ability of 11-beta-hydroxysteroid dehydrogenase (present in the renal tubules) to convert cortisol to cortisone, which doesn't act as a mineralocorticoid.

therealslimshady  Adding some ways to eliminate the other answer choices for good measure: B) ADH can be secreted by small cell lung cancer (SCLC), and would cause SIADH, but that does not manifest with hypertension or hypokalemia. C) Epinephrine can cause hypertension (a1 effect), and hypokalemia (via stimulation of the Na/K-ATPase), but is secreted by pheochromocytomas rather than SCLC. D) PTHrP does not cause hypertension or hypokalemia, and is secreted by squamous cell carcinoma of the lung, not SCLC. E) VIP can cause hypokalemia through diarrhea (see VIPomas in First Aid), but not hypertension, nor is secreted by SCLC.

 +8  (nbme24#44)

Aminoglycosides are nephrotoxic; nephrotoxic chemicals/drugs cause acute tubular necrosis (ATN), characterized by damage to the PCT. ATN causes the formation of brown, muddy, granular casts in the urine. The fact that this patient is a quadriplegic might be suggesting that they have a lower volume of distribution for the drug (and therefore higher blood concentrations).

 +4  (nbme21#46)

Sounds like a case of Li-Fraumeni syndrome - since p53 is a tumor suppressor for a bunch of cell types, mutations in this gene (as in LFS) result in a myriad of familial tumor types.

pparalpha  Li-Fraunemi syndrome = SBLA (sarcoma, breast, leukemia, adrenal gland syndrome) and occurs because of an autosomal dominant inherited mutation of p53 APC: linked to FAP (colorectal cancer) RET: linked to papillary thyroid cancer, MEN 2A, MEN 2B RB1: retinoblastoma
privatejoker  The thing that threw me off was that the only connection in her FH to the above SBLA reference was the mention of a paternal cousin with adrenocortical carcinoma. The other two mentioned had brain cancers, which seem completely outside the scope of the above mnemonic. Then again, as mentioned elsewhere, I suppose the best policy on these is just to rule out the absolute wrong answers. I swear, the NBME is lying when they tell us to choose the "best" answer on some of these. What they actually mean in practice is for us to choose the least shitty.
dbg  ^ this guy cracked the code. nbme ur doomed.
cienfuegos  @privatejoker: I feel the pain. Quick FYI: UW includes brain in the associated tumors.
hyperfukus  we can just make her thing SBBLA and hopefully never get this wrong again
jakeperalta  @privatejoker: according to UW, Li Fraumeni includes SABBB(sarcoma/adrenocortical/breast/brain/blood(leukemia))
ac3  side note: RB1 = retinoblastoma with an increased risk of osteosarcoma
lukin4answer  TP53 associated with SBLA + Brain tumor + Anaplastic Thyroid ca + Transitional cell ca. -UW

 +12  (nbme21#3)

This is a case-control study because it selects first by disease outcome (intellectual disability) and then retroactively looks at exposure/risks (TV usage). Odds ratios are used to evaluate case-control studies; if there was a positive relationship between TV use and intellectual disability, the OR would say something like "Children with intellectual disabilities were 3 times more likely to have 2 or more hours of TV time per day than children without intellectual disabilities."

Relative risk is used for cohort studies, which first define an exposure (TV use) and then look at the outcome (Intellectual disability). A relative risk would be more like "Patients with 2+ hours TV/day are at 3x higher risk to develop intellectual disability than children with <2 hours."

Typically, OR and RR are similar numbers but that assumption breaks down at a certain point, I think when the disease is very rare or something.

drachenx  Following up on Neonem's comment OR = RR when you are dealing with a RARE disease.

