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 +3  (nbme22#21)

Knowing the LR+ value = 10 does not help to solve this Q because estimating where "10" should fall on an axis is arbitrary. Also, the data points are coordinates -- they have an X-value and a Y-value (X, Y).

The way to approach this Q is to know that a high specificity means that a positive result is very, very likely to be a true positive.

Suppose that the specificity is 0.99 -- this is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculate 1-specificity = 1 - 0.99 = 0.10. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A."

You don't even need to know a specific specificity value to solve this problem. All you need to do is understand that if the specificity is extremely high, you will need to find a datapoint that is closest to the origin -- at least for the value in the X-axis in the coordinate of the data point -- because the X-axis corresponds to a calculation of "1-specificity".

link981  Excellent explanation but a minor typo. 1-0.99 = 0.01 not 0.10 :)

 +3  (nbme20#17)

Goljan had a lecture that mentioned that "If a patient has galactorrhea, review every drug they're taking since many drugs cause galactorrhea."

The only thing of possible relevance in this Q-stem is that she takes a medication, therefore the answer of "drug effect" is the most likely reason for her galactorrhea.


 +2  (nbme20#24)

Guyon Canal Syndrome is due to an Ulnar Nerve lesions and is associated with bicycle handlebar use.

Also FINGER abduction and adduction is mediated by ulnar nerve. The patient is having trouble with FINGER abduction and adduction.

The Froment sign is testing ADDUCTOR POLICIS ACTIVITY, which is mediated by the ULNAR NERVE activity. It is NOT testing thumb opposition, which would be mediated by the median nerve.

See Froment sign


 +1  (nbme20#50)

The reason "do not prescribe antibiotics until testing results are available" is incorrect is because we already have a gram stain that shows gram-negative diplococci in pairs. This is Neisseria gonorrhoeae. So, no need to wait for test results come back.

The Q-stem stating that "Testing for Neisseria and Chlamydia" is ordered" after already having done the Gram stain seems to be a distractor.


 +2  (nbme20#44)

Patient's symptoms began 30 min after mowing lawn (i.e. after doing physical activity). He has severe chest pain and is cool, clammy, diaphoretic. He has increased pulmonary artery pressure and increased left atrial pressure. Taken altogether, this is cardiogenic shock.

Cardiogenic shock is a heart pump problem -- the LV isn't working.

When the LV, isn't working, it causes a back up in the direction opposite to how blood normally flows. Therefore, blood will back up in the lungs.

This causes increased capillary hydrostatic pressure --> this drives more fluid into the interstitium --> this causes increased interstitial hydrostatic pressure --> there is now more fluid than normal in the interstitium --> this affects the protein ratio within the interstitum --> this causes decreased interstitial oncotic pressure.


 +0  (nbme20#42)

Patient in hypovolemic shock - the clues are low BP and COOL skin. Hypovolemic shock is caused by fluid loss.

The patient has decreased preload b/c of fluid loss, i.e. there is decreased blood volume returning to heart --> thus decreased preload.

endochondral   why not dec SVR?
sup  @endochondral w/ hypovolemic shock you would see increased systemic arterial resistance as arteries will constrict to try and bring BP back up.

 +1  (nbme20#35)

Spleen is enlarged. Compare it to CT scan showing normal-sized spleen:

http://www.startradiology.com/uploads/scroll/18/14hiu6b3qot5.jpg





Subcomments ...

submitted by sympathetikey(197),

As stated below, the Left crus cerebri was damaged (see what it should normally look like below). This contains the corticospinal tract. Since the corticospinal tract decusates at the medulla, below the midbrain section we're looking at, you would see Contralateral (Right) Spastic Hemiparesis

sympathetikey  http://what-when-how.com/wp-content/uploads/2012/04/tmp15F11_thumb.jpg +2  
hello  What identifies that a cross-section is medulla vs midbrain vs pons? +1  
kernicterusthefrog  @hello I like to pay attention to the Cerebral Aqueduct (diamond/spade shape seen mostly in Midbrain, and transitioning to 4th ventricle in rostral Pons), and then the shape and size of the 4th ventricle as you move down Pons to rostral&middle Medulla, and eventual closing and absence of fluid space at caudal Medulla. +3  
hello  @kernicterusthefrog Thank you. +  