 +4  (nbme21#49)

I think you can know that this is a thalamic stroke rather than cortical because a cortical stroke occurring only in the postcentral gyrus (primary sensory cortex) and involving the entire homunculus without affecting the nearby precentral gyrus (primary motor cortex) is very unlikely.

sahusema  Ya I think this question is trying to test your knowledge between a cortical lesion and a subcortical lesion.
cienfuegos  Central Stroke Syndrome: Neuropathic pain due to thalamic lesions. Initial paresthesias followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysesthesia on the contralateral side. Occurs in 10% of stroke patients. FA 2018 499

 +8  (nbme21#36)

In addition to beeip's comments, FA2018 says that chondrosarcoma is more common in the "medulla of pelvis and central skeleton" while chondromas are more in the small bones of hands & feet... so I guess you could go off of it being in a bigger bone (femur). Or perhaps the pleomorphic histology of the cells, which would be more characteristic of a malignant tumor.

 +1  (nbme21#40)

From centerwatch.com (never heard of it before but seems like a good explanation):

"Phase IV studies, often called Post Marketing Surveillance Trials, are conducted after a drug or device has been approved for consumer sale. Pharmaceutical companies have several objectives at this stage: (1) to compare a drug with other drugs already in the market; (2) to monitor a drug's long-term effectiveness and impact on a patient's quality of life; and (3) to determine the cost-effectiveness of a drug therapy relative to other traditional and new therapies. Phase IV studies can result in a drug or device being taken off the market or restrictions of use could be placed on the product depending on the findings in the study."

seagull  Well, I was not smart and put phase 1 since it was talking alot about adverse effects and withdrawl from the patients. But now I see I have 2 extra chromosomes...my bad.
link981  Phase 1- Determine if drug is SAFE Phase 4- Continous surveillance of a drug that is already on the market. The vignette clearly states the drug is marketed. That means it passed the clinical trials. Marketed drugs have passed Phase 3

 +7  (nbme21#25)

Major risk factor for aortic dissection is hypertension, and in this case might be due to cocaine use, which causes marked hypertension. Dissections cause a tear in the tunica intima -- blood can flow backwards into the pericardium and cause tamponade. This manifests as crackles in the lung due to poor left ventricular function (filling/diastolic problem due to compression).

forerofore  there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this.
temmy  please why is there where a diastolic mumur?
whoissaad  @temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border)
garibay92  Does anyone know why is this patient's tepmerature elevated?
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia
almondbreeze  judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm
almondbreeze  he's only 28 - another clue for marfan?
turtlepenlight  did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection
cmun777  @almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN.
ibestalkinyo  @turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection.

 +9  (nbme21#41)

This is a case of porphyria cutanea tarda. The way I remember this is that it's the only high-yield porphyria that has skin manifestations due to UV. I remember this by "After U (uroporphyrin), it's UV". Apparently it's also associated with Hepatitis C, which could be the reason why there's increased AST & ALT, or it could be due to toxic buildup of intermediates in heme synthesis.

meningitis  Why cant it be protoporphyrinogen oxidase? It was because of that reason (Increased AST and ALT) I thought it wasnt uroporphyrinogen decarb. My train of thought was: "wow, mitochondria are messed up.. there must be a lot of intermediates in there,therefore the Uroporph decarb must OK."
arlenieeweenie  FA 2019 pg. 417, the later on the defect in the heme synthesis pathway is the one more associated with skin findings! Also according to this year's edition uroporphyrinogen synthase is now known as prophobilinogen deaminase
nobody  AMBOSS has estrogen therapy listed as a susceptibility factor for PCT. I could not find a link between elevated AST/ALT and estrogen therapy that would occur 15 years into treatment.

 +8  (nbme21#15)

This is a case of acute gout. Monosodium urate crystals are taken up by neutrophils, leading to an acute inflammatory reaction. T-cells aren't really involved in gout (more rheumatoid arthritis).

hungrybox  Great explanation! So frustrating that I got this wrong, should have been easy.
temmy  the way i thought about it was how did the neutrophils get there? the answer is via increased vascular permeability
nor16  they, unfortunately, did not ask " how did neutrophils get there" but " whats the cause of the swelling " not to confuse with " what causes the swelling "
divya  absolutely right temmy. that's how i thought about it too.