submitted by armymed88(13),

A little math here.. pH is low --> acidosis pCO2 is high --> respiratory Normal compensation should be roughly a 1 (acute) to 4(chronic) increase in bicarb per every 10 increase in pCO2.. Its lower here, so clearly not compensated and indicated additional drop in bicard --> add on metab acidosis

hello  Hm, what do you mean by "normal compensation?" Are you talking about the bicarb should be increased? Are you saying that a normal compensation would be metabolic alkalosis? Would metabolic alkalosis be an increase in bicarb? +1  
kateinwonderland  How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis?? +  
yb_26  normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis +  


submitted by seagull(276),

This is a likelihood ratio. LR+= Sens/1-Specif

Any value greater than 10 (per first aid) indicated "usefulness of diagnostic test" which is comparable to PPV (ruling in a dz). Point "A" is the closest mark to where 10 should be on the Y axis.

brise  The question is asking what point would be the most likely to rule in cancer, and high specificity when positive rules in cancer. The highest specificity value is A, bc the the X axis shows (1-specificity)! +3  
hello  brise is correct. Knowing the LR+ value = 10 does not help in this situation because estimating where "10" should fall on an axis is arbitrary. The way to approach this Q is to know that a high specificity is will mean that a positive result is very very likely to be a true positive. In theory, suppose that the specificity was 0.99. This is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculating 1-specificity = 1 - 0.99 = 0.1. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A." +2  


submitted by bobson150(1),

Is this saying there is vesicoureteral reflux? I could have sworm this same image was on form 20 or 21 and the answer was Wilms tumor

hello  Yes, it was. I think in both vignettes, the picture was basically irrelevant. Or another possible clue -- but definitely not needed to answer the Q. +1  
presidentdrmonstermd  My school uses old "retired" NBME questions for exams and I've also seen this exact same picture multiple times...w/ different scenarios I think. I tried remembering what the questions were but I guess it's mostly irrelevant. +  


The description of bilateral lower limb loss of vibration implies DCML damage, and the absent DTRs + Romberg seem to me to be implying that he possibly has tabes dorsalis from syphilis (or something very similar in presentation).

As for the other answers, A is wrong because his motor function is intact, B is wrong because pain and temperature deficits are not mentioned, C is wrong because it implies a specific nerve is entrapped, but he has lost bilateral sensation in his entire lower extremities

D is the trickiest, and I’m not 100% sure, but I would think radiculopathy of the anterior (ventral) roots would cause motor deficits since they carry motor efferents. You might also expect that motor dysfunction to be unilateral, since it would be unlikely to have a problem with the nerve roots on both sides. also the DCML is not located near the anterior roots of the spinal cord, so if the anterior roots were affected you really wouldn’t expect to see vibratory loss.

So basically process of elimination, I do feel like sensory neuropathy is an extremely vague answer though and I wasn’t a fan of the question.

keycompany  This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral). +3  
hello  Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness. I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function. +2  
niboonsh  Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative? +1  
link981  Great explanation guys +  


submitted by hayayah(284),

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. +2  
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. +1  


submitted by hayayah(284),

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... +1  
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 +2  


submitted by hayayah(284),

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 =/ +3  
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); +5  
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) +2  
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 +1  
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 +1  
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! -_- +1  
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 +  


submitted by sympathetikey(197),

As stated below, the Left crus cerebri was damaged (see what it should normally look like below). This contains the corticospinal tract. Since the corticospinal tract decusates at the medulla, below the midbrain section we're looking at, you would see Contralateral (Right) Spastic Hemiparesis

sympathetikey  http://what-when-how.com/wp-content/uploads/2012/04/tmp15F11_thumb.jpg +2  
hello  What identifies that a cross-section is medulla vs midbrain vs pons? +1  
kernicterusthefrog  @hello I like to pay attention to the Cerebral Aqueduct (diamond/spade shape seen mostly in Midbrain, and transitioning to 4th ventricle in rostral Pons), and then the shape and size of the 4th ventricle as you move down Pons to rostral&middle Medulla, and eventual closing and absence of fluid space at caudal Medulla. +3  
hello  @kernicterusthefrog Thank you. +  


submitted by hayayah(284),

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? +1  
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. +1  
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. +2  


submitted by johnthurtjr(31),

While I can get on board with Adjustment Disorder, I don't see how this answer is any better than Somatic Symptom Disorder. From FA:

Variety of bodily complaints lasting months to years associated with excessive, persistent thoughts and anxiety about symptoms. May co-appear with illness.