 +4  (nbme21#32)

Pathoma says that interstitial (atypical) pneumonia is characterized by diffuse interstitial infiltrates, presents w/ relatively mild upper resp symptoms (minimal sputum & low fever), and is most often caused by viruses, but can be bacterial. However, this question is presenting a chronic case, so I'm assuming that the previous interstitial pneumonia caused a fibrotic response in the lung.

 +4  (nbme21#34)

The sacral micturition center is 1 of 3 components of micturition reflex (other 2 are from pontine reticular formation and cerebral cortex). Sacral mict center = S2-S4 spinal cord level traveling from ventral white matter in the Pelvic nerves, responsible for bladder contraction via the cholinergic nerves (think it acts on the M3 receptor in the bladder detrusor?). If you lose these nerves (i.e. in pelvic fracture), will result in overflow incontinence.

 +3  (nbme21#49)

Thiazide diuretics are the class with the largest risk of hypokalemia.

 +13  (nbme21#43)

Morphine is a mu opioid agonist - one adverse effect of opioids is mast cell degranulation that is IgE-independent. Release of histamine is akin to an anaphylactic reaction --> pruritis, etc.

sympathetikey  Never had heard of that one. Just a good guess. Thanks!
yb_26  IgE-independent mast cell degranulation can also be caused by radiocontrast agents, some antibiotics (vancomycin)
temmy  it was a u world question
mambaforstep  FA 2019 pg 400
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535
mannywillsee  i'm in FA 2019 and pg 400 is blood groups and hemolytic diseases of the newborn. I found this info in page 535
mambaforstep  under mast cells "IgE-independent mast cell degran"! FA 2019 pg 400

 +1  (nbme21#18)

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

thisisfine   Found this difficult because FA characterizes "thoughts of harming baby or self" as postpartum psychosis - which is super rare, and doesn't fit this case. Also, CBT is first line treatment for postpartum depression - so I still like the offer to refer to a therapist as the best choice.
d_holles  Same @thisisfine.
chandlerbas  i see what youre saying but we should make sure that the mother is alive for us to refer to a therapist. remember if shes willing to harm herself most likely also willing to harm the the little cutie baby....so asking for suicidal thoughts screens for progression to post partum psychosis with the aim to prevent the sentinel event: harm to the baby

 +3  (nbme21#4)

"Tennis elbow" is due to radial nerve impingement near the lateral epicondyle of the humerus. Extensor carpi radialis brevis is a muscle of the extensor compartment of the forearm, originates from the lateral epicondyle as well.

ibestalkinyo  The radial nerve is NOT involved with lateral epicondylitis. The underlying pathophys is inflammation of the tendinous bursa and origin of the extensor tendons. Radial nerve involvement would lead to more neurologic deficits such as loss of sensation and weakness rather than tenderness and pain against resisted extension.

 +11  (nbme21#42)

RPR = screening test for syphilis. This is a stocking-glove pattern rash, characteristic of secondary syphilis. Drug of choice for syphilis at any stage is intramuscular Penicillin.

ragacha  PAG 147 FA 2018
teepot123  also says which antibiotic, only 2 in the list, helps narrow down, pen more commonly used

 +1  (nbme20#21)

Cat scratch disease (Bartonella infection in immunocompetent hosts) causes lymphadenitis (especially in the axillary region) characterized by sarcoid-like non-caseating granulomas filled with neutrophils.

 +3  (nbme20#6)

Leukotriene B4 is a potent chemotactic molecule for neutrophils. Selective loss of this would have no effect on platelets, mast cells, or endothelium - these are more responsive to changes in TXA2, complement/arachidonic acid, and PGI2, respectively.

kernicterusthefrog  FA says: "Neutrophils arrive B4 others"

 +4  (nbme20#43)

Cilostazol is a phosphodiesterase inhibitor; leads to increased cAMP which inhibits platelet degranulation/activation while also causing vasodilation. All of the other options work on either vasculature or platelets but not both.

kernicterusthefrog  Just to add: cAMP activates protein kinase A (PKA), which is the more direct mediator of platelet aggregation inhibition, and of myosin light-chain kinase inhibition (which causes inhibition of smooth muscle contraction and thus vasodilation). Just in case there's a question that gets more specific than this one!
brbwhat  wasn’t dypirdamole an option?
fataldose  I believe they also cause vasodilation by decreasing the cellular reuptake of adenosine by endothelial cells and the adenosine causes vasodilation.

 +9  (nbme20#5)

Methotrexate would be a drug of choice for psoriasis refractory to topical creams and light therapy; inhibits dihydrofolate reductase in order to decrease skin cell proliferation and reduce inflammatory response.

69_nbme_420  Cyclosporine can also be used to treat Psoriasis (NOT cyclophosphamide - ans B)
len49  Drugs that can be used for psoriasis include cyclosporine, MTX, TNF-alpha inhibitors including Etanercept, lnfliximab, adalimumab, certolizumab, golimumab according to FA

 +6  (nbme20#36)

Shigella causes an inflammatory diarrhea; it produces a toxin and can invade tissue directly. In addition, it is resistant to acid, so it has a characteristically low infective dose (~10 organisms), which facilitates its fecal-oral (person-to-person) spread especially in settings where hygiene may be compromised, such as in daycare or institutional housing. It can be differentiated from E. Coli (EHEC) because E Coli doesn't have as much person-to-person spread and only causes GI damage by the shiga-like toxin, not direct invasion. Therefore, EHEC wouldn't facilitate as strong of a neutrophilic response.

yotsubato  I assumed all the kids in the daycare had the same lunch, thus got food poisoning, thus all got EHEC.

 +12  (nbme20#50)

This patient likely has some form of upper motor neuron lesion or disease - UMN lesions are characterized by weakness, increased deep tendon reflexes, and spastic paresis. Baclofen is a GABA-B agonist specific to the spinal cord, used ot treat muscle spasticity, dystonia, and MS. GABA-B is a G-protein coupled receptor coupled to Gi, so agonism of this receptor causes hyperpolarization of the neurons and decreased release of excitatory glutamate.

 +2  (nbme20#6)

Alcohol withdrawal leads to a sympathetic-hyperactivity-like syndrome with tremors, HTN, insomnia, GI upset, diaphoresis, and mild agitation 3-36 hours after the last drink. There is a similar, but usually slightly later, overlap of withdrawal seizures 6-48 hours after the last drink.

katsu  Alcohol withdrawal sx (p. 554 FA 2018) Time from last drink: 3–36 hr: tremors, insomnia, GI upset, diaphoresis, mild agitation 6–48 hr: withdrawal seizures 12–48 hr: alcoholic hallucinosis (usually visual) 48–96 hr: delirium tremens (DTs) Treatment: benzodiazepine
baja_blast  p. 558 in FA 2019.

 +2  (nbme20#24)

Most of intrinsic muscles of the hand are innervated by ulnar nerve - chronic compression at the hook of hamate could lead to nerve ischemia

 +1  (nbme20#46)

Obstructive uropathy causes a postrenal azotemia --> when prolonged, tubular damage ensues. This leads to an acute tubular necrosis, characterized by necrotic plugs in the tubular system as seen in the image

meningitis  Does anyone know the relevance of the stem saying: "during this time she also has been crying frequently"?
usmleuser007  Think the postrenal azotemia is d/t her pregnancy. With the increasing in size fetus, the pelvic cavity is being compressed and thus there is pressure on the ureters. This leading to the presentation. As per above --- the crying maybe just d/t her pain and emotional stress caused by worrying about possible complications regarding her fetus.
maxillarythirdmolar  My gut tells me it must be some sort of transient change in placental size with hormonal changes. It's reminiscent of what you might expect for breast changes during the menstrual cycle, imo

Subcomments ...