SSD belongs in a group of disorders characterized by physical symptoms causing significant distress and impairment.

savdaddy  I think part of it stems from the fact that this patients symptoms are occurring within the time-frame for adjustment disorder while SSD seems to have a longer timeline. Aside from that I find it difficult to see why SSD wasn't a possible answer. +  
chillqd  To add to that, I inferred that the obsession with checking temp and with the tingling sensation were signs provided to him by the physicians of recurrence. He is anxious over his cancer recurring, and they are more specific than a variety of body complaints +  
hello  In somatic symptom disorder, the motivation is unconscious. I think for the patient in this Q-stem, his motivation is conscious -- he wants to make sure that recurrence of cancer is not going "undetected". +3  
cienfuegos  I also had issues differentiating these two and ultimately went with SSD, but upon further review it seems that a key differentiating feature was the timeline. His somatic symptoms would have had to have been present for at least 6 months per the DSM criteria https://www.ncbi.nlm.nih.gov/books/NBK519704/table/ch3.t31/ +  


submitted by hayayah(284),

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 +  


submitted by hayayah(284),

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  


submitted by beeip(48),

Thought this would be something regarding "bariatric surgery," but nope, just "no starchy foods, because you're pre-diabetic."

hello  Yep, seems that because the patient has prediabetes, he should avoid eating excessive starchy foods. +  
yotsubato  such a BS question IMO +1  
yotsubato  such a BS question IMO +  
breis  I put nuts thinking of "fats" and that with a bariatric surgery they may have problems with absorption.. +1  


submitted by kentuckyfan(10),

Urea cycle: Decreased citrulline and hyperammonemia can differentiate it from orotic aciduria.

hello  As the poster indicates, the described patient has a defect in the urea cycle, specifically an ornithine transcarbamylase deficiency. Added for clarity to future readers. +  


submitted by drdoom(127),

The more general principle: endothelia vasodilate in the presence of high CO2; you gotta get rid of that acid somehow! Can’t let it accumulate, as lower pH within a “micro-environment” affects structure/efficiency of enzymes, proteins, etc. The more acidic a local environment, the more you expect nearby vasculature to dilate (as a means of increasing flow rate, thereby ferrying off accumulate acid).

The anesthesiologist can exploit this mechanism. By hyperventilating (blowing off CO2), the brain vasculature senses a low CO2 / “hunky-dory state,” which requires no vasodilation. In other words, the vasculature does not need to continue the ATP-consuming practice of synthesizing Nitric Oxide (NO).

hello  But, the Q-stem states the anesthesiologist is HYPOventilating the patient. +1  
drdoom  decreasing respiratory rate = retention of CO2 = vasodilation of brain arteries = more filling of tubes = greater intra-cranial pressure +  
drdoom  @hello shoot, you're right! i ended my explanation with the example of HYPERventilation when i should have done the opposite! (sorry!) ... edit: "By HYPOventilating (retaining CO2), the brain vasculature senses a high CO2 environment and vasodilates = increases intra-cranial filling and pressure!" +  


submitted by loopers(1),

Vomiting blood and cool skin indicates this is a type of hypovolemic shock. To understand shock, remember that 1) BP = TPR x CO 2) CO = SV x HR 3) SV = EDV - ESV In hypovolemic shock, you are losing fluid, so stroke volume is decreased and end diastolic volume is decreased. Decreased EDV means that the "filling volume" is decreased, which also means the preload will be decreased (https://www.cvphysiology.com/Cardiac%20Function/CF007). Also, skin is cool because you're decreasing SV --> decreased CO --> Ang II/ADH/etc is released to vasoconstrict increaseing resistance. Since there is increased resistance, there is less blood flow causing skin to be cold/clammy.

hello  Patient in hypovolemic shock - the clues are low BP and COOL skin. Hypovolemic shock is caused by fluid loss. The patient has decreased preload b/c of fluid loss, i.e. there is decreased blood volume returning to heart --> thus decreased preload. +1