submitted by neonem(452),

I think the reason you need to inject gonadotropins in this case is because you need FSH and LH to produce sperm. FSH stimulates the sertoli cells, which line the seminiferous tubules and help the spermatogonia produce spermatocytes. Testosterone is a product of Leydig cells when they're stimulated by LH, so injecting testosterone would bypass that step but it wouldn't really help with spermatogenesis. However, injecting GnRH also doesn't doesn't really help because you need that pulsatile GnRH at night to make LH and FSH whereas long-acting GnRH analogs actually decrease LH and FSH production.

m-ice  Adding on to the answer above. I was stuck between the gonadotropin injections and clomiphene. But, clomiphene acts to increase activity of GnRH which then exerts its effects on the pituitary. The man in this question had his pituitary removed because of an adenoma. So, he needs the FSH and LH directly. +15  
mousie  agree! Removal of the pituitary would case a deficit in Gonadotropins (LH, FSH) and therefore nothing to simulate the testes to make sperm... replacing the T with a patch would not stimulate the testes to make sperm and if his axis was intact (although its not) this would further down regulate the production of sperm. I eliminated Clomiphene because if he dosent have T to induce negative influence on the hypothalamus he will have increased GnRH and further increasing it with Clomiphene would not correct the deficit in Gonadotropins. +2  
neonem  Oh duh... that makes much more sense. Thanks! P.s. I thought clomiphene was more of a fertility drug for women, since it blocks negative feedback of estrogen on the hypothalamus/pituitary. But in men the system is under feedback due to testosterone, not estrogen. +5  

The disease here is fructose bisphosphatase deficiency. In it, IV glycerol or fructose doesn’t help because both enter the gluconeogenesis pathway below fructose bisphophatase. Galactose on the other hand enters above it. I don’t think you really need to know this to choose the correct answer since the clinical picture of fasting hypoglycemia that is corrected w/ some sort of sugar that can enter the gluconeogenesis pathway should clue you into the right answer.

neonem  I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch. +15  
vshummy  I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process! +17  
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +2  
linwanrun1357  In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase. Therefore, this question makes me confused.... +  
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +  
atbangura  I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke. +1  
lilyo  So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused. +1  
djtallahassee  Its Hereditary Fructose intolerance right? gets sick after fructose and I guess glycerol can jump in via aldolase B on this pathway via page 74 of FA2019. It looked like a fructose thing to me so I just marked out the other ones and moved on. +  
paperbackwriter  @djtallahassee I was wondering same, but hereditary fructose intolerance also results in inhibition of glycogenolysis :/ confusing question. +  
mdrahimi7  See linwanrun1357 because very few amount of fructose metabolize by hexokinase and most of them goes through aldolase b so they need fructose b is phosphatase +  
mdrahimi7  See @linwanrun1357 because very few amount of fructose metabolize by hexokinase and most of them goes through aldolase b so they need fructose bis phosphatase. +  

submitted by brethren_md(73),

tumor of Pineal Gland (Pinealoma) causes Parinaud Syndrome (vertical gaze palsy)

neonem  Due to compression of the superior colliculus in the tectum, I believe +8  
wowo  FA2019 p516 +3  
misterdoctor69  FA2020 p528 +  
qiss  tectum as in the superior colliculus +  

submitted by brethren_md(73),

Chronic Mesenteric Ischemia aka intestinal angina. Main clues are postprangial epigastric pain, weight loss. Usually due to Celiac (a), SMA, or IMA atherosclerosis.

neonem  What's tough about these answer choices though is that you have 2 different viable combos. +  
codyluvr95  The ectatic aorta might also mean AAA below the renals, affecting the IMA, +2  
sherry  Also since there is this ectatic aorta, the arteries involved need to be adjacent to one another. If there is a choice as in celiac and SMA, it could also be correct. +  

submitted by mcl(456),

Methionine is an essential amino acid. All others listed are not.

scalpelofthenorth  Pg 81 Tyrosine is listed as an essential AA. Should be tryptophan for those who got this wrong like me. +  
neonem  But tyrosine can come from phenylalanine, so it's not really essential right? +  
gh889  in FA2019, it is listed as Tryptophan, not Tyrosine. That was corrected. +1  
usmleuser007  Note: Tyrosine is ONLY essential with PKU in children +  
niboonsh  bro FA2018 lists tyrosine as an essential AA. They played us. +1  

submitted by cantaloupe5(61),

For this one you just had to know the glycolysis pathway. Stem told you 2,3-BPG is elevated, which is upstream of pyruvate kinase.

neonem  Right, and that glycolytic enzyme deficiencies lead to hemolytic anemias. +2  
toxoplasmabartonella  I just thought the typical presentation of pyruvate kinase deficiency would be hemolytic anemia of the newborn. +3  

Autoimmune thyroiditis (aka Hashimoto) + pregnant--> Think about possibility of fetal hypothyroidism due to antibody mediated maternal hypothyroidism. Leads to Cretinism. Findings in infant are the 6'P (Pot belly, Pale, Puffy face, Protruding umbilicus, Protuberant tongue, and Poor Brain development.

neonem  I don't understand the last part of this question stem though... if the mother's TSH *increases* during pregnancy? Wouldn't this further increase her (and/or the fetus's) production of T4 and thus counteract the hypothyroidism? +  
poojaym  @neonem no. Autoimmune hypothyroidism is a destruction of the thyroid gland, and a decrease in production of T3/T4. An increase in TSH means that there is not enough T3/T4 to inhibit TRH, and so TSH is being released to stimulate the thyroid gland. +8  
arezpr  TSH, T3, T4 and thyroglobulin cannot cross the placental barrier. +  
chamaleo  @arezpr although those hormones can't cross, the autoantibodies from Hashimoto's can +  
yotsubato  The baby has its own TSH though +  
sbryant6  TSH comes from the pituitary, and act on the thyroid. Autoantibodies attack the thyroid, so TSH doesn't work. +  
kimcharito  no goiter then? +  

My thought process was that post-partum bleeding is usually related to the uterus, and much of the pelvic viscera is supplied by branches of the internal iliac artery.

neonem  This sounds like a case of acute endometritis. In any case, uterus is supplied by uterine artery (branch of internal iliac artery) with collateral flow from ovarian artery (comes right off aorta). I don't think there are any branches of external iliac artery into the pelvis; it becomes femoral artery once it passes under inguinal ligament. +3  
tsl19  Here's a picture that I found helpful [Female Reproductive Tract arterial supply] (https://teachmeanatomy.info/wp-content/uploads/Blood-Supply-to-Female-Reproductive-Tract.jpg) +12  
sympathetikey  @tsl - Thank you! +  
step1soon  uworld Qid:11908 +  

submitted by strugglebus(129),

Pt has polycythemia vera (myeloproliferative disorder) due to chronic hypoxia induced by COPD. Myeloid metaplasia is extra medullary hematopoiesis due to myelofibrosis. Hereditary hemochromatosis would have been proven by a prussian blue stain. Hypersplenism would have caused decreased RBCs, and myelodysplasic syndrome would have shown Auer rods or blasts.

neonem  Right, I think this would be just called "appropriate absolute polycythemia", whereas polycythemia vera is due to a malignant JAK2 mutation and would be termed a type of chronic myeloproliferative disorder. +9  

submitted by strugglebus(129),

As an edit: 108,001 people reported to have side effects when taking Hydrochlorothiazide. Among them, 25 people (0.02%) have Breast discharge

neonem  I think the best way to answer this question was by process of elimination. +  
sympathetikey  That's some bullshit lol +4  
karljeon  Haha I eliminated the answer by process of elimination. +17  
medschul  I eliminated thiazides by process of elimination :( +1  
medstudent65  Shit I eliminated thiazides because of elimination went with HTN thinking intercranial bleed effecting the pituitary +1  

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